Pancreas (Question 1 - 4)

1. The etiology and pathogenesis of chronic pancreatitis. Classification. The clinical

picture of the disease;

Chronic pancreatitis (CP) - chronic polyetiological inflammatory degenerative process in

the pancreas characterized by prolonged course. CP is a result of the activated pancreatic

enzymes in the parenchyma and stroma of the pancreas with permanent destruction,

progressive atrophy, substitution cellular elements of parenchyma by the connective

tissue, occurrence of pseudocysts, calcification of pancreas and disorders in its exo- and

endocrine function (A.A. Shalimov).

The inflammatory component in the development of CP is not the only and even leading, it

is believed to define this disease as “pancreatopathy”.

The incidence of chronic pancreatitis has a constant upward trend and a range from 2 to

10 cases per 100 thousand populations annually, and its overall frequency is from 50 to 75

patients per 100 thousand populations. According to autopsy data, CP occurs from 0.18 to

9%, on average, about 1%. The disease is most often diagnosed at the age of 40-60

years.

Etiology

CP is considered to be a polyetiological disease. Its origin and development are

associated with at least 100 reasons, the main ones of which are:

1) chronic alcoholism

2) gallstone disease

3) injury, incl. operating, with post-traumatic obstruction of the pancreatic ducts 4)

exposure to chemicals, including drugs

5) hyper- and dyslipidemia

6) insufficient protein nutrition

7) genetic predisposition (antitrypsin deficiency and other genetic factors)

8) hyperparathyroidism (hypercalcemia)

9) cystic fibrosis (the most frequent factor in children)

10) idiopathic factors

Gallstone disease and alcohol intake are the most common causes of the development of CP,
amounting to 60-80%. In different countries (geographical regions) and sociodemographic groups of
the population one of these two main causes of CP is leading. The third place in terms of frequency
of occurrence is the so-called idiopathic CP, the etiological factors of which cannot be ascertained.
Idiopathic CP is 10-15% of all patients. All other causes of CP are relatively rare, they account for up
to 10% in total. There are several theories of the pathogenesis of CP, of which enzyme is considered
the most recognized. According to this theory, each of the etiological factors leads to the activation
of enzymes produced by the pancreas, autolysis of the gland, necrobiosis and necrosis of acinar
tissue and stroma of the gland, followed by its replacement with connective tissue and the
development of fibrosis.

The main factors of the pathogenesis of alcoholic CP are:

- toxic metabolic and damaging effects of alcohol on the pancreas;

- dysfunction of the sphincter of the hepato-pancreatic ampoule with duodenopancreaticreflux,

hypertension in the ducts of the pancreas;

- violation of the secretory function of the pancreas: changes in the characteristics of pancreatic
juice, leading to precipitation of the protein in the ductal system and it obstruction;

- enhanced secretion with bile products of free radical oxidation of fatty acids and peroxide
compounds penetrating into the pancreatic duct and supporting the inflammatory process in the
pancreas.

The main mechanism of CP in cholelithiasis, according to the theory of “common channel” is biliary-
pancreatic reflux resulting blocked stone in large papilla of the duodenum, trauma and prolonged
spasm of sphincter hepato-pancreatic ampoule, papillostenosis due to frequent injury papilla by
small stones. ( Normally, pressure in the gallbladder and common bile duct when they are empty is
250 mm of water. And in the main pancreatic duct - 300-500 mm of water. It prevents the
occurrence of bile reflux in the pancreatic duct. The gallstone disease, in particular
choledocholithiasis, complicated by stenotic papillitis may be the cause of CP due to the disruption
of the normal passage of bile and its throwing into the pancreatic ducts). It is also possible the direct
transition of inflammation from the gallbladder, bile ducts to the pancreas through the venous and
lymphatic vessels in the absence of biliary-pancreatic reflux.

CP classification

Since CP is in fact a very heterogeneous disease, having a different etiology, morphological, clinical
variants, the creation of a comprehensive and generally accepted classification is a big problem. A
number of CP classifications have been proposed, which can be grouped as follows:

1. clinical classifications based on the nature of the dominant disease syndrome,

2. morphological, which take into account both the preferential localization of the pathological
process in different parts of the pancreas, and the nature of the morphological changes in the tissue
of the organ,

3. etiopathogenetic, according to which primary and secondary chronic pancreatitis of different

etiologies are distinguished,

4. complex classification schemes based on mixed principles, with this can be taken into account
several parameters: clinic, morphology, the nature of the functional impairment and lesions of
adjacent organs, the degree of activity of the inflammatory process in the pancreas, etc.

One of the most accepted and used classifications of CP is the clinical classification of CP,
proposed by A.A. Shelagurov. According to this classification, there are:

1. Chronic recurrent pancreatitis, characterized by pain crises (exacerbations). The

patient’s condition remains relatively good in the period of remission (the most frequent

form of CP),

2. Chronic pain pancreatitis, occurring with persistent pain,

3. Chronic latent pancreatitis, in which disorders of the external and internal secretion of the
pancreas are determined

4. Chronic pseudotumorous pancreatitis, which is characterized by the lesion of the

pancreatic head mainly with signs of compression of the common bile duct, duodenum

and portal or superior mesenteric veins.

Clinical manifestations of CP

The symptoms of CP are determined by the nature of the lesion of this organ, the stage of the
disease (period of exacerbation or remission), the extent of lesions of the gland and its adjacent
organs, and in some cases other organs and systems, finally, the presence, nature and severity of
complications and consequences of pancreatic lesions.

A.A. Shelagurov (1970) summarized the main symptoms of CP as follows:

1) pain in the upper abdomen;

2) dyspeptic symptoms;

3) weight loss;

4) intestinal disturbances (constipation, diarrhea);

5) fever;

6) jaundice;

7) sometimes glycosuria;

8) ascites;

9) multiple thrombosis;

10) mental and nervous system disorders.

In general all clinical manifestations of CP can be grouped into several syndromes:

1) pain syndrome;

2) syndrome of clinical manifestations of exocrine pancreatic insufficiency - weight loss, stool

disorders - diarrhea, rarely constipation, signs of steato- and creatorrhea;

3) syndrome of clinical manifestations of pancreatic endocrine insufficiency: latent or overt

diabetes of varying severity, less often - hypoglycemic syndrome, in some cases - signs of impaired
secretion of other pancreatic hormones;
4) syndrome of biliary hypertension (cholestasis) with its clinical manifestations (hepaticcolic,
pruritus, jaundice, acholia, Courvoisier’s symptom), as well as a characteristic laboratory picture;

5) syndrome of obstruction of the duodenum;

6) segmental portal hypertension syndrome;

7) symptoms of CNS damage.

In addition clinical manifestations of inflammatory and purulent-septic lesions of the pancreas and
adjacent organs and tissues are often encountered in chronic pancreatitis. 2. Laboratory and
instrumental diagnosis, differential diagnosis of chronic pancreatitis;

Diagnostics

The diagnosis of CP is based on the clinical presentation, laboratory data and instrumental methods
of diagnostics. Diagnosis of CP has the following objectives:

1. Determine whether the patient has CP,

2. To establish the severity of the disease (morphological changes in the parenchyma and ductal
system of the pancreas, adjacent organs, the severity of loss of gland functions),

3. Identify the presence of complications, their nature, 4. Outline a reasonable treatment plan.

Laboratory diagnosis of CP

Uncomplicated CP does not lead to marked changes in laboratory parameters. An increase in the
activity of pancreatic enzymes in the blood and urine indicates an exacerbation of the inflammatory
process in the gland, and leukocytosis can also be detected with a characteristic shift in leukocyte
formula. Laboratory diagnosis of CP is used primarily to study the function of the pancreas and
determine the degree of its exocrine and endocrine insufficiency. For this purpose, the following
methods can be applied:

1. studies of the external secretion of the pancreas

1) analysis of a secret of a pancreas (direct methods). Pancreatic secretion is collected by endoscopic

cannulation of the pancreatic duct, aspiration of the duodenal contents, collection of discharge
through the external pancreatic fistula, and quantitative and qualitative (bicarbonate, enzyme
activity) characteristics of basal and stimulated secretion are assessed;

2) study of the exocrine function of the pancreas as a state of the digestive capacity of its secret
(indirect methods). First of all, these include coprological studies, etc.;

3) determination of pancreatic elastase in feces.

2. studies of the internal secretion of the pancreas -

1) detection of insufficient B-cell endocrine function, i.e. essentially the diagnosis of secondary
(pancreatogenic) diabetes mellitus;

2) identification of hyperinsulinism (hypoglycemic syndrome).

3. determination of tumor-associated antigens for differential diagnosis with pancreatic cancer

Instrumental methods for diagnostics of CP - aimed at identifying structural changes in the

pancreas that are characteristic of this disease - determining the size of the gland, the

severity of morphological changes in the parenchyma and the ductal system of the

pancreas:

1) X-ray examination - general radiography of the abdominal cavity, targeted radiography

of the projection of the pancreas to detect calcification of the organ,

2) ultrasound,

3) endoscopic retrograde cholangiopancreatography, 4) CT,

5) MRI, especially in the mode MRCP,

5) endoscopic ultrasonography,

6) angiography

7) radioisotope scanning,

8) morphological verification of the diagnosis (puncture biopsy).

Differential Diagnoses

• Ampullary Carcinoma

• Cholangitis

• Cholecystitis

• Chronic Gastritis

• Community-Acquired Pneumonia (CAP)

• Crohn Disease

• Intestinal Perforation

• Mesenteric Artery Ischemia

• Myocardial Infarction

• Pancreatic Cancer

• Peptic Ulcer Disease

3. Treatment of chronic pancreatitis. Conservative therapy. Indications for surgical treatment, types
of operations;

Treatment

As already noted, CP is a disease characterized by the development of inflammation and necrosis of

pancreatic tissue, followed by the replacement of the functional gland parenchyma with connective
tissue, which in less than 30-50% of patients leads to severe exocrine and endocrine insufficiency.
These morphological and functional changes are usually irreversible. Only in rare exceptional cases,
under the influence of treatment, can true recovery of morphological changes and improvement of
the function of the damaged pancreas be achieved. As a rule, a favorable outcome of treatment is
the absence of

recurrences, relief of pain and stabilization of the anatomical and functional changes of the
pancreas.

In the treatment of patients with CP two main methods of treatment can be applied conservative
and surgical, each of which has its own goals, indications, possibilities and limitations.

Conservative treatment of CP

Conservative treatment of CP has the following objectives:

1) elimination of the influence of factors that caused the development of CP,

2) relief of CP exacerbations: elimination of pain syndrome, suppression of pancreas

autolysis, reduction of ductal hypertension, improvement of pancreatic juice and bile

outflow, detoxification therapy, elimination of metabolic disorders, prevention of multiple

organ failure,

3) compensation of exocrine and endocrine secretory insufficiency of the pancreas,

4) suppression of degenerative and stimulation of reparative processes in the pancreas, 5)

prevention of exacerbations of CP

To achieve these goals, a complex of measures is needed including normalization of

lifestyle, diet, the use of a whole arsenal of drugs, physiotherapy, sanatorium-resort

treatment and rehabilitation.

Surgical treatment of CP

Surgical treatment of CP can really be aimed at achieving the following goals:

1) elimination of the cause of the disease,

2) relief of pain,

3) treatment of complications of pancreatitis,

4) possible preservation of exocrine and endocrine functions of the pancreas.

All options for the surgical treatment of CP can be grouped as follows (Danilov MV):

I. Operations on organs adjacent to the pancreas:

1. Operations on the biliary tract and papilla major.

2. Gastrointestinal surgery.

II . Direct surgery on the pancreas:

1. Resection of the gland - of various sizes, up to its extirpation;

a) distal resection of the gland, up to subtotal;

b) pancreatoduodenal resection;

c) proximal resection with preservation of the duodenum and distal gland;

d) isolated removal of pancreatic cysts;

e) total duodenopancreatectomy.

2. Internal drainage of the ducts and cysts of the pancreas.

3. Occlusion of the ductal system of the pancreas.

4. External drainage of pancreatic ducts and cysts.

III. Palliative surgery:

1. Operations on the nervous system.

2. Cryogenic on the pancreas.

IV. Endoscopic interventions on the pancreas and its ducts.

V. Closed surgeries performed under the control of ultrasound and CT.

The choice of the optimal method of treatment of CP and the most adequate method of surgical
treatment may at least stop the further progression of the disease.

4. Complications of chronic pancreatitis, clinical features, diagnosis, treatment;

Chronic pancreatitis has the potential to cause numerous complications. You’re at greater risk of
developing complications if you continue to drink alcohol after you’ve been diagnosed.

• Nutrient malabsorption is one of the most common complications. Since your pancreas isn’t
producing enough digestive enzymes, your body isn’t absorbing nutrients properly. This can lead to
malnutrition.

• The development of diabetes is another possible complication. Pancreatitis damages the cells that
produce insulin and glucagon, which are the hormones that control the amount of sugar in your
blood. This can lead to an increase in blood sugar levels. About 45

percent of people with chronic pancreatitis will get diabetes.

• Some people will also develop pseudocysts, which are fluid-filled growths that can form inside or
outside of your pancreas. Pseudocysts are dangerous because they can block important ducts and
blood vessels. They may become infected in some cases.

Pancreatic cysts

Pancreatic cysts are fluid-filled and capsule-limited cavities that can be located both in the
parenchyma of the pancreas (intrapancreatic) and in the adjacent sections of the retroperitoneal
tissue, omental bag (extrapancreatic).

Most often (almost 50%), cyst formation is the outcome of severe forms of acute destructive
pancreatitis. Chronic pancreatitis is combined with cyst formation in 25%, pancreatic injury leads to
the formation of a cyst in 20%, approximately 5% of all cases of cystic lesions of the pancreas are
tumor cyst - cystadenoma and cystadenocarcinoma.

Classification cysts of pancreas

Forming a classification of pancreatic cysts a variety of criteria are used, such as etiology, localization
of the cyst, its wall structure, size, duration of the disease, the presence or absence of complications,
etc. Therefore, there are many classifications of pancreatic cysts. An example of the classification of
pancreatic cysts is the following, according to which pancreatic cysts are distinguished;

1. on the structure of the wall of the cyst and the origin:

- true (have epithelial lining)

a) congenital

b) acquired

- retention (cystic dilatation of the pancreatic duct due to intraductal hypertension), -

parasitic,

- tumor.

- false (pseudocyst)

- inflammatory (due to destruction on the basis of acute or chronic pancreatitis), -

posttraumatic,

- idiopathic.

2. by localization:

- organ (intrapancreatic), located in the parenchyma of the pancreas, in any of its parts,

often have a relatively small size and are often associated with the ductal system of the

pancreas,

- extraorganic (extrapancreatic), located outside the parenchyma of the pancreas (in the

tissue of the retroperitoneal space, in the cavity of the omentum, in the mesentery of the

small intestine or transverse colon), are almost always the outcome of pancreatic

necrosis, often reaching significant sizes.

3. by the presence of complications: - inflammation,

- perforation into the abdominal cavity (less often in the pleural or in the pericardial cavity),

- bleeding into the lumen of the cyst,

- stenosis of the output section of the stomach and (or) duodenum,

- compression of the common bile duct,

- rapid growth of cysts with the threat of perforation.

The classification of pancreatic cysts based on the fundamental classification criteria and

proposed by G.D. Vilyavin and al. (1977). According to this classification cysts of the

pancreas are distinguished

I. By etiology:

1. After inflammatory and destructive pancreatitis:

a) in operated patients;

b) in non-operated patients.

2. Posttraumatic cysts.

3. Parasitic.

4. Tumor (primary and metastatic).

5. Congenital.

II. According to clinical signs:

1. In terms of cyst formation:

a) acute forms (up to 2 - 3 months of cyst existence);

b) subacute forms (3 - 6 months);

c) chronic forms (from 6 months to several years).

2. According to the severity of the cyst:

a) simple;

b) complicated (inflammation, perforation, peritonitis, bleeding, fistula formation, malignant

transformation, etc.).

III. Primary and recurrent cysts. The clinical presentation of pancreatic cysts is determined by its
nature, size, location, presence or absence of complications. To verify the diagnosis, all methods of
laboratory and instrumental studies can be applied, the main of which should be recognized as
methods that allow identifying the anatomical and morphological characteristics of cysts, their
localization, wall structure, complications.

Treatment of cysts of the pancreas

The main method of treatment of cysts of the pancreas is surgical. Single cases of selfhealing of
formed pancreatic cysts cannot justify all the dangers of the passive tactics of their treatment, due
to the high probability (at least in 15-20% of patients) of the occurrence of different and severe
complications. Most of these complications are accompanied by high mortality, even under the
condition of performing emergency operations, and the technical implementation of surgical
interventions against the background of a developed complication is much more difficult, while the
radicalness of the intervention is much less. It is important to remember that cystic formation of the
pancreas, interpreted clinically as a complication of pancreatitis, may actually be a cystic tumor or a
malignant cyst.

Thus, the identification using clinical and instrumental methods in patients with pancreatitis formed
pancreatic cyst should be considered an absolute indication for surgery. More difficult is the choice
of the optimal duration of surgery, as well as the method of treatment, especially in case of
incompletely formed cysts.

Variants of surgery of pancreatic cysts are

1. cysts excision (cystectomy)

2. resection of the pancreas with a cyst,

3. internal cyst drainage, incl. double internal drainage

4. external drainage of the cyst, including marsupialization.

5. closure of the fistulous passage and ductal system of the pancreas. Surgery used for

pancreatic cysts can be

1. emergency and planned;

2. radical and palliative.

It should be understood that the surgical treatment of pancreatic cysts should be pathogenetically
substantiated, i.e. first aimed at eliminating the causes of cyst formation

Abdomen (Question 5 -7)

5. Classification of damage to the stomach. Mechanisms of injury, the pathogenesis of abdominal

injuries;

The closed abdominal trauma is the kind of injury of the abdomen when the skin remains intact.

To determine the size of injures the body is divided into 5 areas:

1) The head, spine and spinal cord

2) Neck

3) Chest

4) Abdomen

5) Musculoskeletal system (extremities and pelvis).

The most frequent ruptures occur in the spleen, kidney, small intestine and its mesentery, liver.

• ISOLATED is an injury of one area only by one factor.

• POLYTRAUMA it is a trauma of internal organs in two or more areas when it is exposed to one
factor.

• COMBINED trauma considered as injury caused by different factors (mechanical and

thermal,mechanical and chemical, mechanical and electrical, etc.).

Causes: traffic injury, household, falling down from high amplitudes (katatravma), industrial and
sports injuries.

Mechanism: direct impact (drop, compression etc.) and shock.

CLASSIFICATION

Without injury of the internal organs:

a) injury of the abdominal wall;

b) Retroperitoneal hematoma.

With injury of the internal organs:

a) hollow organs;

b) parenchymal organs;

c) hollow and parenchymal organs;

d) Retroperitoneal organs.

With injury of the major blood vessels:

a) the aorta;

b) the inferior vena cava;

c) Large mesenteric vessels.

Types of lesion of internal organs in the closed trauma:

a) Contusion of internal organs (hemorrhage);

b) Rupture, breaking and crushing;

c) Contusion, tear, break, crush injury of retroperitoneal organs (pancreas and kidneys), followed by
development of cellulitis or retroperitoneal hematoma. A two-stage lesion of parenchymatous organ
- an injury of organ with the subcapsular hematoma formation at the first and second stage after a
certain time period (hours, days, weeks) hematoma breakthrough into the

peritoneal cavity with intraperitoneal bleeding.

6. The clinical picture of abdominal injuries. Laboratory and instrumental diagnosis, differential
diagnosis;

CLINIC

• Closed abdominal injury without damaging internal organs - hematoma, painful abrasions, bruises
in the anterior abdominal wall.

• The main manifestation of abdominal trauma with internal injuries: shock, bleeding and peritonitis.
The

symptoms of shock and intraabdominal bleeding predominates (common symptoms) in lesions of

parenchymal organs, and peritonitis predominates in lesions of hollow organs (local symptoms).

Signs of damage of the internal organs of the abdomen:

• The person affected shows painful expression on his face;

• impaired consciousness from lethargy leading to stupor and coma;

• Tachycardia and decrease blood pressure, caused by damage and blood loss;

• The frequency, rhythm and depth of breathing are violated parallel to the severity of the injury;
• Dry tongue, white or brown bloom; - pain during abdominal palpation;

• Anterior abdominal wall is not involved in the act of breathing or its movements are limited;

• Rigidity of abdominal muscles with varying severity; - peritoneal symptoms;

• Percussion determines most painful area, the presence of liquid (haemoperitoneum,

hydroperitoneum)

or free gas in the abdominal cavity (pneumoperitoneum);

• Auscultation reveals decreased bowel peristalsis or its absence.

Symptoms:

• Bloomberg - the appearance of pain after the sudden withdrawal of the hands during palpation of

the abdomen;

• Mendel - tenderness to percussion anterior abdominal wall;

• Rosanov - an attempt to change the body position of the patient, he returns to the initial forced
position, usually on the back and on the side with legs bent or tries to sit down;

• Kulenkampf - sharp pain on palpation of soft or slightly tense of anterior abdominal wall;

• Joyce - percussion change when the patient is rotated to one side indicates hemoperitoneum,
preservation blunting indicate retroperitoneal hematoma, or bleeding in the root of the mesentery;

• Disappearance of hepatic dullness indicates the presence of gas in rupture of the hollow organ;

• Dullness in sloping areas of the abdomen is the symptom of hydroperitoneum.

Factors affecting the clinical presentation and timely diagnosis: shock, significant blood loss, a
combination of internal injuries, alcohol and drug intoxication of the patient.

DIAGNOSIS

 Anamnesis, nature and mechanism of injury, it may be asked to medical professionals, relatives
and spectators.

Laboratory methods:

 CBC: reduction of red blood cells, hemoglobin, hematocrit, the proportion with bleeding;
leukocytosis to 35х109/l at admission and bleeding of the hollow organs contents into the peritoneal
cavity. It is necessary to study the dynamics of these indicators in 30-60 minutes.

 Urine analysis: hematuria due to damaged organs of urinary system; raising the level of alpha-
amylase in trauma of pancreas; appearance of bile pigments from biliary tract.

Radiological methods:

 General radiography and fluoroscopy of abdominal organs depending on the severity of injury in
an upright position, sitting, lateroposition: the presence of gas, liquid in the abdominal cavity and
retroperitoneal fat; pneumatization of the stomach and intestines; deformation and displacement of
organs; impaired function, the position and shape of the diaphragm.
 Indirect signs of damage to internal organs: fractures of the lower right and left edges (suspected
damage to the liver and spleen), lower thoracic or upper lumbar vertebrae (suspected damage to
the pancreas and kidney), pelvis (suspected bladder rupture).

 X-rays of the esophagus in cases of suspected injury.

 Cystography for suspected bladder injury.

 Excretory urography is indicated for suspected renal injury.

 Angiography is performed in cases of suspected hematoma of parenchymal organs and it can be

therapeutic method.

 Computed tomography is used in general stable condition of patient when it is necessary to clarify
the status of parenchymal organs, aorta, foci of hemorrhage in the abdominal cavity and
retroperitoneal space.

Instrumental methods:

 Bladder catheterization. In the case of obtaining more than 1 liter of bloody urine, i.e. volume
exceeding the capacity of the bladder due to the flow of fluid from the abdominal cavity, we can
assume its rupture (Zeldovich sign). Lack of urine, like its small amount, with urinary retention is
likely to indicate its accumulation outside the bladder (the patient “urinates inside himself”).

 Ultrasound to determine the presence of free fluid and gas in the peritoneal cavity,

 Retroperitoneal hematoma, lesion of parenchymatous organs.

Invasive methods:

 Laparocentesis allows you to explore the contents of the abdominal cavity.

 Laparoscopy (video laparoscopy) reveals abnormal contents, damage to internal organs,

retroperitoneal

hematoma.

 Laparotomy is indicated when all other methods have been exhausted, and doubts about the
diagnosis remains.

7. Treatment of injuries of the abdomen. Indications for surgery, options for interventions;

Surgical tactics

INDICATIONS

1) The presence of a clinical presentation of the internal bleeding and peritonitis in patients with
abdominal trauma is an indication for urgent surgery.

2) Presence of growing hematoma of the anterior abdominal wall serves as an indication for surgery.

3) Conservative treatment is efficient for patients with bruises, abrasions, stable hematomas of the

abdominal wall, stable intraorgan hematomas of parenchymatous organs and small stable
subcapsular hematomas, as well as the majority of patients with closed kidney injury without
damage of the vascular pedicle.

Surgery
 The growing hematoma of the abdominal wall should be opened, the cavity should be emptied of
blood and clots, the bleeding vessel should be ligated, suturing of the wound, leaving drainage.

 Surgery on damaged organs: suturing of lesion, suturing with fixation of a large omentum, an
organ suture, hepatopexy, a large omentum tamponade, resection and removal of an organ,
removal of the damaged intestine to the anterior abdominal wall, nephrostoma.

Breast/ Chest (Question 8 -11)

8. Classification and clinical breast/chest injury;

Breast injury refers to a violation of the anatomical integrity, physiological functions of the

chest and (or) the organs of the chest cavity due to exposure to a mechanical agent.

All breast injuries are divided into closed and open.

Classification of closed chest injuries (E.A. Wagner, 1981):

1) According to the mechanism of injury : bruise, compression, concussion.

2) By the nature of the anatomical lesions:

- without damage to the skeleton;

- with damage to the bone skeleton;

- without damage to internal organs;

- with damage to internal organs.

3) According to the presence of complications:

- without complications;

- with complications.

4) According to the state of the cardiopulmonary system:

- without symptoms of respiratory failure;

- with the phenomena of acute respiratory failure (I, II, III degree);

- without the phenomena of cardiovascular failure;

- With the phenomena of acute cardiovascular failure (I, II and III degree).

5) Given the severity of the injury : mild, moderate, severe.

Clinical picture of closed chest injuries

The clinical picture of closed chest injuries is determined by the presence of various

injuries of the skeleton, chest organs and other anatomical areas, which leads to

significant polymorphism of clinical manifestations, requires an individual approach in each

case.
1. General manifestations:

- symptoms of traumatic shock (impaired consciousness, persistent hypotension,

tachycardia, oliguria);

- bleeding symptoms (weakness, dizziness, dry tongue, pallor of the skin, sticky sweat,

tachycardia, tendency to hypotension);

- symptoms of respiratory and circulatory disorders (cyanosis, shortness of breath,

marbling, and a decrease in limb temperature).

2. Local signs:

- abrasions, bruises in the form of continuous blue-purple spots or stripes, swelling of the

skin due to blood accumulated under it (hematoma);

- restriction of excursions of the chest when breathing on the side of the injury;

- chest rotation, i.e. the retraction of its fragment during inhalation when the rest of the

chest expands and prolapse on the exhale when the rest of the chest decreases.

- cough with hemoptysis or bleeding from the respiratory tract;

- bone crepitus in the fracture area;

- subcutaneous crepitus with emphysema;

- upon palpation in the area of damage, pain intensifying with deep inspiration and

movement, lack of voice trembling in case of pneumo-, hemotrax;

- during percussion, dullness of sound (hemothorax, contusion of the lung), box sound or

tympanitis, displacement of the borders of cardiac dullness in the opposite direction

(pneumothorax), etc .;

- during auscultation, the absence or weakening of breathing (pneumo-, hemothorax), wet

rales (lung contusion, pneumonia), etc. It should be emphasized that the most common

life-threatening condition is respiratory failure, the main causes of which are:

1. Violation of the biomechanics of respiration.

2. Obstruction of the bronchi.

3. Bronchiolospasm.

4. Reducing the formation of surfactant, a tendency to atelectasis.

5. Changes in hemodynamics in the pulmonary circulation.

6. Inammatory changes in lung tissue (post-traumatic pneumonia)

The combination of several of the above factors leads to the development of severe
respiratory distress syndrome and may be called “shock lung”. In severe types of breast

damage, along with respiratory, cardiovascular failure also develops.

Certain types of closed chest injuries

Fractures of the ribs are the most common damage to a chest injury, which is manifested

by pain, aggravated by breathing, movement and palpation. It should be remembered that

fragments of broken ribs are secondary damaging agents, and with an increase in their

number, the probability of typical pleural (pneumo-, hemothorax) and pulmonary (bruising,

rupture) complications increases proportionally. More often 3-9 ribs break, in the case of

1-3 neurological and vascular injuries are common, and with fractures of 9-12, concomitant

abdominal injury.

Multiple, especially bilateral, terminal rib fractures are accompanied by respiratory failure.

The paradoxical mobility (otation) of the chest wall occurs with multiple fractures of the ribs

along two or more lines (terminal or oating fractures), as well as their combination with a

fracture of the sternum. Finite is called fracture of the ribs along several anatomical lines,

with the formation of a sash (valve) of the chest wall. The otation otates when breathing:

during inspiration, it sinks, during exhalation it prolapses. This leads to a violation of the

biomechanics of respiratory movements and the development of acute respiratory failure.

The main complaint is severe pain at the site of a rib fracture, shortness of breath.

Bruised lung. Morphologically manifested by hemorrhage in the lung parenchyma, which

often causes the development of intrapulmonary hematoma, post-traumatic pneumonia

and lung abscess.

Closed heart damage. Allocate concussion, bruise, rupture. With a concussion, a spasm of

the coronary arteries occurs, followed by myocardial ischemia, which is accompanied by a

violation of conduction, rhythm, and a decrease in blood pressure. In the case of a heart

injury, in addition to spasm of the coronary vessels, hemorrhages occur in the epi-, myo-,

endocardium and are manifested by more signicant disturbances in the function of the

heart. On the ECG, nonspecic changes in the ST segment , blockade of the legs of the

bundle of His in combination with various types of arrhythmias up to ventricular

tachycardia are noted . Contusion (bruising) of the heart is often accompanied by a

fracture of the sternum; at the same time, it can proceed without signicant changes in

hemodynamics and remain unrecognized.

In especially severe cases, ruptures of the myocardium and interventricular septum are

observed, which is accompanied by a clinic of cardiogenic shock.

To diagnose heart damage, it is necessary to study and determine the values of the most

informative symptoms: the nature of chest damage, pulse properties, central venous

pressure, electrocardiographic signs of rhythm disturbance, myocardial ischemia.

Ultrasound can provide valuable information. The differential diagnosis is carried out with

traumatic myocardial infarction (occurs in 6% of cases, more often in elderly people),

which is made taking into account the ECG data in dynamics, laboratory tests (biochemical

markers).

9. Laboratory and instrumental diagnosis, differential diagnosis of breast/chest

injuries;

Diagnosis of breast injuries

Anamnesis: patient complaints and clarication of the nature and circumstances of the

injury. Important information can be provided by medical personnel, relatives of the victim,

eyewitnesses, contained in the accompanying medical documentation.

Laboratory methods:

- UAC: a decrease in the level of red blood cells, hemoglobin, hematocrit, specic gravity

with hemothorax; leukocytosis with bleeding and the entry of the contents of a hollow

organ into the pleural cavity. The denition of these indicators in dynamics is important.

X-ray methods:

a) fluoroscopy and chest radiography are leading diagnostic studies. They allow you to

identify damage to the bone skeleton of the chest; accumulation of air under the skin

(emphysema), pleural cavity (pneumothorax) and in the mediastinum; pleural effusions;

accumulation of blood in the pleural cavity (hemothorax); intrapulmonary hemorrhage.

b) tomography and CT specify the nature and localization of damage to internal organs.

c) angiography reveals damage to the vessels of the chest and mediastinum, pulmonary

embolism.

d) uoroscopy of the esophagus is indicated if it is suspected of being damaged.

Instrumental methods:

- ECG, ultrasound of the heart establish the localization and nature of its damage.

- Ultrasound of the pleural cavity reveals hemothorax, inammatory effusion in the pleural
cavity, and also determines the areas of compaction of the lung tissue.

- Pleural puncture establishes the nature and amount of pathological contents in the

pleural cavity and at the same time is a therapeutic manipulation.

- Thoracoscopy (video thoracoscopy) allows you to identify a signicant amount of damage,

pathological conditions when. The method allows you to adequately assess the

assessment of existing injuries, to complete the rehabilitation of the pleural cavity.

- Tracheobronchoscopy is performed if suspected damage, obstruction of the trachea and

bronchi. It is also performed for therapeutic purposes - - FGDS is performed to exclude

rupture of the esophagus.

Special methods:

- Ruvilua-Gregoire test - coagulation in a test tube of blood poured out of the pleural cavity

indicates ongoing bleeding.

- Determination of the concentration of markers of myocardial damage (CPK, LDH,

troponin).

10. The principles of treatment of breast/chest injuries, especially management of

post-operative period;

Treatment consists of the following principles: anesthesia, restoration of airway patency

and adequate pulmonary ventilation, elimination of pneumo- and hemothorax, elimination

of pathological condition, surgical treatment of injuries of the intra-thoracic organs.

1. Elimination of pain.

Adequate analgesia provides a protective function against traumatic shock, allows the

victim to breathe adequately, which is the basis for the prevention of pneumonia. Of the

drugs, narcotic analgesics (promedol, tramadol), non-narcotic pain medications (ketorolac,

analgin) in combination with diphenhydramine are used. In severe cases, intravenous

administration of analgesics is possible.

An important place in the complex of treatment for patients with closed chest injuries

belongs to epidural anesthesia and various modications of novocaine blockade: “three

places” blockade (medial to the fracture zone, lateral to the fracture zone and in the

fracture zone), prolonged blockade (alcohol-novocaine paravertebral, sternal, etc. ),

constant anesthesia of the fracture zone of the ribs.

2. Elimination of pneumo- and hemothorax.

This is achieved by performing puncture and drainage of the pleural cavity. Puncture of the

pleural cavity, performed according to emergency indications in the 1st minutes of the

victim’s admission, allows confirming or eliminating the accumulation of air or blood in the

pleural cavity even before obtaining the results of the X-ray examination, conducting their

aspiration, which will improve the patient’s condition and will help determine further tactics

of patient management. Drainage is the method of choice for breast injury, accompanied

by an accumulation of air and blood in the pleural cavity. allows not only to completely

remove the pathological contents, but also to promptly display indications for thoracotomy.

3. Restoring airway patency and adequate pulmonary ventilation.

This principle is largely ensured by adequate analgesia. Patients are shown massage,

inhalation, expectorant and sputum-thinning agents, stimulation of cough. In patients with

moderate trauma, the half-sitting position of the patient provides lowering of the diaphragm

and additional adequate breathing due to intercostal muscles. Inhalation of oxygen, even

in passive mode, provides part of the body's oxygen demand.

4. Surgical treatment of injuries of the internal organs of the chest.

Indications for thoracotomy (in some cases video thoracoscopy is possible) with closed

chest injuries are: - pericardial tamponade;

- damage to the vessels of the upper aperture of the chest and vessels of the

mediastinum;

- progressive hemothorax;

- curled hemothorax;

- massive, not having a tendency to decrease pneumothorax; - damage to the tracheobronchial

tract;

- damage to the esophagus;

- damage to the diaphragm.

In relation to chest injuries, as a rule, before performing thoracotomy (video thoracoscopy),

acute respiratory distress is eliminated. For this, drainage of the vocal cavity is performed
immediately upon admission. Further, the patient is given anesthesia with one-lung intubation - an
intact (less) lung is ventilated.

Lung damage. In victims, to achieve hemo- and aerostasis, suturing of lung ruptures is used, atypical
resection using staplers is possible. Performing anatomical resections of the lung is usually not used.
Damage to the trachea, bronchi. In case of incomplete tears, suturing is performed. With a complete
gap (more often, the right main bronchus is torn off at the place of departure from the trachea),
integrity can be restored by forming an anastomosis.

Damage to the heart and large vessels. Such patients are immediately sent to the operating room,
where they perform a thoracotomy, the purpose of which is to stop bleeding, restore the integrity of
damaged organs, eliminate tamponade of the heart, acute respiratory disorders.

Paradoxical mobility (rotation) of the chest. The stabilization of the skeleton of the chest is
performed. Elimination of pathological mobility of the damaged section of the chest wall is achieved
by skeletal traction over the ribs or sternum, osteosynthesis is performed. In recent years,
stabilization with a metal plate according to the type of operation “ Nuss ” is often used for funnel
chest deformities. Sometimes they resort to internal stabilization of the costal “valve” with the help
of prolonged (up to 10-15 days) mechanical ventilation, which is often accompanied by the
development of infectious complications and higher mortality.

Indications for surgery;

1. Chest wall fractures, dislocations and barotrauma (including diaphragm injuries)

Indications for immediate surgery include the following:

• Traumatic disruption with loss of chest-wall integrity

• Blunt diaphragmatic injuries

Relatively immediate and long-term indications for surgery include the following:

• Delayed recognition of blunt diaphragmatic injury

• Development of a traumatic diaphragmatic hernia

2.Blunt injuries of lungs, pleura and aero-digestive tract

Indications for immediate surgery include the following:

• Massive air leak following chest-tube insertion

• Massive hemothorax or continued high rate of blood loss via the chest tube (ie,

1500 mL of blood upon chest-tube insertion or continued loss of 250 mL/hr for 3

consecutive hours)

• Radiographically or endoscopically confirmed tracheal, major bronchial, or

esophageal injury

• Recovery of gastrointestinal (GI) tract contents via the chest tube

Relatively immediate and long-term indications for surgery include the following:

• Chronic clotted hemothorax or fibrothorax, especially when associated with a

trapped or nonexpanding lung

• Empyema
• Traumatic lung abscess

• Delayed recognition of tracheobronchial or esophageal injury

• Tracheoesophageal fistula

• Persistent thoracic duct fistula/chylothorax

3.Blunt injuries to heart, great arteries, veins, and lymphatic vessels

Indications for immediate surgery include the following:

• Cardiac tamponade

• Radiographic confirmation of a great-vessel injury

• Embolism into the pulmonary artery or the heart

Relatively immediate and long-term indications for surgery include the late recognition of a great-
vessel injury (eg, development of traumatic

pseudoaneurysm).

Contraindications for operative intervention

No distinct, absolute contraindications exist for surgery in blunt thoracic trauma. Rather, guidelines
have been instituted to define which patients have clear indications for surgery (eg, massive
hemothorax, continued high rates of blood loss via chest tube).

A controversial area has been the use of emergency department (ED) thoracotomy in patients with
blunt trauma who present without vital signs. The results of this approach in this particular patient
population have been dismal and have led many authors to condemn it.

Postoperative Care

Patients are extubated as soon as feasible in the postoperative period. Monitoring devices are kept
in place while needed but are removed as soon as possible. Intravenous fluids are provided until the
patient has had a return of GI function, at which time the patient can be fed. Patients with severe
associated injuries, especially those in a coma, may require prolonged enteral tube feedings.

Pain control is important in these patients because it facilitates breathing and helps to prevent
pulmonary complications such as atelectasis and pneumonia. Chest physiotherapy and nebulizer
treatments are used as necessary, and the use of an incentive spirometer is encouraged.

Chest tubes are placed for suction until fluid drainage has fallen sufficiently and the lung is
completely expanded without evidence of air leak. Tubes may then be placed to water seal and may
be removed if a chest radiograph demonstrates continued lung expansion.

11. Complications of breast/chest lesions, clinical manifestations, diagnosis,

treatment; Patients with blunt thoracic trauma are subject to myriad complications during the
course of their care.

Wound complications include the following:

• Wound infection

• Wound dehiscence (particularly problematic in sternal wounds)

Cardiac complications include the following:

• Myocardial infarction

• Arrhythmias

• Pericarditis

• Ventricular aneurysm formation

• Septal defects

• Valvular insufficiency

Pulmonary and bronchial complications include the following:

• Atelectasis

• Pneumonia

• Pulmonary abscess

• Empyema

• Pneumatocele, lung cyst

• Clotted hemothorax

• Fibrothorax

• Bronchial repair disruption

• Bronchopleural fistula

Vascular complications include the following:

• Graft infection

• Pseudoaneurysm

• Graft thrombosis

• Deep venous thrombosis

• Pulmonary embolism

Neurologic complications include the following:

• Causalgia (injuries that involve the brachial plexus)

• Paraplegia (the spinal cord is at risk during repair of a ruptured thoracic aorta)

• Stroke

Esophageal complications include the following:

• Leakage of repair

• Mediastinitis

• Esophageal fistula
• Esophageal stricture, late (click here to complete a Medscape CME activity on treating esophageal
strictures)

Complications involving the bony skeleton include the following:

• Skeletal deformity

• Chronic pain

• Impaired pulmonary mechanics

Pleural complications of a chest injury

Pneumothorax. They distinguish between open (free communication of the pleural cavity with the
external environment, in connection with which air enters and leaves through the wound of the
chest wall), closed (air intake occurs at the time of damage and stops due to displacement of soft
tissues) and valve, or tense (occurs
whenviolationoftheintegrityofthebronchiortheformationofavalveintheareaofthewoundofthechest,th
e air entering during the inhalation into the pleural cavity does not exit or partially leaves it upon
exhalation) pneumothorax.

Apical (collapse of the apex of the lung, partial or paracostal (band of air up to the diaphragm),
incomplete (lung collapsed by 1/3 - 1⁄4), total (collapse of the entire pulmonary parenchyma) are
distinguished by the volume of collapse of the lung tissue.

In the case of total pneumothorax, patients are restless, the presence of severe acrocyanosis,
shortness of breath is noteworthy. Breathing shallow, rapid. With a deep breath, the pain intensies
sharply. Compensatory tachycardia is noted, blood pressure is normal or low. When examining the
chest, there is a noticeable restriction of the mobility of the affected half of the chest, gentle
breathing on the affected side, the presence of a wound and emphysema around it, and air suction
through the wound heard from a distance when breathing in and out of the wound when exhaling.
Percussion is determined by tympanitis, and in the presence of hemothorax - dullness over its
surface. Auscultation -a sharp weakening of breathing in the projection of the upper lobe of the lung
and its almost complete absence in the projection of the lower lobes.

The most severe is the total valve pneumothorax in which the mediastinum mixes, the deformation
of large vessels and bronchi occurs, which is accompanied by severe cardiorespiratory failure.
Cyanosis of the skin, and visible mucous membranes, swelling of the cervical veins, tachycardia,
arterial hypotension in combination with a decrease in pulse pressure are noted. Respiratory
movements on the affected side are absent or weakened, tympanitis and a mixture of cardiac
dullness in a healthy direction are determined percussion.

Hemothorax - accumulation of blood in the pleural cavity due to damage to the vessels of the lung,
chest wall, wounded heart and large vessels of the chest. According to P.A.Kupriyanov, on the basis
of direct radiography in a vertical direction along the rear landmarks of the chest wall, the following
are distinguished: small (100–200 ml in the pleural sinuses), medium (up to the level of the scapular
angle - 500–700 ml), large (up to the middle of the scapula - 1000-1500 ml) and total hemothorax
(2000 ml or more).

The condition of victims with moderate to severe hemothorax. Pallor of the skin, frequent shallow
breathing, tachycardia, arterial hypotension are characteristic. With percussion, dullness of sound is
detected, the displacement of the borders of the heart in the opposite direction, with auscultation,
weakening of respiratory sounds.
Hemopneumothorax. Combines the signs of the above conditions.

It should be remembered that a chest injury can be combined with damage to the abdomen, with
tears (a sharp increase in pressure; broken ribs) of the spleen and liver most often occur. In this case,
the clinical picture will present symptoms of acute blood loss, irritation of the peritoneum.

Cardiology (Question 15 -39)

15. Classification of congenital heart defects. Hemodynamic abnormalities, clinical

features and diagnosis of congenital heart diseases;

16. Indications for surgical treatment of congenital heart defects, methods and

timing of surgical interventions. Forecasts, outcomes and prevention;

Classification of congenital heart defects

Creating a single classification of congenital heart defects is associated with certain

difficulties due to the huge number of types of defects and principles that can be put in its

foundation.

All CHD can be divided into groups:

· Vices with a left-to-right shunt (“pale”);

· Vices with a right-to-left shunt (“blue”);

· Cross-discharge;

· Vices with obstructed blood flow;

· Valvular defects;

· Defects of the coronary arteries of the heart;

· Cardiomyopathy;

· Congenital cardiac arrhythmias.

In pediatric practice, Marder (1957) classification is convenient, based on the

characteristic of blood flow in the small circulation and the presence of cyanosis.

Features of

hemodynamics

Presence of cyanosis

Present Absent

Enrichment of the

pulmonary circulation
ventricular septal defect, atrial

septal defect, open arterial duct,

abnormal drainage of pulmonary

veins, incomplete

atrioventricular communication

transposition of great

vessels, hypoplasia of the

left heart,

common arterial trunk,

single ventricle of the heart

Depletion of the pulmonary

circulation

isolated stenosis

pulmonary artery

transposition of the great

vessels + stenosis of the

pulmonary artery, Fallot's

tetrad, tricuspid atresia,

Ebstein's disease,

false common arterial trunk

Obstruction of blood flow

in the systemic circulation

aortic stenosis, aortic

coarctation

According to the degree of hemodynamic disorders

• Without hemodynamic disorders

• Moderate hemodynamic disorders

• With severe hemodynamic disorders

According to the clinical course

• Primary adaptation phase

• Relative compensation phase

• Terminal

• Hemodynamic disorders, clinical presentation, diagnosis of congenital heart

defects.

The majority of congenital defects are heart defects with enrichment of the pulmonary

circulation, occurring predominantly without cyanosis and with the presence of an

arteriovenous shunt. The discharge of blood through a defect is determined by its size and

vascular resistance of the blood circulation circles. Secondary sclerotic changes in the

pulmonary vessels that develop under the inuence of increased pulmonary blood ow and

pressure lead to an increase in pulmonary vascular resistance, leveling the difference

between pulmonary artery pressure and the aorta, changing the direction of the blood ow

(“changing shunt”).

Mild pulmonary hypertension is complicated by chronic or recurrent pneumonia.

Pulmonary hypertension causes hypertrophy and systolic overload of the right heart and

impairs the effectiveness of the surgical correction. With a high degree of pulmonary

hypertension, venoarterial shunt of blood through a defect in the aorta appears and

gradually increases, despite the appearance of cyanosis, this reduces the load on the right

heart and partially relieves the pulmonary circulation. In this situation, the surgical closure

of the defect quickly eliminates this shunt, and the right ventricle has to throw out the entire

stroke volume against high resistance into the pulmonary artery. Therefore, in the acute

situation of a new hemodynamic situation, the right parts of the heart are unable to cope

with the increased load and postoperative acute right ventricular failure develops, which is

fatal. In addition to the higher risk of postoperative mortality, severe pulmonary

hypertension complicates the postoperative course and rehabilitation of patients.

In children suffering from congenital heart disease with the enrichment of the pulmonary

circulation, the formation of pulmonary hypertension goes through three main phases:

hypervolemic, mixed, sclerotic. For the hypervolemic phase, a large arteriovenous

discharge into the pulmonary circulation, hypervolemia of the pulmonary vessels, in

response to which vasospasm occurs, without an increase in the general pulmonary

resistance, is characteristic. The pressure in the pulmonary artery remains normal or

increases moderately. The pulmonary circulation has a depositing ability, an increase in

No significant
hemodynamic

disturbances

dextrocardia, vascular

anomaly,vascular ring - double

aortic arch, Tolochinov - Roget

disease

blood ow 2-3 times may not be accompanied by a signicant increase in pressure in the

pulmonary artery. For the mixed phase, a protective increase in pressure in the pulmonary

artery system caused by a spasm of the pulmonary vessels is

characteristic. Due to this mechanism, the amount of arteriovenous discharge of blood

decreases with increasing pulmonary resistance to blood ow. Hypertension is functional,

mainly due to hypervolemia and increased vascular wall tone due to vasoconstriction and

hypertrophy of the middle lay of the small muscular arteries. After a successful surgical

correction of the defect, the pressure in the pulmonary artery in most patients is almost

completely normalized. For the sclerotic phase, destructive changes in the vascular wall

are characteristic, when, against the background of hypertrophy of the middle sheath of

the small muscular arteries, sclerosis of the inner lining occurs, followed by thinning of the

arterial wall and their generalized dilation with the development of necrotizing arteritis. In

the sclerotic phase, there is a high irreversible pulmonary hypertension, expansion of the

pulmonary artery, persistent cyanosis, and severe hypertrophy with systolic overload of the

right heart, often with manifestations of chronic right ventricular failure. Surgical

intervention, predict the results of surgical correction, the nature of rehabilitation, the

duration and patient quality of life.

Clinical manifestations of CHD:

• Dyspnea;

• Discoloration of the skin (cyanosis, pallor);

• Apathy, restless sleep, indifference to others;

• Lag in physical development;

• Frequent lung diseases;

• Heart hump;

• Various blood pressure indicators in the upper and lower extremities;

• Displacement of cardiac dullness;

• Heart rhythm disturbances;

• Heart murmur;

• An increase in the size of the liver (edema, ascites are observed only in the terminal

stage).

The clinical manifestations of CHD are mainly represented by two syndromes:

arterial hypoxemia and congestive heart failure.

In the formation of arterial hypoxemia in CHD, three main mechanisms may play a role:

intracardiac discharge of blood from right to left and its entry into the aorta; reduced

pulmonary blood ow and reduced pulmonary return of arterial blood to the heart;

separation of large and small circles of blood circulation. With the majority of CHD of the

cyanotic type, arterial hypoxemia is associated with the rst two mechanisms.

