Exam questions for 5 year students

1. Causes of acute abscess of lung.

Lung abscess is defined as a circumscribed area of pus or necrotic debris in lung
parenchyma, which leads to a cavity, and after formation of bronchopulmonary
fistula, an air-fluid level inside the cavity
Lung abscesses have numerous infectious causes. Anaerobic bacteria continue to be
accountable for most cases (The most common anaerobes are Peptostreptococcus
species, Bacteroides species, Fusobacterium species, and microaerophilic
streptococci.). These bacteria predominate in the upper respiratory tract and are
heavily concentrated in areas of oral-gingival disease. Other bacteria involved in lung
abscesses are gram-positive and gram-negative organisms.
Causes
• Primary (aspiration of oropharyngeal secretions, necrotizing pneumonia,
immunodeficiency);
o Dental/peridental infection;
o Para nasal sinusitis;
o Gastro-oesophageal reflux disease;
o Frequent vomiting;
o Intubated patients;
o Patients with tracheostomy;
• Secondary (bronchial obstructions, haematogenic dissemination, direct
spreading from mediastinal infection, from subphrenium, coexisting lung
diseases);
o Abdominal sepsis;
o Infective endocarditis;
o Intravenous drug abuse;
o Infected cannula or central venous catheter;
o Septic thromboembolisms.
o Bronchiectasis;
o Cystic fibrosis;
o Bullous emphysema;
o Bronchial obstruction by tumor, foreign body or enlarged lymph nodes;
o Infected pulmonary infarcts;
o Pulmonary contusion;
o Broncho-oesophageal fistula.

2. Clinical symptoms of acute abscess of lung

• At the first stage of acute abscess the patients complain of general weakness,
headache, malaise, suppressed appetite, moderate chest pain, dyspnea,
subfebrile temperature.
• At the second stage the state of the patients is worsened. The fever rises to as
high as 39-40°С and has a hectic character. At the same time the chest pain
increases, which associates with a troubling cough and dyspnea. The condition
of the patients is worsened and the intoxication increases. One can feel a foul-
 smelling from the mouth at cough. The amount of sputum is small, with a rusty
tone. With the beginning of the draining of destructive cavities through
bronchus the daily quantity of the sputum reaches 500 ml and more. At this
time is possible hemoptysis. The sputum is foul-smelling. At sedimentation it
divides into three layers:
o inferior – resembling a grey mass with detrites and flaps of a pulmonary
tissue;
o medial – purulent, turbid, liquid;
o Upper – mucous foamy layer.
• Further in favourable cases there is a considerable improvement of state of the
patients. The body temperature falls, the signs of intoxication reduce and the
appetite increases.
• The disease grades into the third stage, which is characterized by the regress
of clinical manifestations, up to their complete disappearance.
The physical signs good are well revealed at peripheral localization of the process.
By palpation – weakened vocal fremitus. At percussion – a blunted sound over the
site of the purulent focus and perifocal infiltration (at subpleural location of the
abscess). By auscultation – tubular sound with a moist rales in the zone of purulent
focus. Well-generated subpleural cavities of major sizes can be revealed by
percussion by bandbox sound, on auscultation by moist rales on the background of
amphoric respiration.

3. Clinical picture of chronic abscess of lung.

Chronic abscess of lungs occurs at 12-15 % of cases. It is considered to be chronic at
existence of a pulmonary abscess more than 6-8 weeks. It is characterized by a
cyclic course.
• In the stage of remission the patients complain of a moderate dyspnea, cough
with expectoration of a mucous or mucopurulent discharge.
• The exacerbation manifests by coughing up of 250-500 ml of a purulent foul
sputum, chest pain, dyspnea, hectic temperature with the difference in 1,5-
2°С. Dizziness, suppression of appetite, general weakness which increases
according to intoxication. The skin is pale with moderate cyanosis. The
respiratory rate rises to 28-30 per min.
• In 6-8 months is noticed the clubbing of the fingers and deformation of the
chest. The vocal fremitus is a little bit weakened on the side of lesion
(particularly in peripheral localization of the process).
• The percussion reveals a short sound in projection of pathological process, the
auscultation - a lot of moist rales on the background of amphoric respiration

4. Treatment of acute abscess of lung. Indications for operative treatment.

With the purpose of maximal concentration of drugs in the pathological focus
applied: Antibiotic of choice is Clindamycin for anaerobic microflora. Clindamycin
(600 mg IV on 8 h) and then 300 mg PO on 8 h or combination ampicilin/sulbactam
(1.5-3 gr IV on 6 h). Alternative therapy is piperacilin/tazobactam 3.375 gr IV on 6 h
or Meropenem 1 gr IV on 8 h (33).
For MRSA it is recommended to use linezolid 600 mg IV on 12 h or vancomycin 15
mg/kg BM on 12 h. 2nd generation cephalosporin:cefoxitin, cefotetan
• Injection of antibiotics in the vessels of a pulmonary circulation by means of
catheterization of central veins, pulmonary artery;
• Introduction of medicinal agents into respiratory tracts (in the second stage) –
through the endotracheal microirrigator, nasogastric tube, during
bronchoscopies, endoscopic catheterization of the abscess cavity through the
draining bronchus, in aerosolic inhalations. The composition of medical
admixtures includes: antibiotics, antiseptics (10 % dimexid, dioxydin, microcid
etc.), enzymes;
Evacuation of purulent content of the cavities:
• In natural way by an active sanation of tracheobronchial tree using repeated
fibrobronchoscopies, aspirations through the endobronchial catheter,
installations of medical agents through the microtracheostomy, aerosolic
inhalations;
• Transthoracically by means of repeated punctures or external draining of
peripheral cavities.
Indications for operative management in acute destructive processes of lungs:
• Pulmonary bleeding of ІІ (300-700ml) – ІІІ (more than 700ml) degree;
• Progression of the process on the background of active and appropriate
therapy;
• Tense pyopneumothorax, which is failed to liquidate by the draining of pleural
space;
• Impossibility to rule out the suspicion on a malignant tumour.
Contraindications: decompensation of the vital functions and systems in the
terminal stage, bilateral purulent destruction of lungs, concomitant incurable
malignant tumours

5. Clinic of pulmonary bleeding, treatment.

Pulmonary bleeding arise suddenly, are associated with coughing out of a foamy, red
blood and clots by portions or continuous stream. The most often source of a
pulmonary bleeding are the bronchial arteries and vessels of a pulmonary tissue. The
clinical manifestations of a pulmonary suppuration are accompanied by dizziness,
weakness, dyspnea, chest pain. The hemodynamic disturbances depend on intensity
of the bleeding. The auscultation of lungs from both sides reveals the moist rales
(aspiration). If the pulmonary destruction is present the plain film of the chest shows
the localization of the source of bleeding
I degree – hemorrhage up to 300 ml: Single hemoptysis or Multiple hemoptysis.
This degree manifests by coughing out the sputum tinged with blood, the
hemodynamic disturbance usually absent
ІІ degree – hemorrhage up to 700 ml.
• Single bleeding:
o with fall in arterial pressure and decreasing of hemoglobin;
o without fall in arterial pressure and decreasing of hemoglobin.
• Multiple bleeding:
o with fall in arterial pressure and decreasing of hemoglobin;
 o without fall in arterial pressure and decreasing of hemoglobin.
ІІІ degree - hemorrhage exceeds 700 ml. accompanied with sharp decreasing of
arterial pressure, rapid (more than 100-120 beats/min), small, sometimes thread
pulse, and even its disappearance on peripheral arteries, tachypnea to 40 per 1 min,
hemoglobin to 50-60 g/l. Probable the fulminant course up to the terminal state with
prompt failure of cardiac activity and asphyxia by blood.
Treatments for pulmonary hemorrhage include
• bronchodilators, tracheal suction,
• supplemental oxygen, mechanical ventilation, protective strategies by
decreased involvement of lung, positive pressure ventilation,
• intubation with bronchial tamponade, and reversal of coagulopathy.

6. Clinic of empyema.
• The pain is the sign, which denote the involvement of pleural membranes in
the process. Its intensity increases depending on depth of respiration and body
position.
• The dyspnea arises from accumulation of a purulent content in a pleural space
and exception of particular volume of a pulmonary tissue from respiration. It's
in direct ratio to amount of exudation in a pleural space.
• The cough is manifestation of inflammation or purulent and destructive
process in a pulmonary tissue.
• Fever to 39-40°C, headache, sleeplessness, general malaise, and anorexia – all
these are manifestations of intoxication.
• The forced patient's position and restriction of breathing should be considered
as outcomes of a pain syndrome. The extension of pleural empyema causes the
swelling of thoracic wall, smoothing of intercostal spaces.
• By palpation – diminished vocal fremitus on the part of lesion.
• The data of percussion and auscultation depend on extension of the process and
amount of pus in a pleural space. At percussion over the exudate it is possible
to reveal short sound with oblique upper contour. Above the exudate –
tympanic sound resulting from consolidation of pulmonary tissue. By
auscultation – diminished or absent sound in a great amount of exudate.
• X-ray shows Damosieu line, which is an oblique line that demarcates pus and
normal tissue

7. Indications and technique of pleurocentesis.

Thoracentesis is indicated for the symptomatic treatment of
• large pleural effusions or for treatment of empyemas.
• It is also indicated for pleural effusions of any size that require diagnostic
analysis
• Removal of air with a tight or closed pneumothorax;
• Pumping out pleural effusion;
• Administration of medicinal preparations.
When preparing for puncture of the pleural cavity Necessarily do chest radiography.
The procedure of thoracocentesis is carried out using local anesthesia, for which a
solution of novocaine is used. Anesthetized with puncture soft tissues and intercostal
muscles. Thoracocentesis is performed as follows:
• The patient sits down to rest his back, or lies on a healthy side. The hand from
the side where the puncture will be done is placed on the opposite shoulder or
on the head.
• Puncture of the pleural cavity with hemothorax for removal of blood or with
hydrothorax for pumping out of the liquid is done in the 7th - 8th intercostal
space along the scapular or posterior axillary line. In pneumothorax, puncture
is performed in the 2nd - 3rd intercostal space along the upper edge of the rib
by the mid-incision line.
• On the needle put a transitional rubber tube.
• With hemothorax and hydrothorax, aspiration is performed to remove Pleural
contents. After the tube is full, it is clamped with a clamp, drained and injected
again until the entire contents of the pleural cavity are removed. If the liquid is
difficult to evacuate, then try to achieve an increase in the outflow rate. To this
end, it is recommended to change the position of the patient's body or to
connect a low-pressure suction to the catheter.
• At the end of the procedure, an antibiotic is injected into the cavity.
• The needle is removed with a sharp movement.
• The puncture site is treated with a disinfectant solution, covered with sterile
gauze.
• At the end of the procedure, a chest radiograph is performed to determine if the
pleural cavity is better and no complications have occurred.