Heart failure is a pathological condition in which the heart is unable to provide the blood

circulation necessary to meet the needs of the body. It most often develops either due to

an increased load on the heart by blood volume or pressure, or due to a decrease in

myocardial contractility during hypoxia or an inammatory process in the heart muscle. The

main symptoms of heart failure are tachycardia, shortness of breath, signs of stagnation in

a small or large circle of blood circulation. In young children, heart failure is almost always

biventricular in nature.

Complications of CHD:

· Dystrophy

· Anemia

· Recurrent pneumonia

· Infective endocarditis

· Thromboembolic syndrome

· Disorders of rhythm and conduction

Instrumental diagnostics of CHD

· ECG during which you can identify overload of various parts of the heart,

myocardial changes

· General radiography of the chest organs, where a change in the conguration of

the heart can be noted

ECHO-CG - the main method - allows you to see the morphology of the defect and

determine the functional state of the heart.

The open arterial duct (OAD, PDA) - the presence of a connection between the aorta

and the pulmonary artery, which is considered an anomaly in the postnatal period (Fig. 1).

Anatomic closure or obliteration occurs during the rst 2 weeks of postnatal life. Such

pathological conditions of the neonatal period as the syndrome of respiratory disorders,

congenital pneumonia, birth asphyxia prevent the closure of the PDA. The volume of blood

discharged from the aorta into the pulmonary artery leads to the development of diastolic

overload and dilatation of the left heart, especially the left atrium, hypervolemia in the

lungs with the formation of pulmonary hypertension. The clinical picture of PDA is typical of

the CHD, occurring with the enrichment of the small circle of blood circulation, and will

depend on the size of the duct. With the natural course the life of patients lasts for 20-25

years. After 12 months of age, spontaneous closure of the ductus arteriosus rarely occurs.

The main complications of PDA are heart failure, pulmonary hypertension, infective

endocarditis, aortic aneurysm and / or pulmonary artery.

Surgical treatment involves dressing or intersection with the closure of the aortic and

pulmonary duct ends, but lately catheter endovascular occlusion of the duct has also been

used

Atrial septal defect (ASD) is a group of heart defects that are characterized by abnormal

communication between the atria.

Hemodynamic changes in ASD develop gradually due to the difference in pressurein the

large and small circles of blood circulation, due to which a left-right discharge of blood

through a defect is formed. Due to the receipt of an excess amount of blood in the right

atrium and right ventricle, their dilatation and hypertrophy develop over time. A

hemodynamic (relative) stenosis of the pulmonary artery is formed, the noise of which is

heard during auscultation. Changes in the vessels of the pulmonary circulation occur

according to general laws, but much more slowly than with VSD. It is difficult to suspect

ASD in the neonatal period. Signs of circulatory failure develop, as a rule, much later - at

1-3 years of age, when there is an increase in the motor activity of the child. Indicators of

physical development in children with ASD, as a rule, correspond to the age norm.

Patients of early age are characterized by frequent respiratory diseases, accompanied by

bronchial obstruction. Signs of high pulmonary hypertension develop late — by the age of

16–25.

Treatment of heart failure is carried out according to general principles. Surgical treatment

is a radical correction - plastic of ASD.

Ventricular septal defect (VSD) - occurs most often, both in an isolated form, and as part

of many other heart defects.

There are 3 sections in the interventricular septum: the upper part is membranous,

adjacent to the central brous body, the middle part is muscular, and the lower part is

trabecular. According to these sections, ventricular septal defects are also named, but

most of them have perimembranous localization. In order to properly assess the size of the

defect, its size must be compared with the diameter of the aorta. Minor defects of 1-2 mm

in size, located in the muscular part of the interventricular sept, are called Tolochinov –

Roger disease. Intracardiac hemodynamic disturbances in VSD begin to form sometime

after birth, as a rule, after 3-5 days of life. In the early neonatal period, heart murmur may

be absent due to the same pressure in the right and left ventricles due to so-called

neonatal pulmonary hypertension. A gradual drop in pressure in the pulmonary artery

system and in the right ventricle creates a difference (gradient) of pressures between the

ventricles, as a result of which there is a discharge of blood from left to right (from the high

pressure area to the low pressure area). The additional volume of blood entering the right

ventricle and the pulmonary artery leads to an overow of vessels in the pulmonary

circulation where pulmonary hypertension develops.

If the surgical correction of CHD is not performed, the processes of pulmonary vascular

sclerosis begin to form (high pulmonary hypertension - Eisenmenger syndrome). This

pathological process does not reverse development and leads to a signicant increase in

pressure in the pulmonary artery (sometimes up to 100-120 mm Hg). In the clinical picture

of the disease there are many pathological signs: heart “hump”, the expansion of the

borders of relative cardiac dullness, more to the right. The most characteristic feature of

Eisenmenger syndrome is a gradual increase in cyanosis, rst peripheral, and later diffuse.

This is due to cross-ow of blood in the area of the ventricular septal defect, which, if the

pressure in the right ventricle is exceeded, becomes right-left, i.e. changes its direction.

The clinical picture of VSD is in the symptom complex of heart failure, which develops at
1-3 months of life (depending on the size of the defect). In addition to signs of heart failure,

VSD may manifest pneumonia.

Surgical interventions are divided into palliative operations (narrowing of the pulmonary

artery) and a radical correction of the defect - plastic surgery of an interventricular septal

defect.

Abnormal drainage of the pulmonary veins (ADPV) is a congenital heart disease, which

is characterized by the conuence of the pulmonary veins into the right atrium or into the

caval veins of the greater circulation. Normally, all four pulmonary veins are drained into

the left atrium. With partial abnormal drainage of pulmonary veins, one or two pulmonary

veins ow into the right atrium (or, alternatively, into the superior vena cava, lower hepatic

or portal vein). With total abnormal drainage, all pulmonary veins are not properly drained

(Figure 6). At the same time there is a different degree of severity of stagnation in the

pulmonary circulation and overload of the right atrium, which increases signicantly. To

discharge the latter, the presence of an atrial septal defect, through which blood from the

right atrium will ow into the left atrium, carrying mixedblood there, is a prerequisite. In the

classic version, there is a large secondary atrial septal defect.

The clinical picture depends on the type of defect and, rst of all, on the number of

abnormally draining veins. With total ADPV, the clinical picture is specic and develops

shortly after birth: dyspnea progresses and becomes pronounced, mild cyanosis takes

place, symptoms of biventricular heart failure develop rapidly and increase, there is a

tendency to develop severe pneumonia against the background of marked hypervolemia

of the pulmonary circulation. Children, as a rule, signicantly lag in physical development.

With partial ADPV, the clinical picture develops more slowly and the defect can be

detected by chance, most often in the second year of life. Children tend to develop

satisfactorily. There may be a tendency to broncho-pulmonary diseases.

With total abnormal drainage of pulmonary veins, patients die from refractory heart failure

and high pulmonary hypertension.

Average life expectancy is 2-6 months. Partial abnormal drainage of pulmonary veins is

characterized by a calmer prognosis.

Surgical correction is carried out in different age periods and depends on the type of CHD.

The operative lethality at this defect makes up to 25% in the period of a neonatality and
progressively decreases with age of the child. Newborns sometimes undergo palliative

surgery - balloon atrioseptotomy in order to expand the interatrial message. Radical

surgery is to create a wide anastomosis of the pulmonary veins with the left atrium, closing

the ASD.

Fallot’s tetrad (FT) belongs to the most common heart disease of the blue type (Fig. 7). In

the classic Fallot’s tetrad, there are 4 signs: narrowing of the right ventricular ejection at

various levels, ventricular septal defect, which is always large, high, perimembranous, right

ventricular myocardial hypertrophy and aortic dextraction. Defect refers to the CHD of the

cyanotic type with the impoverishment of the small circle of blood circulation.

There are three clinical and anatomical variants of the defect:

1) FT with atresia of the orifice of the pulmonary artery - “extreme”, form;

2) The classic form;

3) FT with minimal pulmonary stenosis, or “pale”, a cyanotic form of FT.

Fallot’s triad is distinguished when there is no ventricular septal defect. Fallot’s tetrad can

be combined with other CHDs: with the simultaneous presence of ASD, the variant is

called Fallot’s pentad. Most often, FT is combined with PDA, due to which a compensatory

blood supply to the lungs occurs. With the “extreme” form of FT, the defect is “ductus” -

dependent.

The degree of hemodynamic disturbance is determined by the severity of stenosis of the

pulmonary artery. Obstruction may be at the level of the output section of the right

ventricle, at the level of the valve of the pulmonary artery, along the trunk and branches of

the pulmonary artery, and at several levels simultaneously. During systole, blood flows

from both ventricles to the aorta and, in smaller quantities, into the pulmonary artery. Due

to the fact that the aorta is wide and shifted to the right, the blood passes through it without

hindrance, therefore, with the classical form of the Fallot’s tetrad, there is never a

circulatory insufficiency. Due to the large ventricular septal defect, the pressure in both

ventricles is the same. The degree of hypoxia and the severity of the patients correlate

with the degree of stenosis of the pulmonary artery. In patients with the extreme form of

Fallot’s tetrad, the blood enters the lungs through the open arterial duct or through the

collaterals (arteriovenous anastomoses and bronchial arteries), which can develop in

utero, but more often - postnatally. Compensation of blood circulation occurs due to: 1)
right ventricular hypertrophy; 2) the operation of the PDA and / or collaterals; 3) the

development of polyglobulia and polycythemia as a result of prolonged hypoxia; Cyanosis

is the main symptom of Fallot’s tetrad. The degree of cyanosis and the time of its

appearance depend on the severity of stenosis of the pulmonary artery. In children of the

first days of life, only severe forms of the defect — the “extreme” form of Fallot’s tetrad —

are diagnosed on the basis of cyanosis. Basically, the gradual development of cyanosis

(by 3 months - 1 year), which has various shades (from pale bluish to “blue-crimson” or

“iron-blue”), is characteristic: 1st, cyanosis of the lips, then mucous membranes, fingertips,

skin of the face, limbs and trunk. Cyanosis increases with the activity of the child. Early

develop “drum sticks” and “watch glasses”. Permanent symptom is shortness of breath,

which is noted at rest and sharply increasing with the slightest exertion. Gradually

develops a delay in physical development. Almost from birth, a rough systolic murmur is

heard along the left edge of the sternum. A formidable clinical symptom in Fallot’s tetrad,

which is responsible for the severity of the condition of the patients, is undesired cyanotic

attacks. They arise, as a rule, between the ages of 6 and 24 months on the background of

anemia. The pathogenesis of the onset of an attack is associated with a sharp spasm of

the infundibular section of the right ventricle, with the result that all venous blood enters

the aorta, causing the most acute hypoxia of the central nervous system. Blood oxygen

saturation during an attack drops to 35%. The intensity of the noise in this case decreases

sharply until complete disappearance. The child becomes restless, the expression on his

face is frightened, the pupils are dilated, shortness of breath and cyanosis are increasing,

the extremities are cold; followed by loss of consciousness, convulsions, and possible

development of hypoxic coma and death. Attacks vary in severity and duration (from 10–

15 seconds to 2–3 minutes). In the post-attack period, the patients remain sluggish and

adynamic for a long time. Sometimes the development of hemiparesis and severe forms of

cerebrovascular accident is occurred. By the age of 4-6 years, the frequency and severity

of attacks is significantly reduced or they disappear. This is due to the development of

collaterals, through which more or less adequate blood supply to the lungs occurs.

Depending on the characteristics of the clinic, there are three phases of defect:

Phase I - relative well-being (from 0 to 6 months), when the patient’s condition is relatively

satisfactory, there is no physical development lag;

Phase II - dyspnea and cyanotic attacks (6-24 months), characterized by a large number

of brain complications and deaths;

Phase III - transitional, when the clinical picture of vice begins to take on adult features;

With a pale form of FT, the course and clinical signs resemble those with septal defects.

With the natural course of CHD, the average life expectancy is 12-15 years. Causes of

death are unhealthy-cyanotic attacks, hypoxia, disorders of hemo- and liquorodynamics,

cerebral thrombosis, strokes, infective endocarditis.

Surgical correction in patients with FT is divided into palliative operations (imposition of

subclavian-pulmonary anastomosis) and radical correction of CHD. Palliative surgery

allows the patient to survive and grow stronger before carrying out a radical correction,

which is carried out in 2-3 years. Radical surgery involves the simultaneous elimination of

all cardiac abnormalities and is carried out at preschool age.

The optimal age for the surgical treatment of certain congenital heart defects

CHD - critical

1. Open ductus arteriosus with respiratory distress syndrome - 1 month

2. Sharp coarctation of the aorta and Complete obliteration of the aortic arch - Urgent

3. Ventricular septal defect with pulmonary hypertension - 3-6 months

5. Fallot’s tetrad - 3-6 months

6. Total abnormal pulmonary vein drainage - 1 month

CHD - not so critical

1. Coarctation of the aorta - 4-5 years

2. ASD - 5-6 years

3. VSD - 3-5 years

4. PDA- After 6 months

5. Fallot’s tetrad - In infancy palliative treatment and final I 5-7 years

Currently, the vast majority of heart defects are operated on. Operations are usually

classified as palliative and radical. Hemodynamic correction is also isolated. Palliative

operations are resorted to in cases of a serious condition of the patient and / or torpid in

the treatment of congestive heart failure. For example, in CHD, proceeding with the

enrichment of the pulmonary circulation, Muller’s operation is performed - a narrowing of

the pulmonary artery by applying a squeezing cuff to the vessel. Subsequently, a radical
correction of the CHD is carried out. When “ductus”-dependent heart defects perform an

operation to impose a subclavian-pulmonary anastomosis.

Radical heart operations are performed under conditions of arterial blood circulation,

hypothermia, and cardioplegia. Hemodynamic correction is performed when radical

surgery is impossible due to the anatomical features of the heart defect, for example, in

hypoplasia of the left calving, double separation of the vessels from the right ventricle, etc.

17. Methods of diagnosis of acquired heart defects;

Coronary angiography is a method of x-ray examination of coronary arteries using

selective filling them with a contrast agent. Coronary angiography is performed by

puncture of the main artery according to Seldinger (usually the femoral or radial) with the

catheter being guided along the guide proximal to the aortic root and the catheter

positioned alternately at the mouth of the right and left coronary arteries.

Indications:

• Patients with stable angina pectoris I-II FC, who underwent MI

• Patients with post-infarction aneurysm and progressive (left ventricular) heart failure

• Patients with stable angina FC III-IV with inefficiency anti- anginal therapy

• Patients with stable angina pectoris with blockade of the legs of the bundle of His in

combination with signs of myocardial ischemia according to myocardial scintigraphy

• Patients with coronary heart disease combined with aortic valvular disease requiring

surgical correction

• Patients with ischemic heart disease with severe cardiac arrhythmias requiring

clarification of the genesis and surgical correction.

Contraindications:

· fever

· Severe disease parenchymal organs

· Expressed total heart failure

· Acute cerebrovascular accident

· Severe ventricular rhythm disorders.

Ventriculography - contrasting of the left ventricle, is performed during CAG, which

makes it possible to evaluate a number of important hemodynamic parameters:

· Detect regional dysfunctions of the LV (hypo- and akinesia zones)

· Diagnosis of left ventricular aneurysm

· Identify intra-cavitary formations (parietal thrombi and tumors)

· Assess the state of the valvular apparatus of the heart

Evaluate LV systolic function

Functionally significant is the detection of the following symptoms during angiography:

arterial occlusion, stenosis of more than 75%, stenosis of 50% or more (the main trunk of

the left coronary artery).

Intra-coronary ultrasound is an image of the lumen of the coronary arteries with a high

resolution of the transverse section using a piezoelectric crystal rotating through 360 ° or

sequential activation of many crystals of the sensor introduced into the artery lumen.

Initially, the technique was developed as an alternative to angiography, which does not

require radiation exposure and contrast, but at the moment it does not allow replacing the

standard angiographic study.

The main objectives of invasive visualization techniques for examining coronary blood ow

is to determine the morphological substrate of coronary blood ow disorders, which allows

you to determine the tactics and preferred method of re-vascularization. The choice of re-

vascularization method is based on risk stratification. There are two main approaches to

performing coronary re-vascularization: percutaneous transluminal coronary angioplasty

and coronary artery bypass grafting. Each of the methods has soy advantages and

disadvantages.

ECG during which you can identify overload of various parts of the heart, myocardial

hypertrophy;

General radiography of the chest organs, on which a change in the conguration of the

heart can be noted;

Contrast ventriculography of the heart - an x-ray method of studying chambers of the

heart allows to evaluate the contractile function of the ventricular myocardium, to

investigate the condition of the valvular apparatus, to identify the aneurysm in the cavity of

the left ventricle;

ECHO-CG - the main method - allows you to see the morphology of the defect and

determine the functional state of the heart.

18. Artificial coronary support: principles, indications, myocardial protection.

Complications of cardiopulmonary bypass;

Cardiopulmonary bypass - temporary shutdown of the heart from the blood circulation

and the implementation of blood circulation in the body using an artificial blood circulation

apparatus. Used in operations on the heart and aorta. In most cases, cardioplegia is used

during cardiopulmonary bypass - a set of measures aimed at protecting the myocardium

during cardiac surgery, including cardiac arrest and myocardial protection. Cardiac arrest

in the diastole phase reduces myocardial oxygen consumption. Most modern strategies for

cardioplegia are based on the introduction into the coronary bed of cold solutions

containing a high concentration of potassium ions.

Auxiliary blood circulation is a method of partial replacement of cardiac function with the

help of mechanical devices.

A device with a balloon is inserted through the femoral artery, which is installed below the

left subclavian artery. By periodically inflating and deflating the balloon in accordance with

the phases of the cardiac cycle, temporary support of the pumping function of the heart is

provided. The artificial ventricle of the heart is a mechanical device that partially or

completely replaces the function of the heart in heart failure (Fig. 11). The principle of their

work consists in mechanical unloading of the left or right or two ventricles of the heart. In

the case of a bypass of the left ventricle, the cannula is implanted in the apex of the

ventricle or atrium, then blood passes through the pump of the auxiliary device into the

cannula implanted into the aorta. In the case of using the right artificial ventricle, blood

from the right ventricle through the pump enters the pulmonary artery.

The artificial ventricle of the heart can be used temporarily - while the patient is

expecting a donor heart, and the heart’s own pumping function is insufficient, or recovery

of the heart’s function is expected, for example, after an acute myocardial infarction

complicated by cariogenic shock. Long-term therapy is also possible for patients with

contraindications for heart transplantation.

Extracorporeal membrane oxygenation (ECMO) is an invasive extracorporeal oxygen

saturation method in the development of severe acute respiratory failure. Veno-arterial

(blood sampling from a vein, oxygenation, return to the artery) ECMO can be considered

as prolonged extracorporeal circulation, which is used in patients with acutely developed

and potentially reversible respiratory, cardiac or cardiorespiratory insufficiency, which do

not respond to standard therapy.

The mechanical support of the heart is associated with the risk of ischemic and

hemorrhagic strokes, bleeding, the development of local infections and sepsis.

Indications for surgical treatment and types of surgical interventions for acquired heart

defects.

Surgical treatment of patients with aortic insufficiency is indicated for all symptomatic

patients who are in NYHA functional class II or above, as well as with an ejection fraction

of> 20-30%. Patients with damage to the contractile function of the left ventricle have a

higher risk of surgery and postoperative mortality. Aortic valve replacement is indicated for

all patients with aortic stenosis with symptoms of the disease, as well as for patients

without symptoms with a high trans-valvular pressure gradient (greater than 60 mmHg),

opening area ≤ 0.6 cm 2, coronary or other valve pathology, up to of how left ventricular

decompensation develops.

Surgical correction of aortic defect is carried out with the help of its prosthetic mechanical,

biological (Fig. 13) frame and frameless prostheses or cryopreserved allografts.

Indications for surgery for mitral stenosis are determined by the area of the left

atrioventricular orifice. Mitral stenosis with an area of MV ≤1 cm2 is considered

critical. The indication for surgery is a reduction in the area of MV <1.5 cm2 and II and

more functional class NYHA .

The indication for an operation for mitral insufficiency is the area of the effective opening of

regurgitation> 20 mm2, II or more degree of regurgitation, and II - III functional

NYHA class.

Surgical correction of mitral disease is carried out with the help of prosthetics with artificial

mechanical and biological prostheses. In some cases, it is possible to perform

reconstructive operations on the mitral valve. For this, various methods of reconstruction

are used: annuloplasty on hard and soft rings, resection of the valves, implantation of

artificial chords.

The indication for surgery for tricuspid valve stenosis is the effective orifice area <1.5 cm2,

and in case of insufficiency, blood regurgitation to the right atrium of II - III degree.

The main method of correction of relative tricuspid valve insufficiency is

annuloplasty. Ways to reduce the diameter of the tricuspid valve ring consist in holding a
purse-string plastics and using rigid or flexible corrective rings. In some cases, when it is

impossible to perform a corrective surgery, a bioprosthetic valve is used.

TAVI (Transcatheter Aortic Heart Valve ) The prosthesis for TAVI is a tricuspid bovine

pericardial valve, fixed in a metal frame (stent). The folded bioprosthesis inserted into the

femoral artery using a catheter is delivered to the orifice of the affected native aortic valve

and opens up on its own or inflates with a balloon. The operation is performed under x-ray

control. The delivery system is removed, the valve begins to function. TAVI is the treatment

of choice for patients older than 75 years with severe aortic stenosis, who have

contraindications for open surgery.

The implantation of a mitral valve clip is a surgical percutaneous technique, which is

performed to correct severe mitral insufficiency in patients with a high risk of surgical

intervention (Fig. 15). This device is a clip designed to connect the valves at the center of

the mitral valve (an analogue of the open operation Alfieri is the elimination of prolapse of

the anterior valve of the mitral valve with a suture attaching the anterior prolapse to the

unchanged posterior cusp with the formation of a double lumen atrioventricular orifice

ensuring valve tightness). The clip of the mitral valve with the help of the delivery device is

carried out through the femoral vein, then by transseptal access (puncture of the interatrial

septum) is delivered from the right atrium to the left, and then to the mitral valve area.

Fixing the clips to the valve leaflets is carried out under the control of transesophageal

echocardiography.

19. Indications for surgical treatment and surgical interventions with acquired

defects. Prosthetic heart valves. Pre- and post- operative period and outcomes;

Prosthetic heart valves.

Severe lesions of the valve apparatus need replaced valves. Most often carry out the

replacement of the mitral and aortic valves. Mechanical prostheses - made of plastic,

carbon or metal. They are durable and can last long enough. Since blood when in contact

with mechanical valves is prone to the formation of blood clots, patients with such

prostheses should take anticoagulants (warfarin) for life. Biological - made from animal

tissues (xenografts) or from the heart of a human donor (allografts). Patients with

biological valves, as a rule, do not need to take anticoagulants.

Long experience of using artificial mechanical valves of the heart has shown that despite
their reliability and durability, the use of prostheses is not an ideal solution. The

accumulation of experience in the use of bio-prostheses made it possible to assess the

strengths and weaknesses of allo and xeno materials. Along with the advantages, they

have the disadvantage - the fragility caused by the destruction of biological tissue in the

long-term period. On the one hand, this leads to the rejection of the use of bio-prostheses

in patients of middle (up to 65 years) age, on the other, to the search for methods capable

of realizing the use of allografts not as prostheses, but as viable valves or vessels.

When performing prosthetics or plastics of the heart valves, access is usually

sternotomy. Operations are performed under conditions of artificial blood circulation.

Pre- and postoperative period, outcomes.

The preoperative preparation of the patient for surgery on the heart valves is aimed at

conducting the necessary examinations, planning the course of the surgery. Diagnosis of

concomitant pathology is carried out and the degree of its severity is assessed, which is

very important in terms of reducing the risk of developing intraoperative complications and

the probability of a lethal outcome of the event.

If you find any additional somatic problems, you should achieve an optimal general

condition of the patient, in which unwanted negative points will be minimized. Patients

should be, as far as possible, compensated for heart failure.

In the postoperative period, a complex cardiological rehabilitation plays an important role,

which includes assessing the patient’s clinical condition, optimizing pharmacological

treatment, physical rehabilitation — a stepwise and controlled increase in physical activity

adapted to the individual human capabilities, psychosocial rehabilitation, the purpose of

which is to teach the patient to help himself in stress situations emotional states, such as

fear or depression, to develop the ability to psychological adaptation to the effects of the

disease, lifestyle changes, education of patients and their relatives.

Currently, no single implanted biological or mechanical prosthetic heart valve provides the

patient with a lifetime guarantee against his dysfunction.

Prostheses of different designs have individual behavior in the long-term period, which is

characterized by different valve-dependent complications. The development of valve leaf

calcification is characteristic of biological prostheses. On mechanical prostheses, there is a

high probability of pannus and thrombosis. All prostheses are vulnerable to complications
associated with infectious endocarditis.

20. Infective endocarditis, clinical features, diagnosis, treatment, indications for

surgical treatment;

Infectious endocarditis is an infectious lesion of the tissue of the valve apparatus of the

heart and endothelium by various pathogens.

The criteria for establishing the diagnosis of endocarditis are positive blood cultures and

persistent bacteremia, vegetation, abscess or prosthesis discharge in echoCG, new valve

regurgitation, as well as predisposition (predisposing heart disease or drug use), fever,

vascular phenomena (large arterial embolism, septic lung infarction, mycotic aneurysms,

intra-cerebral hemorrhages), immunological phenomena (glomerulonephritis, Osler

nodules, Rota spots).

From the point of view of surgery in the pathogenesis of infective endocarditis, the most

important is the fact of the rapid destruction of the valvular apparatus of the heart. This

leads to a catastrophic increase in heart failure, since the myocardium does not have time

to adapt to a sharp violation of hemodynamics.

The decision about the need for surgical treatment arises, as a rule, with the development

of “complicated infectious endocarditis”: changes in hemodynamic status; persistence and

prevalence of infection; development of metastatic foci of infection; systemic emboli. In

these cases, surgical treatment is more successful than the therapeutic approach.

Indications for surgical treatment - CHF, ineffective antibiotic therapy or sepsis, large,

mobile vegetations or repeated episodes of embolism, abscess of the heart, involvement

in the process of prosthetic valve.

In case of severe damage or destruction of the valve, prosthetics are usually performed. In

some cases, valvo-plasty and vegetation removal are performed.

21. Indications for surgical treatment of coronary heart diseases. The choice of

method of operative benefits, early and late results;

Currently, direct myocardial re-vascularization by percutaneous transluminal balloon

angioplasty (PTBA) and stenting or coronary artery bypass surgery and mammary

coronary artery bypass graft has become the main method of surgical treatment of

coronary heart disease (CHD).

A key factor in studying the topic of surgical treatment is a clear understanding of the
nature of coronary heart disease (CHD). CHD is a myocardial damage caused by a

disorder of the coronary circulation, resulting from an imbalance between the coronary

blood flow and the delivery of oxygen to the heart muscle. CHD is based on organic lesion

of the coronary arteries, in the overwhelming majority of cases caused by stenotic

atherosclerosis, to which thrombosis can join. As a result, the main directions of the

treatment of coronary artery disease are medical therapy aimed at restoring the balance

between myocardial need and oxygen delivery. Indications for surgical treatment occur in

cases where the balance can not be achieved with medication. Such situations may be

urgent (acute coronary syndrome) or develop over a long period of time (stable exertional

angina of high functional class). In addition, surgical treatment is indicated in the

development of complications of coronary artery disease (ventricular aneurysm, the

separation of the valve chord with the development of acute failure, etc.).

Questions of classification, drug therapy and prevention of coronary artery disease are

discussed in detail in the course of internal diseases. More details on the issues related to

surgical care.

The range of surgical interventions for ischemic heart disease is reduced not only to
revascularization issues, but also to the aspect of invasive diagnostics - coronary

angiography, ventriculography, intracoronary ultrasound.

Coronary angiography (CAG) is a method of x-ray examination of the coronary arteries

by selectively filling them with a contrast agent. Coronary angiography is performed by

puncture of the main artery according to Seldinger (usually femoral or radial) with a

catheter guided along the guide wire to the aortic root and positioning the catheter

alternately in the orifices of the right and left coronary arteries.

Indications:

• Patients with stable angina pectoris NYHA I-II, who have had myocardial infarction

• Patients with postinfarction aneurysm and progressive (left ventricular) heart failure

• Patients with stable angina pectoris NYHA III-IV with the ineffectiveness of antianginal

therapy

• Patients with stable exertional angina with blockade of the His’ bundle in combination

with signs of myocardial ischemia according to myocardial scintigraphy

• Patients with coronary artery disease in combination with aortic heart disease, requiring
surgical correction

• Patients with coronary artery disease with severe cardiac arrhythmias requiring

clarification of genesis and surgical correction.

Contraindications:

· fever

· severe parenchymal diseases

· severe total heart failure

· acute disorders of cerebral circulation

· severe ventricular rhythm disorders.

Ventriculography - contrasting of the left ventricle, performed during CAG, which makes it

possible to evaluate a number of important hemodynamic parameters:

• Detect regional LV dysfunction (zones of hypo- and akinesia)

• Diagnose a LV aneurysm

• Identify intracavitary formations (parietal thrombi and tumors)

• Assess the condition of the heart valve

• Evaluate LV systolic function

Functionally significant is the detection of the following signs during angiography: artery

occlusion, stenosis of more than 75%, stenosis of 50% or more (main trunk of the left

coronary artery).

Intracoronary ultrasound is an image of the lumen of the coronary arteries with a high

resolution cross section using a 360 ° rotating piezoelectric crystal or the sequential

activation of a multitude of sensor crystals inserted into the artery lumen. Initially, the

technique was developed as an alternative to angiography, which does not require

radiation exposure and contrast, but at present it is not possible to replace the standard

angiographic study.

The main objectives of invasive imaging techniques for examining coronary blood flow is to

determine the morphological substrate of coronary blood flow disorders, which allows you

to decide on the tactics and preferred method of re-vascularization. The choice of revascularization
method is based on risk stratification. There are two main approaches to

coronary re-vascularization: percutaneous transluminal coronary angioplasty and coronary

bypass. Each method has advantages and disadvantages.

Coronary angioplasty is a minimally invasive procedure in which an adequate lumen of

the artery is restored by performing balloon angioplasty (crushing a plaque with a high

pressure balloon) followed by the installation of a stent (metal mesh tube with or without

drug coating). The introduction and positioning of the balloon and the stent is carried out

using the same technique as angiography - with Seldinger’s puncture of the femoral artery

using different conductors to pass through the narrowing site. The operation is performed

under local anesthesia.

Indications

• Progressive angina .

• ACS or early infarction

• Early post-infarction angina.

• Stable angina with low quality of life on the background of adequate drug therapy.

• High risk of cardiovascular accidents and / or death, as a result of non-invasive

examination methods.

Advantages of stenting

• Minimally invasive access

• Local anesthesia, the patient is conscious.

• Short-term hospitalization.

• Fast to performing in an emergency (with ACS)

• High efficiency (up to 90%).

Disadvantages of stenting

• The risk of thrombosis, heart attack, restenosis (up to 15-60% within 6 months).

• At high risk of restenosis, it is necessary to set expensive stents with a drug coating.

• Despite visible minor injuries, the stent implantation procedure is laborious, especially in

case of severe calcification.

A number of technical limitations: extended narrowing, stenosis in the branching zone of

the arteries, stenosis of the left coronary artery, not applicable for the lesion of small

vessels, prognostically worse for multi-vascular lesions

The direct effect of PTBA in patients with stable angina with proper selection of patients

reaches 95%. In patients with a single vascular lesion, the mortality associated with the

procedure itself is less than 0.2%; with multiple lesions of the arteries - 0.5%, the
frequency of Q-infarction is less than 1%.

The second main method of myocardial revascularization is coronary artery bypass

surgery. This intervention involves the formation of bypass routes of blood flow past the

site of stenosis. Depending on the technical conditions, concomitant pathology, equipment

and skills of the surgeon, various options for this intervention are possible, from standard

coronary artery bypass surgery from a sternotomy with cardiopulmonary bypass to

minimally invasive thoracotomic and endoscopic approaches on the working heart. For the

formation of bypass anastomoses can be used as native arteries (left and right internal

thoracic arteries, gastro-epiploic arteries - which are skeletized, cut off in the distal part,

after which they anastomose with the affected coronary artery distal to the stenosis /

occlusion site), the displaced arteries (usually radial artery) or autovenes (vv. saphena

magna or parva) that anastomose with the aortic root and the affected artery. Arterial

shunts are preferable to venous because of the lower frequency and later periods of

restenosis (10 years after surgery, 90% of the internal mammary artery transplants

continue to function).

Indications for CABG in patients with stable angina pectoris

• The ineffectiveness of conservative drug treatment of coronary artery disease

• Stenosis of the left coronary artery,

• Stenosis of the three coronary arteries (especially with left ventricular dysfunction),

• Stenosis of the proximal left descending coronary artery over 75% with concurrent

damage of at least one artery.

Benefits of CABG

It can be performed with a significant length of vascular lesion.

Can be performed with the defeat of any arteries (including the left coronary trunk)

Does not lead to a limitation when performing MRI (compared with stenting with

holometalic stents)

Disadvantages of CABG

• Extensive preoperative preparation program. Complicated general anesthesia with

invasive monitoring.

• Long duration (up to 6 hours), depending on the method and number of superimposed

shunts.
• Traumatic surgery is difficult to tolerate.

• Higher frequency of hemorrhagic and suppurative complications

• Requires long rehabilitation

• More lifestyle restrictions related to surgery.

Mortality in CABG in patients with lesions of several arteries and severe dysfunction of the

left ventricle reaches 4-5%, about the same incidence of Q-infarction. Currently, there is a

tendency to increase the frequency of operations performed on the working heart and from

the mini accesses, which significantly reduces the frequency of complications.

In conclusion, it should be noted that CABG and stenting in most cases are not

interchangeable with myocardial re-vascularization techniques, but represent separate

surgical approaches for the treatment of coronary artery disease in various clinical

situations.

22. Post-infarction cardiac aneurysm, diagnosis, indications for surgery, types of

operations;

Cicatricle myocardial changes as a result of a heart attack can lead to the formation of

ventricular aneurysms. As a rule, aneurysms occur after extensive transmural infarction, in

rare cases due to trauma or a congenital defect. In most cases, aneurysms are localized in

the apex or on the anterior wall of the left ventricle. The existence of an aneurysm changes

the nature of blood flow in the ventricles, significantly reducing the ejection fraction and the

minute volume, conducting impulses, is accompanied by a high risk of formation and

migration of blood clots.

Clinically, post-infarction aneurysm is manifested by pain in the heart, chest pains,

shortness of breath, interruptions in the work of the heart - i.e. the clinic of angina, due to a

decrease in contractile function of the ventricle. As a rule, patients indicate a history of

heart attack.

Physical examination can reveal a paradoxical pulsation in the fourth intercostal space on

the left, systolic murmur.

Instrumental examination includes radiography of chest (change in the configuration of the

heart shadow due to the sacculate protrusion), ECG (characteristic features of the heart

aneurysm: QS or QR complex, persistent elevation of the interval S-T and negative T wave

in the chest leads), Echo-CG (the location of the aneurysm is clearly defined its size, the
presence of thrombotic masses in the cavity of the aneurysm). Additionally Echo-CG

assess changes in hemodynamic parameters and the state of the valves and papillary

muscles.

Coronarography (with a view to clear diagnosis of lesions in the vascular bed) and

ventriculography (to determine the size of the aneurysm, localization, myocardial changes

due to the pathological process, to evaluate the overall contractile ability of the remaining

part of the left ventricular myocardium) is a mandatory stage of the survey.

With the natural course of the disease, patients with post-infarction aneurysms die within

2–3 years from increasing cardiovascular insufficiency, embolic complications or

arrhythmias.

The presence of a ventricular aneurysm is an independent indication for surgical

treatment, but this often requires the performance of myocardial re-vascularization.

Surgical treatment of a ventricular aneurysm consists in excision of the aneurysm wall with

removal of parietal thrombi and closure of the resulting defect. If necessary, the

intervention is complemented by performing coronary bypass surgery, mitral valve

replacement. Minimally invasive transthoracic techniques of surgical repair of aneurysms

have been developed.

23. Pericarditis, classification, indications and types of surgery;

Pericarditis is inflammation of the pericardium. The pericardium is a bag formed by two

walls and containing in its cavity the heart and roots of the main vessels (aorta, pulmonary

trunk, caval veins). In the pericardium, there are two layers - serous, covering the heart

(epicardium), and fibrous parietal layer. The functions of the pericardium are the fixation of

the heart in the region of the mediastinum, protective function and reduction of friction

during heart contractions. Pericardial diseases can be both isolated and part of systemic

diseases. The following main pericardial lesions are distinguished: pericarditis, pericardial

effusion, cardiac tamponade, constrictive pericarditis, and pericardial thickening.

Classification of pericarditis:

on etiology - primary, secondary;

Depending on the primary etiological cause:

· viral pericarditis;

· bacterial pericarditis;
· tuberculosis pericarditis;

· other infectious pericarditis;

· pericarditis in autoimmune diseases;

· pericarditis in diseases of the heart and adjacent organs;

· pericarditis with metabolic disorders;

· traumatic pericarditis;

· pericardial neoplastic lesions;

· radiation pericarditis;

· idiopathic pericarditis

By the nature of inflammation - acute, chronic.

Pericarditis rarely occurs as an independent disease and is often a complication of other

diseases. In this regard, often there is no specific clinic. However, patients most often

present the following complaints: general malaise, weakness, shortness of breath, chest

pain, heart palpitations and dry cough. As the heart is expelled with an effusion, signs of

impaired cardiac activity increase: cyanosis of the lips and extremities appears, swelling of

the neck veins, severe shortness of breath, and a drop in blood pressure. Given the nature

of complaints, pericarditis always has to be differentiated from CHD, myocardial infarction,

pleuritis, and heart failure.

The main diagnostic tools for the detection of pericarditis are imaging techniques -

radiography, echocardiography, CT. Unfortunately, these techniques do not provide

information on the nature of pericardial inflammation and do not give direct indications and

the need for one or another treatment option. Reliable differential diagnosis can be

accomplished only by invasive pericardiocentesis techniques with obtaining a tissue

sample and effusion, as well as pericardioscopy. In most cases, a subxiphoid incision is

used to perform invasive studies, which is convenient for obtaining diagnostic material.

Invasive diagnostic studies are completed with pericardial drainage to prevent tamponade.

In many cases, a sufficient amount of diagnostic information can be collected using

ultrasound-controlled or X-ray-controlled pericardial puncture. This technique is less

invasive, easier reproducible. Pericardiocentesis in any of its variants should be performed

under instrumental control (ECG, echo-CG, fluoroscopy), since it is accompanied by the

risk of severe complications - puncture of the pleural cavity, heart cavity, liver, development
of pneumothorax, hemothorax, hemopericardium. Such invasive diagnostic procedures

should not be performed in conditions where it is impossible to provide emergency care in

case of complications, except in cases of an immediate threat to the patient’s life.

The treatment of acute pericarditis in most patients takes place in parallel with the

treatment of the underlying disease and according to the same principles: antimicrobial

therapy, heart remedies, painkillers, anti-inflammatory therapy. There are no drugs with

“pericarditis” in the indications for treatment, therefore, prescription of drug therapy is

carried out on the basis of the etiology of the underlying disease, and for primary bacterial

pericarditis - depending on the sensitivity of the pathogen. Surgical care in the treatment of

pericarditis may be necessary in the case of the development of tamponade, constrictive

pericarditis, septic condition.

In case of purulent pericarditis pericardiocentesis is performed. If there is no effect,

surgical treatment is indicated - pericardiotomy with drainage of the cardiac sac.

Drainage of the pericardial cavity with exudative serous pericarditis is possible through

capillary drainage under ultrasound control.

Drainage of the pericardial cavity is necessary after open cardiac surgery, suturing the

wounds of the heart in order to prevent tamponade.

With a recurrent growing effusion (usually malignant), a pericardial window may be

formed - communication between the pericardial cavity and the pleural cavity in order to

prevent tamponade. This intervention can be performed with video

thoracoscopy. This type of drainage is less effective and radical than pericardectomy, but

technically simpler, less traumatic, and have less risk.

Pericardiectomy - open excision of the altered pericardium, usually required for the

treatment of chronic constrictive pericarditis (i.e., in situations where the contractions of the

heart are not limited by effusion in the cavity, but by changes in the pericardial sheets

themselves). Decortication is the most complete, but with preservation of the phrenic

nerves. It is necessary to exempt from the parietal and visceral sheets of the pericardium,

the right atrium, the vena cava, the lower part of the right ventricle. A full pericardectomy

can be performed only from sternotomy access. This operation requires cardiopulmonary

bypass. Although artificial blood circulation is not required to perform pericardectomy, the

intervention may be complicated by injuries (vessels, heart, myocardium), which will

require expansion of the surgery.

24. Surgical treatment of cardiac arrhythmias: diagnosis, methods of correction;

Heart rhythm disorders have a high prevalence in the population. Even normally with a

daily ECG recording, the supraventricular extrasystoles (mostly atrial) are found in

43-63% of cases, ventricular extrasystoles can be caught in 2/3 of people with a healthy

heart. For heart diseases, the number of extrasystoles is usually higher, their nature and

significance are more serious. The clinical significance of extrasystoles is determined by

their negative effect on hemodynamics and the ability to provoke more severe rhythm

disturbances: atrial fibrillation / flutter, supraventricular and ventricular tachycardias. Atrial

fibrillation occurs in approximately 0.4% of the adult population, in individuals older than 60

years - in 2-4% of cases. Atrial fibrillation has a negative effect on cardiohemodynamics, is

characterized by a high risk of thromboembolic complications, which requires its timely

diagnosis and treatment.

Disorders of the conduction of the cardiac impulse are a frequent pathology in persons

with diseases of the cardiovascular system. Often, these disorders limit the possibilities of

drug therapy, putting the doctor in front of the need to determine indications and

contraindications for the surgical treatment of blockades.

Basic concepts

Arrhythmias are changes in the normal frequency, regularity, and source of excitation of

the heart, as well as impulse conduction disorders, communication disorders, and (or) the

sequence between atrial and ventricular activation.

Extrasystoles - premature in relation to the basic rhythm of arousal of the whole heart or

any of its department.

Atrial fibrillation (atrial fibrillation) - chaotic, irregular excitation of certain groups of

atrial muscle fibers with a loss of mechanical atrial systole and irregular excitations and

ventricular contractions.

Atrial flutter - supraventricular tachycardia, characterized by an organized atrial rhythm

with a frequency of usually between 250 and 350 beats per minute.

Blockade - a partial or complete disruption of the movement of an electrical impulse along

the cardiac conduction system.

Etiology of arrhythmias and blockades

1. Diseases of the cardiovascular system (acquired and congenital), resulting in damage to

the cell membranes of cardiomyocytes: ischemic heart disease, arterial hypertension,

myocarditis, cardiomyopathy, heart defects;

2. Violations of the regulation of the cardiovascular system (psychogenic, neurogenic,

reflex influences);

2. Disorders of myocardial metabolism: electrolyte, endocrine (thyrotoxicosis) and

impairment of ABB;

3. Physical and chemical effects: caffeine, nicotine, alcohol, drugs, hypoxia, hypo-and

hyperthermia, mechanical effects.

The clinical manifestations of arrhythmias and blockades and related complaints are

due to two main factors: irregular heartbeats and a decrease in the efficiency of cardiac

output. Patients complain about the feeling of interruptions, pauses, “fading” of the heart,

heart palpitations, sometimes seizures, fast fatigue, weakness, swelling, and sometimes

loss of consciousness.

The diagnosis is made on the basis of clinical data. However, to determine the nature and

form of rhythm disturbances, as well as the complications that prevent some invasive

interventions, it is necessary to perform a list of diagnostic tests: ECG, Holter’s ECG

monitoring, echocardiography, transesophageal electrophysiological examination of the

heart.

Treatment. Treatment of arrhythmias is primarily medical, aimed at reducing the

excitability of the heart, controlling heart rate (cardiac glycosides, β-blockers, calcium

channel blockers) and preventing thrombotic complications (aspirin, warfarin). In some

cases, cardioversion may be performed to restore heart rate. In tachi-arrhythmias (atrial

flutter / atrial fibrillation, WPW syndrome), non-drug treatment is indicated in the following

cases:

• The ineffectiveness of drug therapy

• Relief of paroxysmal supraventricular tachycardia

• Prevention of complications of malignant arrhythmias. Methods of surgical treatment of

tachi-arrhythmias are:

• Transvenous catheter radiofrequency ablation (focus of ectopic activity, mouths of the

pulmonary veins in case of AF, area of the “neck” in TP)

• Destruction of the AV-connection and implantation heart pacemaker

• Catheter modification of the AV connection (without heart pacemaker)

• Implantation of atrial atrioverter-defibrillator.

• Surgical atrial isolation (radiofrequency operations like “corridor”, “labyrinth”)

A pacemaker is a small device (pulse generator), like a pocket watch, which is implanted

under local anesthesia under the skin, near the heart, to control heart rhythm. A modern

device is a complex device made of inert medical titanium alloy, in the case of which a

battery and a microprocessor unit are placed, oriented towards the heart’s own electrical

activity. When the heart rhythm is disturbed, the stimulator begins to generate an electrical

discharge to stimulate contractions of the myocardium, while at a normal rhythm it does

not work. There are single-chamber, two-chamber and three-chamber pacemakers:

single chamber - the active electrode is located only in the ventricle and only its stimulation

occurs (deficiency - the atria contract in their own rhythm, if the atrial and ventricular

contractions coincide, blood flows from the ventricle to the atrium, which can cause serious

consequences);

two-chamber - two electrodes: to the atrium and ventricle, provides consistent reductions

and normal blood flow;

three-chamber (last generation) - three electrodes: to the atrium, to the right and left

ventricles, creates a physiological movement of blood through the chambers of the heart.

Pacemaker implantation: A flexible insulated wire is inserted into the left subclavian vein,

a transvenous endocardial electrode is passed to the heart under x-ray control: the distal

end is attached to the right ventricle, the proximal to a pulse generator (single-chamber

pacemaker); 2 wires are often inserted, the second is attached to the right atrium (twochamber).
The operation lasts 1-2 hours. In the hospital the patient spends 1-2 days.

Modern artificial pacemakers are reliable in operation, their service life reaches 5-10 years,

after which, if necessary, the stimulator bolt can be replaced. A portable pacemaker, the

mass of which usually does not exceed 45 g, is implanted subcutaneously in the

subclavian region.

All modern pacemakers have at least two functions: 1) carry out electrical stimulation of

the corresponding heart section and 2) have the ability to perceive their own electrical

activity of the atria and ventricles, being included in the stimulation mode only in the period
when the critical heart rate decreases or asystole develops (“on demand”).

Some modern artificial pacemakers also have additional functions, for example, the ability

to change the frequency of heart stimulation depending on the size of the load performed

by the patient (adaptive mode) or the possibility of external non-invasive reprogramming of

the pacemaker using special devices or the ability to automatically recognize and stop

tachycardia paroxysm.

The pacemaker is programmed based on the individual parameters of the activity of the

cardiovascular system of each patient.

Catheter ablation is a surgical treatment of arrhythmias based on the intracardial

destruction of pathological pathways causing arrhythmia. It is used in ventricular and

supra-ventricular tachyarrhythmias, additional conduction pathways (WPW syndrome),

atrial fibrillation.

There are several types of catheter ablation:

1. Radio frequency destruction (energy of radio frequency waves). It has become

widespread, since it is well eliminated foci of arrhythmias, and healthy areas of the

myocardium are damaged to a lesser extent.

2. Laser destruction.

3. Electrical destruction (electric current is applied). 4. Ultrasonic destruction.

5. Cryogenic destruction (low temperature).

The operation is performed under local anesthesia. Through the femoral artery or the left

subclavian vein, electrodes are administered under fluoroscopic control into the heart

cavity. Conduct eletrophysiological study of the heart to detect arrhythmic zones. An

intracardiac cardiogram is recorded, which is recorded on a computer monitor. Special

tests that provoke arrhythmia are performed. Having found an arrhythmogenic point, it is

affected by radio frequency energy supplied through one of the electrodes. After 20

minutes, repeat the electrophysiological study to assess the effectiveness of the performed

manipulation. If the therapeutic effect is achieved, the catheters are removed, hemostatic

pressure bandages are applied to the place of punctures. The patient is prescribed strict

bed rest for 24 hours.

Blockade (bradyarrhythmias). Main types

Sinoatrial blockade is a conduction disorder in which impulses produced in the sinus

node are not able to overcome the sinoatrial connection or exit the C-A node more slowly

than normal.

Atrioventricular blockade is a partial or complete impairment of conduction in the path of

impulse movement from the atria to the ventricles. In the clinic, AV blockades are

classified:

I. By stability:

• Acute transient;

• Intermittent;

• Chronic, permanent (fixed).

II. By severity or degree :

• AV blockade of I degree (incomplete),

• AV blockade of the II degree: I and II types (incomplete),

• AV blockade of the III degree (full).

III. By topographic level.

• Right atrium (interstitial tracts)

• AV node (node)

• Common trunk of the His’ bundle (stem)

• Both legs of the His’ bundle (blockade of the legs of the His’ bundle)

• On several levels (combined blockade)

From surgical positions, the following types of bradyarrhythmias are important: sick sinus

syndrome, AV blockade 2 and 3 degrees.

Morgagni – Adams – Stokes syndrome.

A number of bradyarrhythmias (AV-blockade II or III, especially the distal form of complete

AV-blockade) is often accompanied by the development of pronounced hemodynamic

disturbances caused by a decrease in cardiac output and hypoxia of organs, primarily the

brain. Especially dangerous are periods of ventricular asystole, i.e. periods of absence of

effective ventricular contractions resulting from the transition of AV stage II blockade to

complete AV block, when the new ectopic ventricular rhythm driver located below the level

of the blockade had not yet begun to function. In such situations, the period of asystole

may last for a few seconds and be accompanied by a short-term sudden loss of

consciousness of the patient. This phenomenon is called the Morgagni-Adams-Stokes

syndrome (attacks of MAS). This condition may spontaneously become ventricular

fibrillation.

Blockade treatment

In the treatment of sinoauricular and atrioventricular blockade guided by the severity of

clinical manifestations. For bradycardia that is not accompanied by clinical symptoms in

the form of dizziness and fainting, it is possible to restrict yourself to dynamic observation

of the patient or an attempt to administer drugs that improve performance in C-A or A-B

nodes: such as atropine or its analogues (bellataminal), izadrin sublingual, peripheral

vasodilators (reflex tachycardia). In more severe disorders, implantation of a pacemaker is

the only treatment.

Indications for implantation of pacemaker in blockades:

• Sick sinus syndrome

• AV-blockade of the II degree of the Mobitz I type (in rare cases with the development of

hemodynamic disturbances not controlled by medication)

• Class II AV-blockade of the Mobitz II type (since the risk of the development of the full

AV-blockade is high)

• AV blockade with a 2: 1 in the following two cases: o with distal blockade

with the progression of hemodynamic disorders.

• AV block III degree (complete).

• Registered MAS, regardless of the degree of AV blockade recorded on the ECG

Since conduction disturbances with bradyarrhythmias can be the result of not only organic,

but also functional, electrolyte, and drug changes, implantation of a pacemaker is rarely

considered the first treatment method. The first step is to eliminate the influence of

corrected factors, including with temporary cardiac pacing, and only in the absence of

effect is the implantation of a permanent pacemaker indicated.

It should be remembered that staging cardiac stimulation is an invasive procedure with

penetration into the heart chambers and implantation of a foreign body, which is

associated with the risk of complications :

• The displacement of the electrode and the inability to stop the stimulation;

• Thrombophlebitis;

• Sepsis;
• Embolism (air);

• Pneumothorax;

• Perforation of the heart wall.

In view of the severity of possible complications, the implantation of the pacemaker should

be performed exclusively in the conditions of specialized departments.

Currently, implantation of permanent pacemaker is the only effective way to treat severe

chronic brady-arrhythmias. Annually the number of pacemakers implanted worldwide

reaches 300 thousand.

25. Classification of aortic aneurysm, clinical features, diagnosis, indications for

surgical treatment;

26. Complicated forms of aortic aneurysm. Clinical manifestations, diagnosis,

treatment;

Thoracic Aortic Aneurysms

The aneurysms of the thoracic aorta include cases of irreversible local sacciform or diffuse

aortic dilatation of 2 times or more compared with the normal diameter.

Classification.

According to the localization of the aneurysm of the thoracic aorta is divided as follows;

Localization of thoracic aortic aneurysms.

a – Valsalva’s sinus aneurysm;

b - aneurysm of the ascending aorta; in - aortic arch aneurysm;

c - aneurysm of the descending thoracic aorta;

d - aneurysm of the thoracoabdominal aorta.

1.Valsalva’s sinus aneurysms, which include the initial segment of the aorta from the

fibrous ring of the aortic valve to the synotubular sulcus, the line on which the upper points

of the commissures of the semilunar valves of the ascending aorta are projected. These

aneurysms are usually innate in nature. The aneurysms of the ascending aorta - from the

level of the sinotubular sulcus to the mouth of the brachiocephalic trunkAt the suggestion

of D.Cooley, ascending aortic aneurysms, accompanied by expansion of the fibrous ring of

the aortic valve, Valsalva’s sinuses and loss of the synotubular sulcus were divided into a

separate category called “annuloaortic ectasia”;

2. Aortic arch aneurysm, including a segment of the thoracic aorta from the mouth of the
nameless artery to the level of discharge of the left subclavian artery;

3. Aneurysms of the descending aorta, located in the segment of the thoracic aorta

between the left subclavian artery and the aortic orifice of the diaphragm;

4. Thoracoabdominal aortic aneurysms, beginning in the descending aorta and

extending to its abdominal region. To characterize the latter, use the Crawford

classification

Type 1 - the lesion begins in the proximal half of the descending aorta and above the level

of the discharge of the renal arteries

Type 2 - aneurysm also spreads from proximal half of the descending thoracic aorta to a

level below the discharge of the renal arteries,

Type 3 - begins in the distal half of the descending aorta and continues for a different

length in the abdominal aorta

Type 4 - the aneurysm begins at the level of the aortic orifice of the diaphragm and

includes the 6th abdominal aorta

According to etiology

1. Congenital diseases.

- Cardiovascular system (double or single aortic valve, aortic stenosis, coarctation of the

aorta, tortuous aortic isthmus).

- Connective tissue (Marfan, Ehlers – Danlos syndrome, etc.).

2. Acquired diseases.

- Non-inflammatory, degenerative:

a) Atherosclerosis or media degeneration;

b) Postoperative (aortic cannulation sites, suture line of prosthetic anastomoses or aortic

patches).

- Inflammatory:

a) Infectious and non-infectious aortitis;

b) Mycotic;

c) Aortic prosthesis infection.

- Post -traumatic.

- Iatrogenic (aorta catheterization, balloon counterpulsation, etc.).

- Idiopathic (Erdheim’s medionecrosis).

- Hormone-mediated (medionecrosis in pregnant women).

Risk factors for developing aortic aneurysms are considered

1. Hypertension,

2. Age,

3. Smoking

4. Cocaine addiction.

The clinical picture of aneurysms of the thoracic aorta depends on the location and size

of the aneurysm. In approximately 75% of cases, the disease is asymptomatic and is

detected by chest X-ray or CT of the chest, by ultrasound examination. Characteristic

symptoms in aneurysms of the ascending aorta are chest pain due to aortic wall lesions,

compression of surrounding organs, or angina pectoris in coronary arteries. Compression

of the superior vena cava is accompanied by edema of the upper limbs, head and neck.

Symptoms of heart failure are typical for ascending aortic aneurysm due to frequent

concomitant aortic valve disease.

With aneurysms of the arch and the descending part of the thoracic aorta, pain syndrome

can occur both behind the sternum and in the interscapular region. With this arrangement,

aneurysms are more characteristic symptoms associated with compression of surrounding

organs and tissues. Thus, esophageal compression is manifested by dysphagia,

dysphonia occurs during compression of the recurrent nerve, and during compression of

the vagus nerve, bradycardia and salivation occur. Compression of the trachea and the left

main bronchus may be accompanied by shortness of breath, stridor, the development of

congestion in the lungs. The defeat of aneurysmal process branches of the aortic arch

may be accompanied by a clinic of chronic cerebrovascular disease, symptoms of

transient or acute disorders of cerebral circulation.

Aneurysms of the thoracoabdominal aorta are often accompanied by abdominal pain,

especially in the epigastric region; they are characterized by symptoms associated with the

involvement in the process of branches of the abdominal aorta and the development of

ischemia of the relevant organs. These are signs of chronic abdominal ischemia with

lesions of the celiac trunk and superior mesenteric artery, renovascular hypertension, and

ischemia of the lower extremities. Rarely, with occlusion of the intercostal arteries,

ischemic lesions of the spinal cord develop.

Aneurysm rupture. The clinical picture in case of ruptures is characterized, first of all, by

a pronounced collapse often against the background of persisting pain syndrome. The

remaining symptoms are associated with the localization of the gap, for ascending aortic

aneurysms, this is the hemopericardium. For localization of a gap in the descending part or

arch of the aorta, hemothorax is characteristic, less commonly massive esophageal or

pulmonary hemorrhage.

A thoracoabdominal aneurysm is characterized by a rupture into the free abdominal cavity

or retroperitoneal space, less commonly into the stomach or duodenum, when vomiting

with red blood and / or melena is noted. The rarest localization of rupture of aneurysms of

the ascending aorta and the thoracoabdominal department is a breakthrough into the

superior vena cava and the inferior vena cava, respectively. The clinical picture in these

situations is characterized by acutely developing heart failure.

Marfan’s syndrome is a disease of the connective tissue that is inherited in an autosomal

dominant manner and is associated with a defect in the gene responsible for the synthesis

of fibrillin, the main protein component of microfibrils that make up elastin fibers.

The main clinical signs of Marfan’s syndrome:

1. ocular disorders of the subluxation of the lens, occurs in 87% of patients

2. musculoskeletal deformities, funnel chest, elongation of fingers with narrow nail

plates (arachnodactyly - in 77% of patients), increased joint mobility, recurrent dislocations

(shoulder, hip, patella, Steyberg positive sign (maximum reduced thumb protrudes beyond

the rest of the fingers that cover it), joint flexion of the joints, increased length of the lower

extremities relative to the length of the body (dolichostenomelia), tall, scoliosis (in 72% of

women and 50% of men in), protrusion of the acetabulum, extension of the knee joints,

flat-footedness, spina bifida occulata (hidden spina bifida or dural ectasia), kyphoscoliosis,

thoracic lordosis, expansion of the large cistern, lumbosacral meningocele, high arch of

the sky;

3. family history, detected in approximately 75% of patients

4. cardiovascular manifestations associated with mitral valve prolapse (90% of patients);

30-50% of patients have mitral regurgitation. Nearly 80% of patients have aortic root

enlargement, in some cases with aortic regurgitation. Other cardiovascular manifestations

of the syndrome include annuloaortic ectasia, dissection and aortic aneurysm. The severity
of aortic injury increases with age. Usually, aortic dissection begins with the Valsalva’s

sinuses, then dilated, the sinotubular sulcus and further the aortic arch and arc.

The average life expectancy for patients with Marfan’s syndrome is 32 years. The main

cause of death is cardiovascular complications, including 60-80% expansion of the aortic

root (dissection, rupture, valve damage).

The intensity of the expansion of the aorta in Marfan syndrome is inhibited by the use of

beta-blockers. Surgical treatment is carried out primarily in the event of delamination or

rupture. In planned situations, when the normal aortic diameter is twice exceeded or

enlarged to 5 cm or more, the operation is considered absolutely indicated due to the

extremely high risk of a rupture or separation. Indications for surgery are also heart failure

due to mitral or aortic regurgitation.

Aortic dissection is the discrepancy (division) of the aortic media into two layers due to

penetration of the intraluminal blood through the intimal gap and the occurrence of a

pathological connection between the true lumen of the aorta and the channel formed in the

middle layer of the aorta, called the false lumen.

Classification. De Bakey in 1965 divided the aortic dissection as follows

Type 1 - Stratification, and then may extend to any extent;

Type 2 - the bundle captures only the ascending aorta;

Type 3a - dissection begins below the orifice of the left subclavian artery and extends only

within the descending aorta;

3b type - dissection is the same as with type 3a, but extends through the aortic orifice of

the diaphragm to the abdominal aorta.

Stanford Classification:

Type A - exfoliation of the ascending aorta (regardless of the location of the intima strain

and the presence of distal distribution),

Type B - dissection extends only to the descending aorta.

For aortic dissection in the thoracoabdominal region, the Crawford classification is used for

a more detailed description.

Etiology. The main causes of dissection are degenerative aortic media lesion and

hypertension. It is believed that long-standing arterial hypertension can lead to

stratification itself in the absence of degenerative aortic disease, due to the occurrence of
mechanical and metabolic stresses in the aortic wall in response to a pulse wave.

The clinical picture of aortic dissection is characterized by an acute, almost

instantaneous onset of high blood pressure with the development of intense pain

syndrome, expressed so that outwardly, despite hypertension, the patient looks like being

in a collaptoid state (lethargy, gaze fixation, cold sticky sweat, weak peripheral ripple). The

causes of often persistent and severe hypertension are damage to the baro-receptors of

the aorta, the release of catecholamines, and in some cases, as a rule, with involvement in

the bundle of the left renal artery - activation of the renin-angiotensin system. A decrease

in blood pressure leads to the suspension of aortic dissection and a decrease in the

severity of pain syndrome with stabilization of the general condition, but then a wave-like

growth of this process is possible again and again. The causes of hypotension in aortic

dissection, in addition to compensatory mechanisms (vasoplegia due to shock,

redistribution of the BCC), can be heart tamponade, aortic regurgitation, aortic rupture,

coronary artery occlusion. Localization of pain depends on the place of the beginning of

the stratification. With the spread of the bundle, the source of the pain shifts and can reach

the lumbar region, in some cases the stratification is almost asymptomatic, and signs of

ischemia of other organs and systems may be the first symptoms of the

disease.Manifestations of ischemia of other organs are coronary insufficiency, stroke or

transient disorders of cerebral circulation, clinic mesenteric thrombosis, acute renal failure,

acute arterial impassability of the lower extremities. Aortic valve insufficiency is observed

in half of the patients, and in 55% it is pronounced.

Symptoms of chronic dissection and its complications (rupture) are determined by theType

1 - stratification begins in the ascending section, goes through the arc in the descending s

extensiveness of the dissection, the degree of involvement in the process of various parts

of the thoracic aorta. Clinical symptomatology in patients with chronic dissection is

primarily associated with an increase in aortic size.

The natural course of aortic dissection. In acute proximal stratification, mortality during the

first 24 and 48 hours is at least 33 and 50%, respectively, i.e. at least 1% of non-operated

patients die every hour. During the week, 80% die, and during the first month - 95% of

patients with acute proximal aortic dissection. Among patients with chronic proximal

bundles, after 5 years, 10–5% survive. In distal separations, 75% of patients remain alive
within a month.

Surgery.

The choice of the type of operation depends on the prevalence of the aneurysm, the

degree of involvement of the aortic root and aortic valve, comorbidity, the life expectancy

of the patient, the desired status of anticoagulant therapy. For correction of the pathology

of the ascending aorta, operations are performed to replace the aortic segment involved in

the aneurysm with a vascular prosthesis, and for aortic valve pathology, aortic valve

reimplantation or valve-containing conduit are performed.

In the reconstruction of the aortic arch, hypothermic (280C) antegrade cerebral perfusion

through the right subclavian artery and/or additional branches from the aortic artery is used

to protect the brain. Surgical correction of aortic arch aneurysms is most often performed

according to the “hemi arch” method.

Dissecting aneurysm of the thoracic aorta.

Dissecting aneurysm of the thoracic aorta is characterized by an intimal rupture and partial

redirection of blood flow from its natural lumen to a false one, located within the media

between intima and adventitia. A type A dissecting aneurysm is an absolute indication for

surgery. The state of aortic dissection is not a factor influencing the decision about surgical

treatment - in cases of thrombosis of the false lumen there remains the risk of fatal

complications and surgery is necessary. Currently, hybrid interventions are possible: the

ascending aorta and the arch are replaced with a vascular prosthesis if necessary the reimplantation
of the aortic valve is performed, and to reduce the morbidity of the operation

and close the false lumen of the descending thoracic aorta, stentgraft is used.

Aneurysms of the abdominal aorta

Aneurysms of the abdominal aorta (AAA) are in many ways similar to the aneurysmal

changes of the thoracic aorta (especially thoracoabdominal aneurysms, which are a direct

continuation of the enlarged part of the descending aorta), but also have certain

differences. According to the literature data, the frequency of abdominal aneurysms varies

within fairly wide limits, which is caused by the difference in approaches (population

screening, autopsy assessment). In general, abdominal aortic aneurysm is not the most

common disease of the arteries - according to various sources, it ranges from 0.6 to 7%,

and the incidence of the disease increases with age, but AAA occurs in individuals of any
age. However, despite the relatively low frequency, this pathology has a high proportion in

the structure of mortality, since it is characterized by high mortality with the development of

complications. The risk of developing complications of abdominal aortic aneurysm

increases with increasing diameter of the aneurysm. Assessment of the risk of

complications is the main criterion in determining indications for surgical treatment in

uncomplicated course.

The causes of the development of AAA are diverse: atherosclerosis, inflammatory

processes, infection, connective tissue pathology. Unlike thoracic aortic aneurysms, the

proportion of atherosclerotic aneurysms of the thoracic aorta is significantly higher. Until

now, there is no single concept for the development of aneurysms, which allows to explain

the pathogenesis of this disease. Depending on the underlying etiological causes,

pathogenetic changes in the aortic wall, leading to its dilatation, are inflammatory or

degenerative. However, these data were obtained at certain stages of change, while the

true dynamics of changes have not yet been completely studied. In the pathogenesis of

aneurysm development, genetic factors, high blood pressure, sex, and many other causes

and factors play a role.

There is no unified approach to the classification of abdominal aortic aneurysms, which

allows to systematically reflect the essence of the processes taking place. Therefore,

several approaches are used to classify AAA: etiological, pathogenetic, anatomical,

morphological, clinical, etc. The main classification approaches are listed below.

By etiology, AAA is divided into:

• congenital

• acquired

- Non-inflammatory (atherosclerotic, traumatic)

- Inflammatory (syphilitic, infectious, infectious-allergic)

- Posttraumatic / anastomotic.

According to morphological features;

• Bag-shaped.

• Spindly.

According to size:

• Small aneurysm (3-5 cm).

• Medium (5-7 cm).

• Large (over 7 cm).

• Giant (8-10 times the diameter of the infrarenal aorta)

Based on wall structure

• true

• false

According to the clinical course

• Asymptomatic.

• Painless course.

• Pain stage of the disease.

• Stage of complications:

- threatening gap;

- gap, breakthrough;

- stratification;

- non-coronary artery embolization.

By anatomical localization:

• Type I - infrarenal with adequate proximal and distal isthmus

• Type II - infrarenal with adequate proximal isthmus, extending to the aortic bifurcation

(IIa), with the involvement of the common (IIb) and the mouths of the internal iliac (IIc)

arteries

• ІІІ type - juxtarenal

• Type IV - supra-and infrarenal

Clinical picture

In case of uncomplicated abdominal aortic aneurysm, they may not manifest themselves

for a long time, therefore they are often found by chance when screening ultrasound of the

abdominal organs or when searching for a different pathology of the abdominal cavity and

retroperitoneal space. In some cases, patients (especially those with asthenic physique)

independently note the presence of a volume pulsating formation in the abdomen (usually

in the umbilical region) or this formation is detected on palpation of the abdomen by

medical personnel. Much less frequently, AAA is detected by indirect signs of an

abdominal mass formation (dislocation of the shadow of the intestinal loops during
radiography, constipation, etc.). During the physical examination, in addition to the most

pulsating volumetric formation of the umbilical region, a systolic murmur can be

auscultatorily detected above it. In juxtarenal and suprarenal aneurysms, symptoms

characteristic of an abdominal mass in the upper abdomen are possible: signs of

compression of the duodenum, stomach, bile ducts, disturbances in the kidney intestinal

perfusion (ie, abdominal ischemia syndromes). Pain syndrome for uncomplicated

abdominal aortic aneurysms, as a rule, is not typical. The appearance of pain in patients

with an established diagnosis of an aortic aneurysm most likely indicates a partial or

threatening rupture of the wall of the aneurysm.

Complicated AAA is characterized by symptom polymorphism. The most common

complication of AAA is its rupture. The clinic for rupture of the abdominal aortic aneurysm

largely depends on the location of the rupture and the conditions that provoked it

(increased blood pressure, physical exertion). The main clinical manifestations of the

rupture are associated with hematoma formation and tissue stratification, which causes

pain, and loss of BCC. Depending on the location of the gap and hematoma, the pain

syndrome may have a different character. Gaps in the back wall are sometimes

accompanied by moderately severe aching pain in the lumbar region, sometimes even

without falling of the BCC, since the dense tissues of the ligaments of the spine do not

allow the hematoma to spread widely. In such cases, it happens that the patient is

examined for pain for a long time and is operated on in a planned manner, when a rupture

is detected. If the aneurysm ruptures in the soft tissues, an extensive retroperitoneal

hematoma is formed with severe pain in the lumbar region, radicular pain, impaired

innervation of the lower extremities and blood supply, since the hematoma squeezes the

terminal part of the aorta. It often happens that such ruptures occur after lifting weights or

other physical activities, and since they are manifested by severe weakness, especially of

the lower extremities, this condition is mistakenly regarded as a vertebral hernia or an

attack of radiculitis. If the patient has a history of AAA, the complaints described should be

primarily attributed to aneurysm rupture. If there is no history of aneurysm in history, it is

necessary to evaluate the pulsation of the femoral arteries and the appearance of the

lower extremities (when aneurysm ruptures, as a rule, pale cyanotic, marble color,

pulsation is reduced). A rupture of the aneurysm on the front / side surface is usually
accompanied by sharp pain in the abdomen or lower back and the clinic of acute blood

loss. The most severe are tears in the free abdominal cavity or the lumen of a hollow

organ. In both cases, acute blood loss syndrome will prevail, due to the lack of conditions

for restricting hematoma. In case of rupture, there will be a pronounced acute pain

syndrome in the abdominal cavity, in the second case there will be practically no pain

syndrome, but there will be a clinic of acute gastrointestinal bleeding. Severely diagnosed

aneurysms are diagnosed and flow into the lumen of the inferior vena cava, accompanied

by a clinic of acute heart failure and volume overload of the right heart, as well as acute

venous insufficiency.

The stratification of isolated aneurysms of the abdominal aorta occurs relatively

infrequently (more typical for thoracoabdominal aneurysms). In general, ultrasound signs

of delamination, i.e. double contour in the vessel lumen occurs with great frequency.

However, this phenomenon is not caused by intimal detachment, but by the presence of a

thrombotic bowl that performs the cavity of the aneurysm, leaving the central lumen, which

can be shifted from the axis of the vessel, which creates the impression of separation.

True AAA dissection occurs rarely and is characterized by pain in the lumbar region and

the clinic of ischemia of the lower extremities and pelvic organs.

The presence in the aneurysm of the thrombotic bowl can cause non-cardiogenic

thromboembolism of the arteries of the lower extremities with the development of the clinic

of acute ischemia of one or both limbs. Sometimes episodes of noncardiogenic embolism

serve as the first manifestation of aneurysm. Migration of a large segment of the

thrombotic bowl or its complete displacement can lead to aortic thrombosis, i.e. complete

blockage of the lumen. With acutely developed aortic thrombosis, the clinic of acute

ischemia of both lower limbs, pelvic organs in combination with acute heart failure prevails.

Diagnostics

In addition to the described clinical manifestations, the examination of patients with

abdominal aortic aneurysms requires the use of imaging techniques. Ultrasound allows

you to extract AAA, evaluate its lumen and permeability, measure the diameter of the

aneurysm, determine the location relative to the renal arteries, in some cases to identify

the hematoma around the aneurysm (extensive). Being an excellent screening technology,

ultrasound is not able to provide answers to all the questions necessary for planning an
intervention. More reliable information is provided by CT with contrast and MRI (Fig. 6): the

interposition of the aneurysm and neighboring structures, hematoma and its

communication with the lumen, contrast flow, structure, shape and size of the aneurysm,

lumen, intima condition. Ideally, the survey should be performed under MSCT conditions.

Angiography of the aorta and arteries of the lower extremities is somewhat inferior in terms

of the effectiveness of MSCT, but it provides a spatial representation of the lesions of the

vascular bed, which is useful for planning an intervention. The disadvantages of

angiography should not include a clear estimate of the size of aneurysms, since only their

lumen contrasts, and the outer diameter can be estimated with a calcified aortic wall or in

the absence of a thrombotic bowl.

Treatment

The main method of treatment of aortic aneurysms is surgical. In an uncomplicated

course, the main criteria for determining indications for surgical treatment are the size and

shape of the aneurysms and the growth rate. The presence of a bag-shaped aneurysm

serves as an independent indication for surgical treatment, since the risk of rupture of baglike
aneurysms is quite large. With a spindle-shaped aneurysm, indications for planned

surgical treatment will be “medium” and “large” aneurysms (d> 5 cm), since upon reaching

such a diameter, the risk of aneurysm rupture during the year is 5-10%, which exceeds the

risk of surgery (2-3 %). A separate indication for the planned treatment of asymptomatic

aneurysms is an increase in diameter of more than 0.5 cm in 6 months (rapid growth is

usually characteristic of inflammatory aneurysms).

Drug therapy for aneurysms is aimed at reducing the risk of rupture and slowing the

growth of the aneurysm. Depending on the etiology, therapy may include antibacterial

drugs, statins, anti-inflammatory drugs. A mandatory treatment point is the correction of

blood pressure in patients with hypertension, preferably with the use of β-blockers as a

component of therapy (reduce the risk of rupture). But it should be remembered that

therapeutic agents are only ancillary. Patients require regular screening for timely

determination of indications for surgical treatment.

In case of complicated course (rupture, separation, thrombosis), surgical treatment is

necessary for health reasons. Without surgical treatment, mortality for complications of

aortic aneurysms reaches 100%. In the surgical treatment of patients with aneurysm
rupture, mortality reaches 25-75%. Such high rates of mortality and severity of the

postoperative period require, if possible, to purposefully select patients for planned

surgical treatment.

The principal task of surgical intervention for abdominal aortic aneurysms is to turn off the

enlarged portion of the aorta with a thinned wall of blood flow with the formation of a safe

path to the blood supply to the distal bed.

The main methods of surgical treatment of AAA at the moment are resection of the

aneurysm with prosthetics and staging of the stentgraft. In exceptional cases, aortic

ligation is possible against the background of a rupture, however, the mortality rate for

such operations exceeds 90% and at the moment they are practically not performed.

Each of the methods of surgical treatment has its own advantages and disadvantages.

Open resection of the aneurysm with prosthetics is a severe abdominal surgery,

accompanied by severe blood loss, a relatively high incidence of complications, but leaves

ample opportunities for surgical maneuver in case of irregular anatomy, involvement of the

renal arteries, occlusion of the distal channel segments, the need to preserve the lower

mesenteric artery, etc. The operation can be performed in the form of a linear prosthesis

resection of the aortic area, bifurcation prosthetics with the launch of blood flow to the iliac

arteries or femoral, as well as extranatomical shunting of the aortic area off (from the

subclavian artery) with a compromised neck of the aneurysm. Although the immediate

postoperative period during resection of the aneurysm is accompanied by a relatively high

risk of complications, but the distant complications almost does not have. Endovascular

shutdown of the aneurysm with a stent graft implies the performance of the lumen of the

aorta with a stent covered with an impermeable tissue material. This intervention is less

traumatic, however, it requires precise observance of anatomical conditions, individual

graft selection, as well as lifelong observation and control using CT and angiography to

eliminate complications in the long-term period (primarily endolics).

Occlusive-stenotic lesions of the terminal aorta

Occlusive-stenotic lesion of the terminal aorta is a special case of occlusive-stenotic

lesions of the arteries of the lower extremities and, as a rule, is considered as one of the

variants of Leriche syndrome with appropriate clinical symptoms. Separate classification

approaches in this case do not apply. However, there are fundamentally important points
that require separate instructions. First, it is the prognostically more severe character of

the lesion than in the case of even both common iliac arteries, since collaterals along the

lumbar arteries are turned off, which is especially important in acute thrombosis. Mortality

in acute aortic thrombosis is very high. Secondly, chronic occlusion of the terminal part of a

large vessel such as the aorta leads to a significant increase in total peripheral resistance

and the development of heart failure. Therefore, occlusion of the terminal aorta is an

independent indication for surgical treatment, even with a low degree of chronic arterial

insufficiency. And thirdly, endovascular reconstruction with occlusive lesion of the terminal

aortic region is not indicated. Fourthly, when planning surgery, the question clearly arises

as to the need for aortic clamping, which requires an assessment of the function and

reserve of the myocardium, invasive blood pressure monitoring during the operation, as

well as an assessment of the brachiocephalic vessels.

The remaining therapeutic and diagnostic approaches are similar to those used in patients

with occlusive-stenotic lesions of the peripheral bed.

27. Coarctation of the aorta: clinical features, diagnosis, differential diagnosis,

treatment, principles;

Coarctation of the aorta (CA) is a congenital segmental narrowing of the aorta in the area

of the arc, isthmus, lower thoracic or abdominal regions.In most cases in infants,

coarctation is located on the site from the left subclavian artery to the open arterial duct or

immediately after it, called the aortic isthmus.In the fetus and newborn, the aorta isthmus

region is normally narrowed, since during the prenatal period only one third of the blood

volume flows through the descending aorta, the other two thirds pass through the

PDA. Soon after the closure of the PDA, all the blood begins to pass through the isthmus,

it gradually expands and almost reaches the diameter of the descending aorta. In the

presence of pathology, the isthmus region remains narrowed in one or another area. The

constriction may take the form of a constriction (then a membrane with a small opening is

found inside the vessel, but there may be a complete break in the aortic arch) or a tubular

constriction for some distance. In relation to the PDA, aortic coarctation is subdivided as

follows:

1. Narrowing proximal to the site of PDA discharge - preductal coarctation of the aorta;

2. Narrowing at the level of the PDA discharge - juxtaductal coarctation of the aorta;
3. Narrowing distal to the PDA discharge - post-ductal aortic coarctation.

Hemodynamics significantly depends on the type and location of coarctation, the degree of

narrowing, as well as the presence of concomitant CHD. With an isolated spacecraft in the

large circle of blood circulation, two modes of blood circulation are established: proximal

(arterial hypertension) and distal (arterial hypotension and lack of blood flow) of the

narrowing site.

In case of post-ductal coarctation in the case of intrauterine formation of collateral

circulation, the flow of the defect is less severe. Collateral blood flow occurs through the

subclavian, intercostal, internal thoracic, scapular, epigastric, and vertebral arteries, which

over time expand due to increased pressure in them. With inadequate development of

collaterals, blood pressure rises significantly to the site of constriction and blood under

pressure is discharged from the aorta through the PDA into the pulmonary artery. The

amount of discharge depends on the gradient between the aorta and the pulmonary artery

and, as a rule, is significant. In response to the arrival of a large additional blood volume in

the vessels of the pulmonary circulation, pulmonary hypervolemia and hypertension are

developed.

In case of pre-ductal coarctation of the aorta, the direction of blood shunting will depend on

the pressure ratio in the descending aorta and the pulmonary artery. When the degree of

narrowing is pronounced, venous arterial blood shunt is noted, which leads to the

appearance of differentiated cyanosis (there is on the legs, but not on the arms).

When CA is combined with other CHDs, in particular, with VSD, the value of arterio-venous

discharge is very large, and pulmonary hypertension develops faster.The result of longterm
hemodynamic stress is the development of left ventricular fibroelastosis of the

endomyocardium, always accompanied by cardiomegaly, a fall in cardiac output, severe

signs of left ventricular hypertrophy and left atrium refractory to treatment of heart

failure.With postductal CA localization, the clinical picture develops quite quickly - in the

first weeks of life. For children, marked anxiety, shortness of breath, difficulty in feeding,

the development of malnutrition are characteristic. Pale skin, with an ashy tint (especially

during anxiety attacks). The legs in children are always cold to the touch due to a lack of

peripheral blood flow. Chest deformity of the “heart-hump” type may develop. In the lungs,

congestive crepitus are heard, and pneumonia is possible. Cardiac impulse strengthened,
spilled. Borders of the heart are extended left and right, with fibroelastosis -

significantly. When auscultation is always marked tachycardia, sometimes - canter

rhythm. The noise picture is nonspecific - most often systolic or systolic-diastolic PDA

noise is heard. Medium or low intensity systolic murmur in the interscapular region can be

heard. The most specific clinical symptom, by the presence of which coarctation can be

suspected, is a decrease in pulsation in the femoral artery. When measuring systolic blood

pressure there is a significant increase in the upper half of the body. Other clinical signs

may be symptoms of circulatory failure, usually total in young patients.

In case of pre-octal coarctation, along with the above-mentioned symptoms, the presence

of differentiated cyanosis, more pronounced on the legs, is characteristic.

In older children, the clinical picture is significantly different from that in nursing

patients. As a rule, children develop normally. Defect is detected by chance (more often at

school age) when high blood pressure is detected. Characteristic is the appearance of

such children with a developed upper half of the body and an asthenic physique of the

lower half of the body.

At the stage of primary adaptation, a high mortality rate of children due to severe heart

failure and the accession of pneumonia is noted. In the future, the condition of the patients

is stabilized (due to the development of collateral circulation and myocardial hypertrophy,

the closure of the PDA) and they live, on average, to 30-35 years. The main complications

in adults are exfoliating aneurysm and aortic rupture, severe strokes and infective

endocarditis.

Surgical correction consists of excision of the site of aortic narrowing and joining of

the cut ends “end to end”, “side to side”, “end to side”, or subsequent ismoplasty. In

children with coarctation according to the type of internal membrane, balloon angioplasty

surgery can be used.

Blood vessels

28. The etiology and pathogenesis of arterial occlusive diseases, Classification;

Occlusive peripheral arterial disease is blockage or narrowing of an artery in the legs (or

rarely the arms), usually due to atherosclerosis and resulting in decreased blood flow.

Symptoms depend on which artery is blocked and how severe the blockage is.

To make a diagnosis, doctors measure blood flow to affected areas.

Drugs, angioplasty, or surgery is used to relieve the blockage and reduce symptoms.

Occlusive peripheral arterial disease is common among older people because it often

results from

• atherosclerosis (plaque or disease buildup in the wall of the blood vessel), which

becomes more common with aging.)

When people suddenly develop a painful, cool, and pale arm or leg, they should seek

medical care immediately.

• Turbulent Blood Flow

Bypass surgery may be done to treat arteries that are narrowed or blocked. In this

procedure, blood is rerouted around the affected artery—for example, around part of the

femoral artery in the thigh or part of the popliteal artery in the knee. A graft consisting of a

tube made of a synthetic material or part of a vein from another part of the body is joined

to the blocked artery above and below the blockage.

29. Chronic limb ischemia. Classification, clinical picture, diagnosis, differential

diagnosis;

30. Chronic limb ischemia treatment. Indications for surgical treatment, types of

operations;

Chronic limb ischaemia is peripheral arterial disease that results in a symptomatic reduced

blood supply to the limbs.It is typically caused by atherosclerosis (rarely vasculitis) and will

commonly affect the lower limbs (however the upper limbs and gluteals can also be

affected).Around 15-20% individuals over 70yrs have peripheral arterial disease.

The Framingham study demonstrated an increase in the prevalence of the disease from

0.4 per 1000 males aged 35-45yrs to 6 per 1000 males aged >65yrs.

Risk Factors

• Smoking

• Diabetes mellitus

• Hypertension

• Hyperlipidaemia

• Increasing age

• Family history

• Obesity and physical inactivity

Clinical Features

The clinical features of chronic limb ischaemia depend on its severity, as shown in Table 1.

One of the earlier symptoms is intermittent claudication, a cramping-type pain in the calf,

thigh, or buttock after walking a fixed distance (the ‘claudication distance’), relieved by rest

within minutes.

Table 1 – Fontaine classification of chronic leg ischaemia

Buerger’s test involves lying the patient supine and raising their legs until they go pale and

then lowering them until the colour returns (or even becoming hyperaemic). The angle at

which limb goes pale is termed Buerger’s angle; an angle of less than 20

degrees indicates severe ischaemia.

Critical Limb Ischaemia

Critical limb ischaemia is the advanced form of chronic limb ischaemia.

It can be clinically defined in three ways:

• Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia

• Presence of ischaemic lesions or gangrene objectively attributable to the arterial

occlusive disease

Stage I Asymptomatic

Stage II Intermittent claudication

Stage III Ischaemic rest pain

Stage IV Ulceration or gangrene, or both

• ABPI less than 0.5

On examination, the limbs may be pale and cold, with weak or absent pulses.Other signs

include limb hair loss, skin changes (atrophic skin, ulceration, or gangrene), and thickened

nails.

Differential Diagnoses

There are two major differential diagnoses* for a patient presenting with limb ischaemia

symptoms:

• Spinal stenosis (‘neurogenic claudication’)

• Typically have pain from the back radiating down the lateral aspect of the leg

(tensor fascia lata), often have symptoms on initial movement or symptoms

that are relieved by sitting rather than standing

• Acute limb ischaemia

• Clinical features that are less than 14 days duration, often presenting within

hours.

*Acute-on-chronic ischaemia is a more complex condition whereby there is an acute often

embolic event in a patient with previous peripheral arterial disease. These patients are

sub-classified as they typically have a longer duration in which the limb is salvageable.

Investigations

The diagnosis of chronic limb ischaemia is clinical. The ankle-brachial pressure

index (ABPI, Fig. 2) is used to confirm the diagnosis and quantify severity of chronic limb

ischaemia:

Any ABPI value >1.2 should be interpreted with caution, as calcification and hardening of

the arteries may cause a falsely high ABPI.

Any critical limb ischaemia should be investigated initially with a Doppler ultrasound, used

to assess the severity and anatomical location of any occlusion. Further imaging can be

achieved via CT angiography or MR angiography (MRA).

Due to concurrent cardiovascular risk factors seen in patients with chronic limb ischaemia,

patients should also have a cardiovascular risk assessment. This includes blood pressure,

blood glucose, lipid profile and ECG.

In addition, any patient presenting with chronic limb ischaemia <50yrs without significant

risk factors should also have a thrombophilia screen and homocysteine levels* checked.

Severity ABPI

Normal >0.9

Mild 0.8-0.9

Moderate 0.5-0.8

Severe <0.5

*A lower homocysteine level has been associated with reduced risk of cardiovascular

events

The ankle-brachial pressure index (ABPI); a value of less than 0.9 indicates a reduce

blood supply to the lower limbs

Management

1. Medical Management
Most patients with chronic limb ischaemia require cardiovascular risk factor modification:

• Lifestyle advice (smoking cessation, regular exercise, weight reduction)

• Statin therapy (ideally atorvastatin 80mg OD)

• Anti-platelet therapy (ideally clopidogrel 75mg OD)

• Optimise diabetes control

Enrollment into a local supervised exercise programme has been shown to improve

walking distance and claudication distance, and should be used as first line therapy in any

patient without critical limb ischaemia

The course of chronic limb ischaemia is variable and many patients’ symptoms do improve

on lifestyle changes and medical management alone.

2. Surgical Management

NICE guidance states that surgical intervention can be offered in suitable patients if (i) risk

factor modification has been discussed; and (ii) supervised exercise has failed to improve

symptoms.

Any patients with critical limb ischaemia should be urgently referred for surgical

intervention.

There are two main surgical options available:

• Angioplasty with or without stenting (Fig. 3)

• Bypass grafting, typically used for diffuse disease or in younger patients

• A combination such as surgery to clean a specific lesion allowing access for

angioplasty to another region

Amputations are considered for any patients who are unsuitable for revascularisation with

ischaemia causing incurable symptoms or gangrene leading to sepsis.

Complications

Chronic limb ischaemia can result in sepsis (secondary to infected gangrene), acute-onchronic
ischaemia, amputation*, and reduced mobility and quality of life.

*Amputation is eventually required in 1-2% (increases to 5% in people with diabetes)

Over a 5 year period, of those patients with intermittent claudication:

• Most will have stable claudication

• 10-20% develop worsening symptoms

• 5-10% develop critical limb ischaemia

Two years following a below-knee amputation for chronic limb ischaemia, 15% require a

further above knee amputation, 30% have died, and only 40% have full mobility.

The 5 year mortality rate in those diagnosed with chronic limb ischaemia is around 50%

31. Chronic and acute disorders of visceral blood flow. Classification, clinical

picture, diagnosis, differential diagnosis, indications for surgery, types of

operations;

For the first time at autopsy, he revealed and described the asymptomatic occlusion of the

superior mesenteric artery Tiedeman in 1843. Until recently, the incidence of this disease

has not been studied. According to the literature, the frequency of damage to the superior

mesenteric artery is 30–40%, and the celiac trunk is 20–40%. The following forms of

abdominal ischemia are distinguished: acute and chronic.

The cornerstone in emergency departments is the diagnosis and treatment of acute

disorders of mesenteric circulation. This pathology is characterized by high numbers of

mortality, disability of patients. The main cause of acute abdominal ischemia is mesenteric

thromboembolism, due to the presence of a concomitant pathology in the patient. Surgical

treatment of mesothrombosis is the resection of a section of the necrotic intestine. Fogarty

thrombectomy from the main vessels of the mesentery is usually not advisable due to the

low tolerance of the intestine to ischemia. In most cases, patients with mesothrombosis

enter the operating table when irreversible changes in the intestinal wall have already

occurred.

Differential diagnosis of acute violation of mesenteric circulation must be carried out with

all diseases of the "acute abdomen" group.

Chronic disorders of visceral circulation is a disease characterized by ischemic circulatory

disorders of the abdominal cavity caused by impaired visceral artery patency due to extra -

or intravasal causes (A. V. Pokrovsky, 1979). Since the disease manifests itself in

abdominal pain during the maximum activity of the digestive organs in the literature, this

condition is also known as "abdominal toad." The mechanism of pain is identical to angina

pectoris. It is caused by a violation of the ow of oxygenated blood to an actively functioning

organ due to impaired blood ow through the arteries. Extravascular and intravascular

causes lead to circulatory disorders in the abdominal organs. Extravascular causes include

compression of the mesenteric arteries with the crescent ligament of the diaphragm, nerve
ganglia of the solar plexus, medial leg of the diaphragm, tumors. In this case, the celiac

trunk is most often subjected to extravascular compression. The main causes of

intravascular compression is atherosclerosis in the mesenteric vessels, or aorto-arteritis.

At the beginning of the development of the disease, ischemic changes are compensated

by the developed system of collateral organs of the abdominal cavity. Ischemic disorders

in the digestive tract are manifested in incomplete digestion of foods, especially fats. For a

long time, existing ischemia of the intestinal muscle layer is manifested in impaired motor

function, which is clinically manifested by flatulence and constipation. Chronic ischemia of

the abdominal organs is characterized by a triad of symptoms: 1) acute, paroxysmal pain

that occurs some time after a meal 2) impaired intestinal functions, which are expressed in

malabsorption and maldigestion syndromes; 3) progressive weight loss.

The following forms of chronic abdominal ischemia are distinguished: compensated,

subcompensated, decompensated.

The compensated stage is characterized by a slight change in the function of the

gastrointestinal tract, which is manifested by pain. Pain, as a rule, is caused by occlusalstenotic lesion
of the branches of the celiac trunk. It occurs after eating a large volume of

food regardless of its quality (“small portions” syndrome). Also, a pain attack can provoke

prolonged walking or mental stress. The pain is usually localized in the epigastrium. The

attack lasts from several minutes to 1.5 to 3 hours. As a diagnostic criterion, a test with

nitroglycerin can be used. The meaning of which is that when taking nitroglycerin, the pain

syndrome stops.

In the stage of subcompensation, chronic abdominal ischemia is manifested by belching,

vomiting, nausea. Bloating is also characteristic. With occlusal-stenotic lesion of the

inferior mesenteric artery, patients are concerned about constipation, which is due to

hypoperfusion of the terminal intestine. In cases of localization of the pathological process

in the region of the superior mesenteric artery, patients are disturbed by episodic attacks of

diarrhea, unstable stool, which leads to a progressive decrease in body weight. The longterm
symptoms described above lead to the development of astheno-hypochondria

depressive syndrome in patients.

With the development of the decompensated stage of chronic abdominal ischemia, the

patient develops prolonged diarrhea or constipation, which leads to dehydration and

progressive depletion.
In the diagnosis of chronic ischemia of the abdominal organs, an important role is given to

a thorough collection of anamnesis and complaints. When interviewed, patients indicate

the inefficiency of conservative therapy. The use of laboratory diagnostic methods allows

to identify violations of the digestive tract.

If the patient has the entire previously listed symptom complex, the absence of the clinical

effect of conservative treatment, the patient is shown to perform an X-ray contrast study

(angiography) of visceral vessels.

An ultrasound scan of the abdominal organs with duplex angioscanning can also be used

to diagnose chronic ischemia of the abdominal organs.

It is necessary to carry out differential diagnosis of chronic abdominal ischemia with

extravascular compression of blood vessels with tumors of the stomach, hepatobiliary

zone, pancreas, chronic pancreatitis, peptic ulcer, abdominal aortic aneurysm.

Surgical treatment in the rst stage of the disease is not advisable. The most justified is

conservative therapy. Indications for surgical treatment in the stage of sub compensation

and decompensation are set individually, taking into account the severity of the disease

and associated pathology.

Surgical treatment of disorders in the pathways of blood ow to the organs of the abdominal

cavity is carried out in specialized surgical departments. Obstruction of blood ow due to

occlusion-stenotic lesions of the vascular bed are corrected by performing various types of

vascular reconstructions. Surgical access when performing reconstructive interventions on

the celiac trunk and superior mesenteric artery is carried out from the left

thoracophrenolumbotomy in 9 intercostal spaces. To perform decompression of the celiac

trunk and reconstruction of the inferior mesenteric artery, it is most advisable to use

laparotomy. In cases of extravascular compression of the celiac trunk, the medial leg of the

diaphragm is intersected, the median fibrous ligament of the diaphragm is dissected, and

the nerve ganglia of the solar plexus are resected.

With the development of endovascular technologies in clinical practice, balloon dilatation

and stenting of visceral arteries are increasingly being used. The use of these methods of

treatment is more promising in terms of reducing surgical trauma, but they require further

study of the long-term results of treatment.

32. Renovascular hypertension: etiology, and pathogenesis, clinical manifestations,

diagnosis, differential diagnosis, indications for surgery, types of operations;

A form of secondary arterial hypertension due to occlusal-stenotic lesion of the renal

arteries. Renal artery stenosis (SPA) not only leads to the development of vaso-renal

hypertension, but can also cause renal failure, heart failure with pulmonary edema, and

unstable angina pectoris.

The causes of stenotic lesions of the renal arteries can be both congenital and acquired,

the latter are much more common.

Congenital malformations include:

• Fibromuscular dysplasia (SH as the cause 14-25%)

• Hypoplasia renal arteries

• Atresia of renal arteries

• Aneurysms of the renal arteries

• Arteriovenous fistula

The group of acquired diseases includes:

• Atherosclerotic renal artery (as the reason SH 60-83%)

• Nonspecic aortoarteritis (as SH to cause 10%)

• Thrombosis and renal artery embolism

• Extravascular renal vascular compression of various genesis (tumor, scar tissue, etc.).

• Traumatic injuries

There are several clinical signs indicating a high risk of SPA; if they are present, this

pathology is much more common than in the general population:

• Noise in the abdominal aorta (systolic or diastolic);

• Development of hypertension at the age of younger than 20 or older than 55 years;

• Malignant hypertension;

• Refractory or difficult to control hypertension;

• Azotemia in patients receiving angiotensin converting enzyme (ACE) inhibitors;

• Atrophy of the kidney;

• Hypertension and concomitant atherosclerosis;

• renal failure in old age.

In the natural course of SPA, a gradual occlusion of the renal artery occurs over time, loss

of kidney mass and weakening of its function. The rate of progression of SPA, according to
angiographic studies, varies from 39% to 49%. With the most severe stenosis, complete

occlusion develops in 16% of patients.

In a prospective study on the medical treatment of SPA, progression was noted in 42% of

patients (11% developed occlusion). It should be noted that the progression of SPA and

the loss of renal function do not correlate with the possibility of drug control of

hypertension.

Atherosclerotic stenosis of the renal artery, the most common cause of secondary

hypertension, is found in less than 5% of the total hypertensive population, but at the same

time, atherosclerosis, fibromuscular dysplasia and nonspecic aortoarteritis account for

95% of all renal artery lesions.

Vasorenal hypertension is the cause of malignant hypertension in 10 to 45% of patients. In

people older than 50 years, in 5-15% of cases, this leads to renal failure and the need for

dialysis. As a Swedish study showed, in patients with renal artery stenosis more than 50%,

the overall risk of death is 3.3 times higher than in the general population (with equal age

groups), and the risk of death from cardiovascular disease is 5.7 times above.

Stenotic lesions of the renal arteries represent a significant public health problem not only

in the Republic of Belarus but also in foreign countries. So, according to rough estimates,

in the Russian Federation the number of patients with vasorenal hypertension is about 1.5

million people, in the USA, according to 1977, about 1 million people suffered from this

pathology. A number of studies have shown that atherosclerotic lesions of the renal

arteries increase not only cardiovascular, but also overall mortality.

Indications for surgical treatment:

· Refractory hypertension

· Hemodynamically signicant stenosis ( > 75%) of the renal artery

· The development of symptoms of renal failure

Currently, balloon dilatation and stenting of the renal arteries is the operation of choice in

the presence of veried hemodynamically signicant renal artery stenosis with a decrease in

the nitrogen-excreting function of the kidneys. Open surgical procedures are practically not

used due to their great trauma.