8. Classification of posttraumatic hemothorax.

І. According to degree of hemorrhage:
• Small (the loss less 10 % of volume of circulating blood).
• Moderate (loss of 10-20 % of volume of circulating blood).
• Great (loss of 20-40 % of volume of circulating blood).
• Total (exceeds 40 % of volume of circulating blood).
ІІ. According to duration of bleeding:
• With continuing hemorrhage.
• With the stopped bleeding.
ІII. According to the presence of clots in a pleural space:
• Coagulated.
• Noncoagulated.

9. Medical tactic in chest trauma complicated by hemothorax.

Complaints
• In case of small hemothorax clinical manifestations of hemorrhage are slightly
expressed or absent at all.
• Dyspnea, cough, general malaise and dizziness are obvious in moderate
hemothorax. The skin is pale. The hemodynamic disturbances – tachycardia
and decreased arterial pressure are observed.
• The great and total hemothorax are associated with signs of shock.
Physical exam
 • By percussion the dullness is revealed.
• By auscultation - the breathing over the site of hemothorax is sharply
diminished or is not heard.
On X-ray picture of hemothorax the intensive homogeneous shadow on the side of
the lesion with oblique upper contour is observed. The costal sinus does not
visualized.
• In small hemothorax, depending on the degree of intrapleural bleeding, the
shadow observed only in the region of sinus.
• In moderate hemothorax it achieves a scapular angle (on the back surface) or V
rib on anterior surface of the chest wall.
• In great hemothorax this shadow achieves ІІІ rib, and total hemothorax
characterized by complete shadow of a pleural space.
Treatment
• A treatment of small hemothorax requires needle aspiration or drainage of
pleural space and elimination of blood. The manipulation is carried out in 7-8th
intercostal spaces in the postaxillary or scapular lines.
• Total, great or moderate hemothorax with persistent bleeding (positive test by
Revilour-Greguar) requires thoracotomy for liquidation of a bleeding source.
• The bleeding wounds of lungs are sewed up by twist suture. If the pleural space
contains liquid blood, the surgeon carries out its reinfusion. The clots are
removed from pleural space.

10. Diagnostics and treatment of cardiac tamponade.

Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the
pericardial space, resulting in reduced ventricular filling and subsequent
hemodynamic compromise.
Patients with acute tamponade may present with dyspnea, tachycardia, and
tachypnea. Cold and clammy extremities from hypoperfusion are also observed in
some patients. Other symptoms and signs may include the following:
• Elevated jugular venous pressure
• Pulsus paradoxus: abnormally large decrease in stroke volume, systolic blood
pressure and pulse wave amplitude during inspiration. The normal fall in
pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is
referred to as pulsus paradoxus
• Chest pressure or discomfort that's relieved by sitting or leaning forward.
• Decreased urine output
• Confusion
• Dysphoria
• fainting, dizziness, and loss of consciousness
Although echocardiography provides useful information, cardiac tamponade is a
clinical diagnosis. Echocardiography can be used to visualize ventricular and atrial
compression abnormalities as blood cycles through the heart. The following may be
observed with 2-dimensional (2-D) echocardiography:
• An echo-free space posterior and anterior to the left ventricle and behind the
left atrium
• Early diastolic collapse of the right ventricular free wall
 • Late diastolic compression/collapse of the right atrium
• Swinging of the heart in the pericardial sac
• Left ventricular pseudohypertrophy
• Inferior vena cava plethora with minimal or no collapse with inspiration
• A greater than 40% relative inspiratory augmentation of blood flow across the
tricuspid valve
• A greater than 25% relative decrease in inspiratory flow across the mitral valve
Management
Removal of pericardial fluid is the definitive therapy for tamponade and can be done
using the following three methods:
• Emergency subxiphoid percutaneous drainage
• Pericardiocentesis (with or without echocardiographic guidance)
• Percutaneous balloon pericardiotomy

11. Classification of posttraumatic pneumothorax.

Posttraumatic pneumothorax is the presence of air in a pleural space, caused by
mechanical injury of lung or chest wall as a result of trauma.
І. According to extension of process:
• Unilateral.
• Bilateral.
ІІ. According to degree of a lung collapse:
• Partial (collapse of lung to 1/3 of its volume).
• Subtotal (collapse of lung to 2/3 of its volume).
• Total (collapse of lung exceeding 2/3 of its volume).
ІІІ. According to the mechanism of occurrence:
• Closed.
• Open.
• Valvular.

12. Mediastinal emphysema. Methods of treatment.

Mediastinal emphysema is the complication of the blunt trauma of the chest, which is
characterized by entering and accumulation of air in mediastinum. The entry of air in
mediastinum leads to compressing of superior cava vein and right atrium, which
results in the expressed discirculation.
The causes of mediastinal emphysema is partial (damage of a membranous part) or
complete disruptions of trachea, bronchi, esophagus and in some cases – tension
pneumothorax.
Symptomatology and clinical course
• The patients complain of difficult breathing and swallowing, pain behind
breastbone, hoarseness, and cough attacks.
• As a rule, the patient's position is forced – semi-sitting.
• The neck and face are thickened, cervical veins distended, the skin is cyanotic.
• By palpation – the crepitation of neck, face, and shoulder area. By auscultation
heart tones are diminished with tachycardia.
• On X-ray film on the background of enlightenment observed well-defined
contour of a mediastinal pleura. If there is the damage of mediastinal pleural
membrane a pneumothorax (mainly total or intense) is revealed.
Treatment
• The tissues in the mediastinum will slowly resorb the air in the cavity so most
pneumomediastinums are treated conservatively.
• Physical activity should be discouraged and bed rest must be ensured. Pain is
controlled with analgesics, according to the Individual Unit’s protocols.
• Anti-anxiety drugs should also be administered.
• Coughing should be suppressed with relative antitussives.
• Breathing high flow oxygen will increase the absorption of the air.
• If the air is under pressure and compressing the heart, a needle may be inserted
into the cavity, releasing the air.
• Surgery may be needed to repair the hole in the trachea, esophagus or bowel.
• If there is lung collapse, it is imperative the affected individual lies on the side
of the collapse, although painful, this allows full inflation of the unaffected
lung.
• Progressing mediastinal emphysema requires the urgent drainage of anterior
mediastinum in order to prevent external cardiac tamponade.

13. Treatment of posttraumatic pneumothorax.

Symptoms
• The rest dyspnea.
• The chest pain.
• By percussion obtains bandbox sound, or tympanitis.
• By auscultation - weak or absent breathing sounds.
• Lag on affected side.
Treatment
• Aspiration of air by means of thoracentesis, closed drainage of a pleural space
in 2nd to third rib mid clavicular or anterior axillary line
• The absence of effect (incomplete expansion of lung) of active aspiration, and
also valvular closed pneumothorax is the indications to operative management
– suturing of the pulmonary wound

14. Achalasia of the esophagus, classification.

Achalasia of the cardia is the disease, which is characterized by failure of the lower
esophageal sphincter to relax with swallowing.
Classification
Four stages of the disease are distinguished:
• functional spasm without esophageal dilation;
• constant spasm with a moderate esophageal dilation and maintained peristalsis;
• cicatrical changes of the wall with expressed esophageal dilation, the peristalsis
is absent;
• considerable esophageal dilation with sigmoid-shaped elongation and the
presence of erosive changes of esophageal mucosa.
According to Chicago classification
• Type 1 , achalasia with minimal esophageal pressurization: Absence of
peristalsis, no pressurization within the esophageal body, high integrated
relaxation pressure
 • Type II achalasia with esophageal compression: Absence of peristalsis and
contractile activity, panesophageal pressurization> 30mmHg and high
integrated relaxation pressure
• Type III achalasia with spasm: Absence of peristalsis and two or more
spastic contractions with or without periods of compartmentalized
pressurization and a high integrated relaxation pressure

15. Clinical characteristics of achalasia of the esophagus.

• Dysphagia in the onset of the disease wears a temporary intermittent character
with further permanent interchange. The passing of food after several swallows
delayed on the level of a lower part of breastbone. In some cases during meal
the dysphagia arises suddenly without any cause. The majority of the patients
with dysphagia swallow better warm or hot food.
• Esophageal vomiting (regurgitation) is the outcome of accumulation in
esophagus of two and more l. of fluid. In initial stages of the disease the
regurgitation can arise during or at once after meal and is accompanied by
discomfort pain sensations. In advanced stages observed regurgitation with a
rotten smell. The regurgitation can occur during sleeping – the sign "of a wet
pillow".
• Splashing sounds and gurgling behind breastbone are rarely observed.
• The sign of nocturnal cough arises owing to aspiration of fluid from
esophagus into trachea. Thereby, the patients try to sleep in a sedentary
position.
• Pain and sense of tightness in the chest is the result of spasm and esophageal
distention. With the developing of esophagitis, the pain wears a burning
character.
• Loss of weight is the outcome of prolonged disturbed food intake.
• Beak sign on barium swallow
Variants of clinical course and complications
• The bleedings arise owing to complications of erosive esophagitis at long
• The malignancy occurs in the patients with phenomena of a chronic
esophagitis and chronic character of the disease.
• Pneumonia, abscesses, bronchiectases, atelectases and pneumosclerosis are
frequently the outcomes of decreasing pulmonary excursion which results from
compression by dilated esophagus.

16. Treatment of achalasia of the esophagus depending on the clinical

stage.
Diet. The food should be semisoft, without pungent relishes, chemically inactive and
enriched with proteins, fat, carbohydrates and vitamins.

The medicament treatment should include local anesthetics, spasmolytics, and

sedative drugs. The medicament treatment results only in temporary relief.

Cardiodilatation is indicated in І-ІІ stage of achalasia. It is one of the chief

methods of the treatment of this pathology. The treatment is performed as follows:
under local anesthesia by aerosol or solution of anesthetic agent (lidocain, trimecain)
through constricted part of the cardia under roentgenological check cardiodilatator
(metal, pneumatic) is passed. The air is pumped up in balloon making pressure
200-350 mm H2O. Repeated procedure is performed in 2-3 days. The course of
dilatation includes 3-10 procedures, depending on obtained effect.
Surgical treatment is managed in ІІІ-ІV stage of achalasia or in recurrence of
the disease after dilatation.
• Heller's method (esophagomyotomy). Operation is performed through upper
median laparotomy or left thoracotomy in VІІ intercostal space. After exposing
of constricted part of esophagus and taking it on tourniquets a muscular layer
of anterior wall of esophagus dissected down to mucosa. The myotomy
performed from dilated part of esophagus to cardial part of stomach. The
complete transsection of all muscular layer of esophagus, particularly its
circular fibers, is the requirement of relapse prevention. The defect of a
muscular layer of esophageal wall is covered with a gastric fundus or by means
of interrupted suture or diaphragmatic flap.
• Helerovsky's method. The operation is indicated for the patients with ІІІ-ІV
stage of the disease in case of considerable esophageal dilation, when
performance of Heller's operation is impossible owing to cicatrical changes.
However the indication for this operation should be restricted, because of
frequent development of expressed esophagitis in postoperative period. The
same accesses, as in Heller's operation are applied. Constricted part of
esophagus to its dilation exposed and cardial part of stomach is mobilized.
Dilated part of the esophagus is anastomosed with the fundus of stomach.

17. Esophageal diverticula, classification.

The esophageal diverticula are the sacciform outpouchings of the esophageal wall,
which filled with mucus and undigested food.
According to the origin:
• congenital;
• acquired.
According to the histological structure:
• true (have all layers of esophageal wall);
• false (absent muscular layer of esophageal wall).
According to the localization:
• pharyngoesophageal (Zenker's); posterior outpouching of mucosa and
submucosa through the cricopharyngeal muscle
• bifurcational;
• epiphrenic.
According to the clinical course:
• complicated;
• uncomplicated.

18. Clinical characteristics of esophageal diverticula.

The symptomatology of Zenker's diverticula depends on the stage of development
and their size.
 • Salivation, cervical dysphagia, difficult swallowing and cough usually occur in
advanced stages of the diverticulum.
• The dysphagia is frequently caused by congestion of food in diverticulum.
• Also a compressible mass in the neck usually on the left side is frequently
revealed. The patients should press this mass to swallow the food and
sometimes make unusual movements by neck in order to empty the
diverticulum.
• The gurgling sound when the patient is eating and foul-smell from the mouth
resulting from decay of undigested food in diverticulum cause the patient to
alter social activities.
• The sign "of a wet pillow" results from increased salivation and nocturnal
discharge of saliva and mucus from the mouth.
Bifurcational diverticula are usually less 2 cm in size and therefrom rarely
complicated and clinically manifested. At its greater size the complications can arise
rather frequently and determine the course and manifestations of the disease.
The epiphrenal diverticula can achieve considerably size, and more frequently
complicated by diverticulitis. Being filled with food, such diverticulum can compress
cervical organs, and sometimes is complicated with achalasia.
The diagnosis is confirmed by the findings of barium swallow, and also
esophagoscopy

19. Complications of esophageal diverticula.

• Diverticulitis. The anginal pain, or the pain in epigastric region, which can
resemble stenocardia or gastric disorders, belching, are the chief
manifestations. Sometimes observed nausea and vomiting.
• The perforation of diverticulum can be directed into pleural space, trachea,
bronchus or pericardium. The clinical picture depends on the place of
perforation. In part the perforation in trachea or bronchus results in occurrence
of esophago-bronchial fistula. Clinically such complication is commonly
shown by cough during meal. An everlasting esophago-bronchial fistula can
cause the aspiration pneumonia with the further abscessing.
• Bleeding from diverticula frequently results from erosion of esophageal
mucosa on the background of diverticulitis. Nevertheless such bleedings, as a
rule, are not profuse and rather easily stopped by conservative treatment.
• Malignancy rarely occurs and most often as the outcome of recurrent
diverticulites.

20. Treatment of esophageal diverticula.

• The treatment of pharyngoesophageal diverticula is surgical.
• Conservative therapy is indicated in case of severe concomitant pathology, the
patient's refusal of operation or there are no conditions for its performance. In
such cases mechanically sparing diet with washing down of solid food.
• In order to expose pharyngoesophageal diverticula the cervical access along the
anterior border of the sternocleidomastoid muscle is applied; in case of
bifurcational diverticula right-sided posterolateral thoracotomy in ІV
 intercostal space is performed; in epiphrenal diverticula – left-sided
posterolateral thoracotomy in VІІ intercostal space
• The essence of the operation consists of the following: the esophagus
mobilized proximal and distal to diverticulum; after the exposure the latter is
sutured or stapled near its basis and cut off. The line of suturing is covered by
muscular layer of esophageal wall.

21. Classification of esophageal hernia.

Classification
According to the origin:
• congenital;
• acquired.
According to number:
• single;
• multiple.
According to histological structure:
• true (have all layers of esophageal wall);
• false (absent muscular layer of esophageal wall).
According to localization:
• sliding hiatal hernia occurs when the gastroesophageal junction, along
with a portion of the stomach, migrates into the mediastinum through
the esophageal hiatus
• paraesophageal hiatal hernia.also called rolling-type hiatal hernia, the
widened hiatus permits the fundus of the stomach to protrude into the
chest, anterior and lateral to the body of the esophagus; however, the
gastroesophageal junction remains below the diaphragm
• Mixed
According to the clinical course:
• complicated;
• uncomplicated.
International classification Four types of esophageal hiatal hernia are identified:
• Type I: A type I hernia is also known as a sliding hiatal hernia. 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.
• Type II: A type II hernia 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.
• 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.

22. Clinical manifestation of esophageal hernia

The predominant manifestations resulting from sliding diaphragmatic hernia (about
90 % of diaphragmatic hernias) are the signs of gastroesophageal reflux. It is
characterized by the pain behind breastbone or epigastric region. It more often
appears in supine position after meal or after intensive physical exertion.
• Heartburn is the second according to the frequency sign and caused by the
injury of esophageal mucosa by gastric juice as a result in turn of
gastroesophageal reflux.
• Belching by air, as a rule, observed, which commonly results in pain relief and
decrease of arching feeling in epigastric region.
• Regurgitation arises owing to gastroesophageal reflux, which reaches pharynx
and oral cavity. More often observed regurgitation by gastric acid or bitter
liquid or food.
• The sign of "lacing shoes" is expressed when the patient bends down after
liquid food, and the latter is partially poured out into the mouth. It is caused by
incompetence of the lower esophageal sphincter (gastroesophageal junction).
• Nausea and vomiting are rare. The latter some patients cause by themselves to
achieve some relief.
• Dysphagia is rarely observed. More often it is the outcome of complications of
diaphragmatic hernia (esophageal stricture, malignancy).
Roentgenological signs: 1) the sign of "bell"; 2) blunt His angle; 3) lack of air bubble
of the stomach.

23. The treatment of esophageal hernias.

In case of sliding hiatal hernia the method of a choice is the conservative therapy:
• the diet the same, as in peptic ulcer; weight loss
• position of the patient during sleeping – with elevated upside, during
exacerbation – sedentary;
• suppression of gastric secretion by administering of н2-blockers and PPI
• neutralization of gastric acid; antacids
• intensifying of evacuation of the food from stomach;
• avoidance of constipation; laxatives as needed
• anesthetics and sedative agents.
The indication for surgical treatment of sliding diaphragmatic hernia is the
considerable expression of clinical signs, diminish of patient's working capacity, fail
of conservative treatment, bleeding, peptic stricture, malignancy.
• Nissen fundoplication is the most common operation used. This procedure
involves a 360° fundic wrap around the gastroesophageal junction.
• The Toupet procedure is a variant of the Nissen wrap and involves a 180°
wrap in an attempt to lessen the likelihood of postoperative dysphagia.
 • Belsey (Mark IV) fundoplication: This operation involves a 270° wrap in an
attempt to reduce the incidence of gas bloating and postoperative dysphagia.

24. Classification of thyrotoxicosis

Etiology:
• Primary Thyrotoxicosis: Grave’s disease or Diffuse Toxic goitre
• Secondary Thyrotoxicosis: Toxic Multinodular Goitre, postpartum
• Solitary toxic nodule (Toxic Adenoma)
According to severity
• Mild degree is the tachycardia up to 120 per minute, fever as high as 38°С,
satisfactory state of the patient, tachypnea. NSAID/ Opioids
• The moderate gravity of thyrotoxic response manifests by mild psychomotor
excitement. They complain of general weakness, headache, fever sensation,
rapid pulse to 120-140 per minute (rhythmic, tense), and sometimes
extrasystole. Temperature raises as high as 38,5-39°С. Characteristic the
considerable sweating, tachypnea, superficial sleep. Beta blocker, Opiods,
Glucocorticoids
• Severe degree of thyrotoxic response is characterized by expressed
psychomotor excitement. The patients are restless, frequently change
positions in the bed, they complain of considerable sweating, permanent
fever sensation and expressed tremor. Hyperemia of the face, pulsate vessels
of the neck and cyanosis of leaps are evident. The pulse rate usually exceeds
140 per minute, irregular and soft. The breathing is superficial. Body
temperature is 39-40°С. The sleeplessness in such patients is almost
impossible to liquidate by hypnotic and narcotics agents. Give sedative,
beta blocker, oxygen mask, NSAID’s, glucocorticoids, desintoxication,
neuroleptanalgesia.