33. Clinical and instrumental diagnosis of artherosclerotic vascular lesions.

Differential diagnosis;
Atherosclerosis obliterans- a systemic, chronic, slowly progressing, incurable disease,

which is accompanied by deep changes in the arterial wall and impaired patency due to

the growth of atherosclerotic plaque. The main reason for the development of occlusalstenotic
lesions of the arterial bed is atherosclerosis. The development of atherosclerotic

plaques, as a rule, occurs in the arteries of large and medium caliber elastic and muscle

type. It should be remembered that atherosclerosis is a systemic disease that affects the

entire arterial bed of a person, but manifests the disease in one of the most affected

vascular pools. The degree of atherosclerotic lesion of the vascular bed increases with

age. According to scientific studies, atherosclerotic plaques in the vessels begin to form

even in childhood, however, the clinical manifestations of the disease appear mainly in

adulthood. This phenomenon is due to the high adaptive potential of the human vascular

bed. So hemodynamically significant stenosis is considered to be a narrowing of the lumen

of the artery of at least 75% of its diameter. The growth rate of atherosclerotic plaque

depends on many factors, the main of which are smoking, low level of physical activity and

improper eating behavior. In the majority of modern international recommendations for the

treatment of occlusal- stenotic lesions of the vascular bed, the modification of the above

risk factors plays a huge role with a high level of evidence. So hemodynamically significant

stenosis is considered to be a narrowing of the lumen of the artery of at least 75% of its

diameter. The growth rate of atherosclerotic plaque depends on many factors, the main of

which are smoking, low level of physical activity and improper eating behavior. In the

majority of modern international recommendations for the treatment of occlusal- stenotic

lesions of the vascular bed, the modification of the above risk factors plays a huge role

with a high level of evidence. So hemodynamically significant stenosis is

considered to be a narrowing of the lumen of the artery of at least 75% of its diameter. The

growth rate of atherosclerotic plaque depends on many factors, the main of which are

smoking, low level of physical activity and improper eating behavior. In the majority of

modern international recommendations for the treatment of occlusal- stenotic lesions of

the vascular bed, the modification of the above risk factors plays a huge role with a high

level of evidence.

Based on the definition of a WHO expert committee, atherosclerosis is a “variable

combination of changes in intima and media of arteries, consisting of focal accumulation of

lipids, complex carbohydrates, fibrous tissue, salt deposits and blood fragments” [4].

With the development of atherosclerosis in the arteries, a specific proliferation of intima

(accumulation of lipids and smooth muscle cells) occurs in combination with lipid infiltration

and the accumulation of blood elements in an atherosclerotic plaque. Gradually, the wall of

the artery loses its elasticity and becomes like a “bamboo stick”. The disease proceeds for

a long time and imperceptibly, leading to a gradual narrowing of the lumen of the vessel

and impaired blood ow in the organ. Gradually, the development of atherosclerotic plaque

leads to vascular thrombosis. The development mechanism, which is explained by the

Virchow triad: slowing blood ow (due to the presence of a hemodynamically significant

atherosclerotic plaque protruding into the lumen of the artery), damage to the endothelium

(due to destruction of the fibrous capsule of the plaque), a change in the rheological

properties of blood (hypercoagulation).

34. Occlusive diseases: etiology, pathogenesis, pathological anatomy, conservative

treatment;

Nonspecic aortoarteritis is a granulomatous inflammatory disease characterized by a

narrowing of the lumen of the medium and large arteries with a primary lesion of the aorta

and its branches. This pathology is more characteristic of young and middle-aged women

in Asian countries. Frequency of occurrence from 1.2 to 2.6 people per one million of the

population. In 1908, at the XII annual meeting of the Japanese Society of

Ophthalmologists, Dr. Mikito Takiyasu described specific ring-shaped anastomoses in the

vessels of the retina, and Dr. Onisi and Kagoshima at the same meeting reported similar

findings in patients with a pulseless wrist.

The etiology of the disease is still unknown. It is believed that there is a certain genetic

predisposition in people with histocompatibility antigens HLA - B 5, HLA - A 10, HLA - BW

52, HLA - DR 2. In the pathogenesis of the disease, the leading role is played by the

immunological theory.

In Takayasu's disease, the development of the inflammatory process begins in adventitia

( vasavasorum ) and the outer layers of copper on the walls of large and medium arteries.

Inflammatory copper infiltration occurs predominantly by T and B lymphocytes with the

formation of granulomas. In the future, fibrosis of granulomas occurs, sclerosis and tears

of copper, and endothelial hyperproliferation. All this pathological cascade leads to a

narrowing of the lumen of the vessel and the formation of conditions for the development

of a blood clot.

There are 4 anatomical types of disease:

· I type - an isolated lesion of the aortic arch and arteries extending from it, usually

a combination of pathology of the left subclavian and left common carotid artery is noted;

· Type II - an isolated lesion of the thoracic or abdominal aorta and its branches;

· III type - a combined lesion of the aortic arch and its branches with changes in the

thoracic or abdominal aorta;

· IV type - the pulmonary artery, its branches are involved, while a combination with

the I, II or III option is possible.

Most often with non-specific aortoarteritis, subclavian arteries are affected (90%), common

carotid arteries (60%), abdominal aorta (60%), aortic arch (40%). For diagnosis,

ultrasound scan can be used - arteries, CT - angiography, MR - angiography, positron

emission tomography with 18 F-uorodeoxyglucose and contrast angiography, which is the

gold standard for diagnosing Takayasu disease. During angiography, it is determined that

the lesion is localized mainly in the places where the aortic branches discharge, the lumen

of the artery is not uniform and the stenosis sections alternate with the areas of the

unaffected artery. The treatment is mostly conservative using glucocorticosteroids and

cytostatics. Surgical treatment of nonspecific aortoarteritis is indicated only during the first

ve years from the onset of the disease, in an inactive stage and with the development of

stenosis of the main arteries more than 70%. However, it should be remembered that

angiosurgical reconstructions in this case have a limited service life due to intraoperative

trauma to the artery, which leads to the activation of processes of intimal hyperproliferation

with the subsequent development of stenosis or occlusion of anastomoses. For the same

reason, it is imperative to be extremely selective in setting indications for endovascular

methods of treatment.

Obliterating endarteritis is a vascular disease of neurohumoral genesis with a primary

lesion of small and medium caliber arteries of the distal lower extremities. Obliterating

endarteritis takes the second place after obliterating atherosclerosis in the frequency of

damage to peripheral arteries. It affects mainly men aged 30-40 years.

The ratio of men to women is 99: 1.

There are many reasons that lead to the development of obliterating endarteritis. The role

of the trigger mechanism in this disease is played by factors that cause a prolonged

spastic state of peripheral vessels: previous hypothermia or prolonged repeated cooling

(chills) of the lower extremities (men who are fond of winter fishing, drivers, builders),

smoking (vasoconstrictive action of nicotine), impaired innervation (chronic neuritis of the

sciatic nerve, injuries of limbs), some chronic intoxications (e.g. lead). An important role in

the development of obliterating endarteritis has a chronic overstrain of the nervous system

and, first of all, its central departments, because activation of the sympathetic nervous

system leads to prolonged vascular spasms. The autonomic nervous system dysfunction

that develops at the same time is also important, which leads to disorganization of

endocrine activity and a violation of the hormonal function of the sex glands and adrenal

glands. An increase in the incidence was observed during the period of world warriors,

which indirectly indicates the presence of a neuropsychic component in the development

of this pathology.

Pathogenesis obliterating endarteritis is quite interesting. In a simplified form, it can be

represented as follows: first, a long spasm of small and medium caliber vessels develops

against the background of triggering of trigger mechanisms, which subsequently leads to

the development of metabolic acidosis due to tissue hypoperfusion and the accumulation

of free radicals. The destruction of cell membranes and the release of inflammatory

mediators: serotonin, gestamine, kinin, which leads to increased pain impulse and a

number of humoral changes that contribute to thrombosis. On the other hand, as a result

of compression of vasa vasorum by spasmodic muscles of the vessel, blood supply to the

vascular wall suffers, which leads to a violation of its trophism and the development of

degenerative changes in it. Endotheliocytes die, and blood clots also form in parts of the

vessel devoid of endothelium. The pathological process extends not only to the great

vessels, but also to the collateral ones. The defeat of the collateral bed can occur

simultaneously or somewhat later compared to the main. At the beginning of the disease,

collateral circulation is not enough only during exercise of the limb. With the progression of

the pathological process, absolute insufficiency of collateral circulation develops, which

leads to the appearance of severe pains not only when walking, but also at rest,

intensifying in the horizontal position of the limb. At the beginning of the disease, collateral
circulation is not enough only during exercise of the limb. With the progression of the

pathological process, absolute insufficiency of collateral circulation develops, which leads

to the appearance of severe pains not only when walking, but also at rest, intensifying in

the horizontal position of the limb. At the beginning of the disease, collateral circulation is

not enough only during exercise of the limb. With the progression of the pathological

process, absolute insufficiency of collateral circulation develops, which leads to the

appearance of severe pains not only when walking, but also at rest, intensifying in the

horizontal position of the limb.

During obliterating endarteritis, the following stages are distinguished: ischemic, trophic

disorders, ulcerative necrotic, gangrenous.

At the initial stages of the disease, the treatment is conservative with the obligatory

modification of risk factors (bathing, hypothermia, psycho-emotional overload). When

choosing surgical treatment, the most pathogenetically substantiated seems to be the

performance of lumbar sympathectomy. Removal of 1-3 sympathetic ganglia on the

affected side is accompanied by persistent peripheral vasodilation, especially at the onset

of the disease against the background of conservative therapy. The use of

glucocorticosteroid hormones and cytostatics is considered not entirely justified due to the

prevalence in the pathogenesis of the vasospastic component, and not hyperproliferative.

Musculoskeletal dysplasia is a pathology of the arteries that results in the degeneration

of the elastic tissue of blood vessels with the simultaneous growth of fibrous and smooth

muscle tissue, not caused by inflammation or atherosclerosis. Most often, the renal

arteries are involved in the pathological process, less often the branches of the aortic arch,

cerebral vessels.

In view of the rather rare frequency of this disease, the etiology and pathogenesis are still

controversial. Most researchers believe that the pathogenesis of bro-muscular dysplasia is

associated with systemic inflammation syndrome, which is a consequence of congenital

anomalies in the structure of the elastic frame of the vascular wall. Congenital deficiency of

elastic fibers in the walls of the artery leads to the growth of muscle and fibrous tissue.

Such an understanding of the pathological process most logically explains the

angiographic picture of bro-muscular damage to the vascular wall. On the angiograms,

multiple sections of narrowing of the artery are visible, alternating with aneurysmal
dilatations or sections of the unaffected vessel, and the x-ray image resembles a “chain of

beads”.

The treatment of bro-muscular dysplasia is mostly conservative and comes down to the

mandatory lifelong administration of disaggregants (aspirin). Allowed the appointment of

calcium channel blockers, anticoagulants, urokinase, hormonal drugs.

Angiosurgical reconstructions are difficult due to inaccessible localization of the lesion

(renal arteries, upper parts of the internal carotid artery at the base of the skull) and

weakness of the vascular wall, in which it is technically difficult to form anastomoses or

suture arteriotomy holes. The use of endovascular methods of treatment in this situation is

more promising, but there is a high risk of rupture of the vessel.

Congenital malformations of the vessels represent a heterogeneous group of

congenital diseases caused by impaired embryonic development of the vascular system.

The following factors exist that have a teratogenic effect and cause vascular tube

malformations: alcohol, medications (sleeping pills, folic acid antagonists, anticonvulsants),

infectious diseases (rubella, cytomegalovirus, herpes) transferred during pregnancy,

ionizing radiation.

All vascular abnormalities are divided into vascular tumors and malformations, which differ

in their specific structure, pathophysiology, clinical features and treatment tactics. Of the

vascular tumors, the most common hemangioma, which is characterized by endothelial

hyperplasia and is a benign tumor. Most of the vascular malformations are venous, arterial,

lymphatic, capillary, arteriovenous malformations. Malformation is a vascular structure

defect that occurs during embryo and vasculogenesis. Currently, the Classification of the

International Society for the Study of Vascular Anomalies ( ISSVA) is used to classify

vascular anomalies ., 2014). Of fundamental importance is the separation of congenital

anomalies of blood vessels into vascular tumors and malformations.

Classification of the International Society for the Study of Vascular Anomalies ( ISSVA ,

2014)

I. Vascular tumors

Benign

infantile hemangioma

congenital hemangioma (RICH, NICH, PICH)

bundle angioma pyogenic granuloma

epithelial hemangioma Borderline

retiform hemangioendothelioma

capochiform hemangioendothelioma

composite hemangioendothelioma

papillary intralymphatic angioendothelioma

Kaposi's sarcoma

Malignant

Angiosarcoma

Epitheloid hemangioendothelioma

Simple capillary

“wine stain” telangiectasia angiokeratoma venous

II. Vascular malformations

• normal sporadic

• Bean syndrome

• Familial cutaneous and mucous membranes

• Glomangioma

• Mafucci syndrome

lymphatic

• arteriovenous malformations

• arteriovenous stula

combined

CVM, CLM, LVM, CLVM, AVM-LM, CM-AVM

III. Anomalies of large vessels

1. directions

2. quantities

3. lengths

4. diameter (aplasia, hypoplasia, stenosis, ectasia / aneurysm)

IV. convulsive abnormalities associated with other abnormalities

1. syndrome, Klippel-Trenaunay: CM + VM +/- LM + limb overgrowth

2. Parkes Weber Syndrome : CM + AVF + limb overgrowth G

3. syndrome, Servelle-Martorell: limb VM + bone undergrowth

Sturge-Weber syndrome : facial + leptomeningeal CM + eye anomalies +/- bone and / or

soft tissue overgrowth syndrome Maffucci: VM +/- spindle-cell hemangioma +

enchondroma

Macrocephaly - CM (M-CM / MCAP) G

Microcephaly - CM (MICCAP) G

CLOVES Syndrome : LM + VM + CM +/- AVM + lipomatous overgrowth G Proteus

syndrome: CM, VM and / or LM + asymmetrical somatic overgrowth G

Bannayan-Riley-Ruvalcaba sd: AVM + VM + macrocephaly, lipomatous overgrowth

The most common vascular tumor is infantile hemangioma, which occurs in 10% of the

population. Recent studies have shown that they are more common in low-weight girls

born before 37 weeks of gestation, mainly as a result of in vitro fertilization. Congenital

hemangiomas are of 2 types: rapidly involving and generally not involutional. Infantile

hemangioma appears in the first days after birth. It is a clearly defined at red spot on the

skin surface. At this stage, hemangioma can be confused with other vascular diseases,

however, rapid vertical growth allows you to make the correct diagnosis. With intradermal

localization, the hemangioma has a bright red color. In cases where the hemangioma is

located subcutaneously, it loses the clarity of its relief and borders and has a bluish color.

The development of hemangioma has the following stages: growth phase (first weeks and

up to the 3–6th month of life), stabilization phase (from the 6–8th month and up to the 12–

20th month), the regression phase (up to 6–7 years ) With spontaneous involution,

sclerosis of the hemangioma occurs. On the head and neck, the hemangioma is usually

localized in the projection of the trigeminal nerve, and the location in the region of its lower

branch in 60% of cases is combined with pharyngeal hemangioma.

Therapeutic tactics for simple hemangiomas are expectant, with the goal of the onset of

spontaneous sclerosis. In cases of complex hemangiomas characterized by rapid growth,

located on the face, around natural openings, the presence of episodes of bleeding,

ulceration or inflammation, active therapeutic tactics are used. Propranolol is the rst-line

systemic drug in the treatment of hemangiomas. In 2008, it was found that the use of

propranolol in newborns with cardiovascular diseases and concomitant hemangioma led to

a slowdown in the growth of the latter. This observation was confirmed by many studies
that showed a pronounced decrease in tumor size within 1-2 weeks after the start of

therapy. Propranolol is recommended in the treatment of hemangiomas, for which it is

impossible to perform surgery or use wait and see tactics. The most successful use of the

drug in the treatment of volumetric pharyngeal and periorbital hemangiomas. The

mechanism of action has not yet been fully studied. There is an assumption that

propranolol affects vascular growth factor and hemodynamic cytokines.

Despite the relatively high efficiency of propranolol in half the cases, it is nevertheless

necessary to use various degradation options. Currently, surgical excision,

cryodestruction, diathermocoagulation, and laser coagulation of hemangiomas are most

often used.

35. Raynaud’s disease: clinical features, diagnosis, treatment;

A vasospastic disease that is angiotrophoneurosis with a primary lesion of the small

terminal arteries and arterioles. The disease affects mainly the upper limbs. It occurs in

3-5% of the population, mainly female, aged 20-40 years. Women get sick 5 times more

often than men. First described in 1862 by the French physician Maurice Reynaud.

At the heart of the disease is a genetic predisposition. Factors that trigger the onset of the

disease include:

· Frequent and prolonged episodes of hypothermia of the upper limbs,

· Chronic traumatization ngers

· Endocrine disorders (thyroid, gonads)

· Severe emotional stress.

· Professional, production factors (vibration)

· Rheumatic diseases (systemic scleroderma, systemic lupus erythematosus,

rheumatoid arthritis, dermatomyositis, periarteritis nodosa)

Diseases are more common among pianists and typists. In pathogenesis, an important

role is played by increased muscle tone in the distal upper limbs, due to hyperactivation of

the sympathetic nervous system. Often the disease is combined with migraine.

There are 3 main stages of the disease:

1. angiospastic

2. angioparalytic

3. trophoparalytic
In the first stage of the disease, spasms of the vessels of the terminal phalanges of the

fingers are of a short-term nature accompanied by pain. Spasm is quickly replaced by

vasodilation and redness of the skin.

In the second stage of the disease, the hands and fingers acquire a pale, cyanotic color,

and the fingers are pasty.

The trophoparalytic stage is characterized by a tendency to develop panaritium and

necrosis. With the rejection of necrotic tissue, long-lasting non-healing ulcers are formed.

Patients suffering from Raynaud's disease are characterized by a specific reaction to cold,

which manifests itself in the form of chilliness of fingers and pain. Even washing your

hands under cold water can provoke a pain syndrome.

The treatment methods for this disease are divided into two groups: conservative and

operational. Conservative treatment is mainly aimed at stopping the symptoms of the

disease and preventing the causes that cause the onset of the disease. At the first stage of

the disease, the relief of a pain attack is possible by warming the limbs in warm water.

Drug therapy consists in the use of vasodilator drugs. It is recommended that patients

avoid hypothermia of the extremities, chronic trauma and stay in a state of psychoemotional
comfort. With the progression of the disease and the development of trophic

ulcers, various dressings are used depending on the phase of the wound process. In

cases of ineffective conservative vasoactive therapy, surgical treatment is indicated. Since

the main blood ow in the extremities is preserved. The pulsation on the arteries of the

wrists and legs is distinct, and the pathological process is localized at the level of the

capillary bed, only one method of surgical treatment seems to be pathogenetically

substantiated - sympathectomy. Which consists in the removal of 2-3 sympathetic ganglia

on the side of the lesion. As a rule, after surgery, in most patients, a stable remission of the

disease can be achieved with the exception of provoking factors and regular courses of

conservative vasoactive therapy. It should be noted that smoking leads to a rapid

progression of the disease and leveling the achieved positive results from conservative

and surgical treatment. Only after complete cessation of smoking is it possible to perform

sympathectomy. only one method of surgical treatment seems to be pathogenetically

substantiated - sympathectomy. Which consists in the removal of 2-3 sympathetic ganglia

on the side of the lesion. As a rule, after surgery, in most patients, a stable remission of the
disease can be achieved with the exception of provoking factors and regular courses of

conservative vasoactive therapy. It should be noted that smoking leads to a rapid

progression of the disease and leveling the achieved positive results from conservative

and surgical treatment. Only after complete cessation of smoking is it possible to perform

sympathectomy. only one method of surgical treatment seems to be pathogenetically

substantiated - sympathectomy. Which consists in the removal of 2-3 sympathetic ganglia

on the side of the lesion. As a rule, after surgery, in most patients, a stable remission of the

disease can be achieved with the exception of provoking factors and regular courses of

conservative vasoactive therapy. It should be noted that smoking leads to a rapid

progression of the disease and leveling the achieved positive results from conservative

and surgical treatment. Only after complete cessation of smoking is it possible to perform

sympathectomy. after surgery, in most patients it is possible to achieve a stable remission

of the disease with the exception of provocative factors and regular courses of

conservative vasoactive therapy. It should be noted that smoking leads to a rapid

progression of the disease and leveling the achieved positive results from conservative

and surgical treatment. Only after complete cessation of smoking is it possible to perform

sympathectomy. after surgery, in most patients it is possible to achieve a stable remission

of the disease with the exception of provocative factors and regular courses of

conservative vasoactive therapy. It should be noted that smoking leads to a rapid

progression of the disease and leveling the achieved positive results from conservative

and surgical treatment. Only after complete cessation of smoking is it possible to perform

sympathectomy.

36. Stenotic lesions of the terminal aorta, iliac arteries and lower limb arteries:

classification, clinical picture, diagnosis, differential diagnosis, treatment;

Atherosclerosis is the main cause of occlusal-stenotic diseases of the terminal aorta, iliac

arteries and lower limb arteries. Also, non-specific aortoarteritis, thromboangiitis obliterans,

endarteritis obliterans and Raynaud's disease lead to the development of damage to the

arterial bed of the lower extremities and pelvic organs. However, the share of these

diseases in the development of stenotic lesions of the arterial bed is significantly less than

that of atherosclerosis. There is a classification of these diseases according to the degree

of ischemia proposed by A.V. Pokrovsky. The gradation of the development of a chronic

violation of arterial blood flow to the lower extremities effects the distance of painless

walking, the severity of pain and the severity of necrotic changes.

Stage I - asymptomatic lesion of the arteries, which is detected only when using

instrumental examination methods.

Stage II - arterial insufficiency, which occurs during exercise (“intermittent claudication”).

Fundamentally important is the division of this stage. You can start thinking about the

possibility of angiosurgical correction if the patient has stage 2B.

Stage IIA - painless walking distance of more than 200 m.

Stage II B - painless walking distance of less than 200 m.

Stage III - pain occurs at rest.

Stage IV - stage of trophic disorders, usually necrosis of the distal extremities.

It should be noted that the selection of such a term as “critical ischemia” is fundamental. It

includes III and IV stages of classification A.V. Pokrovsky. If the patient has pain at rest or

trophic disorders, the threat of limb loss is maximum.

Occlusion of aortic bifurcation was described and analyzed in detail by R. Lerish in 1923.

The symptom complex described by R. Lerish included five signs: 1) unstable and

incomplete erection; 2) severe fatigue of the lower extremities; 3) diffuse muscle atrophy of

the lower extremities; 4) the absence of trophic disorders; 5) the pallor of the legs and feet,

even in the upright position of the patient. To date, occlusion of aortic bifurcation is called

Lerish syndrome.

The main symptom of chronic arterial insufficiency is the pain that occurs when walking.

First, the pain syndrome occurs with a significant level of physical activity and is

manifested by painful sensations in the muscles of the leg. With a decrease or cessation of

the load, the symptoms disappear. As the atherosclerotic process progresses, the distance

of painless walking decreases, the time required for rest increases. Upon transition to the

stage of critical ischemia, pain at rest is disturbing. Patients sleep with their limbs down or

in a sitting position to relieve pain. However, a prolonged forced position with a limb

lowered down leads to the development of edema, which in turn compresses the

microvasculature and aggravates ischemia.

As the progression of atherosclerotic lesions in the arterial bed, patients lose leg hair.

Atrophy of muscles, skin and subcutaneous tissue occurs. Toenails become brittle,
characterized by fungal infection.

In cases of critical ischemia, ulcers, necrosis on the toes are formed.

The basic principles for diagnosing chronic arterial insufficiency of the lower extremities

are reduced to determining the distance of painless walking, the severity of pain and the

presence of trophic disorders. An important role is played by the determination of the

presence of pulsation on the main arteries of the legs.

Differential diagnosis of chronic arterial insufficiency must be carried out with chronic

venous insufficiency, neuralgia, arthrosis and arthritis. The main symptom of chronic

venous insufficiency is edema, which progressively grows throughout the day. Ripple on

the main vessels preserved. In case of neurological lesions, patients complain of burning,

shooting pains that spread from the buttocks along the lateral surface of the thigh and

lower leg. There is no intermittent claudication and pulsation is preserved on the main

arteries. Pain occurs during palpation of paravertebral points in the lumbar spine, as well

as exit points of the sciatic nerve in the buttocks. With the development of arthritis or

arthrosis, hyperemia in the region of the joint concerned is determined.

As instrumental diagnostic methods, ultrasonic duplex angioscanning is widely used. To

determine the possibility and extent of angiosurgical treatment, the “gold standard” of

diagnosis is radiopaque angiography.

Treatment of occlusal-stenotic lesions of the arterial bed is divided into: conservative and

surgical. All patients with a clinic of chronic arterial insufficiency should be recommended

to walk at least one hour a day under the supervision of relatives. Walking is indicated at

all stages of the disease. It is necessary to explain to patients that at least once every 6

months it is necessary to undergo courses of conservative vasoactive therapy regardless

of the condition of the leg. Only systematic treatment can slow the progression of

atherosclerosis. The main principles of conservative therapy include: leveling risk factors

(categorical smoking cessation), systematic intake of antiplatelet agents (aspirin,

clopidogrel), lipid-correcting therapy (rosuvastatin), activation of metabolic processes

(actovegin, solcoseryl),

An indication for surgical treatment is dissatisfaction with the distance of painless walking

in the presence of hemodynamically signicant damage to the vascular bed. According to

the Fontaine-Pokrovsky classication, the possibility of surgical treatment should be

considered in stages II B - IV .

For open surgical treatment, various types of reconstructive angiosurgical interventions

can be used: reversible endarterectomy, endarterectomy with plastic artery patch, various

types of prosthetics and bypass surgery using autologous or synthetic prostheses.

Endovascular treatment methods include balloon angioplasty and stenting. With limited,

limited hemodynamically signicant stenosis or occlusion, endovascular technologies have

great advantages. It should be noted that the use of hybrid revascularization technologies

signicantly increases the possibilities of angiosurgical correction. Hybrid technologies

include the combined implementation of open angiosurgical treatment of one vascular pool

with endovascular revascularization of another.

37. Etiology and pathogenesis of acute arterial obstruction, classification;

38. Special methods of diagnosis, differential diagnosis of acute arterial

obstruction;

39. Treatment of acute limb ischemia: conservative therapy, indications for surgery,

types of operations;

Acute arterial obstruction - a sudden cessation of arterial blood ow. The main causes are

thrombosis, embolism, angiospasm, injuries of the great vessels.

Thrombosis is a pathological condition characterized by the formation of a blood clot in the

area of the vascular bed.

Embolism is an obstruction of the lumen of an artery with an embolus, which is usually

represented by a part of a blood clot that has torn off from the main source and migrates

with a blood stream through the bloodstream.

The famous Berlin pathologist Rudolf Virchow in the second half of the 19th century

formulated three main reasons for the formation of a blood clot: a violation of the integrity

of the vascular wall, changes in the rheological properties of blood and a slowdown in

blood ow.

Sources:

1) The left half of the heart - atrial fibrillation, post-infarction aneurysm of the left ventricle,

infectious endocarditis with vegetation on the alignment of the valve, stenosis of the mitral

valve, tumor. The greatest embologous danger is represented by episodes of the transition

of the sinus rhythm into fibrillation and vice versa. The most common cause of arterial
thromboembolism is atrial fibrillation.

2) Aorta and large major vessels - separation of fragments of the thrombotic cup of the

aneurysm, a vessel injury that is accompanied by detachment and separation of the

intima, fragmented atherosclerotic plaques;

3) The right heart and veins of a large circle of blood circulation - with extensive defects of

the interventricular and atrial septa. In arterial thromboembolism of the extremities, emboli

are usually localized in the area of bifurcations of the great vessels.

Acute limb ischaemia is defined as the sudden decrease in limb

perfusion that threatens the viability of the limb.

Complete or even partial occlusion of the arterial supply to a limb can lead to rapid

ischaemia and poor functional outcomes within hours.

Etiology

Acute limb ischaemia has an incidence of around 1.5 per 10,000 person years. Its causes

can be classified into 3 main groups:

• Embolisation whereby a thrombus from a proximal source travels distally to

occlude the artery (most common)

• The original thrombus source may be as a result of AF, post-MI muralthrombus, abdominal aortic
aneurysm, or prosthetic heart valves

• Thrombosis in situ whereby an atheroma plaque in the artery ruptures and a

thrombus forms on the plaque’s cap (presenting as acute or acute-on-chronic)

• Trauma (less common), including compartment syndrome

Clinical Features

Classically, the signs and symptoms of acute limb ischaemia can be described using the

6 Ps (the first three here being the most common initial features):

• Pain

• Pallor

• Pulselessness

• Paresthesia

• Perishingly cold

• Paralysis

Acute limb ischaemia is often characterised by a sudden onset of these symptoms. A

normal, pulsatile contralateral limb is a sensitive sign of an embolic occlusion.

In the history, the causes of potential embolisation should be explored. These include

chronic limb ischaemia, atrial fibrillation, recent MI (resulting in a mural thrombus), or a

symptomatic AAA (ask about back/abdominal pain) and peripheral aneurysms.

The later the patient presents to a hospital, the more likely that irreversible damage to the

neuromuscular structures will have occurred (more common >6hrs post-symptom onset),

which will ultimately result in a paralysed limb.

Category Prognosis Sensory

Loss

Motor

Deficit

Arterial

Doppler

Venous

Doppler

I – Viable No Immediate

threat None None Audible Audible

IIA –

Marginally

Threatened

Salvageable,

if promptly

treated

Minimal

(toes) or

none

None Inaudible Audible

Differential Diagnosis

The differential diagnoses for acute limb ischaemia include critical chronic limb ischaemia,

acute DVT (can present as Phlegmasia cerulea dolens and Phlegmasia alba dolens), or

spinal cord or peripheral nerve compression.

Investigation

Routine bloods, including a serum lactate (to assess the level of ischaemia), a

thrombophilia screen (if <50yrs without known risk factors), and a group and save, should

be taken, along with an ECG.

Suspected cases should be initially investigated with beside Doppler ultrasound

scan (both limbs), followed by considering a CT angiography

If the limb is considered to be salvageable, a CT arteriogram can provide more information

regarding the anatomical location of the occlusion and can help decide the operative

approach (such as femoral vs. popliteal incision).

By Milorad Dimic MD [GFDL], via Wikimedia Commons

Management

1. Initial Management

Acute limb ischaemia is a surgical emergency. Complete arterial occlusion will lead

to irreversible tissue damage within 6 hours. Early senior surgical support is vital.

Start the patient on high-flow oxygen and ensure adequate IV access. A therapeutic

dose heparin or preferably a bolus dose then heparin infusion should be initiated as

soon as is practical.

2. Conservative Management

Conservative management can often be considered those Rutherford 1 and 2a;

a prolonged course of heparin may be the most effective non-operative management of

acute limb ischaemia.

Any patient started on conservative management via heparin will need regular

assessment to determine its effectiveness through monitoring APPT and clinical review.

Surgical interventions may be warranted if no significant improvement is seen.

IIB –

Immediately

Threatened

Salvageable if

immediately

revascularised

More
than

toes, rest

pain

Mild/

Moderate Inaudible Audible

III –

Irreversible

Major tissue

loss,

permanent

nerve damage

inevitable

Profound

Profound

paralysis

Inaudible Inaudible

3. Surgical Intervention

Surgical intervention is mandatory for cases presenting in Rutherford 2b

If the cause is embolic, the options are:

• Embolectomy via a Fogarty catheter

• Local intra-arterial thrombolysis*

• Bypass surgery (if there is insufficient flow back)

If the cause is due to thrombotic disease, the options are:

• Local intra-arterial thrombolysis

• Angioplasty (Fig. 2)

• Bypass surgery

Irreversible limb ischaemia (mottled non-blanching appearance with hard woody

muscles) requires urgent amputation or taking a palliative approach.

Most post-operative cases require a high level of care, typically at a high dependency unit,

due to the ischaemia reperfusion syndrome.

*Intra-arterial thrombolysis is often difficult to conduct within 6 hours, therefore often used

for Rutherford 2a

4. Long Term Management

Reduction of the cardiovascular mortality risk in this patient group is key.

Promoting regular exercise, smoking cessation, and weight loss as necessary.

Most cases should be started on an anti-platelet agent, such as low-dose aspirin or

clopidogrel, or even anticoagulation with warfarin or a DOAC. Any underlying predisposing

conditions to the acute limb ischaemia should be treated, e.g. uncontrolled AF.

Cases resulting in amputation will require occupational therapy and physiotherapy, with

a long term rehabilitation plan discussed and transfer to an intermediate rehabilitation

centre.

Complications

Acute limb ischaemia has a mortality rate of around 20%, with the 30-day mortality rate

following the surgical treatment of acute limb ischaemia at 15%.

An important complication of acute limb ischaemia is reperfusion injury; sudden increase

in capillary permeability can result in:

• Compartment syndrome

• Release of substances from the damaged muscle cells, such as:

• K+ ions causing hyperkalaemia

• H+ ions causing acidosis

• Myoglobin, resulting in significant AKI

It is imperative that patients at risk of compartment syndrome are closely monitored and

rapidly treated. Electrolyte imbalance due to reperfusion injury requires close monitoring

and potentially haemofiltration.

Classification of acute arterial insufficiency (V. S. Savelyev)

I stage of ischemia - stage of functional disorders (sensitivity and movement of the limb

preserved, acute pain in the limb, pallor and cooling of the skin, lack of pulse in the

peripheral arteries).

• I A stage - a feeling of cooling, numbness, paresthesia.

• I B stage - pain in the distal extremities joins.

II stage of ischemia - stage of organic changes. Its duration is 12-24 hours. Pain and
tactile sensitivity are absent, active and passive movements in the joints are limited,

muscle contracture develops, and the skin is bluish.

· II A stage - disorders of sensitivity and movements - paresis.

· II B stage - disorders of sensitivity and movements - plegia.

· II B stage - subfascial edema.

III of stage ischemia - necrotic. The duration of the stage is 24-48 hours. Lost all kinds of

sensations and movements. In the end, gangrene of the limb develops.

· III A stage - partial muscle contracture.

· III B stage - total muscle contracture.

The main diagnostic methods: examination, palpation, auscultation, ultrasonic duplex

angioscanning, angiography, examination of the blood coagulation system.

Differential Diagnostics:

1. Acute ileofemoral phlebothrombosis.

2. Diabetic angiopathy.

3. Transverse myelitis.

4. Sciatica

Conservative treatment includes the appointment of direct-acting anticoagulants (heparin,

low molecular weight heparins in therapeutic doses) to prevent further r progression of

thrombosis, antispasmodics (no-spa, papaverine), painkillers, drugs that improve blood

rheological properties (reopoliglyukin) and wet circulation (pentoxifylline). The tactics of

further treatment are determined by the duration of the disease, the prevalence and

localization of the lesion of the vascular bed, the degree of ischemic tissue damage, and

the general condition of the patient. When embolism is performed, an operation is

performed - embolectomy using a Fogarty catheter. The success of this type of surgical

treatment depends on the duration of the disease. The most successful embolectomy in

the first 6 hours after the onset of limb ischemia. Angiosurgical reconstructions are not

performed if the patient has severe concomitant pathology and muscle contracture in large

joints. In the presence of subfascial edema, fasciotomy is additionally performed with the

aim of muscle decompression.

DIAPHRAGM (Question 80- 84)

80. Anatomical and physiological information about the diaphragm, classification of diseases of the
diaphragm.

 The diaphragm is the fibromuscular structure separating the thorax from the abdomen.

 The attachments of diaphragm can be divided into peripheral and central attachments.

 It has three peripheral attachments:

 Lumbar vertebrae and arcuate ligaments.

 Costal cartilages of ribs 7-10 (attach directly to ribs 11-12).

 Xiphoid process of the sternum.

 The parts of the diaphragm that arise from the vertebrae are tendinous in structure, and are
known as the right and

left crura:

 Right crus – Arises from L1-L3 and their intervertebral discs. Some fibres from the right crus
surround the

oesophageal opening, acting as a physiological sphincter to prevent reflux of gastric contents into
the

oesophagus.

 Left crus – Arises from L1-L2 and their intervertebral discs.

 Muscular part consists of skeletal muscle. The muscular part is located on the periphery. It is
divided into the

sternal, costal & lumbar parts.

 The muscle fibres of the diaphragm combine to form a central tendon. This tendon ascends to fuse
with the

inferior surface of the fibrous pericardium.

 Either side of the pericardium, the diaphragm ascends to form left and right domes. At rest, the
right dome lies

slightly higher than the left – this is thought to be due to the presence of the liver.

There are three openings that act as conduit for these structures:

VASCULATURE:

 The majority is provided inferior phrenic arteries, which arise directly from the abdominal aorta.

 The remaining supply is from the superior phrenic, pericardiacophrenic, and musculophrenic
arteries which

branches off from the internal thoracic, as well as six lower intercostal arteries..

 The draining veins follow the aforementioned arteries, azygous & hemiazygous veins and
oesophageal veins.

INNERVATION
 The halves of the diaphragm receives motor innervation from a phrenic nerve.

 The left half of the diaphragm (known as a hemidiaphragm) is innervated by the left phrenic nerve,
and vice

versa.

 Each phrenic nerve is formed in the neck within the cervical plexus, and contains fibres from spinal
roots C3-C5.

CLASSIFICATION OF DISEASES OF THE DIAPHRAGM

Disorders of the diaphragm can be broadly classified as:

1. Disorders of innervation, leading to paralysis of the

diaphragm, with elevation and reduction of thoracic volume

leading to breathlessness.

2. Disorders of anatomy, which are further categorised into:

 Congenital diaphragmatic hernias or

 Acquired hernias, usually secondary to

trauma.

There are two well-recognised congenital sites where

abdominal viscera can herniate into the chest:

 The foramen of Morgagni: a hernia in the anterior

part of the diaphragm with a defect between the

sternal and costal attachments. The most commonly

involved viscus is the transverse colon.

 The foramen of Bochdalek: through the dome of

the diaphragm posteriorly.

3. Traumatic rupture of the diaphragm may occur with blunt trauma.

Unless there is severe bleeding or strangulation of the viscera it is best managed after an interval.

In a severely injured patient being ventilated it can wait until other injuries are dealt with and
weaning from the

ventilator is being considered.

4. Diaphragmatic tumours can be benign or malignant.

When the diaphragm is breached, as in anatomical disorders, repair with either primary closure or
with a mesh is

usually possible via a thoracotomy. Diaphragmatic paralysis, particularly idiopathic unilateral

paralysis, can be
treated by plication, returning the diaphragm to a lower position and improving thoracic volume.

81. Damage and injuries of the diaphragm, causes, clinic, diagnosis, treatment.

Rupture of the diaphragm:

 Traumatic (blunt/ penetrating)

 Iatrogenic causes (medical intervention, for example during surgery to the abdomen or chest)

MECHANISM

 It is proposed that a blow to the abdomen may raise the pressure within the abdomen so high that
the diaphragm

bursts.

 Blunt trauma creates a large pressure gradient between the abdominal and thoracic cavities; this
gradient, in

addition to causing the rupture, can also cause abdominal contents to herniate into the thoracic
cavity.

 Abdominal contents in the pleural space interfere with breathing and cardiac activity.

 They can interfere with the return of blood to the heart and prevent the heart from filling
effectively,

reducing cardiac output.

 If ventilation of the lung on the side of the tear is severely inhibited, hypoxemia (low blood oxygen)
results.

 Usually the rupture is on the same side as an impact. A blow to the side is three times more likely
to cause

diaphragmatic rupture than a blow to the front.

CLINIC

1. Chest and abdominal pain

2. Decreased lung sounds on the side of the rupture

3. Respiratory distress may be present, and the

4. Orthopnea, dyspnea which occurs when lying flat

5. Coughing is another sign.

If herniation of abdominal organs:

1. Signs of intestinal blockage or sepsis in the abdomen may be present.

2. Bowel sounds may be heard in the chest, and shoulder or epigastric pain may be present.

3. When the injury is not noticed right away, the main symptoms are those that indicate bowel
obstruction. These people present months later, with vague symptoms that do not necessarily relate
to an

injury.

 With penetrating trauma, the contents of the abdomen may not herniate into the chest cavity
right away, but they

may do so later, causing the presentation to be delayed

DIAGNOSIS

1. CXR  Half the time, initial X-rays are normal.

In those that are not:

 Hemothorax or pneumothorax is usually present

 The diaphragm may appear higher than normal.

 Gas bubbles may appear in the chest,

 Mediastinum may appear shifted to the side.

 A nasogastric tube from the stomach may appear on the film in the chest cavity; this sign

is pathognomonic for diaphragmatic rupture, but it is rare. A contrast medium that shows up on X-
ray can be

inserted through the nasogastric tube to make a diagnosis.

 The X-ray is better able to detect the injury when taken from the back with the patient upright, but
this is not

usually possible because the patient is usually not stable enough; thus it is usually taken from the
front with the

patient lying supine.

 Positive pressure ventilation helps keep the abdominal organs from herniating into the chest
cavity, but this also can

prevent the injury from being discovered on an X-ray.

2. Computed tomography

3. Thoracoscopy

4. Laparotomy

LOCATION

 Between 50 and 80% of diaphragmatic ruptures occur on the left side

 It is possible that the liver, which is situated in the right upper quadrant of the abdomen, cushions
the

diaphragm.
 However, injuries occurring on the left side are also easier to detect in X-ray films.

 Half of diaphragmatic ruptures that occur on the right side are associated with liver injury. Injuries
occurring

on the right are associated with a higher rate of death and more numerous and serious
accompanying

injuries.

 Bilateral diaphragmatic rupture, which occurs in 1–2% of ruptures, is associated with a much
higher death

rate (mortality) than injury that occurs on just one side.

TREATMENT

 Surgery to repair torn diaphragm  Laparotomy/ Video-assisted thorascopy

82. Hiatal hernias, etiology and pathogenesis, classification, clinic, diagnosis, treatment.

 A hiatal hernia is a type of hernia in which portion of the stomach prolapses through the
diaphragmatic

esophageal hiatus into the middle compartment of the chest.

 Most hiatal hernias are asymptomatic and are discovered incidentally, but rarely, a life-threatening
complication

may present acutely.

 This may result in gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR).

ETIOLOGY

The following are potential causes of a hiatal hernia.

1. Increased pressure within the abdomen caused by:

 Heavy lifting or bending over

 Frequent or hard coughing

 Hard sneezing

 Violent vomiting

 Straining during defecation (i.e., the Valsalva maneuver)

 Pregnancy

2. Being born with an unusually large esophageal hiatus.

3. Injury to the area

The most common risk factors are obesity and older age. Other risk factors include major trauma,
scoliosis, and

certain types of surgery.

CLASSIFICATION

Four types of esophageal hiatal hernia are identified:

Type I: A type I hernia, also known as a sliding hiatal hernia, occurs when part of the

stomach slides up through the hiatal opening in the diaphragm.

 There is a widening of the muscular hiatal tunnel and circumferential laxity of

the phrenoesophageal ligament, allowing a portion of the gastric cardia to herniate

upward into the posterior mediastinum.

 The clinical significance of type I hernias is in their association with reflux

disease.

 Sliding hernias are the most common type and account for 95% of all hiatal

hernias. (C)

Type II: A type II hernia, also known as a paraesophageal or rolling hernia, occurs when

the fundus and greater curvature of the stomach roll up through the diaphragm, forming a pocket
alongside the

esophagus.

 It results from a localized defect in the phrenoesophageal ligament while the gastroesophageal
junction

remains fixed to the pre aortic fascia and the median arcuate ligament.

 The gastric fundus then serves as the leading point of herniation.

 Although type II hernias are associated with reflux disease, their primary clinical significance lies in
the

potential for mechanical complications. (D)

Type III: Type III hernias have elements of both types I and II hernias.

 With progressive enlargement of the hernia through the hiatus, the phrenoesophageal ligament
stretches,

displacing the gastroesophageal junction above the diaphragm, thereby adding a sliding element to
the type II

hernia.

Type IV: Type IV hiatus hernia is associated with a large defect in the phrenoesophageal ligament,
allowing other

organs, such as colon, spleen, pancreas and small intestine to enter the hernia sac.

The end stage of type I and type II hernias occurs when the whole stomach migrates up into the
chest by rotating
180° around its longitudinal axis, with the cardia and pylorus as fixed points.

In this situation the abnormality is usually referred to as an intrathoracic stomach.

CLINIC

In most cases however, a hiatal hernia  Asymptomatic unless have complications.

Called the "great mimic" because its symptoms can resemble many disorders.

1. Dull pains in the chest, shortness of breath (caused by the hernia's effect on the diaphragm)

2. Heart palpitations (due to irritation of the vagus nerve),

3. Swallowed food "balling up" and causing discomfort in the lower esophagus until it passes on to
the stomach.

4. In addition, hiatal hernias often result in heartburn but may also cause chest pain or pain with
eating.

 The pain and discomfort that a patient experiences is due to the reflux of gastric acid, air, or bile.

 While there are several causes of acid reflux, it occurs more frequently in the presence of hiatal
hernia.

5. GORD symptoms  Regurgitation of food/ liquids into the esophagus; Heart burn.

6. Vomiting of blood; Black stool (melaena) from associated esophagitis, erosions (Cameron ulcers),
or a discrete

esophageal ulcer, leading to iron-deficiency anemia

7. In newborns, the presence of Bochdalek hernia can be recognized from symptoms such as
difficulty

breathing, fast respiration, and increased heart rate.

DIAGNOSIS

1. Upper GI series  An upper gastrointestinal series, also called a barium meal, is a series of
radiographs used

to examine the gastrointestinal tract for abnormalities. A contrast medium, usually a radiocontrast
agent such

as barium sulfate mixed with water, is ingested or instilled into the gastrointestinal tract, and X-rays
are used to

create radiographs of the regions of interest.

2. Endoscopy

3. High resolution esophageal manometry

TREATMENT

If asymptomatic/ very little discomfort  no treatment is required.

If there is pain or discomfort  3 or 4 sips of room temperature water will usually relieve the pain.
Symptomatic patients

CONSERVATIVE

1. Modifying lifestyle factors:

 If due to stress  stress reduction techniques

 If overweight  weight loss may be indicated.

2. Elevate the head of their beds and avoid lying down directly after meals.

3. Neutralizing acid: Antacids  Mylanta, Rolaid

4. Antisecretory drugs to reduce acid secretion:

 Proton pump inhibitors  Omeprazole, Lansoprazole

 H2 receptor blockers  Ranitidine, Nizatidine

5. Medications that reduce the lower esophageal sphincter (LES) pressure should be avoided.

SURGERY

Indications

 It is necessary only in the very few patients who have complications of GERD despite aggressive PPI
treatment.

 Esophageal stricture or severe discomfort due to unusually large hiatal hernia or paraesophageal
type. About 5%

of hiatal hernias are paraesophageal.

 If symptoms from such a hernia are severe for example if chronic acid reflux threatens to severely
injure

the esophagus or is causing Barrett's esophagus, surgery is sometimes recommended

Complications from surgical procedures to correct a hiatal hernia may include gas bloat

syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and rarely,
achalasia

Surgical procedures sometimes fail over time, requiring a second surgery to make repairs.

Procedures:

 Surgical treatment involves removing the hernia sac

and closing the abnormally wide esophageal hiatus

+/- Recontruction of LOS (Laparoscopy/

Thoracotomy).

There are 3 major types of surgical procedures that may be

considered are as follows:

1. Nissen fundoplication (or a variant, the Toupet

procedure)

2. Belsey fundoplication

3. Hill repair

Nissen fundoplication the gastric fundus (upper part) of the stomach is

wrapped, or plicated, around the inferior part of the esophagus, preventing

herniation of the stomach through the hiatus in the diaphragm and the

reflux of gastric acid.

The procedure is now commonly performed laparoscopically.

With proper patient selection, laparoscopic fundoplication recent studies

have indicated relatively low complication rates, quick recovery, and

relatively good long term results

83. Diaphragm relaxation: etiology, pathogenesis, clinical features, diagnosis, treatment.

Diaphragmatic paralysis is due to an interruption in its nervous supply. This can occur in the phrenic
nerve, cervical

spinal cord, or the brainstem. It is most often due to a lesion of the phrenic nerve.

ETIOLOGY

Unilateral -Mechanical trauma: ligation or damage to the nerve during surgery

Bilateral-Motor neuron disease (most common): Amyotrophic lateral sclerosis; Post-polio syndrome

Unilateral -Compression: due to a tumour within the chest cavity(e.g., metastatic lung cancer)

Blateral -Thoracic trauma, cardiac surgery

Unilateral -Supraclavicular brachial plexus block Neuropathies: such diabetic neuropathy, multiple
sclerosis

uniilateral -Cervical spondylosis Myopathies: such as myasthenia gravis

uniilateral -Herpes zoster Muscular dystrophy (acid maltase deficiency)

uniilateral -Upper cervical radiculopathies, Hashimoto encephalopathy, and neuromyelitis optica

bilateral -Guillain-Barré syndrome, and Parsonage-Turner syndrome (neuropathy of brachial plexus)

bilateral - Neuropathies: such diabetic neuropathy, multiple sclerosis

bilateral - Myopathies: such as myasthenia gravis

DIAGNOSIS
Physical examination

Unilateral  Dullness to percussion and absent breath sounds over the lower chest on the involved
side.

Excursion on the involved hemithorax is decreased when compared with the healthy side.

Bilateral  Chest examination reveals limitation of diaphragmatic excursions and bilateral lower
chest dullness

with absent breath sounds.

Patients are tachypneic and use accessory respiration muscles.

The diagnostic finding is a paradoxical inward movement of the abdomen with inspiration.

Laboratory Studies & Other Tests

1. Arterial blood gas analysis:

 In px with bilateral diaphragmatic paralysis  Hypoxemia due to hypoventilation from atelectasis

and

ventilation-perfusion mismatching.