25. Diagnostic of thyrotoxicosis

• Thyroid profile – T3 ↑ T4 ↑ TSH ↓
• X ray soft tissue neck Calcification & tracheal deviation
• X ray chest – Retrosternal extension
• ECG:- Stages of development of thyrotoxic arrhythmia
o Multiple extrasystoles
o Paroxysmal atrial tachycardia
o Paroxysmal atrial fibrillation
o Persistent atrial fibrillation not responding to digoxin.
• Radio isotope scan with I131 or Tc99m pertechnitate
• Serum creatin
• Ultrasound scan of the gland.
• Indirect laryngoscopy to rule out symptomless paralysis of vocal cords
• Fine Needle Aspiration Cytologu to confirm the diagnosis.

26. Clinical signs of thyrotoxicosis

Common symptoms of thyrotoxicosis include the following:
• Nervousness
 • Anxiety
• Increased perspiration
• Heat intolerance
• Hyperactivity
• Palpitations
• Tachycardia or atrial arrhythmia
• Systolic hypertension with wide pulse pressure
• Warm, moist, smooth skin
• Lid lag
• Stare
• Hand tremor
• Muscle weakness
• Weight loss despite increased appetite (although a few patients may gain
weight, if excessive intake outstrips weight loss)
• Reduction in menstrual flow or oligomenorrhea
Clinical Eye signs
• Lid lag & Lid retraction
• exophthalmos
• Bilateral proptosis
• Ophthalmoplegia
• Chemosis
Exophthalmos : First abnormality – appearance of sclera above superior Limbus.
Then, eyes propped out and eyelids cannot shut properly.
• Convergence difficult (Moebius sign)
• Can not look down without upper lid lag (von Graefe’s sign)
• No wrinkling of forehead when looking up (Joffroy’s sign)
• Corneal ulceration and loss of vision

27. Treatment of goiter and thyrotoxicosis

Treatment of thyrotoxic crisis
• Block thyroid hormone synthesis: Propylthiouracil 200 to 250 mg every 4
hours or methimazole 30 mg every 6 hours
• Inhibit thyroid hormone release – only after administration of antithyroid
drugs: Lugol’s solution 10 to 15 drops every 8 hours or sodium iodide or
potassium iodide intravenously 0.5 to 1 gram every 12 hours
• Inhibit T4 to T3 conversion: glucocorticoids, e.g. hydrocortisone 200 to 300
mg as a loading dose followed by 100 mg every 8 hours
• Block the effects of T4 and T3 on peripheral tissues: b-blockers, e.g.
propranolol: 0.5-1.0 mg intravenously in 10 minutes followed by 1-3 mg every
hour until concomitantly administered oral propranolol (60-80 mg every 4 to 6
hours) is

28. Indication for coronary angiography

Ukraine Indications for angiography include poorly controlled symptoms;
• abnormal results on stress testing, particularly with a substantial burden of
ischemia (e.g., 1 mm or more of ST-segment depression);
 • ischemia at a low workload (below 5 to 6 metabolic equivalents);
• large, inducible single or multiple wall-motion abnormalities; and substantial
nuclear-perfusion defects.
The indications for coronary angiography (international) have been divided into the
follow clinical categories:
• Assessment of coronary artery disease Persistent angina pectoris Markedly
positive stress test Unstable angina pectoris Positive stress test post infarction
The young patient Variants of angina Complications of ventricular aneurysm
Postoperative coronary surgery problems
• Assessment with valvular heart disease
• Symptomatic diagnostic problem patients
• Resuscitated sudden cardiac death
• Asymptomatic patients Markedly positive stress or thallium test Occupational
safety

29. Indication for coronary stenting

Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a
nonsurgical procedure that improves blood flow to your heart. Overview. PCI
requires cardiac catheterization, which is the insertion of a catheter tube and injection
of contrast dye, usually iodine-based, into your coronary arteries
Clinical indications for PCI or stenting include the following:
• Acute ST-elevation myocardial infarction (STEMI)
• Non–ST-elevation acute coronary syndrome (NSTE-ACS)
• Unstable angina
• Stable angina
• Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
• High risk stress test findings

30. Indication for aorto-coronary by-pass

Coronary artery bypass grafting (CABG) is a type of surgery that improves blood
flow to the heart. During CABG, a healthy artery or vein from the body is connected,
or grafted, to the blocked coronary artery. The grafted artery or vein bypasses (that is,
goes around) the blocked portion of the coronary artery. This creates a new path for
oxygen-rich blood to flow to the heart muscle.
Class I indications for CABG from the American College of Cardiology (ACC) and
the American Heart Association (AHA) are as follows :
• Over 50% left main coronary artery stenosis
• Over 70% stenosis of the proximal left anterior descending (LAD) and
proximal circumflex arteries
• Three-vessel disease in asymptomatic patients or those with mild or stable
angina
• Three-vessel disease with proximal LAD stenosis in patients with poor left
ventricular (LV) function
• One- or two-Vessel disease and a large area of viable myocardium in high-risk
area in patients with stable angina
 • Over 70% proximal LAD stenosis with either an ejection fraction (EF) below
50% or demonstrable ischemia on noninvasive testing
Other indications for CABG include the following:
• Disabling angina (class I)
• Ongoing ischemia in the setting of a non–ST segment elevation myocardial
infarction (MI) that is unresponsive to medical therapy (class I)
• Poor LV function but with viable, nonfunctioning myocardium above the
anatomic defect that can be revascularized

31. Indication for pace-maker implantation

• Acquired AV block: 2nd or 3rd degree
• After myocardial infarction
• Bifascicular or trifascicular block
• Sinus node dysfunction with symptoms as result of long term drug therapy
• Symptomatic chronotropic incompetance
• Hypertensive carotid sinus and neurocardiac syndromes
o Recurrent syncope associated with carotid sinus stimulation
o Asystole of> 3s duration in absence of any medication

32. Dissecting aortic aneurysm, classification, treatment

Aortic dissection (AD) occurs when an injury to the innermost layer of the aorta
allows blood to flow between the layers of the aortic wall, forcing the layers apart.
classification is based on chronicity and labels aortic dissections as hyperacute (<24
hours duration), acute (2–7 days), subacute (8–30 days), and chronic (>30 days)
DeBakey classification
• Type I – originates in ascending aorta, and propagates at least to the aortic arch
and often beyond it distally. It is most often seen in patients less than 65 years
of age and is the most lethal form of the disease.
• Type II – originates in the ascending aorta and is confined to it.
• Type III – originates in the descending aorta and rarely extends proximally, but
will extend distally. It most often occurs in elderly patients with atherosclerosis
and hypertension.
The Stanford classification is divided into two groups, A and B, depending on
whether the ascending aorta is involved.
• A – involves the ascending aorta and/or aortic arch, and possibly the
descending aorta. The tear can originate in the ascending aorta, the aortic arch,
or more rarely, in the descending aorta. It includes DeBakey types I and II.
• B – involves the descending aorta or the arch (distal to the left subclavian
artery), without the involvement of the ascending aorta. It includes DeBakey
type III.
Treatment
• Urgent surgical intervention is required in type A dissections. The area of the
aorta with the intimal tear usually is resected and replaced with a Dacron graft.
• The definitive treatment for type B dissections is less clear. Uncomplicated
distal dissections may be treated medically to control blood pressure. Long-
term medical therapy involves a beta-adrenergic blocker combined with other
 antihypertensive medications. Avoid antihypertensives (eg, hydralazine,
minoxidil) that produce a hyperdynamic response that would increase dP/dt (ie,
alter the duration of P or T waves)

33. The causes of arterial atherosclerosis of the lower limbs.

• Atherosclerosis
• Obliterating endarteritis (obliterative thromboangitis, thrombangiitis obliterans)
• Aorto-arteritis (Takayashu arteritis )
• Diabetes mellitus
• Raynaud's disease
• Group of hypersensitive angiites, autoimmune angiopathy (mixed
cryoglobulinemia, arteritis as a result of collagenous diseases: nodular
periarteritis, dermatomyositis, systemic scleroderma)
• Acute and blunt trauma with artherothrombosis

34. Clinical characteristics of obliterating atherosclerosis of the lower

limbs
• Signs of periodic ischemia. In the patients with atherosclerosis obliterans of the
inferior extremities at physical exertion (prompt walking, run) usually appear
manifestations of a muscle circulation failure, which has the name of
intermittent claudication. Because of occurrence of intensive pain in muscles of
the leg the patient have to stop. In some minutes the pain disappears and he
again can pass the same distance.
• A constant pain (rest pain) appears due to considerably expressed circulatory
insufficiency in legs in condition of functional rest. The pain more often is so
severe, that is frequently it is failed to relieve by narcotic alkaloids. At night, as
a rule, the pain increases. The patient sleeps either with the downcast legs or
during day and night siting with flexed knee.
• After 10-14 days of constant sedentary position the edema of legs and feet
develops. The skin of toes blanched or cyanotic, cold by touch.
• The destructive changes of distal parts of extremity should be regarded as
terminal manifestation of severe arterial ischemia. It could be like focal
necroses, trophic ulcers and gangrene of toes. The development of such
changes usually precedes a long period of the disease, with intermittent
claudication, discoloration, coldness of the skin and its trophic changes as
atresia, atrophy of muscles, loss of hair, dystrophy and disturbance of the nail
growth. The necrotic changes, as a rule, firstly develop on toes.