 Progressive hypercapnia also develops with disease progression.

 The hallmark of patients with diaphragmatic paralysis is hypercapnia and a respiratory acidosis.

 P(A-a) O2 gradients may be normal if there is no underlying parenchymal lung disease.

2. Pulmonary function test  Vital capacity in the upright and supine positions is the most important
part of

the pulmonary function test.

 Lung function tests will show a restrictive deficit.

3. Maximal inspiratory pressures

4. Electromyography & phrenic nerve stimulation  May reveal a neuropathic versus myopathic
pattern

5. Measurement of transdiaphragmatic pressure  This is the criterion standard for diagnosis.

 Measured by placing a thin-walled balloon transnasally at the lower end of the esophagus,
allowing

reflection of the changes in pleural pressure.

 Then, a second balloon manometer is placed in the stomach to measure changes in intra-
abdominal pressure.

 Gastric pressure should become more positive during inspiration. Esophageal pressure should
become more

negative during inspiration, demonstrating an increase in gradient during normal inspiration.

 In cases in which the sniff test is negative and clinical suspicion for diaphragmatic paralysis is still
high,

transdiaphragmatic pressure should be considered.

Imaging Studies

1. Chest radiography  elevated hemidiaphragms, small lung volumes, and atelectasis.

 (Unilateral paralysis can usually be diagnosed with only radiographic studies, unlike bilateral.)

2. Fluoroscopy (fluoroscopic sniff testing)  paradoxical elevation of the paralyzed diaphragm is

observed with

inspiration and confirms diaphragmatic paralysis.

 However, can be misleading as accessory muscle contraction may create the appearance of

diaphragmatic movement.

3. Computed tomography scanning of the chest

4. Magnetic resonance imaging

5. Ultrasonography

TREATMENT

1. Unilateral  the underlying cause must be identified and treated

 Diaphragmatic plication (thoracotomy, video-assisted thoracoscopic surgery (VATS), or

laparoscopy) 

Stabilization by surgical plication

2. Bilateral  mainly depends on the etiology and severity of the paralysis

a) Patients who do not have intrinsic lung pathology  Non-invasive ventilation, such as a CPAP
(continuous

positive airway pressure) machine.

b) In patients with central respiratory paralysis and upper cervical spinal cord injury (lesions above
C3) to wean

them off the ventilators  Phrenic pacing

 Electrodes can be implanted intrathoracically via thoracotomy and, more recently, with VATS.

 Alternatively, electrodes can be placed intramuscularly via a laparoscopic approach.

 In this approach, intramuscular electrodes are placed near the entrance points of the phrenic
nerves using

motor-point mapping techniques.

Negative-pressure systems
c) Patients with mild-to-moderate diaphragmatic weakness usually maintain daytime gas exchange
but worsen

during sleep  Nighttime noninvasive ventilation

d) Patients in whom nasal or oral positive-pressure ventilation is unsuccessful  other forms of

noninvasive

ventilation (e.g., negative-pressure cuirass, pulmonary wrap, rocking bed, positive-pressure

pneumobelt).

e) Patients who are not candidates for less invasive methods or in whom less invasive methods fail 

Tracheostomy with positive-pressure intermittent or permanent ventilation

f) Nerve reconstruction techniques  Neurolysis, nerve grafting, and neurotization for returning
function to

unilateral phrenic nerve injury that occurred as a result of anesthetic procedures and operative and
nonoperative

trauma to the neck.

g) Inspiratory muscle strength and endurance training  lead to increased non-diaphragmatic

inspiratory

muscle recruitment and help those with mild symptoms from diaphragmatic paralysis.

84. Diaphragmatic hernia, classification, diagnosis, treatment principles.

Diaphragmatic hernia is a defect or hole in the diaphragm that allows the abdominal contents to
move into the chest cavity.

Types

1. Congenital diaphragmatic

hernia

 Morgagni's hernia

 Bochdalek hernia

2. Hiatal hernia

3. Iatrogenic diaphragmatic hernia

4. Traumatic diaphragmatic hernia

Pathophysiology

It involves three major defects:

1. A failure of the diaphragm to completely close during development

2. Herniation of the abdominal contents into the chest

3. Pulmonary hypoplasia
CLASSIFICATION

1. True hernia  Have a hernial sac with hernial contents. A hernial sac is composed of parietal
peritoneum,

covered by pleura.

2. False hernia  Without a hernia sac, i.e.the abdominal viscera lying free within the thoracic cavity.

According to the origin of the hernia:

Traumatic

Non-traumatic  false congenital hernias of the diaphragms, true CDH of weak zones, true hernias of
atypical localization, hiatal hernias (esophageal opening, physiological foramen).

a) False congenital hernias of the diaphragm are formed due to failure of the diaphragm to
completely close during embryonic development.

b) True hernias of the weak areas of the diaphragm occur when the intraperitoneal pressure
increases resulting in exit

of the abdominal organs from those sites.

 The most common type, accounting for more

than 95% of cases, is a Bochdalek

hernia/postero-lateral diaphragmatic hernia

(through the lumbo-costal/ foramen).

Bochdalek hernias occur more commonly on

the posterior left side (85%, versus right side

15%). It is more likely to be asymptomatic if

it is on the right side of the chest.

 Accounting for approximately 2% of all

CDH cases are Morgagni

hernia/retrosternal/parasternal hernia). It is

characterized by herniation through

the foramina of Morgagni which are located

immediately adjacent and posterior to

the xiphoid process of the sternum.

 Diaphragm eventration  when there is

abnormal displacement (i.e. elevation) of part

or all of an otherwise intact diaphragm into

the chest cavity. This rare type of CDH

occurs because in the region of eventration

the diaphragm is thinner, allowing the abdominal viscera to protrude upwards.

 Central tendon defects of the diaphragm.

 Common hernial sac contents  omentum, transverse colon, preperitoneal fatty tissue
(parasternal lipoma).

c) True hernias of atypical localization are rare and

differ from diaphragm paralysis by the presence of

hernial gates, and therefore, the possibility of hernia

development.

d) Hiatal hernias are isolated as a separate group, since

they occur most often, have a particular anatomical

structure, clinical manifestations and require certain

treatment principles.

e) Rare hernias of other physiological foramen

(foramen of the sympathetic nerve; hiatus for inferior

vena cava)

CLINIC

Antenatal

The diagnosis of congenital diaphragmatic hernia (CDH) is frequently made antenatally prior to
25 weeks' gestation.

CDH is usually detected in the antenatal period (46-97%), depending on the use of level II
ultrasonography (US)

techniques

Postnatal

 History and clinical findings vary with the presence of associated anomalies and the degree of
pulmonary

hypoplasia and visceral herniation, the degree of lung collapse and displacement of the
mediastinum and the size

and shape of the hernia gate.

 Factors leading to increase intra-abdominal pressure, increase the severity of the symptoms of
the disease.
 In the infant presenting in the neonatal period without antenatal diagnosis, variable
respiratory distress and

cyanosis, feeding intolerance, and tachycardia are noted.

 In the physical examination, the abdomen is scaphoid if significant visceral herniation is

present.

 Auscultation  breath sounds are diminished, bowel sounds may be heard in the chest, and
heart sounds are

distant or displaced.

 Bochdalek hernias are more likely to be asymptomatic if it is on the right side of the chest.

Complaints:

 After heavy intake food Feeling of heaviness and pain in the epigastric region, chest &
hypochondria;

shortness of breath; palpitations

 Regurgitation of recently eaten food brings relief. Increased shortness of breath in a horizontal
position.

 If stomach herniates  paradoxical dysphagia (solid food passes better liquid).

Diaphragmatic hernia can be suspected if there is the above complaints +:

 Reduction in chest movement and smoothing of intercostal spaces on the affected side,

 Retraction of the abdomen with large long-standing hernias (scaphoid chest),

 Presence of dullness or tympanic sound over the affected half of the chest.

 Depending on the degree of herniation of the stomach and intestines, auscultation of intestinal
peristalsis or

splash sound in this area while decreased or completely absent respiratory noises.

 Displacement of the dullness of the mediastinum on the unaffected side.

Late presentation

Above clinical presentation + :

 Patients may present outside of the neonatal period with respiratory symptoms, intestinal
obstruction, bowel

ischemia, and necrosis following volvulus.

 Strangulation of the diaphragmatic hernia is characterized by sharp pains in the corresponding

half of the

chest or in the epigastric region, radiating to the back, scapula.

 Strangulation of a viscera  necrosis and perforation of its walls  development of

pyopneumothorax.
DIAGNOSIS

Clinical pic + Physical examination

Laboratory Studies

Antenatal studies to be considered include the following:

1. Amniocentesis for karyotype analysis should accompany a diagnosis of congenital

diaphragmatic hernia

(CDH)

2. Maternal serum alpha-fetoprotein may be low in cases of CDH

Postnatal studies to be considered include the following:

3. Assess arterial blood gas values  Hypoxemia, hypercarbia, and respiratory or metabolic
acidosis depend

on the degree of pulmonary hypoplasia, persistent pulmonary hypertension of newborn (PPHN),

right-to-left

shunting, and ventricular function

Imaging

4. Chest Radiography

5. CT

6. Ultrasonography and Echocardiography  Antenatal echocardiography may identify cardiac

anomalies

(more commonly, ventricular hypoplasia, atrial septal defects, and ventricular septal defects).

TREATMENT

THE ONLY TREATMENT IS SURGERY.

 Contemporary management of CDH emphasizes management of pulmonary hypoplasia and

persistent pulmonary

hypertension.

Prior to surgery:

 Admission into the NICU (Neonatal Intensive Care Unit)

 Placed on a mechanical ventilator to help breathing.

 If the infant cannot be stabilized using medical treatments and mechanical ventilation, the
alternate pathway

involves putting the infants on a temporary heart/lung bypass machine, called ECMO, which
stands for extracorporeal membrane oxygenation.

 ECMO allows oxygen to be regulated into the blood and then pumps the blood throughout the
entire body.
During ECMO the pulmonary artery has a chance to rest, as it were, thus hopefully reducing the
presence of

pulmonary hypertension, one of the biggest complication of CDH cases. Normally, this machine
is used to

stabilize the baby's condition.

 It is preferred to stabilize the infant prior to surgery, to minimize complications, if possible.

 Window of opportunity is 24-48 hours after birth to achieve normal pulmonary arterial
pressures and

satisfactory oxygenation and ventilation on minimal ventilator settings.

 However, surgical repair can often be safely delayed in stable patients, and the operation can
be scheduled on a

semielective basis. Urgent surgical repair is almost never necessary and may worsen the
pulmonary

hypertension.

 The association of CDH with lethal congenital abnormalities is a relative contraindication for
repair of the

diaphragmatic defect.

Procedure:

 After the baby is stable and his or her state has improved, the diaphragm can be fixed and the
misplaced organs

can be relocated to their correct position.

 That is either done via primary repair where the remaining diaphragm is stretched to cover the
hole, or an

abdominal muscle is split so it can be used to stretch over the hole, and the last option is with a
Gor-Tex patch,

which has higher risks of later infection or re-herniation.

 Any organ displacement is corrected during surgery; the heart and lungs will usually move back
into position on

their own, once displaced organs such as bowel, liver, or stomach, are out of the way.

 The incision is then closed. Sometimes, the incision site will be left open to allow the body to
adjust to newly

moved organs and the pressure associated with that, and then closed later once swelling and
drainage has

decreased.

 Diaphragm eventration is typically repaired thoracoscopically, by a technique called plication

of the diaphragm.
Plication basically involves a folding of the eventrated diaphragm which is then sutured in order
to “take up the slack” of the excess diaphragm tissue.

Prognosis  Congenital diaphragmatic hernia has a mortality rate of 40–62%, with outcomes
being more favourable in the absence of other congenital abnormalities.

Liver (Question 12 - 14)

12. Specific methods of examination of focal liver lesions. Differential diagnosis of liver lesions;

Focal liver lesions can be divided into benign and malignant.

1. Benign - Hemangioma, Focal nodular hyperplasia(FNH), adenoma, liver cysts

2. Malignant - Primary liver carcinomas (HCC, Fibrolamellar carcinoma

cholangiocarcinoma) and Metastasis

Benign liver lesions

1. Hepatic hemangioma

• Benign vascular lesions of the liver and commonest liver tumor (F>M) (30-50 years)

• Range in size from 1cm to 10cm

• Usually asymptomatic

• Hemangioma are compose of many endothelium lined vascular spaces separated by fibrous
septa

• Dx  US, CT (venous enhancement from center to periphery), MRI

2. Focal nodular hyperplasia (FNH)

• Benign nodule formation in liver with no malignant potential.

•2

nd most common benign hepatic lesion.

• More common in young and middle aged women (F>M)

• Usually asymptomatic causing minimal pain

• Dx  US, Doppler imaging, CT(no capsule), MRI

3. Hepatic adenoma

• Rare hepatic tumor. In women aged 20-40 years (associated with oral contraceptive use)

• Solitary. Can be associated with RUQ pain.

• There is risk of rupture, hemorrhage or malignant transformation.

• They are usually resected. Surrounded by a pseudo capsule.

• Dx  CT and MRI

4. Liver cysts
• Maybe single or multiple

• Maybe a part of polycystic kidney disease or biliary hematomas

• Non - specific management required

• Dx  Only US is enough for diagnosis

Malignant liver lesions

1. HCC

• The most common primary liver tumor.

• Rarely occurs before 40 and peaks at 70 (M>F)

• Cirrhosis is the strongest predisposing factor

• Locally invasive - portal vein,IVC and bile ducts

• Can measure alpha-feto protein level (>100mg/ml)

• Dx  CT or MRI in arterial or venous phase

2. Regenerating nodules

• Usually too small to be detected by imaging

• Maybe surrounded by fibrotic septa

• Maybe sideritic regenerating nodules

• Not pre - malignant

3. Dysplastic nodules

• A pre - malignant lesion

• No arterial enhancement

4. Fibro lamellar carcinoma

• Presents in young ptx (5-35)

• Not related to cirrhosis an AFP is normal

• Dx  CT or MRI shows radial scar and calcifications

5. Metastatic disease

• Most common malignant hepatic tumor

• Common primaries are colon, breast, lung, stomach, pancreas, and melanoma

• Mild cholestatic picture

• CT or US guided biopsy for confirmation

• MRI, CT and US features used diagnosed

13. Non - parasitic cysts of the liver. Etiology, pathogenesis, clinical manifestations, diagnosis,
treatment;

1. Simple cysts

2. Multiple cysts arising in the setting of polycystic liver disease (PCLD)

3. Parasitic or hydatid (echinococcal) cysts

4. Cystic tumors

5. Abscesses

 These conditions can usually be distinguished using patient's symptoms, clinical history, and
the

radiographic appearance of the lesion.

 Ductal cysts, choledochal cysts, and Caroli disease are differentiated from hepatic cysts by
involvement of the

bile ducts and are not reviewed in this article.

 In patients with simple liver cysts, it is generally agreed that laparoscopic unroofing offers the
best balance

between efficacy and safety.

 How patients with PCLD should be treated remains less clear because the failure rates for
laparoscopic

unroofing and fenestration are high. Liver resection, though more effective, carries higher risks.

 Treatment of hydatid cysts continues to be controversial. As more experience is reported in

the literature,

indications for PAIR (puncture, aspiration, injection, reaspiration) versus surgery are delineated.

Simple cysts

• The cause of simple liver cysts is not known, but they are believed to be congenital in origin.

• The cysts are lined by biliary-type epithelium, and perhaps result from progressive dilatation of
biliary

microhamartomas.

• Because these cysts seldom contain bile, the current hypothesis is that the microhamartomas
fail to develop

normal connections with the biliary tree.

• Typically, the fluid within the cyst has an electrolyte composition that mimics plasma. Bile,
amylase, and white

blood cells are absent.

• The cyst fluid is continually secreted by the epithelial lining of the cyst. For this reason, needle
aspiration of

simple cysts is not curative, and recurrence is the norm.

Polycystic liver disease

• Adult PCLD (AD-PCLD) is congenital and is usually associated with autosomal dominant
polycystic kidney

disease (AD-PKD).

• Mutations in these patients have been identified in PKD1 and PKD2 genes.

• Occasionally, PCLD has been reported in the absence of polycystic kidney disease (PKD). In
these patients, a

third gene, protein kinase C substrate 80K-H (PRKCSH), has been identified.

• Despite these differences in genotype, patients with PCLD are similar phenotypically.

• In patients with PKD, the kidney cysts usually precede the liver cysts. PKD often results in renal
failure,

whereas liver cysts only rarely are associated with hepatic fibrosis and liver failure.

Neoplastic cysts

• Liver tumors with central necrosis visualized on imaging studies are often misdiagnosed as liver
cysts. True

intrahepatic neoplastic cysts are rare.

• The cause of cystadenomas and cystadenocarcinomas is unknown, but they may represent
proliferation of

abnormal embryonic analogs of the gallbladder or biliary epithelium.

• These cystic tumors are lined with biliary-type cuboidal or columnar cells and are surrounded
by ovarian like

stroma.

• Cystadenoma is a premalignant lesion with neoplastic transformation to cystadenocarcinoma

confirmed by

tubulopapillary architecture and invasion of the basement membrane.

In a retrospective study, Kim et al investigated the value of quantitative color mapping of the
liver’s arterial

enhancement fraction (AEF) in the detection of hepatocellular carcinoma (HCC).

• The investigators determined that when the color maps were analyzed in combination with
multiphasic
computed tomography (CT) scans, the mean sensitivity for HCC detection reached 88.8%, in
comparison with

71.7% sensitivity for HCC detection using the multiphasic CT scans alone.

Hydatid cysts

• Hydatid cysts are caused by infestation with the parasite Echinococcus granulosus.

• The adult tapeworm lives in the digestive tract of carnivores, such as dogs or wolves.

• Eggs are released into the stool and are ingested by the intermediate hosts, such as sheep,
cattle, or humans.

The egg larvae invade the bowel wall and mesenteric vessels of the intermediate host, allowing
circulation to

the liver.

• In the liver, the larvae grow and become encysted. The hydatid cyst develops an outer layer of
inflammatory

tissue and an inner germinal membrane that produces daughter cysts.

• When carnivores ingest the liver of the intermediate host, the scolices of the daughter cysts
are released in the

small intestines and grow into adult worms, thus completing the life cycle of the worm.

Hepatic abscesses

• Hepatic abscesses can be amebic or bacterial in origin.

• Entamoeba histolytica is the causative agent in amebic abscesses. It is contracted by ingestion

of food or

water contaminated by the cyst stage of the parasite. Amebiasis generally only involves the
intestine but

can invade the mesenteric venules resulting in liver abscesses. Its only host is the human.

• Pyogenic abscesses can be a result of instrumentation but are most often caused by ascending
cholangitis in

the setting of biliary obstruction. Microorganisms isolated are most often bowel flora. Other
routes of

contamination include the portal vein and hepatic artery.

• Patients with intra-abdominal infections may present with liver abscesses with extension of
bacteria through

the portal venous system. Hematogenous spread via the hepatic artery in patients with
septicemia is rare.

Laboratory Studies

Little preoperative laboratory workup is required for these patients.

1. Liver function test (LFT) results, such as transaminases or alkaline phosphatase, may be mildly
abnormal, but

bilirubin, prothrombin time (PT), and activated partial thromboplastin time (aPTT) are usually
within the

reference range.

In the setting of polycystic liver disease (PCLD), greater abnormalities in LFT results are found,
but liver failure

is uncommon.

2. Renal function test results, including blood urea nitrogen (BUN) and creatinine levels, are
often abnormal and

should be performed on initial evaluation.

3. GBA - In the presence of hydatid cysts, eosinophilia is noted in approximately 40% of patients,
and echinococcal

antibody titers are positive in nearly 80% of patients.

With cystic tumors, as with simple cysts, LFT results are normal. There may be mild
abnormalities in some patients.

4. Carbohydrate antigen (CA) 19-9 levels are elevated in some patients. Cyst fluid can be sent for
CA 19-9 testing at

the time of surgery as a marker for cystadenoma and cystadenocarcinoma.

Patients with hepatic abscesses can usually be easily identified on the basis of the clinical
presentation.

Leukocytosis is generally present.

5. Enzyme immunoassay (EIA) test detects specific antibodies to E histolytica.

Imaging Studies

The clinician has a number of options for imaging the liver in patients with hepatic cysts.

1. Ultrasonography is readily available, noninvasive, and highly sensitive.

2. CT (see the image below) is also highly sensitive and is easier for most clinicians to interpret,
particularly

for treatment planning.

3. Magnetic resonance imaging (MRI), nuclear medicine scanning, and hepatic angiography have
a limited

role in the evaluation of hepatic cysts.

 Simple cysts have a typical radiographic appearance. They are thin-walled with a homogenous
lowdensity interior.
 PCLD is confirmed by means of ultrasonography or CT, with multiple liver cysts identified at the
time

initial of evaluation.

 Central necrosis of large solid neoplasms can mimic cystic hepatic tumors, in that this area of
necrosis appears

cystic.

 Cystadenoma and cystadenocarcinoma usually appear multiloculated with internal septations,

heterogeneous

density, and irregularities in the cyst wall. Unlike many tumors, cystadenoma and
cystadenocarcinoma are rarely

associated with calcifications.

A practical problem in the evaluation of a patient with a cystic hepatic lesion is differentiating
cystic neoplasms

from simple cysts.

1. Cystic neoplasms tend to have thicker, irregular, hypervascular walls, whereas simple cysts
tend to be

thin-walled and uniform.

2. Simple cysts tend to have homogenous low-density interiors, whereas neoplastic cysts usually
have

heterogeneous interiors with septa and papillary extrusions.

MEDICAL THERAPY

Simple cysts

 No medical therapy has proved effective in reducing the size of simple hepatic cysts.

 Percutaneous aspiration guided by ultrasonography or computed tomography (CT) is

technically simple but

has been abandoned because the recurrence rates are nearly 100%.

 Aspiration combined with sclerosis with alcohol or other agents has been successful in some
patients but has

high failure and recurrence rates. Successful sclerosis depends on complete decompression of
the cyst and

apposition of the cyst walls. This is not possible if the cyst wall is thickened or if the cyst is large.

 Percutaneous catheters should not be placed to drain simple cysts, because the cavity
becomes contaminated,

leading to the development of hepatic abscess.

 Unlike the typical pyogenic hepatic abscess, this problem is difficult to resolve with repeated
catheter placements

because of continued secretion from the cyst epithelium.

Polycystic liver disease/neoplastic cysts

No options are available for the medical treatment of PCLD or cystadenocarcinoma because of
the malignant

potential of cystadenoma, no medical therapy for this lesion.

Hydatid cysts

1. First  surgical or percutaneous therapy

 PAIR (puncture, aspiration, injection, reaspiration) is a percutaneous treatment technique for

hydatid

disease.

 In this minimally invasive method, a needle is introduced into the cyst under ultrasonographic
guidance.

Cyst fluid is aspirated and analyzed. Hypertonic saline or ethanol is then injected and
reaspirated.

 PAIRD (puncture, aspiration, injection, reaspiration, drainage) is similar to PAIR except that a
catheter is

left in place after completion of the procedure. PAIRD is most often used for large cysts.

 Patients should be followed clinically after PAIR treatment. Recurrence is increased in more
complicated

cysts, including those with multiple daughter cysts.

 PAIR should only be performed in highly specialized centers with appropriately trained and
experienced staff.

 In addition, an anesthesiologist should be present for monitoring and treatment in the event of
anaphylactic

shock. Surgeons should be notified immediately in case of complication.

2. Medical adjuvant treatment with antihydatid agents (albendazole and mebendazole).

 In surgical patients, antihydatid agents are generally given perioperatively; and continued only
in those

who have spillage of cyst fluid at the time of operation or to those with cyst rupture.

 Antihydatid agents are used with percutaneous treatment. Medical therapy should be started
4 days before

percutaneous treatment and continued either for 1 month (albendazole) or for 3 months
(mebendazole).
Hepatic abscesses

 Patients with liver abscesses are immediately started on antibiotics/amebicides.

 If abscesses are small, patients may respond to medications alone.

 More likely, these patients will require the addition of percutaneous drainage for eradication.

SURGICAL THERAPY

Simple cysts

Most patients with simple cysts are asymptomatic and require no treatment. When the cysts
become large and

cause symptoms, such as pain, treatment is warranted.

Surgical treatment of simple liver cysts involves

 "Unroofing" the cyst by excising the portion of the wall that extends to the surface of the liver.

 Excision of this portion of the cyst wall at the liver surface produces a saucer-type appearance
in the

remaining cyst so that any fluid secreted from the remaining epithelium leaks into the peritoneal
cavity

where it can be absorbed.

 Although ablating the remaining epithelium with electrocautery or an argon beam coagulator
is possible, this

generally is not required because the volume of fluid secreted each day can be absorbed by the
peritoneum

without any consequence. Furthermore, ablation of the cyst wall can lead to bleeding or bile
leak secondary

to injury to underlying vessels and bile ducts.

 The cyst wall should be sent to pathology to confirm the diagnosis and exclude cystadenoma
or

cystadenocarcinoma as these lesions require enucleation or formal resection in the setting of

cancer.

 Can be done via laparotomy, but today, cyst unroofing can be successfully performed
laparoscopically.

Polycystic liver disease

 In adult PCLD (AD-PCLD), enlargement of the liver occurs slowly and only rarely compromises
liver function.

Only those patients with clearly disabling pain should be considered for surgery.

 In patients with PCLD, the surgical goal is to decompress as much of the cystic liver as possible.
This can be
accomplished by a combination of unroofing and fenestration or, in selected patients, by
resection of the

involved portion of the liver

 Recurrence of symptoms with either procedure is high as new cysts replace those that have
been resected. Small

numbers of patients have been treated with liver transplantation.

Neoplastic cysts

 Several surgical methods for treatment of cystadenoma and cystadenocarcinoma have been
described.

Regardless of surgical technique, all surgical options should result in complete ablation of the
tumor.

 Enucleation and formal resection usually done.

 Fenestration and complete fulguration have also been implemented, although, in this method,
complete

ablation cannot be confirmed by pathology.

Hydatid cysts

All patients with hydatid disease should be considered for percutaneous or surgical treatment
because of the risk of

life-threatening complications of untreated disease.

More complicated cysts are better managed surgically.

Treatment of hydatid cysts is associated with two technical problems:

1. Risk of anaphylaxis from spillage of cyst fluid containing eggs and larvae into the peritoneal
cavity and

2. Recurrence caused by residual eggs in incompletely removed germinal membranes.

 To prevent these problems, most surgeons use a technique in which the cyst contents are
aspirated and replaced

with a hypertonic saline solution to kill residual daughter cysts in the germinal membrane before
unroofing and

pericystectomy.

 The goal of the latter procedure is to excise the germinal membrane, leaving the inflammatory
and fibrous

components of the cyst wall in situ. Attempts to excise the entire cyst wall or to perform formal
hepatectomy

for hydatid cysts have largely been abandoned because of increased surgical morbidity.
Hepatic abscesses

 Usually, by antibiotics and percutaneous drainage.

 If abscesses persist despite attempted percutaneous drainage, surgical drainage is indicated.

 Other surgical indications include large cysts at risk of rupture and abscesses not anatomically
amenable to

percutaneous treatment.

POSTOPERATIVE CARE

 In patients undergoing laparoscopic unroofing of simple hepatic cysts, the orogastric and
bladder catheters

can be removed before the patient awakens from anesthesia.

 A light diet is offered the evening of surgery, and most patients can be discharged home the
following day.

 Generally, recovery is rapid, and most patients resume full activity within 1 week.

 Patients can shower with the waterproof dressings in place the day after surgery. The
dressings can be

removed after 2-3 days.

Complications

 Complications of laparoscopic unroofing of simple liver cysts are uncommon.

 Trocar-site infection is a rare occurrence.

 Unexpected leakage of bile from the cut edges of the cyst can lead to a subhepatic or
subphrenic fluid

collection or, rarely, bile ascites.

 In patients with PCLD, unroofing and fenestration procedures should be performed with care
to avoid injury

to biliary or vascular structures in the compressed hepatic parenchyma between the cysts.

 In patients with hydatid cysts, spillage of cyst contents into the peritoneal cavity, which may
cause

anaphylaxis, is best avoided.

Long-Term Monitoring

 After successful laparoscopic unroofing of a simple liver cyst, the patient is seen at a follow-up
visit within 2

weeks and again 6 weeks after surgery to assess symptomatic relief and to identify
complications, such as

wound infection or ascites.

 Routine radiographic studies are not obtained unless symptoms recur.

14. Liver abscesses: etiology, pathogenesis, clinical manifestations, diagnosis, treatment;

- Refer Question number 13 –

14. Liver abscesses: etiology, pathogenesis, clinical features, diagnosis, and treatment.

A liver abscess is a mass filled with pus inside the liver.

Common causes are abdominal conditions such as appendicitis or diverticulitis due to

haematogenous spread

through the portal vein.

It can also develop as a complication of a liver injury

TYPES

There are several major forms of liver abscess, classified by cause:

1. Pyogenic liver abscess, which is most often polymicrobial, accounts

2. Amoebic liver abscess due to Entamoeba histolytica accounts for 10% of cases. The incidence
is much

higher in developing countries.

3. Fungal abscess, most often due to Candida species, accounts for less than 10% of cases.

4. Iatrogenic abscess, caused by medical intervention

PYOGENIC LIVER ABSCESS

 The most common organisms are Streptococcus milleri and Escherichia coli, but other enteric
organisms such

as Streptococcus faecalis, Klebsiella and Proteus vulgaris also occur, and mixed growths are
common.

 Opportunistic pathogens include staphylococci,

 Common causes 

1. Biliary stone disease + ascending cholangitis. Enterobacteriaceae are especially prominent

when the

infection is of biliary origin. Abscesses involving K pneumoniae have been associated with
multiple

cases of endophthalmitis

2. Instrumentation

3. Other routes of contamination include the portal vein and hepatic artery (sepsis).
a) Haematogenous spread through the portal vein: Other causes of intra-abdominal sepsis 
intraabdominal infections, including appendicitis or diverticulitis

A large pyogenic liver abscess is presumed to be the result of appendicitis

b) Hematogenous spread via the hepatic artery in patients with septicemia is rare.

c) Staphylococcus aureus abscesses usually result from hematogenous spread of organisms

involved

with distant infections, such as endocarditis.

 Increased incidence in the elderly, diabetics and the immunosuppressed.

CLINIC

 Right upper quadrant pain

 Fever (either continuous or spiking)

 Chills

 Anorexia

 Malaise

 Cough or hiccoughs due to diaphragmatic irritation may be reported. Referred pain to the right
shoulder may

be present.

DIAGNOSIS

 Easily identified on the basis of the clinical presentation.

 GBA Leukocytosis is generally present.

 Ultrasound or CT scan  Multiloculated cystic mass

 Aspiration for culture and sensitivity  Confirms dx

TREATMENT

 Patients with liver abscesses are immediately started on antibiotics

 First-line antibiotics  penicillin, aminoglycoside and metronidazole or a cephalosporin and

metronidazole

 If abscesses are small, patients may respond to medications alone.

 More likely, these patients will require the addition of ultrasound-guided percutaneous
drainage for

eradication. Often repeated aspirations may be necessary

 Percutaneous drainage without ultrasound guidance should be performed with caution as an

empyema

may follow drainage through the pleural space.

 If abscesses persist despite attempted percutaneous drainage, surgical drainage is indicated.

 Other surgical indications include large cysts at risk of rupture and abscesses not anatomically
amenable to

percutaneous treatment.

AMOEBIC LIVER ABSCESS

CA  Entamoeba histolytica. It spread by the faecal–oral route.

CLINIC

The most common presentation is with dysentery, but it may also present with an amoebic
abscess, the common

sites being paracaecal and in the liver.

DIAGNOSIS

 Isolation of the parasite from the liver lesion or the stool and confirming its nature by
microscopy.

 Enzyme immunoassay (EIA) test detects specific antibodies to E. histolytica

TREATMENT

 Often patients with clinical signs of an amoebic abscess  Empirical tx with metronidazole
(400–

800 mg t.d.s. for 7–10 days) and investigated further only if they do not respond.

 Resolution of the abscess can be monitored using ultrasound.

 For abscess that is expected to rupture  Aspiration; also helps the penetration of
metronidazole.

72. Topographic anatomy of the mediastinum;

Topographic anatomy of the mediastinum.

Mediastinum - part of the chest cavity, bounded by the rear surface of the sternum - in

front; thoracic spine - back; right and left mediastinal pleura - on the sides; the upper

aperture of the chest - above and the diaphragm - below.

The mediastinum is divided along the horizontal plane through the upper edge of the III rib,

into the upper and lower. By a conventional plane passing frontally through the trachea

and the main bronchi, the mediastinum is divided into anterior and posterior.

The anterior mediastinum contains: the thymus gland, superior vena cava and its

tributaries - brachiocephalic and unpaired, ascending part and aortic arch, pulmonary

trunk, pulmonary veins, phrenic nerves, lymph nodes, trachea and main bronchi; in its
lower section is the heart and pericardium.

In the posterior mediastinum are located: esophagus, lymphatic duct, thoracic aorta,

unpaired and semi-unpaired veins, vagus nerves, sympathetic trunks, pectoral aortic

plexus.

The mediastinum is innervated by the thoracic aortic plexus and its derivatives - the

cardiac, esophageal and pulmonary plexuses.

Blood supply to the mediastinum is carried out by numerous arterial branches originating

directly from the aorta - mediastinal, bronchial, esophageal, pericardial, and from its

branches of the posterior intercostal arteries, from the internal mammary arteries.

The outflow of venous blood occurs in unpaired, semi-unpaired, and internal chest veins.

Lymphatic vessels from the mediastinal organs go to the following lymph nodes:

periosternal, prepericardial, prevertebral, anterior and posterior mediastinal.

73. Etiology and classification of mediastinitis;

74. Clinical features, diagnosis, differential diagnosis, principles of treatment of

mediastinitis;

MEDIASTINITIS CLASSIFICATION

A. By etiology and pathogenesis:

I of . Primary or traumatic;

II . Secondary

- contact (tonsillogenic, odontogenic); - metastatic.

B. By prevalence:

1. Acute lymphadenitis with inflammation of Fiber.

2. Limited inflammation of the mediastinal tissue - abscesses.

3. Spilled (phlegmon).

C. By the nature of the exudate and the causative agent of infection:

1. Serous.

2. Purulent.

3. Putrid.

4. Anaerobic.

5. Gangrenous.

D. Localization:
1.The front.

2. The rear.

3. Total.

E. According to the clinical course:

I Acute mediastinitis:

- fulminant form;

- acute form;

- simple form.

II . Chronic mediastinitis (tuberculosis, syphilitic):

- primarily chronic;

- secondarily chronic.

CAUSES

1. Traumatic mediastinitis due to open and closed injuries; intraoperative injuries, damage

to the esophagus, trachea

2. Odontogenic and tonsillogenic mediastinitis due to inadequate or untimely treatment of

neck phlegmon - 67%.

Clinic of anterior mediastinitis

1. Throbbing pain behind the sternum.

2. The intensification of pain when striking the sternum. Intensive pain

3. Edema in the jugular notch.

4. The appearance of putrefactive and anaerobic forms of crepitus in the jugular cavity.

5. The jugular symptom of Ravich-Shcherbo (retraction in the jugular cavity during

inhalation).

Clinic of posterior mediastinitis

1. Throbbing pain behind the sternum.

2. The intensification of pain when striking the sternum. Intensive pain

3. Edema in the jugular notch.

4. The appearance of putrefactive and anaerobic forms of crepitus in the jugular cavity.

5. The jugular symptom of Ravich-Shcherbo (retraction in the jugular cavity during

inhalation).

6. The appearance of putrefactive and anaerobic forms of crepitus over the clavicle.
7. Paravertebral symptom of Rawicz-Shcherbo and Steinberg (the appearance of rigidity of

the long muscles of the back).

8. Symptoms of compression, mainly of the unpaired and semi-unpaired veins: expansion

of the intercostal veins, effusion in the pleural cavity and in the pericardium.

9. Extension of the boundaries of dullness on both sides of the lower thoracic vertebrae.

10. Compression of the esophagus or cramping it.

11. X-ray - shadows in the posterior part of the mediastinum, with perforation of the

esophagus - leakage of barium from the esophagus into the mediastinum.

Pathogens.

Mixed aerobic and anaerobic microflora - 74%; 26% - only aerobic flora.

Associations of microorganisms included from 2 to 8 types of bacteria - in 87% of cases.

Diagnostics:

- radiography of the neck, chest organs;

- endoscopic research methods (esophagoscopy,bronchoscopy); - uoroscopy and a

graph of the esophagus;

- puncture of the pleural cavities;

- MRI;

-CT.

The treatment of acute mediastinitis is surgical.

1. In case of damage to the upper mediastinum - cervical access, proposed by V.I.

Razumovsky.

2. In case of anterior mediastinitis - rib-sternal drainage from the jugular notch to the

xiphoid process.

3. With total mediastinitis - right-sided thoracotomy, mediastinotomy, ushing drainage of

the mediastinum and pleural cavity.

4. In case of damage to the supraphrenic part of the esophagus - transperitoneal sagittal

diaphragmotomy according to Savinykh-Rozanov.

5. With low located abscesses of the posterior mediastinum, posterior mediastinotomy

according to II Nasilov is most effective.

The most universal and reliable way is mediastinotomy via right-sided thoracotomy.

Only with spontaneous rupture of the esophagus is left-sided thoracotomy.

75. Tumors of the anterior mediastinum, etiology, pathological anatomy, diagnosis,

treatment;

76. Tumors of the posterior mediastinum, etiology, pathological anatomy, diagnosis,

treatment;

Mediastinal tumors are relatively uncommon and there are many different types.

CLASSIFICATION- PATHOLOGICAL

• NEUROGENIC TUMOURS

- MOST COMMON : NEUROFIBROMA, NEURILEMOMA, GANGLIONEUROMA,NEUROBLASTOMA,

NEUROSARCOMA

- OTHERS : CHEMODECTOMA, PARAGANGLIOMA

• THYMOMA - BENIGN, MALIGNANT

• LYMPHOMA – HODGKINSDISEASE ,

• T AND B IMMUNOBLASTIC SARCOMA, SCLEROSING FOLLICULAR CELL

• GERM CELL TUMOURS- , TERATODERMOID(BENIGN AND MALIGNANT)

SEMINOMA, NONSEMINOMA (EMBRYONAL,CHORIOCARCINOMA,ENDODERMAL )

Mediastinal Tumors

Incidence of Mediastinal Tumors is low

– Many years are needed to develop adequate clinical experience Includes a wide variety

of lesions

Clinical presumptive diagnosis is a matter of pattern recognition

– This is inherently difficult

– The approach used by authors is the opposite of what the clinician needs

Approach to Mediastinal Tumors

❖ Known clinical data, always available:

• Age, gender

• Mediastinal compartment location

• Radiographic characteristics

❖ Often available:

• Duration of symptoms

❖ Sometimes available:

• Characteristic presentation: (Myasthenia Gravis, “B” symptoms, associated diseases)

• Laboratory identifiers

Symptoms and associated disorders

❖ Benign/slow growing neoplasms are often asymptomatic

❖ Malignant lesions are frequently symptomatic

❖ Local signs/symptoms Cough Chest pain SVC syndrome Dyspnea, Dysphagia

Cardiac tamponade Associated paraneoplastic diseases (MG, PRCA, Hypogamma,

SLE)

❖ Systemic signs/symptoms B symptoms Fever Night sweats Weight loss Symptoms

and associated

Mediastinum: diagnostic techniques

❖ Non-invasive (Imaging)

• CT • CT/PET • MRI

❖ Minimally-invasive pathologic staging techniques

• Blind TBNA • EBUS-TBNA • EUS-TBNA

• TTNA

❖ Surgical techniques

• Mediastinoscopy • Mediastinotomy

• TEMLA, VAMLA • VATS

Anterior Mediastinum Tumors

• Predominantly Thymoma and substernal Thyroid lesions

• Especially in women, esp. in older age groups

• A few are lymphoma (HD, MLC NHL > LB NHL)

• A few are teratoma in age 40-49 ü ~15% comprised of miscellaneous rare tumors

Anterior Mediastinum Tumors

Thymoma

• Incidence 2.5-3.2/1.000.000 person

• Age onset: 30-40 yrs (with MG); 60-70 yrs (without MG)

• Histotypes: Thymoma (5 subtypes), Thymic carcinoma (TC) and NETT

• Slow onset of symptoms (exception TC/NETT), 30% asymptomatic ü 30-50% associated

Myasthenia Gravis

• Paraneoplastic syndrome (PRCA, Hypogamma, SLE)

• CT signs suggestive for diagnosis

Lymphoma

• Commonly situated in anterior mediastinum Commonest Hodgkin's lymphomas Common

in 40-60 yrs Non Hodgkin’s affects any age.

• Symptoms: fever, wt loss, night sweats, compressive symtoms like pain, dyspnoea,

wheezing, SVC syndrome and pleural effusion.

• Investigations : x-ray , CT scan, cervical lymph node biopsy

• Treatment: Combination chemotherapy Surgery not usually done.

Posterior Mediastinal Tumors: Neurogenic Tumors

❖ Nerve sheath (adults, almost all benign)

• Benign, Neurilemmoma,Neurofibroma, Melanotic schwannoma, Granular cell t.

• Malignant, Neurofibrosarcoma

❖ Ganglion cell (children, young, 2/3 malignant)

• Benign, ganglioneuroma

• Malignant, Neuroblastoma, ganglioneuroblastoma (children)

❖ Paraganglionic tissue

• Benign, chemodectoma, pheochromocytoma

• Malignant, malignant pheochromocytoma

Management - Potentially malignant tumors

• Multiple neurofibromatosis, pain, radiographic signs

• Chest CT; if close to spinal canal

• MRI

• Other imaging (EUS, PET – not well defined)

• Resection, consider multimodality approach

• Long term survival is unusual

Management - Clinically benign, but NeuroFibromatosis:

• If solitary lesion, resect prophylactically

• If multiple, difficult to resect

• Observation

• Poorly defined whether problem is rate of malignant degeneration or development of

new malignant tumor

• Rate of growth of benign lesions is hard to predict

Conclusion

• Optimal evaluation and diagnosis of mediastinal tumors require an integrated clinical,

radiological and histological approach

• Clinical approach includes consideration of the following: age, sex, presence/duration of

symptoms and associated paraneoplastic conditions

• Radiological approach includes CT scan with intravenous contrast; CT scan is essential

to assign the tumor to one of the mediastinal anatomic compartments. MRI and PET-CT

are used on a selective basis.

• Histological confirmation is most often needed for suspected lymphomas and in locally

advanced/unresectable thymic tumors

• More than half of the tumors are in the anterior region, the remaining are equally

distributed in the visceral and paravertebral regions

• In the anterior region the most common tumors are thymomas in adults and lymphomas

in patients < 40 years. GCTs are mostly seen in young males

• In the visceral region more than half of the tumors are cysts. The remaining are

mediastinal involvement from lung cancer and granulomatous diseases.

• In the paravertebral region almost all tumors are from nervous structures. Malignant

forms are typical of infancy or in case of familial neurofibromatosis

OESOPHAGUS (Question 90 - 100)

90. Anatomical and physiological information about the esophagus. Classification of

esophageal diseases. Special methods of examination. General symptoms of

esophageal diseases;

The length of the esophagus depends on age, head position, body length and gender,

fluctuating in women within 23-24 cm, and in men within 25-30 cm. Currently, it is believed

that the length of the esophagus in an adult is on average 25 cm .

The beginning of the esophagus is normal in a 2-year-old child located at the level of 4

cervical vertebra, by the age of 12 - C5, in an adult - C6, and in the elderly - C7. The lower

border is at the level of Th10-11. The cardia is projected onto the anterior surface of the

chest at the level of the VII left rib. The width of the lumen of the esophagus at the level of
the upper border is usually 18 mm, at the level of the lower - 22 mm, and at the level of the

thoracic region 21-25 mm. The thickness of the esophagus wall is on average 3-4 mm.

The entrance to the esophagus is formed from the inside by a lip-shaped fold due to the

excessively developed part m. cricopharynxgeus.

Topographically, 3 sections of the esophagus are distinguished: cervical, thoracic and

abdominal. However, it seems fair to single out the fourth, functionally important

department - the diaphragmatic (physiological cardia).

The cervical esophagus begins at C6 and ends at Th2. This rather short section of the

esophagus (5-6 cm), is completely covered with a layer of loose connective tissue that

passes into the tissue of the upper mediastinum, which makes it quite mobile and supple

when swallowed. In this section, 2 / 3-3 / 4 foreign bodies get stuck. The anterior surface

of this section of the esophagus is adjacent to the trachea and the left lobe of the thyroid

gland, the posterior to the spinal column (C6-Th2.), The lateral to the thyroid gland, carotid

arteries and return nerves.

The thoracic esophagus begins at the upper border of the posterior mediastinum (Th2)

and is pumped at the entrance to the esophageal opening of the diaphragm at the level of

Th9-10. This longest section of the esophagus (16 - 18 cm) is closely adjacent to the

mediastinal pleura and is separated from the prevertebral fascia with a thin layer of loose

fiber. From Th2-6, the esophagus lies to the left of the trachea, at the level of Th3 in front it

crosses with the aortic arch, at the level of Th6 - with an unpaired vein. At a height of Th5,

the esophagus is quite closely adjacent to the left main bronchus and tracheal bifurcation

The embryological community of the trachea and esophagus results in dense connective

tissue and muscle bundles. Underdevelopment or congenital weakness of these elements

contribute to the formation of both congenital and acquired tracheoesophageal fistula. To

the left of the esophagus at this level are the thoracic lymphatic duct, recurrent nerve,

aortic arch, or subclavian artery. At the level of bifurcation, the left and right behind the

esophagus are the vagus nerves. Below the esophagus is adjacent the posterior wall of

the left atrium, separated by the pericardium. 2-3 cm above the diaphragm near the

surface of the left ventricle, the esophagus deviates to the left at an angle. Mediastinal,

paravertebral, para-aortic, and especially tracheobronchial and bifurcation lymph nodes

are adjacent to the esophagus along the entire thoracic region.

The diaphragmatic esophagus , the shortest (1.5-2.5 cm), is located at the level of the

esophagus and very rarely at the level of the general aortic-esophagus, normally at a level

of Th9-10 2-3 cm in front of the spinal column and 1 cm to the left of the midline of the

body. The bro-muscular ring involved in the opening of the cardia ensures its tightness,

and the rather loose fiber inside the diaphragm provides the esophagus with mobility in the

longitudinal direction. This functionally important part of the esophagus, which does not

have a lumen at rest, is called epicardium.

The subphrenic (or abdominal) section of the esophagus , referred to in the literature as

the vestibule of the cardia, has an average length of 3-4 cm (1-7 cm). Its length depends

on the standing of the domes of the diaphragm, the breathing phase, the mobility of the

diaphragmatic esophagus, intrathoracic or intra-abdominal pressure, and other factors.

This section between the dome of the diaphragm and the anatomical cardia is adjacent to

the posterior surface of the left lobe of the liver and is covered in the front and sides of the

peritoneum. In the surrounding loose fiber are the lymph nodes of the cardia and branches

of the vagus and sympathetic nerves. The diaphragmatic and abdominal esophagus are

functionally united and, according to most authors, are physiological cardia.

The outer lower border of the cardia is considered to be the acute angle of the esophagus

entering the stomach, usually formed by the end of the first year of life, - the

angle of His. It represents the angle of transition of one side wall of the esophagus into a

large curvature of the stomach, while the other side wall smoothly passes into a small

curvature. It is believed that functionally this place prevents regurgitation and its

effectiveness directly depends on the severity of the angle of His. The internal lower border

of the cardia is usually recognized as a fold of the mucous membrane (plica cardiaca). The

air bladder of the stomach and intragastric pressure contribute to a snug t of the valve of

the mucous membrane to the right wall, thereby preventing the contents of the stomach

from being thrown into the esophagus. Together with plica cardiaca the antireflux function

is performed by the muscular structures of the cardia at the Z-line level and the cardia

outlet.

Currently, there are 4 physiological narrowing of the esophagus (reduction in diameter by

more than 1/3). In places of narrowing, foreign bodies are more often delayed, injuries,

esophagitis, scars and neoplasms occur. The first narrowing is formed at the entrance to
the esophagus by the pharyngeal-esophageal sphincter at level C6. The second

narrowing, aortic, is less noticeable, its origin is explained by the pressure of the aortic

arch on the esophagus at the Th3 level: this narrowing becomes more pronounced at the

time of passage of food or with aortic sclerosis. At the level of Th5, there is a third

narrowing, due to the depression of the left main bronchus into the wall of the esophagus.

The fourth narrowing is caused by a squeezed esophagus with the legs of the diaphragm

at the level of - Th10. This zone (epicardia) can in pathological cases increase to 7-8 cm.

Esophageal vascularizationin comparison with other parts of the digestive tract, it is less

pronounced due to the lack of a single esophageal artery. The cervical esophagus is

supplied with branches of the lower thyroid and partly the left subclavian arteries. The

thoracic section is vascularized by the branches of the bronchial and intercostal arteries

and the thoracic aorta. The abdominal section covered with the peritoneum is better

supplied with blood than others, receiving food from the lower diaphragmatic and left

gastric arteries (Figure 2). The intramural vasculature is most developed in the

submucosa, from which the arterial plexus nourishes the mucous membrane and muscle.