35. Classification of chronic arterial ischemia of the lower limbs

Classification of artherosclerosis obliterans
❖ І stage (asymptomatic)– complete compensation (coldness, fatigue,
paresthesias);
❖ ІІ stage –functional circulatory insufficiency (a leading sign - intermittent
claudication);
 o II A st. - intermittent claudication 200-500 m
o II B st. - intermittent claudication less than 200 m
❖ ІІІ stage – ischemia of extremity at rest (a leading sign – rest or night pain);
o III A st. - ankle pressure less than 50 mm Hg
o III B st. - ankle pressure less than 30 mm Hg
❖ ІV stage – considerably expressed destruction of tissues of the distal parts of
extremity (ulcers, necrosis, gangrene).
Rutherford classification for chronic limb ischemia

Grade Category Clinical description Objective criteria

0 0 Asymptomatic—no Normal treadmill or reactive

hemodynamically significant hyperemia test
occlusive disease

1 Mild claudication Completes treadmill

exercise; AP after
exercise > 50 mm Hg but at
least 20 mm Hg lower than
resting value
I 2 Moderate claudication Between categories 1 and 3
3 Severe claudication Cannot complete standard
treadmill exercise, and AP
after exercise < 50 mm Hg
II 4 Ischemic rest pain Resting AP < 40 mm Hg, flat
or barely pulsatile ankle or
metatarsal PVR;
TP < 30 mm Hg
III 5 Minor tissue loss—nonhealing Resting AP < 60 mm Hg,
ulcer, focal gangrene with diffuse ankle or metatarsal PVR flat
pedal ischemia or barely pulsatile;
TP < 40 mm Hg
6 Major tissue loss—extending Same as category 5
above TM level, functional foot
no longer salvageable
Wound

Grade Ulcer Gangrene

0 No ulcer No gangrene
Grade Category Clinical description Objective criteria

1 Small, shallow ulcer on distal No gangrene

leg or foot; no exposed bone,
unless limited to distal phalanx

2 Deeper ulcer with exposed Gangrenous changes limited

bone, joint, or tendon; generally to digits
not involving the heel; shallow
heel ulcer, without calcaneal
involvement

3 Extensive, deep ulcer involving Extensive gangrene

forefoot and/or midfoot; deep, involving the
full-thickness heel forefoot/midfoot; full-
ulcer ± calcaneal involvement thickness heel
necrosis ± calcaneal
involvement

36. Methods of the diagnostic of obliterating atherosclerosis of the

lower limbs
Functional tests
• Functional test of Burdenko. Atherosclerosis is interfaced to stagnant processes
in vessels. When bending a foot in a knee, foot (sole) becomes covered by
marble vascular drawing. It testifies to bad outflow of blood from an extremity.
• The hyperemic Shamova/Sitenko’s test. For identification of atherosclerotic
violations in work of vessels for a while 3-5 minutes on a shoulder or a hip the
special cuff is imposed. It squeezes surrounding vessel, interfering with normal
blood circulation. Normal blood supply (and respectively and pink color)
fabrics in norm comes back 25-35 seconds later. If vessels are struck with
atherosclerosis — can be demanded about one minute – one and a half and
more, depending on extent of narrowing of the channel of a blood vessel.
• The functional test of Moshkovich for an assessment of a plantarny symptom.
The patient accepts a prone position. Then raises vertically up feet, without
bending them in knee joints. In such position of the patient ask to remain for
two-three minutes. Then the patient adopts the standing provision. In norm, at
the healthy person skin turns pale in the first situation as there is an outflow of
blood from the lower extremities and as soon as rises — blood supply is
restored, and skin accepts a natural pinkish shade within 8-10 seconds or
quicker again. At patients with atherosclerosis of it it is not observed. Skin of
30 and more seconds is capable to keep pale color, marble vascular drawing,
etc.
Lab and instrumental
 • For establishment of expressiveness of violations of blood circulation resort to
dopplerography of vessels.
• Laboratory measurements of cholesterol: LDL, HDL, triglycerides etc.
• The X-ray analysis gives the chance to establish localization and the sizes of
occlusions of vessels.
• Transcutaneous determination of pO2 and pCO2.

37. Methods of the operative treatment of obliterating atherosclerosis

of the lower limbs
The indications for repairing operations are determined by the gravity of ischemia of
extremities, local alterations, degree of operative hazard.
• Reconstruction of vessels carried out, as a rule, in ІІ- ІІІ stages, sometimes –
in ІV stage of ischemia. To such type of operations a bypass graft and
prosthetic repair are referred.
• For improvement of blood supply of ischemic tissues of the inferior extremities
the endarterectomy of a deep femoral artery with subsequent
profundoplastics is of major value. The latter is carried out through the
arteriotomy in the site of derivation of a deep femoral artery and after
removing of atherosclerotic plaques that obstruct the lumen and accomplished
by the autovenous lateral plastics.
• If necrotic changes of extremities are present, it is necessary to prefer
autoplastic methods of repairing (endarterectomy, autovenous bypass), thus
avoiding of synthetic vascular prostheses, which are always dangerous for
infection.
• The gangrenous changes of the extremity are the direct indication for
amputation.

38. Methods of the conservative treatment of obliterating

atherosclerosis of the lower limbs
Conservative therapy is indicated in І - ІІ stage of a chronic ischemia, and also in the
patients with high hazard of complications and atherosclerotic lesion of arterial
system of the lower limbs, which are not suitable for operative treatment.
• Liquidation of a vasomotor spasm is achieved by application of vasodilating
agents (papaverine, platyphyllin, halidor, no shpa).
• Special exercises, massage or physical procedures stimulate the development
of a collateral circulation.
• For the improvement of microcirculation are instituted the agents, which dilate
vessels and improve the nutrition of ischemic tissues (nicotinic acid, xantinol,
vasaprostan, trental, rheopolyglucin).
• Besides these, it is advisable to use the agents for the normalization of
neurotrophic and metabolic processes (vitamins of group В1, C, Е, hormone
therapy, testosteron).
• Also the agents, which influence on atherogenesis are administered: the agents,
which reduce adsorption of cholesterol (cholestyramine); stop the synthesis
cholesterol-lipid complexes (clofibrate); and which accelerate the elimination
of the lipids from organism. Statins.
 • A positive influence have also the agents, that change blood rheology:
antiaggregants (curantyl, aspirin, rheopolyglucin); indirect anticoagulants
(phenilin,pelentan) and direct anticoagulants (heparin).
• Physiotherapeutic and sanatorium treatment (barotherapy, hyperbaric
• oxygenation, photoradiotherapy, magnetotherapy, diadynamic current by
Bernard, etc.) is also necessary to regard as effective agents in this plan.

39. Complications of obliterating atherosclerosis of the lower limbs

• The acute thrombosis of arterial trunks develops on the background of a
chronic discirculation of the extremity, which exists during several years.
During the development of this complication the pain in extremity appears
which intensity gradually increases. The skin on the onset of an acute occlusion
is blanched, later its coloring acquires a marble character. Temperature of the
skin simultaneously decreases, and the sensory disorders develop: firstly pain
and tactile sensitivity disappears, and then the deep sensitivity. The
development of necrotic changes in tissues manifests by rigidity and
contracture of muscles, morbidity at palpation and passive movements,
subfascial edema as well.
• Ulceration and gangrene frequently complicate advanced or severe
arteriosclerosis obliterans. These complications usually follow infection,
loosening, and sloughing of the nail and firstly appear on the ends of digits,
often around the nails. In ischemic toes, ulceration or gangrene may result from
normal pressure from shoes in ordinary walking. Ulceration of the foot or leg is
usually the result of trauma, either mechanical or thermal, or some type of
pyogenic infection of the skin. Gangrene may involve the distal part of toe, an
entire toe, several toes, the entire foot, and even the leg as high as the knee.
Ischemic ulcers and minor gangrenous lesions of the toes usually produce no
evidence of systemic toxicity unless the margins become infected. More
extensive gangrene involving the foot or leg, particularly when it develops
rapidly after acute thrombotic occlusion of a major artery may cause from mild
to moderate toxemia with fever, tachycardia, mental confusion, and even renal
or hepatic failure.

40. The causes of arterial thrombosis and embolism.

Arterial embolisms can consist of various materials, including:
• Thromboembolism – embolism of thrombus or blood clot
• Cholesterol embolism - embolism of cholesterol, often from atherosclerotic
plaque inside a vessel.
• Fat embolism – embolism of bone fracture or fat droplets.
• Air embolism (also known as a gas embolism) – embolism of air bubbles.
• Septic embolism – embolism of pus containing bacteria.
• Cancer embolism
Causes
• smoking
• hardening of the arteries from high cholesterol
• surgery that affects blood circulation
 • injuries to the arteries
• heart disease
• atrial fibrillation — a type of rapid and irregular heartbeat
• Anti-phospholipid syndrome
• Fracture of bones

41. Clinical characteristics of arterial thrombosis and embolism.

You may notice some of the following symptoms in an arm or leg after an embolism
has formed:
• coldness
• lack of pulse
• lack of movement
• tingling or numbness
• pain or spasms in the muscles
• pale skin
• a feeling of weakness
• These symptoms will likely be asymmetrical, appearing only on the side of
your body with the embolism.

42. Classification of acute arterial insufficiency.

43. Differential diagnosis of acute thrombosis and embolism of major

arteries.
Thrombosis of the heart symptoms:
❖ Sudden chest pain that is radiating to the left arm or left side of the neck
❖ Shortness of breath
❖ Nausea and vomiting
❖ Anxiety
❖ Feeling of indigestion
❖ Palpitations
❖ Unexplained sweating
Thrombosis of the kidney symptoms:
❖ Presence of blood clot in the lungs
❖ Decreased urinary output
❖ Presence of blood in urine
 ❖ Low back pain
❖ Weight loss
Thrombosis of the brain symptoms:
❖ Confusion and stupor where a patient experience episodes of drowsiness and
unable to respond to outside stimuli. The patient will also have the inability to
remember or recall familiar personality and events.
❖ Patient will experience symptoms of stroke such as weakness on one side of
the face and inability to move one or more limbs.
❖ Headache is the most common symptom of cerebral thrombosis which may
tend to worsen over time. Headache may also occur suddenly or the
thunderclap headache.
❖ Swelling of the optic disc may occur due to intracranial pressure and patient
may have a decrease in level of consciousness.
Thrombosis of the arms and legs symptoms:
❖ Warm sensation in the arm or leg depending on the location of blood clot
❖ Sharp pain is felt when the arm or foot is flexed
❖ Redness and swelling over the affected area
❖ Aching throb on the calves when walking

44. Indications for conservative treatment of arterial thrombosis and

embolism, drugs that are used.
It is the first line treatment if patient is hemodynamically stable, or in beginning
stages of the disease
Medications include: Antithrombotic medication. These are commonly given because
thromboembolism is the major cause of arterial embolism. Examples are:
• Anticoagulants (such as warfarin or heparin)
• antiplatelet medication (such as aspirin, ticlopidine, and clopidogrel) can
prevent new clots from forming
• Thrombolytics (such as streptokinase, urokinase,altepase, retepase) can
dissolve clots
• Desensitizing agents (dimedrol, pipolphen, diazolin, suprastin, tavegil) block
the influence of histamine and result in vasodilating effect, reducing thus a
permeability and brittleness of a vascular wall.
• To the drugs, which influence on the blood rheology, should be regarded
dextrans (rheopolyglucin, polyglucinum).
Painkillers given intravenously
Vasodilators to relax and dilate blood vessels: vasaprostan, pentoxyphillin
Appropriate drug treatments successfully produces thrombolysis and removal of the
clot in 50% to 80% of all cases.
Antithrombotic agents may be administered directly onto the clot in the vessel using a
flexible catheter (intra-arterial thrombolysis). Intra-arterial thrombolysis reduces
thromboembolic occlusion by 95% in 50% of cases, and restores adequate blood flow
in 50% to 80% of cases
 45. Control methods for coagulation system.
There are many anticoagulants, including:
• heparin.
• warfarin (Coumadin)
• rivaroxaban
• dabigatran
• apixaban
• edoxaban
• enoxaparin
• fondaparinux
Common antiplatelets include:
• clopidogrel
• ticagrelor
• prasugrel
• dipyridamole
• dipyridamole/aspirin
• ticlodipine
• eptfibatide
thrombolytic agents include:
• Eminase (anistreplase)
• Retavase (reteplase)
• Streptase (streptokinase, kabikinase)
• t-PA (class of drugs that includes Activase)
• TNKase (tenecteplase)
• Abbokinase, Kinlytic (rokinase)

46. Surgical treatment of arterial thrombosis and embolism.

Arterial bypass surgery to create another source of blood supply
Embolectomy, to remove the embolus, with various techniques available:
• Thromboaspiration
• Angioplasty with balloon catheterization with or without implanting a stent
• Balloon catheterization or open embolectomy surgery reduces mortality by
nearly 50% and the need for limb amputation by approximately 35%.
• Embolectomy by open surgery on the artery
If extensive necrosis and gangrene has set in an arm or leg, the limb may have to be
amputated

47. The causes of thrombophlebitis.

Thrombophlebitis mean complete, or partial occlusion of major veins, which forms
on the background of inflammatory response of a venous wall.
Causes is blood clot
• The most often cause of thrombophlebitis of the lower extremities is the
varicosity (varicose thrombophlebitis).
• The contributory factors may be mechanical local damages (mechanical
traumas), long application of contraceptions, infections (influenza, pneumonia,
 typhoid, hematosepsis and other). Pregnancy, obesity, family history of
thrombophlebitis
• The deep and superficial thrombophlebites of legs can also arise in patients
with malignancies, which compress major veins, and also on the background
of leukoses, thromboangitis obliterans and collagenous diseases.

48. Clinical characteristics of thrombophlebitis.

• Superficial thrombophlebitis. These pathology, as a rule, resulting from a
varicose disease of inferior extremities. The onset is sudden. The patients
complain of a burning pain in the extremity. The expressiveness of pain
depends on involvement in inflammatory process of adjacent tissues. A morbid
dense cord with local erythema is defined down the course of great or small
saphenous veins. The general state changes a little. The patients feel moderate
general weakness, chills, the temperature is risen from subfebrile to 38-40°С.
No edema or cyanosis
• Migrating thrombophlebitis is the special form of a superficial
thrombophlebitis. It usually develops in a great saphenous vein as a result of
malignancies or other systemic diseases (thrombangiitis obliterans). It
manifests by a dense formation of a spherical or oval form with signs of
inflammation (morbidity, rising of local temperature, hyperemia of skin). The
common clinical signs are usually absent. During a progression of disease the
formation frequently spreads onto interior surface of a thigh up to a place of a
saphenofemoral juncture. In such situation there is an actual threat of formation
of a floating thrombus with its separation and pulmonary embolism. The
process of migration of a thrombogenesis also could be the cause of iliofemoral
thrombosis.

49. Differential diagnosis of thrombophlebitis and deep vein

thrombosis.
• DVT occurs in the deep veins while thrombophlebitis occurs in the superficial
veins.
• DVT is more life threatening than thrombophlebitis.
• DVT presents with pain, edema and cyanosis whereas thrombophlebitis
presents with just pain, hyperemia, local increase of temperature along varicose
vein
• DVT is diagnosed with ultrasound while thrombophlebitis is diagnosed
through assessment.
• .DVT is treated with blood thinners and compression stockings while
thrombophlebitis is treated with anti-inflmmatories and pain medications.

50. Conservative treatment of thrombophlebitis, drugs that are used.

The treatment of thrombophlebitis of any localization and degree should be begun
from conservative therapy. The agents of the therapy may be divided on passive and
active. The bed regimen should last 7-8 days.
• injection of a blood-thinning (anticoagulant) medication, such as low molecular
weight heparin or fondaparinux (Arixtra), will prevent clots from enlarging.
 After the initial treatment, taking the oral anticoagulant warfarin (Coumadin,
Jantoven, others) or the newer rivaroxaban (Xarelto) for several months
continues to prevent clots from enlarging.
• For improvement of a blood rheology is desirable rheopolyglucin,
polyglucinum, rheogluman, and with the purpose of activization of tissue
microcirculation - niacin, trental. These patients are advisable also drugs of
antiinflammatory activity (butadion, rheopyrin, venoruton).
• Active methods of conservative treatment are aimed on fibrinolytic therapy,
which is most effective during the first 4-5 days from the beginning of the
disease. With this purpose streptokinase is used. For prevention of a bleeding
intravenously trasylol are injected. The application of urokinase, as a direct
plasminogen activator, may be effective.

51. Surgical treatment of thrombophlebitis.

• incision and drainage of the clot should be attempted to alleviate pain.
• Saphenectomy
• Crossectomy with phlebectomy of collaterals or perforating veins

52. The causes of deep vein thrombosis.

• Thrombophlebitis
• Trauma
• Pregnancy
• Operations and postoperative period
• Prolonged bed regimen
• Stroke with paralysis
• Sensitization of the organism, autointoxication, allergic reactions
(immunization, antibiotics, blood transfusion, flu, rheumatic diseases,
complications of varicosity: eczema, cellulitis)
• Infection (trophic ulcers)

53. Clinical characteristics of deep vein thrombosis.

Symptoms of DVT occur in the leg affected by the blood clot and include:
• A firmness or thickening of the vein called a "cord"
• Arching pain of the leg
• Edema of the leg
• Cyanotic skin
• Painful muscle palpation of the leg
• Homans’ sign - tibial muscle pain after maximal dorsiflexion of foot.
• Lowenberg’s test - tibial muscle pain under the pressures of 80-100 mm Hg by
imposing on the leg a cuff of sphygmomanometer.
• Many patients, however, experience no symptoms at all.
• Illeofemoral DVT: Clinic of DVT plus edema of thigh and whole leg. White
phlegmasia. Blue phlegmasia - the total thrombosis of deep, superficial and
pelvic veins which can result in venous gangrene.
• Paget-Shrotter syndrome: DVT of subclavian vein. Arching pain of the arm.
Edema of the arm. Cyanotic skin. Painful muscle palpation of the arm
 • Thrombus that involves the iliac bifurcation, the pelvic veins, or the vena cava
produces leg edema that is usually bilateral rather than unilateral. High partial
obstruction often produces mild bilateral edema that is mistaken for the
dependent edema of right-sided heart failure, fluid overload, or hepatic or renal
insufficiency.
Diagnosis
• D-dimer testing: usually increase in thromboembolism
• Coagulation studies (eg, prothrombin time and activated partial thromboplastin
time) to evaluate for a hypercoagulable state
• Duplex ultrasound, venography, dopplerography

54. Differential diagnosis of thrombophlebitis and deep vein

thrombosis.
• DVT occurs in the deep veins while thrombophlebitis occurs in the superficial
veins.
• DVT is more life threatening than thrombophlebitis.
• DVT presents with pain, edema and cyanosis whereas thrombophlebitis
presents with just pain, hyperemia, local increase of temperature along varicose
vein
• DVT is diagnosed with ultrasound while thrombophlebitis is diagnosed
through assessment.
• .DVT is treated with blood thinners and compression stockings while
thrombophlebitis is treated with anti-inflmmatories and pain medications.