Blood flows through the venules into a rather complex structure of the venous plexus, the

main collector of which is the central submucosal plexus, lying next to the arterial. The

main venous arteries in the cervical spine are the thyroid and bronchial, in the chest -

paired and unpaired (system of the superior vena cava), in the abdominal - veins of the

stomach and liver (portal vein system). Thus, the veins of the thoracic and abdominal

region create an important portocaval anastomosis in clinical practice.

Esophagus lymph nodes are conditionally divided into 5 groups: lymph nodes of the

common carotid artery, jugular and subclavian veins, bifurcation, paraaortic and cardiac

nodes. Lymphatic drainage is carried out through well-developed lymphatic plexuses in the

mucosa and submucous membranes. For the lymphatic system of the esophagus, a

longitudinal orientation is characteristic, i.e., outflow of lymph either up towards the

pharynx or down towards the stomach. In this regard, metastases in cancer of the

esophagus initially spread intramurally and only later are found in regional lymph nodes.

Sometimes the lymphatic vessels open directly into the thoracic duct, which should

be taken into account in the diagnosis and surgical treatment of cancer. Usually, the lymph

of the cervical esophagus is sent to regional nodes near the trachea (paratracheal nodes)
or along the jugular vein. Lymph of the middle third of the esophagus flows into the

mediastinal, bifurcation and tracheobronchial lymph nodes. From the lower esophagus,

lymph is directed along the organ, so with cancer of this part of the esophagus, cardia or

upper stomach, metastasis to the supraclavicular lymph nodes is possible. The common

development of the esophagus and stomach is also confirmed by the outflow of lymph

from the lower segments of the esophagus to the lymph nodes of the upper stomach and

the frequent development of cardio-esophageal cancer.

The innervation of the esophagus is complex and peculiar. Parasympathetic innervation is

carried out through the vagus and recurrent nerves, sympathetic through the nodes of the

border and aortic plexuses, branches of the pulmonary and cardiac plexuses, the fibers of

the solar plexus and ganglia of the subcardia. Numerous nerve branches form the

superficial anterior and posterior plexuses of the esophagus. The anterior one is formed

mainly by the fibers of the right vagus nerve, the posterior by the left. It is considered

proven the existence of many anastomoses between the nerve structures in the plexuses.

The intramural nervous system consists of 3 closely interconnected plexuses -

adventitious, intermuscular and submucosal. They have peculiar ganglion cells (Dogel

cells) that determine autonomous internal innervation and local regulation of the motor

function of the esophagus. The vagus nerves, with their meat fibers, are connected with

the intramural plexuses, and the non-vagus nerves with other intraparietal plexuses. Some

of the soft fibers are pumped into muscle cells. Thus, the esophagus, like the heart, has its

own autonomous nervous system. Reflex self-regulation is carried out mainly by intramural

plexuses.

The cervical part of the esophagus is innervated by the recurrent nerve, the pectoral part

by the branches of the vagus and sympathetic nerves, and the lower celiac nerve. The

fibers of the recurrent nerve innervate the striated muscles, the sympathetic - the smooth

muscles of the esophagus. Efferent nerve fibers, in addition to muscles, innervate the

glands of the esophagus, and afferent fibers (Th5-7) carry out sensory innervation. The

mucous membrane of the esophagus is sensitive to thermal, pain and tactile irritations,

with the most susceptible distal segments and cardia. The area of the mouth of the

esophagus and the place of physiological constrictions are most sensitive to mechanical

irritation. Sensory innervation is carried out by the vagus nerve, the main regulator of
esophageal motility. The sympathetic nervous system controls the tone of the esophagus.

In this way, the esophagus and cardia contain their own intramural neuromuscular

apparatus, regulated by the central and autonomic nervous system. The innervation of the

legs of the diaphragm, especially the right one, is provided by the branches of the phrenic

nerves.

Histology. The wall of the esophagus consists of 4 layers - the mucosa, submucosa,

muscle and adventitia. Adventitia of the abdominal esophagus passes into the serous

cover.

The mucous membrane of the esophagus consists of 20-25 layers of stratified squamous

epithelium. Its thickness is 0.5-0.8 mm. Closer to the lumen are layers of rejected cells,

scaly cells are located deeper, and behind them are layers of prickly cells on a thin

basement membrane. The esophagus epithelium lies on a thin elastic connective tissue

plate, which in turn is separated from the submucosa by the smooth muscle layer with a

longitudinal arrangement of muscle fibers. Due to the elasticity of the mucous membrane

and its larger surface, in comparison with a powerful annular muscle layer, 3-4 longitudinal

folds are formed in it, most pronounced in the middle and lower parts of the organ.

In the area of transition of the squamous epithelium of the esophagus into the cylindrical

epithelium of the stomach, a dentate border is often located above the anatomical cardia.

The folds of the mucous membrane are collected in the form of a socket and close the

cardia. In the mucous membrane of the thoracic esophagus are small shallow branched

tubular glands that secrete mucus. In their excretory ducts, islets of ciliated epithelium can

be observed, similar to airway epithelial cells. In the distal esophagus,

most often in the abdominal part, there are cardiac glands containing pepsin-producing

parietal cells (similar to the cardiac glands of the stomach). Parts of the mucous

membrane of the esophagus containing hormone-active glands such as ectopic islets of

the gastric epithelium are of great importance in the development of peptic ulcers and

strictures.

The submucous membrane is a layer of loose connective tissue with less mobility, but with

a more powerful network of blood vessels, nerves and glands than the mucous membrane.

In the upper segments of the esophagus, the submucosa contains about 200 deep, or

true, glands. Their long excretory ducts open caudally at an angle into the lumen of the
esophagus. These glands secrete thick mucus that has protective properties. The

submucous membrane has sufficient extensibility, therefore, suturing during surgery does

not affect the mobility and folding of the mucous membrane.

The muscular membrane, the most massive (up to 0.2 cm thick), consists of 2 layers - a

powerful circular and twice as thin longitudinal. Blood vessels and the intramuscular nerve

plexus are located in a small layer of connective tissue. The longitudinal muscle layer of

the esophagus is a continuation of a similar layer of the pharynx and, in turn, passes into

the external muscle layer of the stomach, forming a single functional system. The fibers of

this layer communicate with the vessels supplying them with the muscles of the left main

bronchus and mediastinal pleura. The muscular membrane of the upper third of the

esophagus consists of striated fibers, the lower of smooth muscle, and the middle of mixed

fibers. Occasionally, as a result of genetic or congenital disorders, the musculature of the

esophagus is represented only by striated fibers or only smooth muscles. This structure

predisposes to the development of intramural muscle tumors. Such muscle tumors can

probably arise from islands of “dormant” muscle germ cells, which begin to grow rapidly at

a certain stage.

The thickenings of the circular and spiral-like muscle fibers that are quite visible in the

sections, performing the function of the pulp, are located at the entrance to the esophagus

(pharyngeal-esophageal sphincter) and in the area of diaphragmatic narrowing

(diaphragmatic sphincter). The pharyngeal-esophageal sphincter protects against

retrograde throwing of food into the throat, and the pharyngeal muscle prevents air from

entering the stomach during breathing - the “air-tight sphincter”. The existence of an

independent sphincter in the area of the anatomical cardia has not been conclusively

established.

The outer connective tissue membrane consists of interwoven bundles of collagen and

elastic fibers through which the blood, lymph vessels and nerves supplying all layers pass.

Advent occurs in the periophageal tissue and connective tissue of adjacent organs of the

posterior mediastinum. In the thoracic region, the esophagus is connected to neighboring

organs by its already mentioned muscle formations - esophageal-bronchial, esophagealaortic

and esophageal-pleural muscles. In the distal and abdominal segments covered with

peritoneum, the esophagus is fixed by a powerful muscular-tendon sheath.

The physiological role of the esophagus consists in carrying food from the pharynx to the

stomach. The swallowing process is divided into 3 consecutive phases. The first phase is

to push liquid or chewed solid food from the mouth into the throat. It is proved that as soon

as an arbitrarily swallowed lump of food passes the base of the tongue and palatine

arches, swallowing becomes uncontrollable and the second purely reflex phase of

swallowing begins. The center of the swallowing reflex lies in the medulla oblongata and

the brain bridge. With lesions of these parts of the brain, a violation of the second, reflex,

phase of swallowing is manifested by regurgitation of food in the nasal cavity, mouth and

its aspiration. The third phase is the passage of food through the esophagus through the

cardia into the stomach. The function of the esophagus at this stage seems very simple

and understandable, but in fact it remains to this day the subject of heated debate.

The main importance is given to the advancement of food along the esophagus by the

energy supply created by the spraying effect of the pharynx, others consider gravity and

the hydrostatic pressure of food as the main ones, while others recognize only the role of

active wall contraction. At present, the action of all these factors is recognized with a

predominance of each depending on the quantity and quality of food, body position,

condition of the neuromuscular apparatus of the esophagus and the whole organism. So, a

sip of water quickly, in 2-3 seconds, slips into the stomach, significantly ahead of the active

motility of the esophagus. If you drink a lot of fluid in one gulp, then the esophagus and

cardia gape for a long time without movement and only after the last sip does a peristaltic

wave appear, covering the lumen of the esophagus and cardia. Believed that the third

phase of the act of swallowing liquid food is provided mainly by gravity, hydrostatic

pressure and the injecting effect of the pharynx. The experiment with nerve transection

causing the swallowing reflex and the injecting effect, and observations of the astronauts

in zero gravity showed that the act of swallowing under such conditions does not suffer

significantly and is provided by independent active motility of the esophagus. Further

studies (esophagometry, X-ray cinematography, esophagotonokimograya, etc.) proved the

important role of esophageal motility in promoting any food. The leading role of the

peristaltic wave is clearly manifested when a dense or viscous food lump passes through

the esophagus - swallowing slows down 3-5 times and lasts from 6 to 15 seconds. From

the open mouth of the esophagus, it spreads to the walls of the esophagus, causing a
propulsive peristaltic wave directed towards the stomach. The walls of the esophagus in

front of the food lump open and close behind it. The segmented segmental contraction is

5-6 cm long; ahead of him, an expansion of the lumen of the esophagus is noticeable. The

contraction of the longitudinal muscles causes the food lump to move towards the

stomach, and the ring of circular muscles, contracting behind the lump, does not allow it to

go back. Thus, the advancement of the food lump is ensured by a uniform and consistent

reduction of the muscle layers of the esophagus. The average velocity of the peristaltic

wave is 3-5 cm / s, the duration of the reduction of the upper section is about 2 seconds,

and the lower one is about 3 seconds. The segmented segmental contraction is 5-6 cm

long; ahead of him, an expansion of the lumen of the esophagus is noticeable. The

contraction of the longitudinal muscles causes the food lump to move towards the

stomach, and the ring of circular muscles, contracting behind the lump, does not allow it to

go back. Thus, the advancement of the food lump is ensured by a uniform and consistent

reduction of the muscle layers of the esophagus. The average velocity of the peristaltic

wave is 3-5 cm / s, the duration of the reduction of the upper section is about 2 seconds,

and the lower one is about 3 seconds. The segmented segmental contraction is 5-6 cm

long; ahead of him, an expansion of the lumen of the esophagus is noticeable. The

contraction of the longitudinal muscles causes the food lump to move towards the

stomach, and the ring of circular muscles, contracting behind the lump, does not allow it to

go back. Thus, the advancement of the food lump is ensured by a uniform and consistent

reduction of the muscle layers of the esophagus. The average velocity of the peristaltic

wave is 3-5 cm / s, the duration of the reduction of the upper section is about 2 seconds,

and the lower one is about 3 seconds. the advancement of the food lump is ensured by a

uniform and consistent reduction of the muscle layers of the esophagus. The average

velocity of the peristaltic wave is 3-5 cm / s, the duration of the reduction of the upper

section is about 2 seconds, and the lower one is about 3 seconds. the advancement of the

food lump is ensured by a uniform and consistent reduction of the muscle layers of the

esophagus. The average velocity of the peristaltic wave is 3-5 cm / s, the duration of the

reduction of the upper section is about 2 seconds, and the lower one is about 3 seconds.

In a calm state, a relatively stable pressure of about 10 cm of water is maintained in the

esophagus. Art. Upper and lower physiological sphincters separate this zone of
weakly negative pressure from positive pressure in the pharynx and stomach. The tonic

tension of the circular fibers of these sphincters normally creates the upper and

lower zones of increased resting pressure (20-30 cm water column). Swallowing is

accompanied first by a sharp increase in pressure in the area of the upper sphincter for

tenths of a second, and then within 1 second, a drop in pressure not lower than

atmospheric. The resulting primary peristaltic wave creates an average pressure of 70-90

cm

of water. Art., ranging from 30 to 140 cm of water. Art. As food moves through the

esophagus, the pressure and speed of the peristaltic wave weaken to a minimum. The

lower zone of high pressure creates the abdominal segment of the esophagus. The

pressure in this zone is usually 10 cm water. Art. higher pressure in the cavity of the

stomach. The lower elevated pressure zone is a powerful anti-regurgitation barrier due to

its one-way cross-country ability. If the pressure of 5 cm of water is enough to pass food

from the esophagus into the stomach. Art., then for the artificial reproduction of reflux, it is

necessary to raise the pressure to 100 cm of water. Art. This explains the

absence of gastroesophageal reflux with sharp abdominal compression, upside down

positions and space frights. If the pressure of 5 cm of water is enough to pass food from

the esophagus into the stomach. Art., then for the artificial reproduction of reflux, it is

necessary to raise the pressure to 100 cm of water. Art. This explains the absence of

gastroesophageal reflux with sharp abdominal compression, upside down positions and

space frights. If the pressure of 5 cm of water is enough to pass food from the esophagus

into the stomach. Art., then for the artificial reproduction of reflux, it is necessary to raise

the pressure to 100 cm of water. Art. This explains the absence of gastroesophageal reflux

with sharp abdominal compression, upside down positions and space frights.

Usually, the lower esophageal sphincter opens reflexively 3-5 seconds earlier than the

primary wave of esophageal motility. Recently, much attention has been paid to the

hormonal regulation of the digestive system. Some authors associate the pathology of the

cardiac sphincter with the hormones of the APUD system - gastrin and secretin. Gastrin

increases the tone of the sphincter and further increases the level of high blood pressure.

Intravenous infusions of secretin, on the contrary, reduce the pressure and tone of the

cardiac sphincter. Thus, the functioning of the esophagus is regulated not only by the
central and autonomic nervous system, but also by the endocrine system of the digestive

tract. This ensures a normal act of swallowing, coordination of the activity of sphincters

and muscle, layers of the esophagus, creating propulsive peristalsis. Outside of the act of

swallowing, a secondary peristaltic wave can occur in the esophagus, inferior in amplitude

and force to the primary. This non-swallowing peristalsis is called “purifying” or “sentinel”. It

occurs in response to irritation of the esophagus by food debris, foreign bodies or

retrogradely abandoned contents. The function of the esophagus is affected by mental

factors and somatic suffering of the organs of the abdominal and thoracic cavities
(viscerovisceral and vago-vagal reflexes). The type of food or thoughts about it, fear, fright, joy

change the tone of the esophagus and sometimes lead to its motor dysfunction. Irritation

of the trachea and bronchi of the stomach, duodenum, gall bladder, diaphragm and other

organs can be accompanied by dyspeptic disorders of the esophagus.

Classification of diseases of the esophagus

I. Congenital diseases of the esophagus:

1. Atresia.

2. Strictures.

3. Idiopathic expansion.

4. Cardiac failure or chalasia.

5. Doubling the esophagus.

6. Undescended stomach or short esophagus.

II. Acquired diseases of the esophagus:

1. Functional diseases of the esophagus:

a) achalasia or cardiospasm;

b) esophageal spasm or dyskinesia of the esophagus;

c) chalasia or cardia failure.

2. Esophageal diverticula:

a) pharyngeal-esophageal (Zencker diverticulum);

b) the esophagus proper (bifurcation, supraphrenic). 3. Varicose veins of the esophagus.

III. Esophagus injuries:

a) closed and open injuries of the esophagus; b) foreign bodies of the esophagus;

c) chemical burns of the esophagus:

· Concentrated acids;

· Concentrated alkalis.

IV. Benign and malignant tumors of the esophagus.

Special methods for examining the esophagus

1. X-ray method. This is a simple, safe and quite physiological method. It allows one to

study with great confidence the topography, anatomical structure and, in particular, the

functional state of the esophagus. A standard X-ray examination has no contraindications.

It can be performed even in patients in an extremely serious condition, when the use of

other instrumental methods is completely excluded. In all cases, the radiologist must

adhere to the principle of “from simple to complex” and strive with a minimum of methods

to get the most information.

An X-ray examination begins with an overview uoroscopy of the organs of the chest and, if

necessary, the abdominal cavity (first stage). The purpose of a chest x-ray in patients with

a suspected esophageal disease can be the identification and evaluation of concomitant

pathological changes in the lungs and heart, as well as the detection of foreign bodies and

signs of organ wall perforation. This tactic of pre-contrast research often reveals important

radiological symptoms.

The next stage is a contrast polypositional study of the esophagus, combining uoroscopy

and radiography. Contrasting of the esophagus should begin with the use of a regular

liquid barium suspension of sour cream-like consistency (100 g of barium sulfate in 100 g

of water). Good pneumorelief and contrast of the esophagus can be obtained by asking

the patient to drink liquid barium suspension in one gulp, in large sips or in small portions,

like hot tea. Sometimes for a more detailed study of the relief it is necessary to examine

patients in the positions of Trendelenburg or Quincke (the pelvis or legs are located above

the head). For better visibility of the folds of the esophagus, substances that increase its

viscosity (gum arabic, etc.) are added to the barium suspension.

An important place is the study of the general appearance of a tightly contrasted

esophagus. When using the “tight lling” method with liquid barium suspension, such

organic lesions of the esophagus as strictures, ring-shaped narrowing, tumors, diverticula,

nodes of varicose veins, paraesophageal and sliding hernias of the esophageal opening of

the diaphragm, ulcerative defects of the mucous membrane are well detected. More
precisely, the localization and size of foreign bodies can be determined. To detect

perforation of the wall of the esophagus, the use of water-soluble contrast is

recommended.

Since the use of X-ray examination is especially useful in assessing the contractility of the

esophagus, i.e., its peristalsis, it provides significant assistance in the diagnosis of

gastroesophageal reux disease, cardiac achalasia and cardiospasm. In this case, the aim

of the study is to identify the ability of the cardia to open in response to swallowing, to

detect spontaneous or provoked gastroesophageal reflux, which indicates cardiac

insufficiency, and to evaluate the speed and effectiveness of expelling the reflux contrast

mass, the esophageal clearance, from the esophagus.

When using the double contrasting technique by using a suspension of finely dispersed

barium, which has more pronounced adhesive properties, and simultaneously spraying the

organ with gas, it is possible to more accurately assess the relief of the mucous

membrane, to reveal small erosions and ulcers, to diagnose not only pronounced, but also

moderate and even initial forms of esophagitis of various etiologies.

Functional X-ray diagnostics (pharmacodiagnostics, thermodiagnostics, respiratory tests,

pressure tests, etc.) by influencing regulatory mechanisms makes it possible to objectively

interpret the physiology and pathophysiology of the esophagus in the clinic. Diagnostic

(single) intake of neuro- and myotropic substances allows to identify a number of

functional disorders and promotes early recognition of anatomical lesions of the

esophagus. In practical work, the following pharmacological tests are more often

used: morphine (0.25-0.5 ml of a 1% solution intravenously or 0.75-1 ml of a 1% solution

subcutaneously with an examination of the esophagus after 7-10 minutes), atropine (1-1, 5

ml of a 0.1% solution subcutaneously with a study after 10-15 minutes), metacin (2-4 ml of

a 1% solution subcutaneously or intramuscularly with a study after 15 minutes),

prostigmine (1 ml)

2. Endoscopic examination of the esophagus.With the help of broesophagoscopy, it is

possible to most objectively assess the condition of the esophageal mucosa: to determine

the severity of inflammatory changes, mechanical and chemical damage, to identify ulcers

and erosion, fistulas, and metaplasia zones of the epithelium. The method is highly

informative in identifying benign and malignant neoplasms, including in the early stages of
their development. Significant help in this can be provided by chromoscopy - the use of

various dyes (Lugol's solution, indigo carmine, toluidine blue) in order to contrast the

surface of the mucous membrane. Thanks to this technique, areas with altered epithelial

lining become more visible. The indisputable advantage of endoscopy is the ability to

perform targeted biopsies from clearly pathologically altered or suspicious sections of the

mucosa and obtain material for histological and cytological studies. In addition, during the

study, the elasticity and extensibility of the wall of the esophagus can be determined,

which is especially important in the diagnosis and determination of treatment tactics for

strictures of various origins.

With esophageal strictures, an esophagoscope can be used to conduct an Eder-Pustow

bougon guide, and then the esophagus is dilated and dilated. For the treatment of postburn
strictures, lidase can be injected directly into the scar tissue through an endoscope.

Sometimes, with mechanical stenosis of different etiologies, a hollow tube is inserted

through an endoscope to facilitate nutrition through a narrowed area. Endoscopic sclerosis

of the dilated veins of the esophagus is widely used by chipping the bed of a vessel or

intravenous administration of a sclerosing drug. Electrocoagulation of the source of

bleeding, polypectomy is also performed through an endoscope according to clinical

indications.

An especially valuable advantage of endoscopy is the ability to extract foreign bodies of

the esophagus with exciting forceps, loops, baskets, scissors and other special devices.

3. The manometry of the esophagus. It is rarely used in practice, however, with its help it

is possible to quantify the speed and amplitude of peristaltic waves, the duration of the

opening of the lower esophageal sphincter, obtain information about the length and tone of

the lower esophageal sphincter, its localization with respect to the diaphragm, and in some

cases reveal a sliding hernia of the esophagus aperture. Thus, the method is very useful in

the differential diagnosis between diseases such as insufficiency of the lower esophageal

sphincter in gastroesophageal reflux disease, cardiac achalasia and cardiospasm, diffuse

esophageal spasm, scleroderma.

4. Sample with a solution of methylene blue. This is a less sensitive than pH meter

methodology for the qualitative detection of gastroesophageal regurgitation. The study

consists in aspirating the esophageal contents through a probe after introducing a glass of
liquid through it into the cavity of the stomach, tinted with 3 drops of a methylene blue

solution. The appearance of stained contents in the esophagus indicates cardiac

dysfunction and gastroesophageal reflux.

5. CT. With the help of CT, which allows to obtain a series of images of transverse

sections of the neck, chest, upper floor of the abdominal cavity, the depth of structural

damage to the esophagus wall can be most reliably estimated, which is especially

important when determining the local spread of the tumor process. In this case, computed

tomography with great accuracy reveals metastases in distant organs. This allows you to

more accurately determine both the stage of the malignant neoplasm, as well as

indications for surgical and combined treatment methods, to evaluate the effectiveness of

the therapy in repeated studies. In addition, with the help of CT, benign formations of the

esophagus (polyps, leiomyomas, fibromas, neurobromas, adenomas, cysts), foreign

bodies, organ compression from the outside can be detected.

6. Endoscopic sonography- endoscopic ultrasound surpasses computed tomography

in the ability to determine the stage of a tumor according to TN classification. With

significantly greater reliability, it is possible to identify enlarged periesophageal lymph

nodes. The accuracy in determining the T and N stages of esophageal carcinoma with

endoscopic sonography reaches 85% and 75%, respectively, and with CT - 60% and 74%.

The method owes its accuracy to the analysis of the details of the image of the five- layer

structure of the wall of the upper gastrointestinal tract. The disadvantages of the method

include the impossibility of holding the instrument further than the proximal edge of the

lesion site in case of severe stenosis of the esophagus, as well as low specificity in

assessing the benign or malignant nature of enlarged lymph nodes. Besides,

7. pH Metrics of the esophagus. The method can be used both for a monitor study of the

intraesophageal medium, and for various functional tests characterizing the motor activity

of the esophagus and the effectiveness of the cardiac closure mechanism. 24-hour

intraesophageal pH monitoring is the most sensitive and specific test for the diagnosis of

gastroesophageal reflux disease and is considered the “gold standard”. At present, 6- and

12-hour monitor studies are also used with sufficient accuracy.

8. Radionuclide scintigraphy of the esophagus is a non-invasive method for diagnosing

disorders of the motor function of the esophagus and its transport ability. The researcher is
given a drink of a colloid labeled with technetium (99mTc) diluted in water. Using a gamma

camera connected to a computer, a series of scintigrams of the segments of the

esophagus and stomach are performed. Only as a result of this study is it possible to

quantify gastroesophageal reflux and the rate of emptying of the esophagus. The

sensitivity of the method reaches 90%. Thus, radionuclide scintigraphy is the most

sensitive non-invasive test for the quantitative demonstration of reflux.

9. Acid perfusion test . It was proposed in 1958 by Bernstein and Baker, which serves to

elucidate the causes of the appearance of typical symptoms of esophagitis and the

differential diagnosis of cardiac and esophageal genesis of pain. A 0.9% solution of sodium

chloride is injected into the esophagus of the subject at a rate of 6-7.5 ml / min for 15-30

minutes. Then the solution is replaced with 0.1N hydrochloric acid. The test is considered

positive if the administration of 0.1 N hydrochloric acid causes pain, heartburn and other

typical symptoms of esophagitis, and with the repeated administration of a 0.9% sodium

chloride solution, these complaints disappear.

As follows from the foregoing, a fairly wide range of diagnostic methods are currently used

for instrumental examination of the esophagus, from which it is necessary to choose the

necessary in each specific clinical situation.

General symptoms of esophageal pathology

Dysphagia is a disorder of any phase of the act of swallowing. Esophageal dysphagia is a

disorder of the third phase of swallowing. Extra-esophageal and intra-esophageal

dysphagia are distinguished.

Extra-esophageal dysphagia is divided into upper, middle and lower.

Upper esophageal dysphagia is caused by diseases of the thyroid gland, lymph nodes,

muscles, spine and other organs, as well as numerous central and peripheral disorders of

the nervous regulation of the functions of the mouth, pharynx and mouth of the esophagus.

Muscular discoordination, paresis or paralysis of one or more muscles involved in the act

of swallowing leads to its disorder. Nutrition, especially the intake of liquid food, in such

patients is difficult due to its easier throwing into the nose or respiratory tract. Swallowing

is impaired by hypofunction of the salivary glands, xeroses, or an overdose of atropine and

its derivatives. This often painful dysphagia should be called dry. After the abolition of

atropine, dysphagia and pain quickly disappear.

Often dysphagia occurs in hysterical individuals. Sometimes such psychogenic dysphagia

is accompanied by exhaustion due to an imaginary fear of food. Emotions, stressful

moments, eating dry food or in a hurry and other factors can cause even a healthy person

a short-term attack of dysphagia (episodic or functional dysphagia). Upper dysphagia often

becomes a secondary manifestation of the underlying disease and is observed in the

practice of neuropathologists, otorhinolaryngologists, psychiatrists, and oncologists.

Middle extra-esophageal dysphagia is usually an indirect symptom of the pathology of the

posterior mediastinal organs (vessels, nerves, lymph nodes, heart, pleura, connective

tissue, etc.). Expansion of the heart chambers (to a “bovine heart”), atriomegaly with mitral

defect, abnormalities of the heart, aorta, subclavian artery, tumors and pericardial cysts,

mediastinum are usually accompanied by mild dysphagia, and malignant tumors and

metastases make dysphagia a formidable cardinal sign of the disease.

Tumors and cysts of the diaphragm, Bohdalek hernia, hepatomegaly, splenomegaly cause

lower extra-esophageal dysphagia.

Intraesophageal dysphagia has a similar division.

Spasms of the mouth of the esophagus (pharyngoesophageal achalasia), Zenker

diverticula, foreign bodies, acute and chronic inflammations of the oral mucosa, pharynx

and larynx, xerosis, Plummer-Winson syndrome, and others are mildly severe mild

dysphagia lead to upper intraesophageal dysphagia. , which causes a conditioned reflex

fear of food in patients.

Average intraesophageal dysphagia can be caused by both functional neuromuscular

disorders and organic lesions (esophagitis, ulcers, strictures, tumors, diverticula, etc.).

Dysphagia after ingestion of any food is more characteristic for esophagitis, after liquid -

for functional pathology, after solid - for organic narrowing of the lumen by a tumor,

stricture, stenosis.

Lower intraesophageal dysphagia often reflects chalasia and achalasia, hiatal hernia,

reflux esophagitis, ulcers, strictures, including circular stricture of the esophagus, tumors,

transcardial displacement of the mucous membrane, epiphrenic diverticuli, and others from

rare , hernias and tumors) there is a special type of dysphagia with variable intolerance to

hot, cold, sour, fatty, solid or liquid food.

The paradoxical dysphagia, in which solid food passes better than liquid, and large pieces
of food is better than small ones, is described in the literature as a symptom of

Lichtenstern. Scleroderma esophagopathy is usually accompanied by increased

dysphagia with a horizontal position of the body, although this symptom is also

characteristic of chalasia, hernias, esophagitis, and cancer. It is important to emphasize

that dysphagia does not always indicate cancer stenosis, however, it should always cause

the thought of cancer. When dysphagia appears, patients tend to panic, identifying it with

cancer. Dysphagia caused by cancer is progressing, it is stable and pronounced.

Typically, patients refuse first solid and rough food (second courses), then from porridge

and soups (first courses) and, finally, from liquids (third courses). Sometimes in the

dynamics of dysphagia can weaken or even disappear, allowing you to completely eat

lunch, which is explained by ulceration and decay inside the tumor. This “bright” period of

false remission is usually short-lived, and dysphagia again becomes a cardinal clinical

manifestation of the disease.

Pain is a frequent manifestation of both functional disorders and organic lesions of the

esophagus and cardia. Painful sensations are usually localized at the level of the lesion -

usually behind the sternum, occasionally with radiation to the neck, jaw, shoulder, back,

epigastric region (pain abdominal syndrome). Pain along the esophagus can be

associated with eating and be accompanied by dysphagia, occur on an empty stomach,

after eating, spontaneously or at night.

Functional disorders are accompanied by pain behind the sternum during meals or in

stressful situations. It is fundamentally important to exclude angina pectoris or myocardial

infarction in such cases. Dysphagia and pain with dysfunction are not associated with

physical activity, the ECG is normal, taking nitroglycerin does not help. Esophageal hernia

or large epiphrenic diverticulum when filled with food leads to afternoon pain. Reflux

esophagitis and esophagitis are accompanied by pain after taking acidic or spicy foods,

after belching with eaten food, in a prone position. With achalasia, pain can occur either on

an empty stomach in the morning or at night in the form of prolonged pain crises and

combined with dysphagia. The decompensated stages of achalasia weaken the pain

syndrome until it completely disappears (an important difference from cancer), apparently

due to a decrease in the sensitivity of the mucous membrane. Pain in cancer of the
esophagus can occur during or immediately after a meal, localizing above the tumor (prestenotic
esophagitis and cramping) or be constant, localizing below the tumor

(periesophagitis and mediastinitis, vagus nerve compression). Germination of a tumor in

the mediastinal tissue causes irradiation of pain and the interscapular region, and

germination in the nerve trunks is accompanied by intercostal neuralgia. Constant pain

along the esophagus is sometimes explained not by a tumor of the organ itself, but by

metastases to the spine. Constant pain or its constant irradiation with cancer of the

esophagus indicates a neglected pathological process. localized below the tumor

(periesophagitis and mediastinitis, vagus nerve compression). Germination of a tumor in

the mediastinal tissue causes irradiation of pain and the interscapular region, and

germination in the nerve trunks is accompanied by intercostal neuralgia. Constant pain

along the esophagus is sometimes explained not by a tumor of the organ itself, but by

metastases to the spine. Constant pain or its constant irradiation with cancer of the

esophagus indicates a neglected pathological process. localized below the tumor

(periesophagitis and mediastinitis, vagus nerve compression). Germination of a tumor in

the mediastinal tissue causes irradiation of pain and the interscapular region, and

germination in the nerve trunks is accompanied by intercostal neuralgia. Constant pain

along the esophagus is sometimes explained not by a tumor of the organ itself, but by

metastases to the spine. Constant pain or its constant irradiation with cancer of the

esophagus indicates a neglected pathological process.

Heartburn is a burning sensation behind the sternum in the xiphoid process. Heartburn

happens on an empty stomach or after a hearty meal, a lot of sweets, spices or spicy

dishes. Often it appears in a horizontal position, with physical work and a bent state,

during pregnancy. The mechanism of the occurrence of heartburn has not been fully

clarified, but it is considered the response of an already irritated wall of the esophagus (for

example, with esophagitis) to retrogradely abandoned stomach contents (often acidic).

In most cases, heartburn is a sign of reflux esophagitis, chalasia, scleroderma, hiatal

hernia, occurs after inadequate surgical correction of the cardia, pylorocardial

discoordination syndrome, and other conditions. Alkalis, alkaline mineral waters and

adsorbents relieve heartburn, but often it soon arises with renewed vigor. Heartburn

associated with alkaline reflux (with achilic gastritis, after gastrectomy) is relieved by weak
solutions of organic acids or diluted hydrochloric acid. Using pH-metry and

esophagotonokimograi it was shown that in patients suffering from heartburn, the pH in the

stomach is reduced to 3-5.

It is fundamentally important to distinguish heartburn from a sensation of heat behind the

sternum in coronary insufficiency. Functional tests with nitroglycerin or soda can help

diagnose. The progressive disappearance of heartburn and the occurrence of dysphagia

are prognostically unfavorable, indicating the development of peptic stricture as a result of

reflux esophagitis or cancer in the presence of chronic esophagitis

Belching and regurgitation - involuntary sharp ejection of air or a mixture of air with gastric

contents into the mouth from the esophagus or stomach cavity. Often this unpleasant

process for the patient is accompanied by a loud sound. Belching is close to belching, i.e.,

belching with food and air, more often observed in children.

Belching with air after a plentiful meal, carbonated drinks is physiological. In neuropaths,

and sometimes in healthy individuals, with salivation, forced feeding of lying, diseases of

the abdominal cavity (peptic ulcer, tumors, cholecystitis), aerophagy causes a sonorous

burping of air.

Belching usually occurs spontaneously 10-20 minutes after eating. It can be acidic in

hyperacid conditions or due to fermentation acids in the absence of hydrochloric acid in

the stomach. Bitter belching reflects biliary duodenogastroesophageal regurgitation, and

belching with rancid oil reflects fermentative dyspepsia of the stomach. The putrid smell of

belching is due to the decomposition of tissue and food debris with stenotic cancer of the

esophagus, cardia or stomach.

Bad breath - can be a sign of not only a tumor, but also esophagitis, peptic ulcer and

stricture, hernia, diverticulitis, achalasia. Since a person is able to distinguish up to 10,000

odors, one should reckon with the patient's subjective perception of the smell from his

mouth.

Subjective cacosmia means a constant or periodic sensation by the patient himself of bad

breath (rot, rotten eggs, etc.), but objectively the source of bad breath is not detected. With

objective cacosmia, a real source of unpleasant odor is clinically revealed (caries,

periodontal disease, stomatitis, sinusitis, purulent tonsillitis, lung destruction, esophagitis,

esophageal cancer, chalazia, etc.).

Rumination is a rare form of regurgitation of food in humans and frequent in mammals. It

consists in re-chewing and swallowing food thrown from the stomach into the mouth in

humans or into the cavity of the room (the initial part of the stomach) in ruminants.

Sometimes the term is called regurgitation of food only in infants, recognizing this

symptom as physiological for newborns and pathological for adults.

Esophageal vomiting represents a combined state of expulsion (filling) and expulsion of

the esophagus (expulsion), i.e., emptying of the filled esophagus. True esophageal

vomiting is performed by the antiperistaltic contractions of the muscles of the enlarged

esophagus with organic cardia stenosis (tumor, ulcer, achalasia). The upper esophageal

sphincter does not withstand the pressure created by a sharp spasm with a distorted

longitudinal orientation. In fact, this is chalazia of the mouth of the esophagus with

achalasia of the cardia. Fountain vomiting more often occurs after a hearty meal with the

last piece of food or when going to bed, tilting the body, straining. Esophageal vomiting

indicates a neglected pathology of the cardia. Sometimes cardia failure, pyloric stenosis

cause vomiting similar to esophageal, but in these cases it is accompanied by nausea and

occurs with the participation of the muscles of the stomach.

Esophagus bleeding- This is a spontaneous discharge from the mouth of red blood. The

ejection of a small amount is an eructation of blood, and abundant ejection is bloody

vomiting. With esophageal bloody vomiting, a real source (varicose veins, cancer, ulcer) of

bleeding is located in the esophagus itself, profuse bleeding from the mouth with relatively

little pronounced chalk occurs, bleeding begins at night or after a hearty meal (increased

blood ow). A similar picture can be given by cardia cancer, ruptures of the mucous

membrane of the gastroesophageal junction (Mellory – Weiss syndrome), hypochromic

anemia (Plummer – Winson syndrome), infringement of a paraesophageal hernia, covered

aortic aneurysms, tracheoesophageal fistulas. Esophageal varicose nodes are the most

common cause, but profuse bleeding can cause damage to the lungs, blood vessels, and

even capillaries.

Hiccups in patients with damage to the esophagus indicate involvement of the phrenic

nerve. Most often this happens with cancer of the esophagus, but can be observed with

esophagitis, achalasia, complicated hernias, scleroderma esophagopathy, when the

mediastinal tissue is affected (periesophagitis). In cancer of the cardia, hiccups can be

caused by damage to the branches of the vagus nerve.

Many diseases of the esophagus are accompanied by a number of secondary, nonspecific

local and general clinical manifestations that are closely related to the underlying disease:

hypersalivation with esophagitis, hoarseness of the voice during germination of the

recurrent laryngeal nerve tumor, heaviness in the chest, shortness of breath, weakness,

loss of appetite, exhaustion in cancer, attacks of nocturnal cough with achalasia, nervous

tic with dyskinesias.

91. Chemical burn of the esophagus: etiopathogenesis, classification, clinical

picture, diagnosis, differential diagnosis;

92. Complications of esophageal burns: clinical features, diagnosis, treatment;

93. Chemical burns to the esophagus. Clinic of the acute period. First aid and

treatment guidelines in the acute period;

Damage to the esophagus caused by ingestion of acids or alkalis is called toxic toxic

esophagitis. These substances are taken for the purpose of suicide or by mistake. Acids

cause coagulation necrosis of tissues with the formation of a dense, dry scab of curled

proteins, which protects the deeper layers of the organ from damage. Caustic alkalis

cause coalification necrosis with the destruction of neutral fats and complex lipids by the

type of saponification, therefore such burns are deeper with a more unpleasant prognosis.

The severity of the burn depends on the concentration, amount, chemical nature of the

substance taken, the duration of its contact with the esophagus wall, the degree of filling of

the stomach at the time of poisoning, the timing of first aid.

When the esophagus chemical burns can occur simultaneously burns of the mouth, larynx,

from e to the lung, acute respiratory failure. This is observed in at e IU acetic acid and

ammonia because of their volatility and vapor when exposed to concentrated acids.

Pathological anatomy . The most pronounced changes occur in places of physiological

narrowing - in the epiglottis, pharyngeal-esophageal sphincter, at the level of tracheal

bifurcation, over physiological cardia.

As a result of a chemical burn, the mucous membrane of the oral cavity, pharynx,

esophagus, and stomach is damaged. Followed by hyperemia and e com mucosa tissue

necrosis occurs rapidly. By the end of the 1st week, the rejection of necrotic areas from the

underlying tissues begins and the formation of superficial or deep ulcerations. Superficial
ulcerations epiteliziruyutsya (1 - 2 months yatsa ) deep - to heal with the formation of

granulation tissue and connective tissue (2 - 6 months ). Cicatricial narrowing of the

esophagus is formed more often in several places; the surrounding tissue is often involved

in the process. The cicatricial-ulcerative process in the esophagus after chemical burns

can last for years. As a result, in individual patientscicatricial narrowing of the esophagus

occurs even after 10 to 20 years from the time of the burn.

Thus, with a burn, four stages of pathological changes can be distinguished:

Stage I - hyperemia and of the mucous membrane

Stage II - necrosis and ulceration

Stage III - the formation of granulations

Stage IV - scarring.

Clinic and diagnosis . The clinical picture of a chemical burn of the esophagus consists of

symptoms caused by the local action of chemically active substances, and manifestations

of intoxication.

Four stages of the clinical manifestations of the disease are distinguished:

Stage I - acute (period of acute corrosive esophagitis);

Stage II - stage of chronic esophagitis (stage of "imaginary well-being");

Stage III - the stage of stricture formation (organic narrowing of the esophagus);

Stage IV - stage of late complications (obliteration of the lumen, perforation of the

esophagus wall, the development of cancer).

According to the severity of acute phase in three degrees isolated esophageal burn: light

(first), moderate (second) strand(third).

The first degree burn is the result at e ma inwardly a small amount of caustic agent in a

low concentration. In this case, the surface layers of the epithelium are damaged in a

larger or smaller section of the esophagus.

The second degree of burn is characterized by more extensive necrosis of the epithelium

to the entire depth of the mucous membrane.

The third degree of burn - necrosis captures the mucous membrane, submucosal and

muscle layers, spreads to para-esophageal fiber and neighboring organs.

The defeat of esophageal acid may be accompanied by lesions of the stomach, and initial

jejunum with the emergence of areas of necrosis and perforation of that Veda e t to the
development of peritonitis in acute as well as scar deformity of the stomach afterwards.

The I acute phase (5 - 10 hours) in patients after at e ma acid or caustic appear severe

pain in the mouth, pharynx, chest, epigastric, profuse salivation, frequent vomiting,

dysphagia due to esophageal spasm in the burn area and by mucosa. Swallowing is

difficult or impossible. Patients excited, scared. The skin is pale, moist. Breath is frequent,

there is a tachycardia. Shock manifestations of various degrees are noted: agitation or

lethargy, lethargy, poor reaction to the environment, drowsiness, acrocyanosis,

tachycardia, decreased blood pressure, dull heart sounds, decreased urine up to anuria. A

few hours after the burn along with symptoms of burn shock symptoms of toxemia:

increase in body temperature to 39 ° C , lethargy replaced excitation sometimes arise

delirium, muscle under. Respiration is frequent, shallow, pulse rate up to 120 - 130 per

minute, blood pressure is reduced due to hypovolemia. In patients painful thirst appears as

a result of dehydration, with electrolytemia. During a blood test, leukocytosis, a shift of the

leukocyte formula to the left, an increase in ESR, an increase in hematocrit, hypo- and

dysproteinemia are noted. The cord e mated cases there is hyperkalemia, hyponatremia

and chloropenia, metabolic acidosis.

Diseases and damage to the esophagus

With concomitant burn larynx and the vocal cords may be hoarseness, difficult g Goes

breath asphyxia. The cord e mated cases develops toxic damage of parenchymal organs

(acute printed e night and renal failure). Poisoning with vinegar essence can cause the

development of intravascular hemolysis. In patients jaundice appears, urine acquires the

color of meat slops, says bilirubinemia, hemoglobinuria, anemia increases. As a result of

aspiration, patients may develop tracheobronchitis, pneumonia. With direct damage to the

vessels in the burn area, early bleeding occurs.

Sometimes on 5 - 7 hours developing psychosis (due to trauma, pain, burn toxemia).

Stage II - the stage of "imaginary well-being" (lasts from 7 to 30 days). By the end of the

1st week, the rejection of necrotic tissues of the esophagus begins. Ingestion of liquid food

becomes somewhat freer, bleeding is possible. With deep necrosis, perforation of the

esophagus occurs with the development of symptoms of mediastinitis, pericarditis,

empyema of the pleura, esophageal-bronchial fistula. Amplified chest pain and back pain,

shortness of breath and tachycardia increases body temperature becomes hectic nature,
chills replaced by heavy sweats, formation of subcutaneous emphysema, cough

appearance at at e IU of liquid food. Aspiration that occurs in the acute period can be

manifested by symptoms of acute tracheobronchitis, pneumonia, lung abscess. The cord

gIn rare cases, in the presence of extensive wound surfaces on the walls of the

esophagus, sepsis may develop. The latent period is characterized by dysfunction of the

parenchymal organs, which is due to dystrophic changes, protein starvation.

By the end of the month (stricture formation step) under the influence of treatment of

burned esophageal areas heal. In 10 - 15% of patients with the X-ray examination show no

longitudinal folding mucosa, single or multiple sections of different narrowing of the

esophagus Length. In 20% of cases, by the end of the month, the phenomena of

"intermittent" dysphagia increase. At esophagoscopy celebrate different Length areas

where healing occurs slowly. The wound surfaces are covered with a dense scab, bleed

easily.

Scar formation is possible in the last few months.

In the long term (up to 2 - 3 years) after a burn (stage of late complications), dysphagia

comes first in the clinical course. From starvation, the patient's condition progresses with

willow worsens. In addition to strictures, the development of cancer, perforation of the

esophagus wall and complications such as pneumonia, lung abscess, bronchiectasis,

diverticula, esophageal-bronchial fistula are possible.

Emergency care for chemical burns of the esophagus and treatment in the acute period

Treatment should begin as early as possible.

First aid is the early administration of analgesics, neutralization and excretion of a

chemical substance. To reduce salivation and relieve esophageal spasm, atropine,

papaverine, ganglion blockers are administered. It is advisable to rinse the mouth, the

appointment of antihistamines (diphenhydramine, suprastin, etc.). An important measure is

gastric lavage with a rubber probe. Depending on the nature of the received substances

for gastric lavage using weak solutions or acid. When the drink is expedient burn acids 2%

- sodium hydrogen carbonate, magnesium oxide (LJ g hydrochloric magnesia) Almagelum

at Poisoning alkalis - 1 - 1.5% acetic acid solution. In the first 6 to 7 hours, antidotes are

administered.

Inpatient treatment consists in carrying patients antishock and disintoxication therapy

(used glucose-novocaine mixture neuroleptics reopoligljukin, albumin, zhelatinol, plasma,

electrolyte solutions).

To normalize the activity of the cardiovascular system, cardiac glycosides, corticosteroids

are prescribed. The correction of metabolic acidosis is carried put g m of 5% sodium

bicarbonate solution. To combat hypovolemia, parenteral nutrition is carried out for 3 to 4

days. For the prevention of secondary infection and pneumonia, broad-spectrum

antibiotics are prescribed.

In order to prevent esophageal cicatricial narrowing of patients with 1st day given every 30

- 40 minutes to 1 - 2 Throat Medicine, containing s sunflower oil, benzocaine, 5%

novocaine solution, an antibiotic, a 3rd of the day they are fed Cooling food. When taking

medicine and food early, it’s as if carrying out a “soft” bougienage of the esophagus. The

appointment of corticosteroids (cortisone, prednisone) also prevents the formation of

scars. It is now recognized expedient to hold early (9 - 11 days) bougienage esophagus for

1 -1.5 months in combination with subcutaneous administration of lidase or ronidase for 2

weeks. Too early, before this term started probing yes e t the opposite effect, causing an

exacerbation of inflammation in the esophagus and increased scarring. Before starting the

bougieurage, it is necessary to perform an esophagoscopy, which will establish the degree

of burn, the absence of neotrotic necrotic tissue.

Gulping of the esophagus is unsafe and may be complicated by its perforation with the

development of purulent mediastinitis and pleurisy, therefore it should be carried out with

great care.

For the prevention of cicatricial stenosis of the esophagus is applied hyperbaric

oxygenation, which reduces the depth of necrosis zone delimits leukocyte infiltration

contributes to the clearance of the wound surface and causes epithelialization e g the end

of 1 month. Hyperbaric oxygenation inhibits the formation of connective tissue, which leads

to the development of a more loose, thin and elastic scar of the esophagus.

If early bleeding occurs, hemostatic therapy is performed.

In case of poisoning with vinegar essence and the development of intravascular

hemolysis, alkalizing therapy (5% sodium bicarbonate solution) and forced diuresis are

necessary.

With the development of acute renal failure, hemodialysis is indicated.

With damage to the larynx and the development of asphyxia , a tracheostomy is applied to

patients . With perforation of the esophagus, urgent surgical intervention is necessary.

94. Cicatricial narrowing of the esophagus: location and shape of the constriction,

clinic, diagnostics, treatment. Indications for probing. bougienage methods;

Cicatricial narrowing of the esophagus. Post-burn strictures have significant Length and

often located in areas of physiological narrowing of the esophagus. Depending on the

depth of damage esophageal wall are formed of different stricture Length. Allocate Space

strictures that are thin membrane thickness of a few millimeters, annular - thickness of 2 -

3 cm, tubular - length of 5 - 10 cm and more, subtotal and total. The strictures can be

single or multiple, complete or incomplete. The course of the stricture is often tortuous,

eccentrically located. With sharp narrowing, a suprastenotic expansion of the esophagus

occurs.

Clinic and diagnosis . The main symptom of post-burn stricture is dysphagia, which

appears from 3 to 4 weeks after the onset of the disease. At first, dysphagia is not

pronounced, it occurs sporadically, accompanied by unpleasant sensations behind the

sternum. Over time, narrowing of the esophagus progresses, as the surface of the

narrowed area is exposed to food trauma, which is accompanied by an inflammatory-scar

process. The severity of dysphagia increases, complete obstruction of the esophagus may

develop. Food retention causes chest pain and regurgitation. With high stenosis of the

esophagus, food during ingestion can enter the respiratory tract, causing laryngospasm,

painful coughing and suffocation.

When long-existing narrowing of the distal esophagus, accompanied by his suprastenotic

extension, the contents of the esophagus is exposed to chemical and bacterial

degradation, which causes an inflammatory process leading to greater esophageal

stenosis, development. Regurgitation in these cases occurs after a considerable period of

time after eating. Among other symptoms of post-burn narrowing of the esophagus often

have chest pain when under g food IU, increased salivation, belching, heartburn. As a

result of malnutrition, patient exhaustion progresses .

One of the most common complications of cicatricial narrowing of the esophagus is

obstruction of the esophagus with food, which requires emergency medical attention

(esophagoscopy to remove the food lump). Chronic inflammatory diseases of the bronchi
and often develop l e soft due to regurgitation and aspiration of food e g in the respiratory

tract. As a result of longitudinal cicatricial shortening of the esophagus, the formation or

increase of a hiatal hernia is possible. Perhaps the development of a cancerous tumor in

the area of stricture. In patients with stenosis, more often than in healthy people,

perforation of the esophagus is observed during instrumental studies.

The diagnosis of esophageal stenosis is confirmed by anamnesis and X-ray examination

with a liquid and a thick contrast medium (Figure 3) . The narrowing of the esophagus has

a tubular shape, the relief of the mucous membrane in the area of narrowing is absent,

peristalsis is not determined. As a result of scarring and inflammation, the lumen of the

esophagus in the narrowing area has an irregular shape. Above the stricture, there is often

suprastenotic expansion, increased peristalsis occurs.

With esophagoscopy, the presence of esophagitis, pockets, scars is detected.

Both methods allow the investigation to clarify the extent, location, Length narrowing its

course, the presence of suprastenotic expansion esophageal- bronchial fistula.

Treatment . The main method of treating esophageal stricture after a chemical burn is

bougieurage, which leads to a stable recovery of 90 - 95% of patients.

Unlike the early one, later bougienage is carried out in order to expand the already

developed narrowing of the esophagus. Begin bougienage from 7 weeks. Bougienage

shown all patients with post-burn esophageal strictures when conduct through the

constriction metallic conductor. Contraindications to bougieurage: mediastinitis,

esophageal-bronchial fistula. To achieve a persistent clinical effect, treatment with

bougienage must be carried out for many weeks and even months . Apply:

1) "blind" walk through the mouth;

2) expansion of the esophagus by radiopaque hollow plastic bougie along a metal

conductor;

3) bougieurage under the control of an esophagoscope;

4) bougieuding on the principle of "bougieuding without end";

5) retrograde bougieurage.

Probing blindly through the mouth it is indicated in small-Length annular strictures of upper

and middle chest esophagus. Treatment is carried out using a special set of bougie. If the

bougie is easy, bouge is carried out next to the thickness of the number.
The method of bougieument was improved with the use of metal conductors and

radiopaque hollow bougie. They provide the opportunity for x-ray control to determine the

course of stricture and advance the bougie along the esophagus, which increases the

effectiveness of the procedure and reduces the risk of perforation of the esophagus.

Probing under the control of an esophagoscope is indicated with an eccentrically placed

stricture, a convoluted narrowing channel, a pronounced suprastenotic expansion, when

difculties arise when conducting a conductor.

"Probing without end" is used in the presence of gastrostomy in patients with tubular,

convoluted or multiple strictures, enter constant derived through the mouth and through

the gastrostomy tube is attached rubber tubes of different diameters. Stretching, they are

carried out through the narrowed area and left for several hours. Retrograde bougienage

through the gastrostomy is safer and easier for patients to tolerate .

In some cases, mechanical expansion of the cicatricial strictures of the esophagus can

lead to the formation of esophagitis. A dangerous complication of bougienage is

perforation of the esophagus and the development of mediastinitis.

At present, balloon plastic surgery of cicatricial narrowing of the esophagus under the

control of endoscopy or uoroscopy is actively used as an alternative to bougie. Apply

electrical dissection of rigid strictures.

Indications for surgery for cicatricial strictures of the esophagus: 1) complete obliteration of

the lumen of the esophagus;

2) repeated unsuccessful attempts to conduct a bougie through stricture; 3) rapid

recurrence of scar strictures after repeated bougieurage;

4) the presence of esophageal fistula with trachea or bronchus;

5) expressed extends stricture;

6) repeated perforation of the esophagus during bougieurage.

In COG g scrap depletion for feeding patients applied gastrostomy as the rst stage of

treatment.

When choosing a method of operation take into account the age and general condition of

the patient , location and Length narrowing of the esophagus. In most cases , one-stage

plastic surgery is performed. Multi-stage plastic surgery is performed in debilitated patients

.
With segmental strictures, various types of partial plastics of the esophagus are produced.

When defeat lower esophagus or gastric cardia used: overlay bypass gastroesophageal

anastomosis resection hitting g nnogo portion and its replacement by a tube formed from a

large curvature of the stomach, the graft from the small or large intestine. With damage to

the pharynx, cervical or cervicothoracic esophagus, proximal partial plasty is performed.

Use transplants from the small or large intestine. One end of the graft is anastomosed with

the esophagus above and the other below the narrowing. With extensive strictures, the

total plasticity of the esophagus with pre- sternal or intrathoracic (retrosternal, intrapleural,

posterior mediastinal) transplant from the small or large intestine is shown.

The creation of an artificial esophagus should not be started earlier than 2 years after the

burn. Only after this period, the degree of scarring of the esophagus can be revealed and it

becomes clear that the formed scar tissue will not allow to expand the lumen of the

esophagus by conservative methods.

95. Cardiospasms (achalasia): etiology and pathogenesis, classification, clinic,

diagnostics, treatment. Indications for surgical treatment, types of operations;

Achalasia of the cardia (cardiospasms) is a neuromuscular disease of the esophagus,

manifested by a violation of the passage of food masses into the stomach due to

persistent disturbance of the reflex opening of the cardia during swallowing, changes in

peristalsis and weakening of the tone of the esophagus wall.

The incidence rate is 0.5-0.8 cases per 100,000 population. The first symptoms of the

disease are more likely to occur at the age of 20-40 years. More often women are ill.

Etiology. Etiological factors are:

• Innate malformations esophagus nervous system (degeneration intermuscular ( A

uerbahova) plexus);

• Constitutional neurasthenia with the occurrence of neurogenic discoordination of the

motility of the esophagus;

• Reflex esophageal dysfunction;

Infectious toxic lesions of the nerve plexuses n the esophagus and cardia.

Pathogenesis. In the area of the esophageal-gastric transition there is a sphincter - a

physiological cardia. In healthy people, he is at rest in a state of tonic contraction, and after

swallowing, he relaxes.
With cardiospasm, increased cardia pressure is observed, the gradient of esophagealgastric
pressure can reach 20 mm Hg. Art. and more at a rate of 10 + 3 mm RT. Art. The

initial stages of cardiospasm are characterized by increased non-propulsive motility of the

esophagus. Morphologically, degenerative-dystrophic changes are found in the

preganglionic neurons of the dorsal nuclei of the vagus nerves and, to a lesser extent, in

the postganglionic neurons of the Auerbach plexus of the esophagus. It is believed that

due to a violation of central innervation during cardiospasm, the smooth muscles of the

lower esophageal sphincter become more than usual sensitive to its physiological

regulator - endogenous gastrin. Thus, with this variant of the course of the disease, a true

spasm of the cardia is observed.

With achalasia of the cardia, on the contrary, mainly postganglionic neurons are affected,

as a result, the reflex of opening the cardia to the throat falls out. Manometrically and a

normal or even reduced gradient of esophageal-gastric pressure, there is a significant

weakening of the motility of the esophagus. With achalasia, there are no conditions for the

occurrence of increased sensitivity of the smooth muscles of the lower esophageal

sphincter to gastrin - the central innervation is preserved.

Therefore, the main differences between cardiospasm and achalasia of the cardia are

different levels of parasympathetic nervous system damage and the related changes in the

sensitivity of the smooth muscles of the lower esophageal sphincter to its main

physiological hormonal regulator - endogenous gastrin.

Clinic and diagnosis . A triad of symptoms is characteristic: dysphagia, regurgitation, pain.

Dysphagia is the main and in most cases the first symptom of the disease. It can occur

suddenly, as if in the midst of full health, or develop gradually. Strengthening of dysphagia

in the majority of patients is observed after neural stimulation, during a hasty meal, while at

g IU dense, dry and bad living or e bathroom food. Sometimes paradoxical dysphagia is

observed: dense food passes into the stomach better than liquid and semi-liquid.

A number of patients dysphagia depends on the temperature of the food: bad passes or

does not pass t e Playa food, and cold runs, or vice versa. Patients gradually adapted to

facilitate the passage of food into the stomach via the series for g mov (walking, gymnastic

exercises, saliva and swallowing of air when g m large amount Ploy water, etc.). Severe

cachexia is rarely observed.

Regurgitation with a small expansion of the esophagus occurs after several sips of food,

with a significantly expanded esophagus it is more rare, but plentiful and is due to strong

spastic contractions of the esophagus that occur when it is full. Regurgitation at position l g

Ms and under strong torso content due to mechanical pressure on the esophageal

sphincter pharyngoesophageal and stretching. Night regurgitation is associated with a

slight decrease in the tone of the pharyngeal-esophageal sphincter.

The pain behind the sternum is diverse. It may be associated with spasm of the

esophageal muscles and eliminated by e IOM nitroglycerin, atropine. However, in most

patients, pain occurs when the esophagus is full and disappears after burping or passing

food into the stomach. In some cases , there were sporadic attacks of pain in the chest on

the type of pain crises Such pain is more often observed in the initial period of the disease,

sometimes the development of dysphagia and regurgitation, which are not always

removed by atropine or nitroglycerin, which suggests their connection with a progressive

dystrophic process in the intramural nerve plexus of the esophagus. Pain on an empty

stomach or after vomiting is often caused by esophagitis and is relieved by eating.

Belching by air, nausea, increased salivation, burning along the esophagus, bad breath

are also caused by esophagitis.

The most common complication of the disease is congestive esophagitis, which occurs

with prolonged retention of food masses in the esophagus. The L g mild cases, it is

manifested by hyperemia and e com mucosa, more COG g mated - presence of rough and

uneven folds, erosions, ulcers, which usually are located slightly above the necked portion.

In the future, bleeding, perforation of the esophagus, periesophagitis may develop.

Chronic esophagitis can cause cancer of the esophagus and cardia.

Common complications are repeated aspiration bronchopneumonia, lung abscesses,

pneumosclerosis. These complications are especially common in children. Complications

caused by compression of the enlarged esophagus of the recurrent nerve, right main

bronchus, superior vena cava, vagus nerve, etc. are described.

B. In Petrovsky identies four stages of the disease:

Stage I - functional intermittent spasm of the cardia, expansion of the esophagus is not

observed;

Stage II - stable spasm of the cardia with an unsharp expansion of the esophagus;
Stage III - cicatricial changes in the muscle layers of the cardia with a pronounced

expansion of the esophagus;

Stage IV - pronounced stenosis of the cardia with dilatation of the esophagus, often Sshaped,
and esophagitis.

The main diagnostic methods are X-ray examination, esophagoscopy,

esophagotonokimograya, pharmacological tests.

With a non-contrast radiological examination of the chest, an additional bulging of the right

mediastinal contour, the presence of a fluid level in the projection of the posterior

mediastinum, and the absence of a gas bubble of the stomach are revealed. Basic

radiographic signs - narrowing of esophagus with terminal h e IMT, smooth and flexible

circuits ( "ame pens g rnutoy candle", "Mouse tail"). The folds of the mucous membrane in

the narrowing area are preserved. The first sips of barium can freely enter the stomach,

then the contrast mass is retained for a long time in the esophagus. A layer of liquid and

food debris are determined above the barium suspension. The expansion of the

esophagus over the site of its narrowing is expressed to varying degrees. In a number of

patients lengthening and curvature of the esophagus.

The peristalsis of the esophagus in all patients is sharply impaired: contractions are

weakened, have a spastic character and insufficient amplitude. With the development of

esophagitis, changes in the relief of the mucous membrane of the esophagus are visible:

granularity, thickening and tortuosity of the folds

Esophagoscopy allows you to conrm the diagnosis, identify complications and conduct a

differential diagnosis with other diseases accompanied by dysphagia. The endoscopic

picture depends on the duration of the disease. At the beginning of the disease esophagus

widened slightly, as the disease progresses the lumen Sun g more expanded and in some

patients it becomes crimped. The mucous membrane has signs of inflammation: the folds

are thickened, the arteries and veins are enlarged, and areas of hyperemia, erosion,

leukoplakia, and ulceration are often visible. Typically, the end esophagoscope navigate

through the narrowed portion, which supports advantageously the functional nature of the

changes in the esophagus. The mucous membrane at the site of narrowing is most often

not changed.

Esophagotonokimographic research is the main method of early diagnosis, as violations of

the contractility of the esophagus and physiological cardia occur much earlier than the

clinical symptoms of the disease. The study is carried out using a special multichannel

probe with rubber cartridges or "open" catheters that record reductions in the esophagus

and changes in the esophageal pressure. Normally, after swallowing, a peristaltic wave

propagates through the esophagus, the cardia at this moment opens

and the pressure decreases. After the passage of the peristaltic wave, the cardia closes

again. With cardiospasm (cardiac achalasia), there is no reflex relaxation of the cardiac

sphincter during swallowing, and intraluminal pressure remains at the previous figures.

In doubtful cases, pharmacological tests are used to confirm the diagnosis. Nitroglycerin

reduces the tone of the esophagus and physiological cardiac sphincter, which facilitates

the passage of the contents of the esophagus into the stomach. The introduction of

cholinotropic drugs (acetylcholine, carbocholine, mecholilus) has a stimulating effect on

the muscular layer of the esophagus wall and on the cardiac sphincter. With

cardioesophageal cancer and organic stenosis of the esophagus, both samples are

negative.

Treatment . Conservative treatment is used only in the initial stages of the disease, and is

also used as an addition to cardiodilation and in preparing patients for surgical treatment.

Food should be mechanically and thermally gentle, rich in proteins, vitamins. The food is

fractional, the last meal 3 to 4 hours before bedtime. Reducing dysphagia in I - II stages of

disease can achieve put g m nitro application of preparations - nitroglycerin, amyl nitrite

With symptoms of esophagitis is used stagnant rinse esophagus weak solution

antiseptics . The therapeutic effect is noted after physiotherapeutic procedures :

electrophoresis (iontophoresis) with novocaine, deep diathermy in the region of the cardia,

long-wave diathermy, etc.

The main method of treatment is cardiodilation, which consists in violent stretching and

partial tearing of the muscles of the distal esophagus and cardia. Cardiodilation can be

performed at any stage of the disease.

Contraindication to the use are, portal hypertension with esophageal varices, expressed

esophagitis, blood diseases, accompanied by bleeding disorders. Surgical treatment is

aimed at eliminating the obstruction of the esophageal-gastric transition. Indications for it

are:
1) the inability to carry out cardiodilation;

2) lack of therapeutic effect after repeated courses of cardiodilation;

3) diagnosed esophageal ruptures that occur during expansion of the cardia;

4) pronounced peptic strictures that developed after overstretching of the cardia and are

not amenable to conservative therapy and bougieurage;

5) a sharp expansion, S-shaped curvature of the esophagus in combination with cicatricial

changes in the cardia.

Currently, operations based on extra mucosal cardiomyotomy are used. Heller

extramucous cardioplasty is performed from abdominal access, producing a longitudinal

dissection of the muscular membrane of the terminal esophagus along the front and back

walls for 8 - 10 cm.

Heller's surgery is combined with esophagofundoraphia or Nissen fundoplication to

prevent the development of peptic esophagitis. Intervention is performed both from

traditional open access and using laparoscopic techniques.

96. Esophagism: etiopathogenesis, classification, clinical picture, diagnosis,

treatment, indications for surgery, types of operations;

Esophagospasm is a disease of the esophagus due to spastic contractions of its wall

during normal cardia function. More often men are ill, mostly middle and old.

Etiology . Idiopathic (primary) and reflex (secondary) esophagospasm are distinguished.

The cause of primary esophagospasm is a violation of the function of the nervous system

and innervation of the esophagus. Secondary esophagospasm is caused by viscerovisceral

reflexes and is combined with other diseases (peptic ulcer, neoplasms of the

esophagus and stomach, cholecystitis, peptic esophagitis, hiatal hernia, atherosclerosis,

angina pectoris, etc.).

Clinic and diagnosis. The clinical picture is dominated by pain behind the breastbone that

appears during the passage of food through the esophagus, has a different intensity, may

radiate to the back, jaw, neck, arms and others. The pain can occur is when yo food ma,

feigning an attack of angina pectoris. For esophageal spasm is characterized by unstable

dysphagia and often e e paradoxical character, which allows to differentiate this disease

from cancer, esophageal stricture and achalasia, in which less dense food passes and

zapivanie e e relieves water. During severe spastic contractions of the esophagus, there
may be regurgitation of a small amount of just taken food in the mouth.

X-ray investigation reveals changes of the esophagus as "h e current",

"pseudodiverticulum", "spin" (Figure 5) . The diameter of the esophagus above and below

the narrowed areas is not changed, the walls of the esophagus are elastic, the folds of the

mucous membrane are longitudinal, the peristalsis is uneven and irregular. Repeated x-ray

examinations usually preserve the same type of peristalsis disorder.

Esophagoscopy is uninformative and is important only to exclude organic diseases of the

esophagus.

An esophagotonokimographic study reveals spastic contractions of the esophagus in the

form of waves of various shapes and amplitudes, while peristaltic contractions are also

recorded. The reflex relaxation of the cardiac sphincter is constantly determined.

A pharmacological test with acetylcholine and carbocholine is negative.

Treatment . Comprehensive treatment of patients with idiopathic (primary)

esophagospasm includes prescribing a sparing diet, antispasmodic and sedative drugs,

vitamins, and physiotherapeutic procedures. In the absence of a positive effect from

conservative therapy, esophagomyotomy (according to the type of Heller operation) is

performed to the level of the aortic arch. Treatment of secondary esophagospasm should

be aimed primarily at eliminating the root cause, then it is necessary to influence the

corresponding links of pathogenesis.

97. Esophageal diverticula: classification, clinical picture, diagnosis, indications for

surgery, options for operations;

The diverticulum of the esophagus is a saccular protrusion of its wall.

Classication. According to the pathogenetic origin, diverticula are divided into pulsion,

traction and mixed.

Pulsed diverticulums are formed due to protrusion of the esophageal wall under the action

of high intraesophageal pressure that occurs during its contraction.

Traction diverticulums are formed due to the involvement of the esophagus wall in

inflammatory and adhesion processes that develop in the mediastinal tissue , most often

against the background of tuberculosis or nonspecific lymphadenitis.

The traction mechanism is observed at the very beginning of the development of the

diverticulum, then the pulsion factors join, as a result of which the diverticulum becomes
pulsion-traction.

According to the topographic the principle at the distinction faringoezofagealnye (border)

Zenker's diverticulum, bifurcation (epibronhialnye) and epifrenalnye (supradiaphragmatic)

diverticula of the esophagus.

Distinguish congenital and acquiring diverticula esophagus true (retaining body structure)

and false (lacking the tunica muscularis). False diverticula at substantially are hernia

(protrusion mucosa through weaknesses muscular wall), which indicates that their

acquired character.

Clinic and diagnosis. Pharyngeal-esophageal diverticula (Figure 7) are observed in men 3

times more often than women, they come from the posterior pharyngeal wall at the level of

the cricoid cartilage of the trachea, where between the constrictors there is an area that is

not covered by muscles (the Lanier-Hackerman triangle), and are by the mechanism of

occurrence of pulsion. Purely esophageal diverticula are less commonly observed in this

area. They come from the Lymer triangle, which is bounded above by the cricoidpharyngeal
muscle, and from below and on the sides by bundles of longitudinal muscles of

the esophagus.

An increase in pressure in the pharyngeal cavity and in the area of the “mouth” of the

esophagus can lead to the formation of a diverticulum along with the discoordination of

muscle contractions. With small sizes, the diverticulum bag is located behind the pharynx

and esophagus, large diverticuli, reaching significant sizes, are localized to the left of the

midline. Traction diverticulums of this area, developing after operations on the neck

organs, are also described.

The Zenker diverticulum in the initial stage may not show anything, sometimes patients are

disturbed by a feeling of awkwardness, “scratching” in the throat while eating - then such

patients are mistakenly treated for diseases of the pharynx or larynx. As the diverticulum

progresses when food enters it and the esophagus is compressed, characteristic

symptoms appear - dysphagia, regurgitation (often during sleep, which can lead to

aspiration), halitosis. With large diverticula in the region of the left half of the neck, elastic

protrusion can be detected, with pressure on which a characteristic “rumbling” is

determined. Sometimes symptoms of compression of neighboring structures are also

observed (swelling of the cervical veins, shortness of breath, palpitations, hoarseness of

the voice, etc.). With the development of diverticulitis and peridiverticulitis, pain occurs in

the neck, back of the head, behind the sternum.

Bifurcation diverticulums (Figure 8) are located mainly on the anterior or anterior-right wall

of the esophagus and, as a rule, are traction by the mechanism of occurrence.

Inflammatory processes in the lymph nodes and other formations of the mediastinum lead

to the development of adhesions, scarring and stretching of the wall of the esophagus.

This is confirmed by operational ndings, in which dense adhesions of the diverticulum with

lymph nodes, trachea, and bronchi are always revealed. Bifurcation diverticuli are smaller

in size than the Tsenker diverticula.

Small bifurcation diverticula, usually asymptomatic, are detected as an accidental finding

in an X-ray contrast study. With more or less large diverticulums with a long and narrow

neck that prevents their emptying, characteristic chest pain (sometimes simulating angina

pectoris), back pain, hypersalivation, belching, less often dysphagia (segmental

esophageal spasm) appear. Pain can be associated with both diverticulitis and

peridiverticulitis, and with the development of segmental esophagitis in the neck of the

diverticulum. Symptoms of compression of neighboring organs are also detected -

palpitations, shortness of breath. Bifurcation diverticula are often combined with a cardiac

hernia of the esophageal aperture of the diaphragm and reflux esophagitis, with symptoms

characteristic for this suffering (heartburn, belching, regurgitation, epigastric pain). With the

development of diverticulitis, severe ulceration and perforation of the diverticulum can

occur (mediastinitis, esophageal-respiratory fistula). Perforation of the diverticulum can

occur in the superior vena cava or aorta, causing fatal bleeding.

Epiphrenic diverticula, first described by Deguis in 1804, are pulsional and are often of

considerable size, usually located on the anterior or anterior-right wall of the lowest third of

the esophagus. It is believed that the main role in their occurrence is played by congenital

weakness of the esophagus wall in this area. Here he deviates to the right of the midline,

and then to the left, so the food lump, constantly acting on the right wall of the esophagus

more than the left, can lead to the formation of a diverticulum. The pulsed mechanism of

the occurrence of epiphrenic diverticula is confirmed by the fact that they are often

combined with cardiospasm and hiatal hernia (Figure 9).

Epiphrenal diverticula with small sizes and a wide neck may not manifest clinically. With
large diverticulums, especially complicated by diverticulitis, the clinical picture becomes

bright: chest pain is characteristic (sometimes as with angina pectoris), less often -

belching, regurgitation, dysphagia, esophageal bleeding. With perforation, the

esophagealrespiratory and esophageal-mediastinal fistulas often develop. Similar complications
arise

when foreign bodies get into the diverticulum. In approximately 20% of patients with such

diverticulums, other diseases simultaneously exist (cardiospasm, reflux esophagitis),

which must be taken into account when developing a treatment plan. Against the

background of chronic diverticulitis, a cancerous tumor may also occur.

In the diagnosis of all types of esophageal diverticulums, the main role is played by a

polypositional radiopaque study, which makes it possible to accurately identify the

localization, size, shape of the diverticulum, and concomitant diseases. If barium

suspension is retained in the cavity of the diverticulum for more than 2 minutes, then

development of diverticulitis can be assumed. A thorough examination of the diverticulum

wall allows you to exclude the diagnosis of a tumor (polyp, cancer), as well as various

complications (fistula). The exact localization of the diverticulum, as well as the condition

of the cardia, is necessary for the selection of rational surgical access (it is known that a

combination of a diverticulum with a cardiac hernia of the esophageal opening of the

diaphragm is possible).

An esophagoscopic examination undoubtedly clarifies the diagnosis, reveals changes in

the mucous membrane of the esophagus and the diverticulum itself, localization, size of

the neck, and the presence of various complications - bleeding, fistula, polyp, and cancer.

Treatment.Conservative treatment is indicated for small, easily emptying diverticulums

without diverticulitis, a poor clinical picture, and also if there are contraindications for

surgery (severe concomitant diseases, especially cardiopulmonary diseases). The

meaning of conservative treatment is to reduce the possibility of developing diverticulitis or

to eliminate it in cases where the operation is contraindicated. The patient is prescribed a

sparing diet - optimal temperature food, well-machined, not causing irritation of the

mucous membrane of the esophagus (spicy foods and alcohol are excluded). For

mechanical purification of the diverticulum, it is recommended to take vegetable oil before

meals, and after a meal to drink several sips of water. With a combination of a diverticulum

with a hiatal hernia and reflux esophagitis, appropriate treatment is performed.

With pharyngeal-esophageal (Tsenkerovsky) diverticulum, the operation is performed by

cervical access. The diverticulum is isolated, excised, the wound is sutured in the

transverse direction in layers on a thick probe inserted into the esophagus to prevent

stenosis. Sometimes, staplers are used to remove the diverticulum, with which the neck is

stitched in the transverse direction, and then the clips are covered with a second row of

interrupted sutures. For the prevention of relapse, it is also advisable to cross in the

longitudinal direction the lower constrictor of the pharynx along the posterior wall below the

neck of the diverticulum.

For surgical treatment of bifurcation diverticulums, diverticulectomy and Girard

invagination are used. The operation is performed by transpleural access. Perform rightsided
thoracotomy in the fifth or sixth intercostal space. Having highlighted the diverticulum

from all sides, its base is stitched either with the help of staplers, or a U- shaped catgut

seam is applied. When applying U-shaped catgut sutures after removing the diverticulum,

the mucosa is stitched again with the same thread. Then impose nodal sutures on the

muscular membrane of the esophagus. The seam lines can be strengthened with a pleural

flap, diaphragm, and alloplastic tissues. Diverticulum invagination is used for small

diverticula, which when immersed in the lumen can not cause narrowing of the lumen of

the esophagus. The diverticulum is invaginated using a purse-string or single-row nodal

suture,

Surgical treatment of epiphrenic diverticulums. Currently, the operation of choice is a

diverticulectomy. Use left or right access on the seventh-eighth intercostal space. Dissect

the mediastinal pleura, distinguish a diverticulum; the diverticulum neck is stitched with a

mechanical (preferably) or continuous catgut suture or synthetic suture with an atraumatic

needle. The second row of sutures is applied to the muscular membrane of the

esophagus. The line of sutures is strengthened by a flap of the diaphragm, mediastinal

pleura, lung, alloplastic tissues. Since epiphrenic diverticula are sometimes combined with

cardiac achalasia, in such cases the removal of the diverticulum is supplemented by

Heller's esophagocardioplasty.

98. Foreign bodies of the esophagus: clinical features, diagnosis, treatment;

Foreign bodies are a rather frequent and dangerous pathology of the esophagus. Most

often, sh, meat and bird bones, dentures, coins, buttons, pins, nails get stuck in the
esophagus. The main reasons for foreign bodies to enter the esophagus are hasty food

with swallowing poorly chewed pieces of food, bones, careless cooking with leaving bones

or other foreign bodies in food, professional habits of shoemakers, tailors, carpenters to

keep nails, needles, pins in their mouths when working. , oral pathology in elderly patients

(poorly fitted false jaws, decreased sensitivity of the oral mucosa), children's habit of taking

random objects in their mouths, intentional ingestion e.

A swallowed foreign body can pass from the esophagus to the stomach and exit naturally

or linger in the esophagus (this can be facilitated by various pathological conditions -

strictures, tumors, diverticula, cramps, achalasia). However, in more than 90% of cases,

foreign bodies are found in a healthy esophagus. The predominant localization of foreign

bodies in the esophagus is the place of physiological constriction. Most often, foreign

bodies linger at the level of the jugular notch of the sternum. Less commonly, delay occurs

at the level of the aortic arch and bifurcation of the trachea and cricopharyngeal narrowing.

Clinic.The clinical picture largely depends on the size, shape, localization, duration of a

foreign body in the esophagus. After ingestion of a foreign body, the patient notes pain, a

feeling of compression in the throat or behind the sternum, which intensifies when

swallowing. Pain can be absent with foreign bodies with a at, smooth surface. The pain

radiates to the back, between the shoulder blades. In addition to pain, dysphagia,

regurgitation, and salivation are characteristic. If the esophagus wall is injured, bleeding

may occur. In rare cases, with large foreign bodies, complete obstruction of the esophagus

occurs. This is largely facilitated by concomitant muscle spasm and inflammatory edema

of the mucous membrane. Sometimes the clinical picture is dominated by signs of sudden

suffocation. With damage to the wall of the esophagus and the attachment of inflammatory

phenomena, there is constant pain in the neck, back, behind the sternum. Dysphagia is

rapidly increasing. The general condition of the patient worsens, the temperature rises,

chills appear. On the neck, more often on the left, there is a painful swelling, crepitus. The

patient’s appearance is characteristic, which, depending on the location of the foreign

body, tends to occupy a forced position. With foreign bodies in the upper third of the

esophagus, he extends his neck, tilts his head down. When a foreign body is retained in

the thoracic region, the body is tilted down, the patient prefers to lie in a bent position.

When swallowing, a painful expression appears on the face. painful swelling, crepitus is
noted. The patient’s appearance is characteristic, which, depending on the location of the

foreign body, tends to occupy a forced position. With foreign bodies in the upper third of

the esophagus, he extends his neck, tilts his head down. When a foreign body is retained

in the thoracic region, the body is tilted down, the patient prefers to lie in a bent position.

When swallowing, a painful expression appears on the face. painful swelling, crepitus is

noted. The patient’s appearance is characteristic, which, depending on the location of the

foreign body, tends to occupy a forced position. With foreign bodies in the upper third of

the esophagus, he extends his neck, tilts his head down. When a foreign body is retained

in the thoracic region, the body is tilted down, the patient prefers to lie in a bent position.

When swallowing, a painful expression appears on the face.

Diagnostics. The examination begins with an instrumental examination of the pharynx and

pharynx with the help of a laryngeal mirror. Sometimes in this way it is possible to detect a

foreign body in the pear-shaped sinuses. After examination, the pharynx proceeds to an Xray
examination of the esophagus. X-ray contrast metallic foreign bodies (coins, needles,

pins, etc.) are easily recognized.

For negative X-ray data, a contrast agent test is used. With negative data from an X-ray

examination and persistent persistent complaints of the patient for pain, dysphagia, with

the onset of inflammatory phenomena, esophagoscopy is indicated.

Treatment. The presence of a foreign body in the esophagus serves as an indication for its

immediate removal. For this purpose, esophagoscopy using special forceps is used. In

adults, it is performed under local anesthesia, in children and excited patients under

anesthesia. If it is impossible to remove a foreign body using esophagoscopy, surgical

methods are used. When localizing a foreign body in the cervical region, at a distance of

25 - 26 cm from the edge of the upper incisors, esophagotomy is used by cervical access

on the left. Foreign bodies of the thoracic esophagus are removed using thoracotomy or

dorsal mediastinotomy.

99. Benign tumors of the esophagus: clinical features, diagnosis, indications for

surgical treatment;

Benign tumors of the esophagus are histologically divided into tumors of epithelial and

non-epithelial origin. The first group includes polyps, adenomas, papillomas and cysts of

the esophagus, the second - leiomyomas, bromas, lipomas and lymphangiomas,

neurobromas, neuromas, osteochondroma, and esophageal myoblastomas. The value of

a benign tumor can range from the size of the cherry to the tumors, which occupy a

signicant part of the esophagus.

In frequency, the first place among benign tumors of the esophagus is occupied by

leiomyoma (50-70% of all benign tumors of the esophagus). Other tumors are very rare.

Leiomyomas in most cases are localized in the lower third of the esophagus, less often in

the middle third. Most often, leiomyomas occur between the ages of 20-60, although cases

of this tumor have been described in children and senile individuals. More often,

leiomyoma occurs in men.

The second most common benign tumor of the esophagus is esophageal cysts.

Depending on the origin of the esophagus cysts are divided into the following groups:

1) retention cysts;

2) cystic, or follicular esophagitis;

3) publication cysts;

4) cysts formed from islets of the gastric mucosa;

5) enterogenic cysts of the esophagus;

6) bronchogenic cysts of the esophagus;

7) dermoid cysts;

8) parasitic cysts.

The esophagus cyst is a thin-walled formation of a round shape, the cavity of which is

lined with epithelium and contains a yellowish liquid.

By the nature of the growth of the tumor (inside the lumen of the esophagus or inside its

wall), their division into intraparietal and intraluminal is based. The rst group includes

leiomyomas, cysts, vascular tumors, the second - fibromas, lipomas, adenomas,

papillomas.

Clinic.Due to their small size, intra-esophageal tumors of the esophagus often do not give

any symptoms and are an accidental finding during an X-ray examination. In clinically

pronounced cases, the main symptoms of intradenal tumors of the esophagus are

dysphagia, pain behind the sternum or in the epigastric region, dyspepsia, and

respiratory disorders. The first two symptoms are most common, although their severity
varies widely. Dysphagia in most cases is negligible, but slowly grows as the tumor grows.

The pain is usually localized behind the sternum or in the epigastrium. Some patients

report irradiation along the edges. Dyspeptic symptoms are reduced to

belching, nausea, vomiting, sensations of fullness in the epigastric region. Some patients

complain of coughing, shortness of breath, pain in the heart, frequent inflammatory

diseases of the bronchi and lungs. Pulmonary symptoms are usually the result of

regurgitation of food masses into the bronchial tree or the result of compression of the

tracheo-bronchial tree by a tumor. Occasionally, vomiting of blood and melena is noted as

a result of ulceration and bleeding from the tumor.

Most intraluminal tumors are localized in the upper half of the esophagus. Single tumors

are more common. In many cases, these tumors are asymptomatic. With large sizes, they

usually manifest with certain symptoms. Patients may have dysphagia, regurgitation, loss

of appetite, salivation, constant sensation of a foreign body in the esophagus. Respiratory

symptoms include coughing, shortness of breath, hoarseness. Pain is usually not

characteristic. Sharp pain may appear when the legs of the tumor are twisted. The most

unpleasant and life-threatening patient is the ejection of a tumor on a long leg during

vomiting in the mouth. A tumor can block the entrance to the larynx, cause an asthma

attack or even death. Complications of benign tumors include bleeding due to ulceration of

the mucous membrane covering the tumor,

Diagnostics.The main diagnostic methods for benign tumors of the esophagus are x-ray

examination and esophagoscopy. A characteristic radiological sign of an intramural tumor

is a semi-oval filling defect with clear contours or a spindle-shaped expansion of the

esophagus. In this case, part of the defect extends into the lumen of the esophagus, and

the other part is located outside it, against the background of the posterior mediastinum.

The severity of each of these symptoms depends on the location of the tumor in relation to

the axis of the esophagus. The relief of the mucous membrane over the filling defect is

usually little changed or smoothed due to the stretching of the mucous membrane by the

tumor. The elasticity and peristalsis of the walls of the esophagus are preserved. It is

characteristic that suprastenotic expansion is usually absent and appears in rare cases

only with stenosis of the lumen of the esophagus. With an uneven tuberous surface of the

tumor, the filling defect has uneven contours. The lateral projection is characterized by a
sharply defined angle between the edge of the tumor and the unchanged wall of the

esophagus. When swallowing, a synchronous shift in the shadow of the tumor is observed.

Intra-luminal tumors are characterized by the presence of a filling defect with clear, even

contours, located in the lumen of the esophagus and changing its location. The folds of the

mucous membrane near the tumor are usually not changed and bend around its base. In

difficult cases, in addition to conventional research methods, pneumomediastinography

and CT can be used, in which the shadow of the tumor and its relation to surrounding

organs are clearly visible. When swallowing, a synchronous shift in the shadow of the

tumor is observed. Intra-luminal tumors are characterized by the presence of a filling

defect with clear, even contours, located in the lumen of the esophagus and changing its

location. The folds of the mucous membrane near the tumor are usually not changed and

bend around its base. In difficult cases, in addition to conventional research methods,

pneumomediastinography and CT can be used, in which the shadow of the tumor and its

relation to surrounding organs are clearly visible. When swallowing, a synchronous shift in

the shadow of the tumor is observed. Intra-luminal tumors are characterized by the

presence of a filling defect with clear, even contours, located in the lumen of the

esophagus and changing its location. The folds of the mucous membrane near the tumor

are usually not changed and bend around its base. In difficult cases, in addition to

conventional research methods, pneumomediastinography and CT can be used, in which

the shadow of the tumor and its relation to surrounding organs are clearly visible.

Esophagoscopy is indicated for all patients with a tumor of the esophagus. A typical

esophagoscopic picture with esophageal leiomyoma is the intact unchanged mucous

membrane of the esophagus above the tumor protruding into the lumen. The lumen of the

esophagus can be narrowed on the one hand and compensatory widened on the other, so

that the esophagoscope can usually be held below the tumor. Sometimes pathology with

esophagoscopy is not determined. This may be due to the fact that the esophagoscope

displaces the tumor and freely passes by.

Treatment . Surgical treatment of benign tumors. In this case, five types of operations are

used:

1) removal of the tumor through the mouth;

2) endoscopic removal of the tumor;

3) tumor enucleation;

4) excision of the tumor with a section of the wall of the esophagus; 5) resection of the

esophagus.

Removal of a tumor through the mouth is used for polyps in the initial esophagus.

Endoscopic removal of the tumor is resorted to with small polyps on a narrow leg. The

operation consists in crossing the tumor leg with a loop and removing it with forceps. In

case of intraparietal tumors and large polyps, especially on a broad base, cervical,

transpleural, or abdominal access is used depending on the location of the tumor. In the

case of a cervical tumor, the esophagus is exposed with a cut along the front edge of the

left sternocleidomastoid muscle. With tumors of the upper 2/3 of the thoracic esophagus,

right-sided thoracotomy in the fifth intercostal space is convenient, with tumors in the lower

third of the esophagus, left-side access in the seventh intercostal space is usually used.

Tumors of the abdominal esophagus are removed through abdominal access.

100. Traumatic damage to the esophagus: causes, clinical features, diagnosis,

treatment principles. Spontaneous rupture of the esophagus;

Damage to the esophagus is divided into closed (internal) from the mucous membrane

and open (external) with penetrating wounds of the neck and chest.

Closed injuries of the esophagus are possible during the implementation of diagnostic and

therapeutic measures (esophagoscopy, gulping of the esophagus, cardiodilation). Damage

to the esophagus can occur from the inside when foreign bodies enter it. Pressure ulcers

of the esophagus wall occur when the probes are in it for a long time, from the pressure of

the cuff of the endotracheal or tracheostomy tube. Perforation of the wall of the esophagus

can occur with its various diseases: tumors, peptic ulcer, chemical burns. Closed injuries of

the neck, chest and abdomen can lead to malnutrition and necrosis of the esophagus wall

as a result of squeezing it between the sternum and vertebral bodies. In this case, damage

to neighboring organs is often noted. Direct trauma to the esophagus can occur during

operations on the mediastinal organs and lungs.

Open (external) esophageal injuries in peacetime are rare. Usually they are combined with

multiple injuries of neighboring organs (thyroid gland, trachea, heart, lungs, large vessels,

etc.).

Clinic. When the cervical esophagus is injured, patients complain of pain when
swallowing, subcutaneous emphysema occurs on the neck. Esophagitis, periesophagitis

and mediastinitis are gradually developing.

In case of damage to the thoracic esophagus, patients note a sharp pain behind the

sternum, aggravated by inhalation, coughing, swallowing, increased salivation, a foreign

body sensation in the esophagus. Characteristically forced position - the body is tilted

forward. There is vomiting with an admixture of blood, a subtle emphysema of the neck,

symptoms of mediastinitis, pericarditis, pleurisy.

Injuries to the abdominal esophagus can lead to peritonitis.

There are cases of spontaneous rupture of the esophagus (Boerhaave syndrome,

described in 1724 - there is a rupture of the lower thoracic esophagus during an attack of

spontaneous or artificially induced vomiting due to a sharp increase in esophageal

pressure (the pressure in the stomach during vomiting can increase to 200 mm Hg. ). A

rupture of the esophagus can also occur when trying to artificially suppress an attack of

vomiting (the syndrome is described in the literature under the name “banquet injury”). The

rupture often takes the form of a linear wound, can spread to the stomach. azvivaetsya

acute mediastinitis, mediastinal pleura is damaged - its empyema in spontaneous rupture

of the esophagus pain occurs suddenly (usually during vomiting) in the xiphoid, may

radiate to the epigastric region, back, left shoulder noted hematemesis,.. mediastinal and

subcutaneous emphysema, shock develops, body temperature rises. With damage to the

mediastinal pleura, hydro-pneumothorax symptoms occur.

Diagnostics.X-ray examination is the main method for diagnosing damage to the

esophagus. It starts with a review uroscopy and radiography, in which you can detect

mediastinal emphysema, the expansion of its shadow, hydro-pneumothorax, neck fiber

emphysema. In the absence of air in the mediastinum, the esophagus with a contrast

agent is examined in the patient's position, lying on his back, on the right and left side, on

his stomach. If there is a suspicion of a defect in its wall due to rupture or perforation,

water-soluble contrast agents should be used, since a suspension of barium, leaving the

defect in the esophagus wall into the mediastinal tissue, imbibes it and makes subsequent

studies uninformative. In addition, it as a foreign body contributes to the development of

infection. Iodine-containing water-soluble compounds (verographin, cardiotrust, etc. )

easily penetrate through small defects in the wall of the esophagus, do not cause an
inflammatory reaction of the surrounding fiber, are quickly absorbed. Often this study is

enough to determine the location and size of the perforation hole. In doubtful cases,

esophagoscopy is used.

Treatment . Conservative treatment (parenteral nutrition, the appointment of antibiotics,

anti-inflammatory drugs) is carried out: 1) until a final diagnosis is established and when

the delivery of the patient to the surgical hospital is delayed;

2) with superficial injuries of the cervical esophagus;

3) as an addition to surgical treatment.

Surgical treatment (radical and palliative) is indicated for extensive damage to the

esophagus, the presence of messages of its lumen with the mediastinum,

tracheobronchial tree, and pleural cavity.

Radical surgical treatment consists in suturing the defect with prescription of damage to

the esophagus up to 1 day. Suturing of the defect in the wall of the esophagus produce

two rows of sutures in the longitudinal direction. The tightness of the sutures and their

isolation from the infected mediastinum and pleural cavity is provided by hemming around

them depending on the location of the defect in the muscles of the neck, parietal pleura,

pericardium, diaphragm, and the bottom wall of the stomach. The mediastinum and pleural

cavity are drained for aspiration of exudate, the introduction of antibiotics, antiseptics,

proteolytic enzymes.

Palliative operations (esophagostomy, gastrostomy, jejunostomy, mediastinotomy, drainage of

the cellular spaces of the neck, pleural cavity) are indicated for through wounds of the
esophagus, when time for radical surgery is missed, and for severe concomitant diseases.

Recently, with perforation of the esophagus, the method of active and tight drainage of the
mediastinum has become widespread. In this case, a mediastinotomy is performed taking into
account the place of damage to the esophagus, often from an incision in the neck, and a double-
lumen drainage tube is brought to the perforation site, which is removed away from the surgical
wound. The surgical wound is sutured in layers. The method is based on the principle of
simultaneous infusion of a mediastinum of an antiseptic solution into the area of the destroyed
and inflamed periophageal fiber and aspiration of this solution together with the contents that
accumulate in the area of post-traumatic purulent inflammation.

Respiratory System (Question 40 - 51)

40. The etiology and pathogenesis of suppurative pulmonary diseases and pleura.

Classification;
Classification of purulent lung diseases:

I. Infectious destruction of the lungs.

According to the nature of the pathological process:

a) abscess purulent or nagrenozny;

b) lung gangrene.

By the presence of complications:

a) uncomplicated;

b) complicated (pyopneumothorax, empyema, pleural effusion, sepsis).

II . Staphylococcal destruction of the lungs.

III . Suppurative cysts of the lungs.

Etiology and pathogenesis. Ways of occurrence: bronchopulmonary, hematogenousembolic,

lymphogenous, traumatic.

41. Acute abscesses and gangrene. The way of emergence, development

mechanisms.;

42. The clinical course and diagnosis of acute suppurative diseases of the lungs;

43. Complications of acute pulmonary suppurations. Diagnosis and differential

diagnosis;

44. The principles of treatment of acute pulmonary suppurations, indications for

surgery, types of interventions;

Etiology and pathogenesis. Ways of occurrence: bronchopulmonary, hematogenousembolic,

lymphogenous, traumatic.

Acute lung abscess

Clinic and diagnosis:

Two phases: before the breakthrough of the abscess in the bronchus and after its

breakthrough.

The clinical and radiological symptoms of the first phase are typical for croupous or focal

pneumonia. Kryukov’s symptom is pain when pressing and tapping on the part of the chest

located above the forming abscess.

In the second phase, more typical symptoms appear: separation of purulent sputum,

sometimes with an admixture of blood. Sputum, settling, is divided into three layers: pusserous
fluid-foam.

Diagnostic methods for suppurative lung diseases: laboratory blood and sputum tests,
external respiration tests, X-ray methods, computed tomography, bronchobroscopy,

thoracoscopy, biopsy, angiography.

Lung Gangrene

Clinic: fetid exhaled air, severe shortness of breath, fetid sputum of the form: meat slops ”,

hemoptysis. Radiological - diffuse dimming of part or all of the lung.

Differential diagnosis: - lung cancer;

- bronchial adenoma; - tuberculosis;

- bronchiectasis;

festering pulmonary cysts;

- suppuration echinococcus of the lung; - lung actinomycosis.

Treatment:

1. Increasing the resistance of organism (mode, nutrition).

2. Improving the conditions of drainage of the abscess: expectorants, proteolytic enzymes,

exercise therapy.

3. Remediation of the bronchial tree.

4. Rational antibacterial therapy.

5. Normalization of cardiac activity.

6. Immunocorrective therapy.

Conservative treatment is futile with abscesses with a diameter of more than 6 cm, a very

thick capsule of an abscess, intoxication, not inferior to a full-edged complex therapy.

Complications in the acute period: a breakthrough of the abscess into the pleural cavity

with the development of intense pneumothorax; bleeding into the bronchial tree with

possible asphyxia; aspiration of pus into the unaffected areas of the bronchial tree and the

development of new abscesses; the formation of ulcers in distant organs, more often in the

brain.

45. Chronic lung abscess: the development, clinical course and differential

diagnosis;

46. Diagnosis and treatment of chronic lung abscess;

An abscess that has not been eliminated in 2 months is regarded as chronic.

Etiology:

1. Features of the pathological process: large, with a diameter of more than 6 cm cavities
in the lung; the presence of sequestration in the cavity; poor drainage conditions; sluggish

reaction of the body to the inammatory process.

2. Errors in the treatment of the patient: inadequate antibiotic therapy; poor drainage;

insufcient fortifying treatment.

Pathological anatomy. Clinic. Two types:

First type - Against the background of remission of the lung abscess, frequent relapse of

the disease occurs in 1-2 weeks. They lead to the phenomena of purulent bronchitis,

intoxication, degenerative changes in the lungs.

The second type -

An acute period

without%remissiongoesintothechronicstage.Severeintoxicationanddystrophyofparenchyma

lorgansdeveloprapidly.Complications are possible (bronchiectasis, pleural empyema,

pulmonary hemorrhage, septicopyemia). Patients die from progressive pulmonary heart

disease.

Symptoms

- cough;

- hemoptysis;

- chest pain;

- shortness of breath;

- sweating;

- thickening of the nail phalanges (drumsticks);

- osteoarthropathy.

Treatment: conservative is often ineffective. Prompt: removal of a lobe or entire lung.

47. Acute empyema and pleural empyema. The clinical course. Diagnosis and

differential diagnosis;

48. The principles of treatment of acute pleural empyema. Indications for surgical

treatment, types of operations;

49. Chronic empyema, the clinical course, diagnosis and treatment;

Empyema is a condition that affects the space between the outermost layer of the lungs

and the layer touching the chest wall, known as the pleural space. This space exists to

help the lungs expand and contract.The pleural space naturally contains a small amount of
fluid. Empyema happens when extra fluid begins to collect in the pleural space.Different

strains of bacteria cause fluid and pus to build up in the pleural space. Very

often, pneumonia causes empyema.

Symptoms of empyema may include:

• having a case of pneumonia that does not improve

• a fever

• chest pain

• a cough

• pus in mucus

• difficulty breathing

• a crackling sound from the chest

• decreased breathing sounds

• dullness when tapping chest

• fluid in the lungs (visible with a chest X-ray)

Empyema can progress through three stages if a person does not receive treatment.

Stage 1: Simple (the exudative phase)

The first stage of empyema is called simple empyema. It occurs when extra fluid begins to

build up in the pleural cavity. This fluid can become infected and may contain pus.