55. Treatment of deep vein thrombosis, drugs that are used.

Drugs
• Heparin. Treatment for DVT usually begins with heparin (or LMWH) therapy.
Standard heparin is given intravenously (injection into a vein) while LMWH
enoxapirin is given by subcutaneous injection under the skin.
• Heparin (or LMWH) therapy is usually followed by 3 to 6 months of warfarin,
which is taken orally.
• Factor Xa inhibitors used in the treatment of DVT include the following:
Fondaparinux, Rivaroxaban
• Direct-thrombin inhibitors (DTIs) include recombinant hirudin, argatroban, and
bivalirudin.
• Thrombolytics (streptokinase). In some cases, your doctor may recommend
using thrombolytics. These clot-dissolving medications are injected via a
catheter directly into the blood clot and are used only when there is an
extremely high risk for pulmonary embolism.
Surgery
• Thrombus removal with catheter-directed thrombolysis
• Mechanical thrombectomy
• Angioplasty
• Stenting of venous obstructions

56. Clinical characteristics of injuries of the arteries.

In arterial external bleeding blood of bright red ciliur effuses by pulsative spurt.
"hard" signs of arterial bleeding
• Bruit or thrill:
• Active or pulsatile hemorrhage
• Pulsatile or expanding hematoma
• Signs of limb ischemia and elevated compartment pressure including the 5
"P's:" Pallor, paresthesias, pulse deficit, paralysis, and pain on passive
extension of the compartment." Pain on passive extension is the earliest and
most sensitive physical finding.
• Diminished or absent pulses: This is not a sensitive prognostic finding, as up to
25% of patients with major vascular injuries requiring repair have normal
pulses distal to the injury.
The following "soft" signs are much less useful in predicting or excluding major
vascular injuries that require intervention.
• Hypotension or shock
• Neurologic deficit due to primary nerve injury occurs immediately after injury.
In contrast, ischemic neuropathy is delayed in onset, developing within
minutes to hours after injury.
• Stable, nonpulsatile or small hematoma
• Proximity of the wound to major vascular structures

57. Clinical characteristics of injuries of the veins

• Low pressure dark blood external bleeding
• Non expanding hematoma
• Shock is rare unless accompanied with arterial injury

58. The signs of internal and external bleeding

General symptoms are the same for all types of bleeding, including inner
bleeding in various cavities. They are observed in heavy loss of blood and consist
of appearance of acute anemia (paleness, dizziness, syncope, trembling small
pulse, progressing decrease of blood pressure).
The local symptoms are various.
At bleedings in empty space of a gastrointestinal tract the blood in a stomach changes
the color. In ample quantity of its accumulation a vomiting, like “ground coffee”
(hematemesis), is originated. Further or at a bleeding from underlaying departments
of a gastrointestinal tract it is observed weak tarry stool in large quantity(melena).
This is example of explicit bleeding.
Occult bleeding – this is hemorrhage without any clinical symptoms. For example,
there is bleeding from ulcer of stomach or duodenum. This type of heamorrhage
doesn’t have clinical symptoms. Such bleeding is possible to reveal only by
laboratory method. This is research of occult blood in feces. Continued long time
concealed hemorrhages which are not revealed, may result in development of an
anemia.
Some kinds of internal bleeding have specific name:
• Haemobilia – haemorrhage from diliary ducts;
• Haematuria - haemorrhage from kidneys and urinary system;
• Haemoperitoneum - haemorrhage in abdominal cavity;
 • Haemothorax - haemorrhage in pleural cavity;
• Haemopericardium - haemorrhage in pericardial cavity;
• Haemartrosis – haemorrhage in joint cavity;
• Metrorrhagia – uterine bleeding;
• Proctorrhagia – rectal bleeding;
• Hemorrhagic insult – cerebral hemorrhage.
External bleeding can be seen

59. Methods of temporary hemostasis

Mannual Pressure of wound or main artery to area. See points of pressure below

o An applying a arresting bleeding tourniquet;

o Digital compression of artery;
o The maximal flexion or a raised position of an extremity;
o A pressure bandage;
o A tamponade of a wound;
o Applying clamp on bleeding vessel;
o A temporarily shunting.

60. Clinical characteristic of the hemorrhagic shock

According V.I.Struchkov and E.W.Lutzevich there four levels of blood loss.
• I level – easy degree – blood loss is even to 10 – 12% of blood circulating
volume (500 – 700 ml). Haemorrhage is causing little changes to
hemodynamic. The general condition of patient is satisfactory. Pulse is slightly
quickened, arterial pressure is normal (standart). Blood hemoglobin is rised
 above 100 g/l (10 g %). During capillaroscopy: background is rosy, 3 – 4
capillary loops with quick gomogenous bloodstream are determined.
• II level – middle degree - blood loss is even to 15 – 20 % of blood circulating
volume (1000 – 1400 ml). Apparent bleeding is distinguished. The general
condition is medium-scale difficalty. Limpness, dizziness, hyperhidrosis,
syncope are observed. Coverlet is pale. Respiration is accelerated. Reflexes are
decrease. Single vomitting or melena may be observed. Pulse become
noticeably more rapid (90 – 100 per min.). Arterial pressure is decreased to 90
mm Hg. Leucocytosis, deviation of the differential count to the left are
determined. Hematocrit is 0,38 – 0,32, hemoglobin is 80 – 100 g/l (8 – 10 g
%). Quantity of urination is decreased.
• III level – heavy degree – blood loss is 20 – 30 % of blood circulating volume
(1500 – 2000 ml). The general condition of patient is bad (grave condition).
Paleness of skin, cold sweat is observed. Rapid vomiting and melena are
determined. The bleeding is accompanied by syncope. Visible mucous
membranes are colourless. The patient yawns, feels thirst. Pulse is rapid and
thready. Arterial pressure is decreased to 60 mm Hg. Hematocrit is 0,30 – 0,32,
hemoglobin is 50 – 80 g/l (5 – 8 g %). Oliguria is observed.
• IV level – massive blood loss – loss of blood is more then 30 % of blood
circulating volume (more than 2000 ml). Plentiful bleeding with prolonged loss
of consciousness may be observed. The general condition of patient is very
grave, preagony. Pulse and arterial pressure are not fixed. Hematocrit is 0,23
and lower, hemoglobin is 50 g/l and lower. Anuria is observed.

61. Treatment of the hemorrhagic shock. Indications for

hemotransfusion
All measures in the treatment of hemorrhagic shock should be directed to stop the
bleeding.
• Local hemostatics (hydrogen peroxide, aminocapronic acid, tranexamic acid,
aprotinin, desmopressin, fibrinogen, vitamin K)
• Surgical
After the bleeding stops, or simultaneously with it (during surgery) spend infusion-
transfusion therapy. Infusion engaged in 2-3 veins. Originally spend puncture of
peripheral veins, and perform catheterization main veins (subclavian, jugular or great
saphenous vein of the lower extremities, etc.). Massive infusion therapy performed
under the control of central venous pressure (CVP). All solutions should be warm.
• 1st degree: Start restoration of blood volume: Rapid infusion of crystalloid 1-2
liter and modified gelatin to 1-1.5 liters . Max infusion of 2l. Shock 1-2
degrees - speed 100-200 ml / min.
• 2nd degree: Start restoration of blood volume: Rapid infusion of crystalloid 2
liter and modified gelatin to 2-2.5 liters . Fresh frozen plasma 250ml, red cell
mass 250ml. Max fluids 3litres
• 3rd degree: Start restoration of blood volume: Rapid infusion of crystalloid 2
liter and modified gelatin to 2-2.5 liters . infuse fresh frozen plasma 750ml, and
red cell mass 750ml. Max infusion of 4l. Shock 3-4 degrees - speed 200-300
ml / min.
 • 4th degree: blood transfusion
Indication for blood transfusion
• symptomatic anemia (causing shortness of breath, dizziness, congestive heart
failure, and decreased exercise tolerance),
• acute sickle cell crisis,
• acute blood loss of more than 30 percent of blood volume
• Patients of hereditary disorders like Haemophilia and Thalassaemia.
• Severe burn victims.
• Major surgery

62. Surgical tactics in injuries of the arteries and veins

• Ligating a vessel in a wound;
• Ligating a vessel at a distance;
• Under-running a bleeding vessel;
• Vasoversion, a crush of a vessel;
• Tamponade of a wound (cavity), a pressure bandage (serves as a temporary
method, but sometimes - as a final method to control bleeding);
• Embolization of vessel;
• Special methods (splenectomy at a parenchymatous bleeding from a lien, a
resection of a stomach at a bleeding from a ulcer or a tumor, a lobectomy at a
pulmonary bleeding, Blaekmor’ probe, etc.);
• A vascular seam, reconstruction of vessels.

63. Etiology and pathogenesis of varicosity.

The varicose veins is the disease which is characterized by nonreversible progressing
changes in superficial, perforating and deep veins, and clinically manifests by the
dilation of superficial veins of the inferior extremities. Varicose veins are veins that
have become enlarged and twisted

64. Clinical characteristics of varicosity.

Complaints
• The compensated varicosity usually does not manifest. Some patients after
physical exertion feel a heavy, dull sensation in legs. At inspection of such
patients in a standing position it is possible to note a little bit expressed
varicose veins of tributaries of great and small saphenous veins. At functional
examination the valves are not affected.
• In the stage of subcompensation the patients complain usually of a heavy
sensation and fatigability of legs, their swelling or edema, burning pain in the
region of varicosity and night cramps of tibial muscles. During examination of
the patient in standing position it is possible to note a considerable varicosity
of superficial veins of the inferior extremities. The skin of lower legs more
often is not changed. The functional examination of the valves reveals valvular
incompetence of superficial or perforating veins.
• In the stage of decompensation the chief complaints of a constant gravity in
legs, pain, prompt fatigue, edema and cramps of tibial muscles. This is
associated with pigmentation, induration and trophic ulcer with localization in
 the lower third of leg. A large protruding veins are common for these patients.
At functional examination it is possible to determine valvular incompetence of
superficial, perforating and deep veins.