Stage 2: Complicated (the fibrinopurulent phase)

In complicated empyema, the fluid in the pleural cavity begins to thicken and form

“pockets.”

Stage 3: Frank (the organizing phase)

Finally, the infected fluid causes scarring to the inner layers that line the pleural cavity in

the lungs. This causes difficulty breathing as it stops the lungs from inflating properly.

Causes

Pneumonia is the most common cause of empyema. People who have undergone

thoracotomies, or chest surgeries, might also be at risk of developing empyema if bacteria

get into the wound.

Risk factors

The biggest risk factor for empyema is having had pneumonia recently.

• being older than 70

• having been in the hospital recently

• having had chest surgery or trauma

In low-risk populations, empyema was generally less severe, and people were more likely

to have developed empyema outside of a hospital.

Statistically, people with the following conditions are also more likely to develop empyema.

• diabetes

• heart disease

• previous cancer

• chronic obstructive pulmonary disorder (COPD)

• lung disease

• intravenous drug use (in simple empyema cases)

Diagnosis

The first step to diagnosing empyema is a chest X-ray. An X-ray can only identify

empyema when there is a specific amount of fluid in the pleural cavity, however.

If the doctor suspects there is liquid in the pleural cavity after a chest X-ray, they will carry

out an ultrasound. Ultrasounds are more sensitive and better at detecting fluid in the

pleural cavity.

CT scans are also a useful method of detecting empyema. This allows doctors to see the

“pockets” of liquid in the pleural cavity.

Treatment

Treatment for empyema can include:

Antibiotics

Doctors usually prescribe antibiotics as the first treatment for simple cases of empyema.

Because different strains of bacteria cause empyema, finding the right antibiotic is crucial.

Antibiotic treatment typically takes 2 to 6 weeks to work.

Drainage

Draining the fluid is essential to prevent simple empyema progressing to complicated or

frank empyema. It also helps keep the condition under control.

To drain the fluid, a doctor performs a tube thoracostomy, which involves inserting an

ultrasound or computer-guided tube into the chest cavity and removing the liquid from the

pleural space.
Surgery

A doctor may recommend surgery for advanced empyema.

For advanced cases of empyema, surgery may be the best treatment option. One study

found that a surgery called decortication yielded better results than tube drainage in

people with advanced empyema.

Decortication involves removing the pus “pockets” and fibrous tissue from the pleural

space, which helps the lungs expand properly.

There are two types of surgeries available. In most cases, a surgeon will perform a videoassisted
thoracotomy (VATS). This procedure is less invasive, less painful, and has a

shorter recovery time than an open-thoracotomy, which requires a surgeon to open the

chest.In some cases, however, a surgeon will perform an open-thoracotomy.There are no

specific criteria to decide when surgery is necessary for empyema. One study found that

those with symptoms lasting less than 4 weeks had better surgery results than people who

had symptoms lasting more than 4 weeks.

Fibrinolytic therapy

A doctor may also recommend fibrinolytic therapy, which uses drugs known as fibrinolytic

agents. The therapy helps to drain pleural fluid, and doctors may use it in combination with

a tube thoracostomy. A 2018 study assessing the effectiveness of VATS surgery in

comparison to fibrinolytic therapy after tube thoracostomy found that both methods are

highly effective.

Rare complications

Possible complications of empyema include:

• Fibrosis, which is when damaged lung tissue causes difficulty breathing that affects

a person’s quality of life. If breathing difficulty continues 6 months after infection,

decortication surgery may improve symptoms.

• Empyema necessitatis, which is an extension of the infection into the chest wall

and soft tissue. This is very rare and requires immediate medical attention.

Outlook

Getting early medical attention can stop empyema from becoming a more severe

condition.

Treatment for empyema can vary depending on the severity of a person’s symptoms.
Antibiotics and drainage are the first steps, followed by surgery in more advanced cases.

50. Bronchiectasis. Classification, the indications for surgical treatment.

Definition of a concept. Etiology, pathogenesis (rarely congenital, often acquired after

measles pneumonia, whooping cough, bronchitis, foreign body aspiration).

Clinic: long course; cough, sputum, pulmonary hemorrhage, chest pain, shortness of

breath, pain in limbs (Marie-Bamberger syndrome).

Diagnostic methods: examination (chest lag in breathing), percussion (dullness),

auscultation (wet rales); X-ray examinations (atelectasis), bronchography. Development

stages:

- initial stage)

- stage of suppuration of bronchiectasis:

a) clinically as purulent bronchitis with exacerbations in the form of extravmonia)

b) with severe symptoms of bronchiectasis, stage of destruction;

c) severe course with severe purulent intoxication)

g) the same, as well as severe disorders of cardiac, respiratory, liver, renal failure.

Differential diagnosis:

- lung abscess;

- central lung carcinoma;

- pulmonary tuberculosis.

Treatment:

Stage I - conservative;

II - III and stage - operational (removal of the affected part of the lung); Stage III -

conservative.

51. Cyst of the lung. Etiology, clinical features, diagnosis, indications for surgery,

types of operations;

lung cysts -- sacs of tissue filled with air or fluid. Treatments can help, but your options

depend on which type you have.

The symptoms are similar, so your doctor may suggest you get an imaging test called

high-definition computed tomography (CT) to figure out which cystic lung disease you

have. If that doesn't work, you may need to get a lung biopsy. Your doctor will remove a

small piece of tissue from your lung and send it to a lab for testing.
Other conditions can look like cystic lung disease, such as emphysema and honeycomb

lung. To confirm that you have it, your doctor will check things like how much air your lungs

can hold. He'll also look at the size, wall thickness, shape, and location of your cysts.

Cystic lung disease is rare. Most adults who get it have one of these four types:

Lymphangioleiomyomatosis (LAM)

LAM happens when muscle cells in the lung tissue grow out of control and form cysts,

which eventually damage your lung tissue. It mostly affects women between ages 20 and

40.

There are two types: TSC-LAM and sporadic LAM.

TSC-LAM is when you have LAM and a rare disease called tuberous sclerosis

complex (TSC). Sporadic LAM means you have LAM but not TSC.

Both kinds are thought to be due to changes in the tuberous sclerosis gene.

Doctors believe that estrogen plays a part in both types of LAM. The disease may get

worse during menstruation and pregnancy, and after using birth control pills with estrogen.

The most common symptoms of LAM are:

• Chest pain

• Tiredness

• Coughing a lot (may be bloody)

• Shortness of breath

• Wheezing

You may also have fluid collect in the space between your lungs and chest wall, a problem

called pleural effusion. It can make it hard to catch your breath. Fluid can also build up in

your belly, legs, and feet.You might get a collapsed lung if a cyst tears through the lining of

your lung. A collapsed lung happens when air leaks into the space between your lung and

chest wall and flattens part of your lung. This is an emergency and needs treatment right

away.

LAM doesn't have a cure, but you can treat it with sirolimus (Rapamune), a medicine that

can slow the disease and may even improve how well your lungs work.You could also

take bronchodilators, medicines that can help open up your airways and

make breathing easier.LAM can get worse over time. If it does, you may need oxygen

therapy, which means you take in oxygen from a tank or machine.

Pulmonary Langerhans Cell Histiocytosis (PLCH)

PLCH mostly shows up in young adults who are smokers or former smokers. In the early

stages, you may not have any symptoms, but if you do, they might include mild shortness

of breath and a cough. Later, you could have problems like:

• Chest pain

• Fever

• Night sweats

• Tiredness

• Weight loss

PLCH begins when chemicals in cigarette smoke cause cells to grow abnormally in your

lungs. As the disease gets worse, scars form and the tissue becomes stiff and thick. You

may find it harder to breathe in enough air, and you'll get short of breath, even during

normal activities.

PLCH can cause a lung to collapse, sometimes more than once. Your doctor may suggest

you get a procedure called a pleurodesis. It closes up the space between your lungs and

chest wall and stops air or fluid from filling the space.It's not clear if PLCH is a cancer or an

immune disorder.

Either way, the first and most important treatment is to quit smoking. PLCH may stop

getting worse and even get better when you quit.You may also take a steroid medicine to

reduce inflammation. Some people with PLCH take a chemotherapy drug if steroids don't

help. If you're very short of breath, you may need to get extra oxygen from a machine or

tank.

Birt-Hogg-Dubé Syndrome (BHD)

BHD is caused by an abnormal gene that you inherit from a parent who has the disease.

You might also get BHD if there are changes to one of your genes, called a gene mutation.

Genetic tests can show whether you have it.

Symptoms usually happen when you're in your 20s or 30s. Small skin bumps on your face

are the most common signs of BHD. These bumps are benign tumors (not cancer) in

the hair follicles. You may also have them on your neck, ears, or upper body.About 80% of

people with BHD have lung cysts. The cysts usually don't cause symptoms, and your lungs

work normally.Up to a third of people with BHD can have repeated lung collapses, and
15% to 30% can get kidney tumors. The tumors are usually slow growing and are

diagnosed at around age 48 to 50. You should get regular CT scans of your belly to find

any kidney tumors early, when treatment works best.

The treatment for BHD depends on the symptoms you have. For example, your doctor

may remove skin bumps with a laser. If you have frequent lung collapses, he may

recommend a pleurodesis. Surgery can remove kidney tumors.

Lymphoid Interstitial Pneumonia (LIP)

LIP is extremely rare. Doctors believe it's both a disease and a reaction to something in

the environment or to another disease.

LIP may happen if you also have an autoimmune disease, especially Sjögren’s syndrome.

In that condition, your immune system -- the body's defense against germs -- attacks the

glands that make your tears and saliva.About twice as many women as men get LIP. It's

typically diagnosed when you're between ages 52 and 56. The usual symptoms are

a cough that gets worse and shortness of breath.

Your doctor may suggest you treat it with steroids to lessen inflammation. If steroids aren't

helpful, you may need to take medicine that tamps down the actions of your immune

system.

SPLEEN (Question 77 -79)

77. Anatomical and physiological information about the spleen. Classification of surgical diseases
of the

spleen.

ANATOMY

Size: The weight of the normal adult spleen is 75–250 g and it measures up to 10 × 7 × 3 cm.

Localization: It lies in the left hypochondrium between the gastric fundus and the left
hemidiaphragm, with its long

axis lying along the 10th rib.

Topography:

 The hilum sits in the angle between the stomach and the kidney and is in contact with the tail
of the pancreas.

The concave visceral surface lies in contact with these structures, and the lower pole extends no
further than the
mid-axillary line.

 There is a notch on the inferolateral border, and this may be palpated when the spleen is
enlarged.

Arterial BS:

 The tortuous splenic artery arises from the coeliac axis, usually from a common stem with a
hepatic artery, and

runs along the upper border of the body and tail of the pancreas, to which it gives small
branches.

 The short gastric and left gastroepiploic branches pass between the layers of the gastrosplenic
ligament.

 The main splenic artery generally divides into superior and inferior branches, which, in turn,
subdivide into

several segmental branches.

Venous drainage:

 The splenic vein is formed from several tributaries that drain the hilum.

 The vein runs behind the pancreas, receiving several small tributaries from the pancreas
before joining the

superior mesenteric vein at the neck of the pancreas to form the portal vein.

 The splenic pulp is invested by an external serous and internal fibroelastic coat which is
reflected inwards at the

hilum onto the vessels to form vascular sheaths.

Lymphatics:The lymphatic drainage comprises efferent vessels in the white pulp that run with
the arterioles and

emerge from nodes at the hilum. These nodes and lymphatics drain via retropancreatic nodes to
the coeliac nodes.

Innervation: Sympathetic nerve fibres run from the coeliac plexus and innervate splenic arterial
branches.

PHYSIOLOGY

 The splenic parenchyma consists of white

and red pulp that is surrounded by serosa

and a collagenous capsule with smooth

muscle fibres.

 These penetrate the parenchyma as

trabeculae of dense connective tissue

fibres rich in collagen and elastic tissue.

 These, with the reticular framework,

support the cells of the spleen and

surround the vessels in the splenic pulp.

 The white pulp comprises a central

trabecular artery surrounded by nodules

with germinal centres and periarterial lymphatic sheaths that provide a framework filled with
lymphocytes and

macrophages.

 Arteries from the central artery and the peripheral‘penicillar’ arteries pass into the marginal
zone that lies at

the edge of the white pulp.

 Plasma-rich blood that has passed through the central lymphatic nodules is filtered as it passes
through the

sinuses within the marginal zone, and particles are phagocytosed.

 Immunoglobulins produced in the lymphatic nodules enter the circulation through the sinuses
in the marginal

zone, beyond which lies the red pulp, which consists of cords and sinuses.

 Cell-concentrated blood passes in the trabecular artery through the centre of the white pulp to
the red pulp cords.

 Red cells must elongate and become thinner to pass from the cords to the sinuses, a process
that removes

abnormally shaped cells from the circulation.

 As 90% of the blood passing through the spleen moves through an open circulation in which
blood flows from

arteries to cords, and thence sinuses, splenic pulp pressure reflects the pressure throughout the
portal system.

 The remaining 10% of the blood flow through the spleen bypasses the cords and sinuses by
direct arteriovenous

communications. The overall flow rate of blood is about 300 mL/min.

FUNCTIONS OF THE SPLEEN

1. Immune function.

 The spleen contains 66.5% and 10–15% of the body’s total T and B lymphocyte population,
respectively.
 It processes foreign antigens and is the major site of specific immunoglobulin M (IgM)
production.

 The non-specific opsonins, properdin and tuftsin, are synthesised.

 These antibodies are of B- and T-cell origin and bind to the specific receptors on the surface of
macrophages

and leukocytes, stimulating their phagocytic, bactericidal and tumoricidal activity.

2. Filter function.

 Macrophages in the reticulum capture cellular and non-cellular material from the blood and
plasma.

 This will include the removal of effete platelets and red blood cells.

 This process takes place in the sinuses and the splenic cords by the action of the endothelial
macrophages.

 Iron is removed from the degraded haemoglobin during red cell breakdown and is returned to
plasma.

 Removed non-cellular material may include bacteria and, in particular, pneumococci.

3. Pitting.

 Particulate inclusions from red cells are removed, and the repaired red cells are returned to
the circulation.

 These include Howell–Jolly and Heinz bodies, which represent nuclear remnants and
precipitated

haemoglobin or globin subunits, respectively.

4. Reservoir function.

 This function in humans is less marked than in other species, but the spleen does contain
approximately 8%

of the red cell mass.

 An enlarged spleen may contain a much larger proportion of the blood volume.

5. Cytopoiesis.

 From the fourth month of intrauterine life,some degree of haemopoiesis occurs in the fetal
spleen.

 Stimulation of the white pulp may occur following antigenic challenge, resulting in the
proliferation of T and

B cells and macrophages.

 This may also occur in myeloproliferative disorders, thalassaemias and chronic haemolytic
anaemias.

6. Hormonal (inhibition of bone marrow function)

7. In metabolism (metabolism of iron, fatty, lipoid, carbohydrate)

8. Plays a role in the endocrine system (connection with the thymus, thyroid, and sex glands - for
example, in

women, splenomegaly leads to the cessation of menstruation, and splenectomy returns this
function)

CLASSIFICATION OF SURGICAL DISEASES OF THE SPLEEN

1. Malformations (absence of spleen, lobed spleen, additional spleen, vagus spleen)

2. Traumatic injuries:

a) Open - closed

b) Isolated - combined

3. Acute diseases of the spleen (inversion of the spleen, spontaneous rupture, heart attack due
to embolism or

thrombosis of the splenic artery, necrosis, abscess of the spleen)

4. Neoplasms of the spleen

78. Splenic cysts, etiology, clinical features, diagnosis, treatment.

According to etiology:

1. Non-parasitic (Congenital cysts; Neoplasms; Secondary cysts  Trauma, Hormonal changes,

Splenic

hemaoma)

2. Parasitic

1. Nonparasitic cysts:

 True (internally coated with endothelium). True cysts congenital and occur due to a violation
of

embryogenesis.

 False (not having endothelial lining). False cysts  acquired and arise most often after injuries,
infectious

diseases and as a result spleen infarction.

According to number:

 Single

 Multiple.

Their volume varies from several tens of milliliters to 5 liters or more.

According to cyst contents

 Serous
 Hemorrhagic character.

NON-PARASITIC CYSTS.

CLINIC

1) Persistent dull pain in the left hypochondrium with radiation to the left shoulder and shoulder
girdle.

2) With large sizes of cysts, pain can increase significantly, symptoms of compression and
displacement of

adjacent abdominal organs appear (stomach, colon)

 HTN; GIT distress; Chest pain; SOB

3) During physical examination,  bulging in the left hypochondrium, some asymmetry of the
abdomen,

palpate enlarged smooth, painless spleen.

4) If cyst is located in the lower the spleen pole  symptom of fluctuation.

DIAGNOSIS

In the diagnosis of spleen cysts, the same methods are used as for abscesses of the spleen

1) Ultrasound scanning

2) Computer tomography  clearly defined low density formation

3) Radioisotope spleen scan

4) Additionally: Celiacography  radiopaque examination of the vessels of the spleen. In this

case, an

avascular zone is determined on an x-ray in the projection of the spleen, displacing its intraorgan
vessels.

TREATMENT

 Surgical  Splenectomy

PARASITIC CYSTS

 Echinococcus is the most common.

 Cysticercus, significantly less often

 Alveococcus, extremely rare

 Ways of penetration of the parasite into the spleen is hematogenous, less commonly
lymphogenous.

 Disease duration ranges from several to 15 years or more.

 As the parasite develops  displacement of adjacent abdominal organs, atrophy of spleen

tissue.
CLINIC

1) Similar to nonparasitic cysts.

2) Complication of splenic echinococcosis  suppuration with the development of clinical

manifestations of

spleen abscess.

DIAGNOSIS

1) Above mentioned methods.

2) Casoni reaction and latex test.

3) Serology  Hemagglutination test; ELISA

TREATMENT

 Surgical  Splenectomy + Albendazole

79. Spleen infarction, clinic, diagnosis, treatment.

Decreased BS to the spleen will result in partial or complete infarction.

ETIOLOGY:

1) Vascular occlusion produced by previous surgical intervention (such as spleen-preserving

distal

pancreatectomy), pancreatic disease, Splenic vein thrombosis, Sickle cell disease.

2) Clots – in infections , thrombophilia, metastasis and malignancy

3) Embolic disorders – Atrial fibrillation, Mitral stenosis, Cholesterol embolus, Patent foramen
ovale, Bacterial

septic endocarditis

4) Splenomegaly - Massively enlarged spleen from myeloproliferative syndrome, Portal

hypertension,

Gaucher disease, Sickle cell crisis in patients with sickle cell anemia, Vasculitis & DIVC

CLINIC

1) The infarct may be asymptomatic. or give rise to left upper quadrant and pain.

2) If symptomatic  begins suddenly with intense sharp pains in the left hypochondrium,
sometimes radiating

to left shoulder tip.

3) Accompanied by fever, expressed tachycardia, vomiting, and intestinal paresis.

 The severity of the clinical picture depends on the size of the infected area of the organ.

4) Minor heart attacks can occur with minimal clinical manifestations or may be asymptomatic.
 In most patients, self-healing occurs with the organization and scarring of the infarcted zone.
Less often, an infected

and purulent fusion of the infarcted zone is observed with the formation of an abscess of the
spleen, sometimes a false spleen cyst develops in the infarction zone.

DIAGNOSIS

 Contrast-enhanced CT will show the characteristic perfusion defect in the enlarged spleen

TREATMENT

 Treat the underlying cause

 Treatment is conservative  Pain relief

 Splenectomy should be considered only when a septic infarct causes an abscess

TRANSPLANTOLOGY (Question 60 - 65)

60. Definition of basic concepts: the transplantation, the recipient, donor, transplant

classification;

61. The immunological basis of Transplantation. Legal and ethical issues of organ

transplantation;

In accordance with the law of the Republic of Belarus dated July 13, 2012, a living donor is

a person who voluntarily gave consent in accordance with the established procedure for

the collection of organs and (or) human tissues for transplantation of organs and (or)

human tissues to a recipient. Organ harvesting - a medical intervention to remove organs

and (or) human tissues from a living or deceased donor.

Living donors cannot be:

minors (except in cases of bone marrow collection),

persons recognized as legally incompetent, as well as persons suffering from mental

disorders (diseases), persons with a disease that is dangerous to the life and health of the

recipient, Pregnant women, orphans left without parental care.

Organ harvesting for transplantation from a living donor is permitted subject to the

conditions:

• written warning of the donor by the attending physician to the state healthcare

organization about the possible deterioration of his health, organs for transplantation;

• the availability of the voluntary consent of the donor for the collection of organs,
expressed in writing, notarized;

• conducting a comprehensive medical examination of this living donor and the presence

of the conclusion of a consultation of medical specialists on the possibility of collecting

organs from him for transplantation.

The bone marrow is taken from a minor who has not acquired full legal capacity, with the

written consent of his legal representative, notarized, and the guardianship authority. In

case of written or oral objection of a minor, bone marrow is not allowed.

Only one of the paired organs, a fragment of an unpaired organ, tissue, the absence of

which does not cause irreversible processes in the body, can be taken from a living donor

for transplantation.

Forcing a person to consent to the removal of his organs is prohibited.

Before organ harvesting, a living donor has the right to receive complete and objective

information about his state of health and the consequences that may arise in connection

with organ harvesting.

Consent to organ harvesting can be revoked at any time, unless the doctors have already

started organ harvesting and its termination or return to its original state is impossible or is

associated with a threat to the life or health of a living donor.

Brain death is denied as the permanent loss of all brain functions in a beating heart

subject. Brain death is the result of a complete stop in cerebral circulation. At the same

time, the function of the remaining organs is preserved if the correct intensive therapy

continues, adapted to new conditions. Brain destruction stops the central commands of

spontaneous respiration, as well as the regulation of circulatory homeostasis, thermo- and

endocrine regulation. This explains the lack of spontaneous breathing, arterial

hypotension, hypothermia and diabetes insipidus.

A detailed history and clinical neurological examination are without a doubt the basis for a

diagnosis of brain death. These data must be recorded in writing.

The US Presidential Ethical Medicine Research Company in the United States formulates

the concept of “brain death” as follows: “Irreversible termination of the entire function of the

whole brain, including the cortex and brain stem, denied in accordance with accepted

medical standards.”

62. Kidney transplantation: historical information, the principles of donor selection,

preoperative preparation, surgery, postoperative management;

The list of data on the history of mandatory methods for examining a potential living kidney

donor (RLD) includes: ultrasound of the abdominal cavity, kidney, bladder, prostate, pelvic

organs. For a kidney recipient, the same examinations and dopplerography of the iliac

vessels are necessary.

An absolute contraindication to intravital kidney donation is: an established diagnosis of

hypertension and decreased kidney function (GFR less than 80 liters per minute)

Criteria for selecting potential cadaveric kidney donors for transplantation: severe

traumatic brain injury, cerebral hemorrhage.

Contraindications are: over 65 years of age and younger and 50 years old, bacterial

sepsis, active viral or bacterial infection (HIV, syphilis), chronic kidney disease, primary

kidney disease, oliguric acute renal failure, systemic disease with kidney damage,

malignant neoplasms.

A relative contraindication is: age over 60 years, arterial hypertension, treated infections,

including hepatitis, neoliguric acute renal failure, diabetes mellitus, covered intestinal

perforation, prolonged cold ischemia, poor hypodynamics (hypotension less than 50-60

mm Hg. ), oligourim within 24-48 hours.

The list of necessary studies for a living kidney donor: tissue typing, determination of

glomerular infiltration, intravenous urography, renography, renal arteriography.

Contraindications for kidney transplant recipients: a donor transplant is not

immunologically suitable for transplantation, the presence of malignant tumors of the

kidneys, if treatment has not been carried out or less than two years have passed since

the radical removal, the presence of infection in the body, decompensation of chronic

diseases of any organ (heart failure, UBJ, sugar diabetes), failure to follow the doctor’s

instructions (regular use of immunosuppressants is necessary), all kinds of psychoses with

personality changes.

Assessment of renal transplant (TP): topometry of TP, assessment of the state of the

perinephric space, color and spectral Doppler ultrasound. When assessing the state of TP,

the contour of the kidney, the uniformity and echogenicity of the parenchyma, the state of

the renal sinus, ChLS and the ureter are evaluated. The cortical layer is calculated by

three measurements at the poles and in the middle segment, the height of the pyramids,
the size of the central echocomplex are estimated, the sizes of the cups, pelvis and ureter

are measured. Assessment of the condition of the perinephric space includes the search

for free fluid around TP, which can be observed with the formation of hematomas, urine,

and lymphocele. CDK allows you to assess the patency of the main vessels of TP, arteries

and veins, as well as the uniformity and degree of perfusion of the vascular bed up to the

interlobular arteries (especially in the presence of multiple TP vessels, requiring

intraoperative reconstruction). With spectral Doppler ultrasound, the systolic, diastolic

blood ow velocity and the resistance index of the main, lobar, segmental, arc and

interlobular arteries are determined.

Ultrasound examination of TP is carried out at 1, 3, 5, 7, 10, 14, 21, 30, 60. 90 days.

Clinical observation is carried out 1 time in 30 days during the rst year according to clinical

indications - more often).

With spectral Dopplerography, RI is less than 0.7 clinically - adequate diuresis and a

decrease in serum creatinine. With a decrease in blood ow velocity indicators and an

increase in RI to 0.8, the clinical condition of TP is assessed as reduced and is

characterized by a slowdown in the normalization of creatinine level or its stably increased

indicator. When RI is greater than 0.8, the clinically functional state of TP is denied as

unsatisfactory and is characterized by an increase in creatinine and a decrease in diuresis.

An increase in RI of more than 0.8 is a reliable criterion that makes it possible to ascertain

a violation in the operation of TP. At the same time, a decrease in RI is a good prognostic

sign. The causes of the acute reaction of rejection of TP are: acute tubular necrosis, acute

cyclosporin nephrotoxic infection, tubolo- inertial nephritis.

TP rejection reaction:

- super acute several hours after transplantation, not amenable to treatment; - acute

rejection crisis from 4 days may occur repeatedly;

- chronic vascular reaction of rejection of TP 3-4 weeks after transplantation.

Complications after transplantation are: bleeding, failure of the anastomosis of the ureter

with the bladder and the formation of urinary fistulas, infection of the wound and bed of the

kidney, the rejection reaction of TP and complications.

63. Heart transplantation: indications, donor selection criteria, postoperative

management;
Classification of heart failure Strazhenko-Vasilenko:

Stage I. Initial latent circulatory failure, which manifests itself only during physical exertion,

at rest, these manifestations disappear, hemodynamics is not impaired.

Stage II. Severe prolonged circulatory failure, hemodynamic disturbances in the small and

large circles of blood circulation are expressed at rest.

Period A. Signs of circulatory failure are moderate at rest, moderate hemodynamic

disturbances, moderate hemodynamic disturbances only in one of the sections of the

cardiovascular system (in the large or small circle of blood circulation).

Period B.'s period the end of a long stage, the expressed hemodynamic disturbances in

which all cardiovascular system is involved (and big and small circles of blood circulation).

Stage III. The final dystrophic with severe hemodynamic disorders, persistent metabolic

changes and irreversible changes in the structure of organs and tissues. Functional

Classification of the New York Heart Association (NYHA).

Class I: no restrictions: primary physical activity is not accompanied by rapid fatigue,

shortness of breath or palpitations.

Class II: slight limitation of physical activity: at rest, there are no symptoms, habitual

physical activity is accompanied by fatigue, shortness of breath or palpitations.

Class III: a marked limitation of physical activity, at rest there are no symptoms, physical

activity of lower intensity, in comparison with usual loads, is accompanied by the

appearance of symptoms.

Class IV: the inability to perform any physical activity without the appearance of discomfort;

symptoms of heart failure are noted at rest and intensify with minimal physical exertion.

Indications for inclusion in the waiting list on the vehicle are divided into:

- generally accepted - maximum oxygen consumption <10 ml / kg / min with the

achievement of anaerobic metabolism; severe myocardial ischemia, limiting normal activity

and not amenable to revascularization; symptomatic age-related ventricular arrhythmias

refractory to all therapeutic methods of treatment;

- probable - maximum oxygen consumption <14 ml / kg / min and a significant limitation of

patient activity; recurrent unstable angina that is not amenable to revascularization,

unstable uid balance, which is not associated with the patient's observation of body weight

control, intermittent intake of diuretics and restriction of sodium chloride;

- inadequate LVEF <20%, FC III-IV according to NYHA classification, previous ventricular

arrhythmias, maximum oxygen> 15 / ml / kg / min.

In 50% of the recipients included in the waiting list, the average life expectancy according

to generally accepted indications for DCMP was 5.6 ± 2.7 months, and for coronary artery

disease - 4.8 ± 2.7 months.

Surgical Heart Transplant Techniques

PARASITIC INFECTIONS (Questions 85- 89)

85. Amoebiasis. Clinic, diagnosis, treatment, indications for surgical treatment.

 AKA amoebic dysentery.

 Amoebiasis is caused by Entamoeba histolytica.

Epidemiology

 The disease is common in the Indian subcontinent, Africa and parts of Central and South
America, where almost

half the population is infected.

 The vast majority of carriers are asymptomatic

 The mode of infection is via the faeco-oral route, thus insanitary conditions and poor personal
hygiene encourage

transmission of the infection

 Therefore, the population from the poorer socioeconomic strata are more vulnerable.

 Patients who are immunocompromised and alcoholics are more susceptible to infection.

 Amoebic liver abscess, the commonest extraintestinal manifestation, occurs in less than 10%
of the infected

population and, in endemic areas, is much more common than pyogenic abscess.

Pathogenesis

 In the small intestine, the parasite hatches into trophozoites, which invade the submucosa to
produce flask-shaped

ulcers.

 In the portal circulation, the parasite causes liquefactive necrosis in the liver, producing an
abscess, the commonest

 extraintestinal manifestation.

 The majority of abscesses occur high in the diaphragmatic surface of the right lobe of the liver.
 One possible explanation for the more common involvement of the right lobe of the liver is
that blood from

the superior mesenteric vein runs on a straighter course through the portal vein into the larger
lobe.

 This may cause pulmonary symptoms and chest complications

 The abscess cavity contains chocolate-coloured, odourless, ‘anchovy sauce’-like fluid that is a
mixture of

necrotic liver tissue and blood.

 There may be secondary infection of the abscess which causes the pus to smell.

 While pus in the abscess is sterile unless secondarily infected, trophozoites may be found in
the abscess

wall in a minority of cases.

 Untreated abscesses are likely to rupture.

 Chronic infection of the large bowel may result in a granulomatous lesion along the large
bowel, most commonly

seen in the caecum, called an amoeboma.

 A mass in the course of the large bowel may indicate an amoeboma

CLINICAL FEATURES

Usually asymptomatic carriers.

INTESTINAL MANIFESTATIONS  Amoebic dysentery

1. Gradual in onset, with symptoms presenting over 1-2 weeks  cramping abdominal pain,
watery or bloody

diarrhea, and weight loss or anorexia, fever

2. Bloody mucoid diarrhea (raspberry jelly) in a patient from an endemic area or following a
recent visit to

such a country

 Intestinal amebiasis may mimic acute appendicitis

EXTRAINTESTINAL MANIFESTATIONS  Hepatic abscess present within 2-4 weeks of infection

The typical patient with amoebic liver abscess is a young adult male

1. Insidious onset of non-specific symptoms  abdominal pain, anorexia, fever, night sweats,
malaise,

cough and weight loss.

2. Gradually progress to more specific symptoms  pain in the right upper abdomen and right
shoulder
tip, hiccoughs and a non-productive cough.

Hospital Surgery F.S. Noordeen

Examination

1. Patient is toxic and anaemic.

2. The patient will have upper abdominal rigidity, tender hepatomegaly, tender and bulging
intercostal

spaces, overlying skin oedema, a pleural effusion and basal pneumonitis – the last feature is
usually a late

manifestation.

3. Occasionally, a tinge of jaundice or ascites may be present.

4. Rarely, the patient may present as an emergency due to the effects of rupture of an abscess
into the

peritoneal, pleural or pericardial cavity

DIAGNOSIS

Laboratory tests

1. Serological tests (very sensitive)  indirect haemagglutination (IHA), indirect

immunofluorescence and

enzyme-linked immunosorbent assay (ELISA), PCR.

2. Stool microscopy  Cysts in stool

3. Rigid sigmoidoscopy using a disposable instrument  rectosigmoid show shallow skip lesions
and ‘flaskshaped’ or ‘collar-stud’ ulcers, punctuate hemorrhages.

4. These can be biopsied or scrapings can be taken along with mucus for immediate microscopic

examination. The presence of trophozoites distinguishes the condition from ulcerative colitis.

5. GBA &BBT  presence of a chronic infective process: anaemia, leukocytosis, raised

inflammatory markers –

erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) – hypoalbuminaemia

6. Liver function tests  Deranged, particularly elevated alkaline phosphatase.

Imaging techniques

1. US

2. CT

3. MRI

 Diagnostic aspiration is of limited value except for establishing the typical colour of the
aspirate, which is sterile
and odourless unless it is secondarily infected.

TREATMENT

Medical treatment is very effective and should be the first choice in the elective situation, with
surgery being

reserved for complications.

CONSERVATIVE TREATMENT

 Metronidazole and tinidazole.

 Follwed by  diloxanide furoate, which is not effective against hepatic infestation, for 10 days
to destroy any

intestinal amoebae.

EXTRA:

Amoeboma

 This is a chronic granuloma arising in the large bowel, most commonly seen in the caecum.

 It is prone to occur in chronic amoebic infection that has been treated intermittently with
drugs without

completion of a full course, a situation that arises from indiscriminate self-medication,

particularly in

resource-poor countries. Hence this is more often seen in such countries.

 This can easily be mistaken for a carcinoma.

 An amoeboma should be suspected when a patient from an endemic area with generalised ill
health and

pyrexia has a mass in the right iliac fossa with a history of blood-stained mucoid diarrhoea.

 Such a patient is highly unlikely to have a carcinoma because altered bowel habit is not a
feature of rightsided colonic carcinoma.

 While iron deficiency anaemia is a classical elective presentation of a caecal carcinoma, the
same is present in

an amoeboma because of chronic malnutrition.

Hospital Surgery F.S. Noordeen

 For abscess that is expected to rupture  Aspiration; also helps the penetration of
metronidazole.

 If there is evidence of secondary infection, appropriate drug treatment is added.

 The threshold for aspirating an abscess in the left lobe should be lower because of its proximity
to the pericardium.

SURGICAL TREATMENT
Only for complications  rupture into the pleural (usually the right side), peritoneal or pericardial
cavities; severe

haemorrhage and toxic megacolon in LI (but these are rare)

1. Rupture into the pleural (usually the right side), peritoneal or pericardial cavities 
Resuscitation,

drainage and appropriate lavage with vigorous medical treatment are the key principles.

2. Toxic megacolon  surgical emergency, the principles of management being the same as for
any toxic

megacolon.

 Resuscitation is followed by resection of bowel with exteriorisation.

 Then the patient is given vigorous supportive therapy.

 All such cases are managed in the intensive care unit, as would any patient with toxic
megacolon whatever

the cause.

3. An amoeboma that has not regressed after full medical treatment  colonic resection,
particularly if cancer

cannot be excluded.

86. Echinococcosis (Hyatid disease). Clinic, diagnosis, treatment, indications for surgical
treatment, types

of operations.

 Hydatid disease is caused by Ecchinococcus granulosus, commonly called the dog tapeworm.

 Close contact with an infected dog, sheep or cattle causes contamination by the oral route,
with the ovum thus

gaining entry into the human gastrointestinal tract.

 The parasite can affect any organ or several organs in the same patient. The liver is the organ
most often affected.

The lung is the next most common. Can also affect the spleen, brain, heart and kidneys,

CLINICAL FEATURES

 The disease may be asymptomatic and discovered coincidentally at postmortem or when an

ultrasound or CT

scan is done for some other condition.

 Symptomatic disease presents with a swelling causing pressure effects.

1. LIVER  enlarging painful mass in the right upper quadrant with the physical findings of a liver
swelling.
Dull pain from stretching of the liver capsule.

2. Daughter cysts may communicate with the BILIARY TREE  obstructive jaundice and its usual
clinical

features.

3. LUNGS, if cyst is large enough  dyspnea, cough, expectoration, fever, chest pain and
sometimes

haemoptysis. Silent cysts may present as an emergency due to rupture or an allergic reaction.

4. BRAIN  Features of raised intracranial pressure or unexplained headaches in a patient from a

sheeprearing community

 The patient may present as an emergency with severe abdominal pain following minor trauma,
when the CT scan

may be diagnostic.

 Rarely, emergency presentation  anaphylactic shock due to rupture of cyst. Such a patient
may subsequently

cough up white material that contains scolices that have travelled into the tracheobronchial tree
from rupture of a

hepatic hydatid on the diaphragmatic surface of the liver.

Hospital Surgery F.S. Noordeen

DIAGNOSIS

1. Serological tests  ELISA and immunoelectrophoresis, PCR.

2. Ultrasound and CT scan are the investigations of choice.

3. GBA  raised eosinophil count;

TREATMENT

LIVER

 Surgical treatment  PAIR (puncture, aspiration, injection of scolicidal agents and reaspiration).

 This is done after adequate drug treatment with albendazole/praziquantel to prevent

secondary peritoneal

echinococcus accidental spillage of fluid during PAIR or to minimize cyst size before surgery.

 Scolicidal agents  hypertonic saline (15–20%), ethanol (75–95%) or 1% povidone iodine

(although some use a

10% solution). This may cause sclerosing cholangitis if biliary radicles are in communication with
the cyst wall.

 Radical total or partial pericystectomy with omentoplasty or hepatic segmentectomy

(especially if the lesion is in
a peripheral part of the liver) are some of the surgical options.

 A laparoscopic approach to these procedures is being tried

 Cysts in other organs need to be treated in accordance with the actual anatomical site, along
with the general

principles described.

 An asymptomatic cyst which is inactive (group 3) may be left alone.

LUNGS

 Main  Surgery +/- chemotherapy (albendazole/mebendazole)

 The principle of surgery is to preserve as much viable lung tissue as possible.

 The exact procedure can vary: cystotomy, capittonage, pericystectomy, segmentectomy or

occasionally

pneumonectomy.

87. Alveococcosis. Clinic, diagnosis, treatment, indications for surgical treatment, types of
operations.

PULMONARY HYDATID DISEASE

 Caused by  Ecchinococcus granulosus; Echinococcus (Alveococcus) multilocularis

 The lung is the second commonest organ affected after the liver.

 The size of the cyst can vary from very small to a considerable size.

 The right lung and lower lobes are slightly more often involved.

 The cyst is usually single, although multiple cysts do occur and concomitant hydatid cysts in
other organs, such

as the liver, are not unknown.

CLINICAL FEATURES

1. May be asymptomatic and found incidentally.

2. Symptomatic patients’  dyspnea, cough, expectoration, fever, chest pain and sometimes
haemoptysis.

3. Silent cysts may present as an emergency due to rupture or an allergic reaction.

EXTRA;

Laparoscopic management

 Laparoscopic marsupialization of the cyst (de-roofing), consisting of removal of the cyst

containing the endocyst
along with daughter cysts, is the most common procedure.

 In the initial steps, the cyst is aspirated, taking care not to spill any contents, using povidone
iodine or hypertonic

saline as a scolicidal agent.

 Any communication with the biliary tree is oversewn and pedicled omentum is sutured to the
margins of the cyst.

 If the cyst is small, superficial and in the left lobe, cystopericystectomy is performed at centres
experienced enough

to do more advanced surgery, removing the entire cyst intact.

Hospital Surgery F.S. Noordeen

DIAGNOSIS

Rupture into the pleural cavity results in pleural effusion.

1. Serological tests  ELISA and immunoelectrophoresis, PCR.

2. CXR  Uncomplicated cysts present as rounded or oval lesions.

 Erosion of the bronchioles results in air being introduced between the pericyst and the
laminated membrane

and gives a fine radiololucent crescent, the ‘meniscus or crescent sign’.

 This is often regarded as a sign of impending rupture.

3. CT scan  when the cyst ruptures, the crumpled collapsed endocyst floats in the residual fluid,
giving rise to

the ‘water-lily’ sign.

Ultrasound and CT scan are the investigations of choice.

4. GBA  raised eosinophil count;

TREATMENT

 MAIN  Surgery +/- chemotherapy (albendazole/mebendazole)

 The principle of surgery is to preserve as much viable lung tissue as possible.

 The exact procedure can vary: cystotomy, capittonage, pericystectomy, segmentectomy or

occasionally

 pneumonectomy.

 Medical treatment is less successful and considered when surgery is not possible because of
poor general

condition or diffuse disease affecting both lungs, or recurrent or ruptured cysts.

88. Opisthorchiasis. Clinic, diagnosis, treatment, indications for surgical treatment, types of
operations.
 Liver flukes: Opisthorchis (specifically, Opisthorchis viverrini and Opisthorchis felineus).

 Chronic infection may lead to cholangiocarcinoma, a malignant cancer of the bile ducts.

Pathology

 In humans, the parasite matures into the adult worm in the intrahepatic biliary ducts where
they may reside for

many years  causing chronic inflammation of the bile ducts  dilation of intrahepatic bile ducts,
with

epithelial hyperplasia and periductal fibrosis.

 These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and
dreaded

complication of this parasitic infestation.

 The eggs or dead worms  stone formation in the gallbladder or common bile duct, which
becomes

thickened and much dilated in the late stages.

 Intrahepatic bile duct stones are also caused by the parasite producing mucin-rich bile.

 The dilated intrahepatic bile ducts may lead to cholangitis, liver abscess and hepatitis.

CLINIC

The disease may remain dormant for many years. Most infected persons are asymptomatic and
exhibit no physical

signs.

Symptomatic:

1. Non-specific symptoms  mild fever, malaise, anorexia and upper abdominal discomfort.

2. Heavier infection  The complete clinical picture can consist of fever with rigors due to
ascending

cholangitis, lack of appetite (anorexia), fatigue, obstructive jaundice, biliary colic and pruritus
from stones

in the common bile duct.

 Acute pancreatitis may occur because of obstruction of the pancreatic duct by an adult worm.

Heavy chronic infections/Advanced stage 

1. Accumulation of fluid in the legs (edema) and in the peritoneal cavity (ascites);

2. Enlarged non-functional gall-bladder

3. recurrent pyogenic cholangitis Periductal fibrosis

4. Cholecystitis & cholelithiasis

Hospital Surgery F.S. Noordeen

5. Obstructive jaundice, hepatomegaly and/or fibrosis of the periportal system

6. CHOLANGIOCARCINOMA  chronic hepatobiliary damage, inflammation, periductal fibrosis

and/or

cellular responses to antigens from the infecting fluke.

DIAGNOSIS

Lab Tests

1. GBA  Oesinophilia

2. Stool analysis (Kato techniques)  Eggs

3. ELISA  antigen 89 kDa of Opisthorchis viverrini

4. PCR

Instrumental Tests

1. Ultrasound scan of the hepatobiliary system  dilatation of intrahepatic bile ducts with only
minimal

dilatation of the common hepatic and common bile ducts, (but latter are much more dilated
when the

obstruction is caused by stones).

The thickened duct  foci in the bile ducts representing the worms or eggs.

2. Endoscopic retrograde cholangiopancreatography (ERCP)

TREATMENT

CONSERVATIVE TX

Curative in the early stages

Antihelminthic treatment  Praziquantel: single dose of 40 mg/kg is effective against

opisthorchiasis

Alternative  Albendazole

SURGERY

 Surgical treatment is cholecystectomy, exploration of the

common bile duct and some form of biliary–enteric bypass

 Repeated washouts are necessary during the exploration, as

the common bile duct is dilated and contains stones, biliary

debris, sludge and mud.

 This should be followed by choledochoduodenostomy.

 Since disease has a prolonged and relapsing course, some

surgeons prefer to do a Roux-en-Y choledochojejunostomy.

 The Roux loop is brought up to the abdominal wall, referred

to as ‘an access loop’, which allows the interventional

radiologist to deal with any future stones

89. Ascariasis. Clinic, diagnosis, treatment, indications for surgical treatment, types of
operations.

 Ascaris lumbricoides, commonly called the roundworm.

Epidemiology

 It is the commonest intestinal nematode affecting humans.

 Typically found in a humid atmosphere and poor sanitary conditions, hence is seen in the
tropics and

resource-poor countries

Pathogenesis

 Larvae cause pulmonary symptoms; adult worms cause gastrointestinal, biliary and pancreatic
symptoms

 Distal ileal obstruction is due to a bolus of worms; ascending cholangitis and obstructive
jaundice from

infestation of the common bile duct

 Acute pancreatitis occurs when a worm is lodged in the pancreatic duct

 Perforation of the small bowel is rare.

CLINICAL FEATURES

1. The larval stage in the lungs causes pulmonary symptoms Loeffler’s syndrome: dry cough,
chest pain,

dyspnoea and fever.

2. The adult worm can grow up to 45 cm long.

3. Small intestine  malnutrition, failure to thrive, particularly in children, and abdominal pain.

 Small intestinal obstruction can occur, particularly in children, due to a bolus of adult worms
incarcerated

in the terminal ileum. This is a surgical emergency.

 Rarely, perforation of the small bowel may occur from ischaemic pressure necrosis from the
bolus of
worms.

4. Common bile duct  Ascending cholangitis and obstructive jaundice.

5. Pancreatic duct  Acute pancreatitis

6. Allergies  Ascariasis may result in allergies to shrimp and dustmites due to the shared
antigen, tropomyosin;

this has not been confirmed in the laboratory.

7. Others  Ascaris have an aversion to some general anesthetics and may exit the body,
sometimes through the

mouth, when an infected individual is put under general anesthesia

A high index of suspicion is necessary so as not to miss the diagnosis:

If a person from a tropical country, or one who has recently returned after spending some time
in an endemic area,

presents with pulmonary, gastrointestinal, hepatobiliary and pancreatic symptoms, ascariasis

should be high on the

list of possible diagnoses.

Complications  acute abdomen; upper GI bleeding; small-bowel obstruction; volvulus and

intussusception,

peritonitis; biliary colic; acute cholecystitis; acute pancreatitis; acute cholangitis; hepatic abscess.

As such, ascariasis could be considered a potential cause of surgical emergency

DIAGNOSIS

Laboratory Tests

1. GBA  Eosinophilia

2. Stool examination (Kato technique)  may show ova.

Instrumental Tests

PULMONARY TESTS

1. Sputum or bronchoscopic washings  may show Charcot–Leyden crystals or the larvae.

2. Chest radiograph may show fluffy exudates in Loeffler’s syndrome.

GIT TRACTS

3. A barium meal and follow-through may show a bolus of worms in the ileum or lying freely
within the small

bowel.

4. Ultrasound may show a worm in the common bile duct or pancreatic duct.

Hospital Surgery F.S. Noordeen

5. Magnetic resonance cholangiopancreatography (MRCP)  an adult worm may be seen in the
common

bile duct in a patient presenting with features of obstructive jaundice.

Intestinal obstruction:

6. Plain abdominal radiograph  may show tubular structures within dilated small bowel,
denoting the

presence of worms.

7. Contrast CT scan  worms show up as curvilinear structures.

TREATMENT

CONSERVATIVE TX

1. Pulmonary phase  usually self-limiting and requires symptomatic treatment only.

2. Intestinal disease  patients should ideally be under the care of a physician for treatment with
anthelmintic

drugs.

Anthelmintic drugs: Albendazole, mebendazole, levamisole and pyrantel pamoate.

Other effective agents include tribendimidine and nitazoxanide.

 Certain drugs may cause rapid death of the adult worms and, if there are many worms in the
terminal ileum,

the treatment may actually precipitate acute intestinal obstruction from a bolus of dead worms.

3. Children who present with features of intermittent or subacute obstruction should be given a
trial of conservative

management in the form of intravenous fluids, nasogastric suction and hypertonic saline
enemas.

The last of these helps to disentangle the bolus of worms and also increases intestinal motility.

SURGERY

 Indications: Surgery is reserved for complications, such as intestinal obstruction that has not
resolved on a

conservative regime, or when perforation is suspected.

1. At laparotomy, the bolus of worms in the terminal ileum is milked through the ileocaecal valve
into the colon

for natural passage in the stool. Postoperatively, hypertonic saline enemas may help force out
the worms.

2. Strictures, gangrenous areas or perforations  resection and anastomosis.

3. If the bowel wall is healthy  enterotomy and removal of the worms may be performed.
4. Rarely, when perforation occurs  the parasites may be found lying free in the peritoneal
cavity. It is safer to

bring out the site of perforation as an ileostomy because, in the presence of a large number of
worms, the

closure of an anastomosis may be at risk of breakdown from the activity of the worms.

5. Common bile duct or pancreatic duct obstruction from a roundworm  by endoscopic

removal, failing which

laparoscopic or open exploration of the common bile duct is necessary. Cholecystectomy is also
carried out.

 When a patient is operated upon as an emergency for a suspected complication of roundworm

infestation, the

actual diagnosis at operation may turn out to be acute appendicitis, typhoid perforation or a
tuberculous stricture,

and the presence of roundworms is an incidental finding. Such a patient requires the appropriate
surgery depending

upon the primary pathology.

A FULL COURSE OF ANTIPARASITIC TREATMENT MUST FOLLOW ANY SURGICAL

INTERVENTION