65. Classification of varicosity.

I) According to etiological factors:
• Primary (essential) and secondary varicosity;
2) According to anatomy:
• Varicosity of a great saphenous vein;
• Varicosity of a small saphenous vein;
• Varicosity of superficial veins;
3) According to the form of varicosity:
• Cylindrical form;
• Diffuse, tortuous form;
• Mixed form;
4) According to stages of the development of disease:
• Compensated;
• Subcompensated;
• Decompensated;
5) According to state of the valves of veins:
• Without valvular incompetence;
• With valvular incompetence;
6) According to manifestation of incompetence of a venous stasis
• I, ІІ, III degree.

66. Diagnostic of varicosity.

Tests for definition of valvular incompetence of superficial veins
• Troyanov-Trendelenburg's test. The patient lies supine with the elevated
extremity, and superficial veins is emptied. A rubber tourniquet is applied
around the upper third of thigh. The patient stands up. If in a vertical position
(with a tourniquet and after its releasing) the veins are slowly filled from below
upward, the test is considered as negative. At prompt filling of veins mainly
from above downward the test is positive.
• Hackenbruch's test. In upward position, the great saphenous vein is
compressed with fingers and the patient is asked to cough. In incompetence of
venous valves, particularly ostial, it is possible to feel a retrograde wave of a
blood, which is transmitted by vessel below the finger.
Tests for evaluation of a valvular incompetence of perforating veins
• Pratt's test. After the veins have been emptied the patient lie supine and
elevating the lower limb vertically the elastic bandage is applied from toes to
groin. The superficial veins are compressed with a rubber tourniquet in the
upper third of thigh. The patient stands up. The imposed bandage is released
gradually from above downward, and simultaneously another elastic bandage
is applied from inguinal region downward thus between them there is a space
5-6 cm. In place of incompetent valves of perforating vein is a protruding of
superficial veins.
 • Sheinis' test. Around the leg, after the emptying of superficial veins by
elevating the extremity, three tourniquets are applied: around the thigh just
below oval fossa, above the knee and around upper leg. The patient is
recommended to stand up. The veins are gradually filled up by a blood. If the
vein in any region is promptly dilated, in this place it is necessary to consider
the incompetence of valves of perforating veins.
• Talman's test is the modification of previous. For performance of this test a
rubber tourniquet of 2-3 m in length is used. It is imposed on the leg of patient
after emptying of superficial veins. Further the patient is asked to stand and the
tourniquet is released. Observing for the filling of veins inform about the
incompetence of valves of perforating veins, as at Sheinis' test.
Tests for estimation of deep veins patency
• Mayo-Pratt's test. In a laying position of the patient around the upper third of
thigh of the elevated extremity a tourniquet is applied and superficial veins are
compressed. Then the extremity is imposed by elastic bandage from toes to the
groin. The patient is asked to stand up. If after that he feels the pain in leg,
sense of compressing and fullness, it is possible to think, that deep veins are
obstructed.
• Delbet-Perthes' test (march test). At the patient, that stands, for the stopping
of blood flow in superficial veins above the knee joint a rubber tourniquet is
applied. After that, he is recommended to walk during 3-5 min. If the
superficial veins after are constricted, it reveals satisfactory patency of deep
veins.
Plan of investigation
• Coagulogram
• Functional tests for definition of the state of a valvular system of Superficial,
deep and perforating veins. See above tests
• Sonography
• Dopplerography
• Phlebography

67. Treatment of varicosity.

Self-care — such as exercising, losing weight, not wearing tight clothes, elevating
your legs, and avoiding long periods of standing or sitting — can ease pain and
prevent varicose veins from getting worse.
Compression stockings Wearing compression stockings all day is often the first
approach to try before moving on to other treatments. They steadily squeeze your
legs, helping veins and leg muscles move blood more efficiently.
Additional treatments for more-severe varicose veins
• Sclerotherapy. In this procedure, your doctor injects small- and medium-sized
varicose veins with a solution that scars and closes those veins. In a few weeks,
treated varicose veins should fade.
• Foam sclerotherapy of large veins. Injection of a large vein with a foam
solution is also a possible treatment to close a vein and seal it. This is a newer
technique.
 • Laser surgeries. Doctors are using new technology in laser treatments to close
off smaller varicose veins and spider veins. Laser surgery works by sending
strong bursts of light onto the vein, which makes the vein slowly fade and
disappear. No incisions or needles are used.
• Catheter-assisted procedures using radiofrequency or laser energy. In one of
these treatments, your doctor inserts a thin tube (catheter) into an enlarged vein
and heats the tip of the catheter using either radiofrequency or laser energy. As
the catheter is pulled out, the heat destroys the vein by causing it to collapse
and seal shut. This procedure is the preferred treatment for larger varicose
veins.
• High ligation and vein stripping. This procedure involves tying off a vein
before it joins a deep vein and removing the vein through small incisions. This
is an outpatient procedure for most people. Removing the vein won't adversely
affect circulation in leg because veins deeper in the leg take care of the larger
volumes of blood.
• Ambulatory phlebectomy: removes smaller varicose veins through a series of
tiny skin punctures. Only the parts of your leg that are being pricked are
numbed in this outpatient procedure. Scarring is generally minimal.
• Endoscopic vein surgery. You might need this operation only in an advanced
case involving leg ulcers if other techniques fail. Your surgeon uses a thin
video camera inserted in your leg to visualize and close varicose veins and then
removes the veins through small incisions. This procedure is performed on an
outpatient basis.
Surgery names
• Troyanov-Trendelenburg's operation. A great saphenous vein just at
saphenofemoral juncture is ligated and cut.
• Babcock's operation. A great saphenous vein is removed by means of a vein
stripper which inserted in its distal end.
• Cocket's operation. A suprafascial ligating and cutting of perforating veins.
• Linton's operation – a subfascial ligating and cutting of perforating veins.

68. Classification of pulmonary embolism.

According to risk
• High risk: associated with shock and or hypotension
• Intermediate risk: patients appear hemodynamically stable but have evidence
of right ventricular dysfunction and or myocardial injury
• Low risk: normal hemodynamics, normal RV size and function
According to classes:
• Massive pulmonary embolism: Large emboli compromise sufficient
pulmonary circulation to produce circulatory collapse and shock.The patient
has hypotension; appears weak, pale, sweaty, and oliguric; and develops
impaired mentation.
• Acute pulmonary infarction: These patients present with acute onset of
pleuritic chest pain, breathlessness, and hemoptysis. Although the chest pain
may be clinically indistinguishable from ischemic myocardial pain, normal
electrocardiogram findings and no response to nitroglycerin rules it out.
 • Acute embolism without infarction: Patients have nonspecific symptoms of
unexplained dyspnea and/or substernal discomfort.
• Multiple pulmonary emboli: The first subset has repeated documented
episodes of pulmonary emboli over years, eventually presenting with signs and
symptoms of pulmonary hypertension and cor pulmonale. The second subset
has no previously documented pulmonary emboli but has widespread
obstruction of the pulmonary circulation with clot. They present with gradually
progressive dyspnea, intermittent exertional chest pain, and, eventually,
features of pulmonary hypertension and cor pulmonale.

69. Clinical manifestations of pulmonary embolism.

• Massive pulmonary embolism: Large emboli compromise sufficient
pulmonary circulation to produce circulatory collapse and shock.The patient
has hypotension; appears weak, pale, sweaty, and oliguric; and develops
impaired mentation.
• Acute pulmonary infarction: These patients present with acute onset of
pleuritic chest pain, breathlessness, and hemoptysis. Although the chest pain
may be clinically indistinguishable from ischemic myocardial pain, normal
electrocardiogram findings and no response to nitroglycerin rules it out.
• Acute embolism without infarction: Patients have nonspecific symptoms of
unexplained dyspnea and/or substernal discomfort.
• Multiple pulmonary emboli: The first subset has repeated documented
episodes of pulmonary emboli over years, eventually presenting with signs and
symptoms of pulmonary hypertension and cor pulmonale. The second subset
has no previously documented pulmonary emboli but has widespread
obstruction of the pulmonary circulation with clot. They present with gradually
progressive dyspnea, intermittent exertional chest pain, and, eventually,
features of pulmonary hypertension and cor pulmonale.

70. Diagnostic of pulmonary embolism

• Dyspnea, pleuritic or atypical chest pain and syncope
• Pleuritic chest pain and hemoptysis
• Palpitations, cough, anxiety, light headedness
• Elevated d-dimer, elevated cardiac troponins, brain natriuretic peptide
• ECG: sinus tachycardia, right axis deviation, ST-T abnormalities, incomplete
or complete right bundle branch clock
• Chest radiograph: loss of lung volume with elevation of ipsilateral
hemidiaphragm, enlarged cardiac shadow, pulmonary infiltrated, increased
radiolucency of affected lungs
• Pulmonary angiography is the gold standard for diagnosis: direct evidence of
embolism or amputation of pulmonary arterial branch
• Echo: right heart dilation, RV hypokinesis, tricuspid regurgitatiom
• CT: partially or complete occluded artery
Wells score is used as clinical prediction of pulmonary embolism
 Clinical Characteristic Score

Previous pulmonary embolism or deep vein thrombosis + 1.5

Heart rate >100 beats per minute + 1.5

Recent surgery or immobilization (within the last 30 d) + 1.5

Clinical signs of deep vein thrombosis +3

Alternative diagnosis less likely than pulmonary embolism +3

Hemoptysis +1

Cancer (treated within the last 6 mo) +1

Clinical Probability of Pulmonary Embolism Score

Low 0-1

Intermediate 2-6

High ≥6

71. Treatment of pulmonary embolism

accepted indications for thrombolytic therapy include hemodynamic instability or
right ventricular dysfunction demonstrated on echocardiography.
• Hemodynamic and respiratory support
Anticoagulation
• Unfractioned heparin bolus 80u/kg
• Low molecular weight heparin: fondaparinux 5mg/kg once/day, enoxaparin
1,5mg/kg/day, dalteparin 200u/kg once/day
• Warfarin
• New oral anticoagulants: Dabigatran 150mg bid, rivaroxaban 15mg tid,
apixaban 10mg bid
Thrombolytic therapy (first line in patients with cardiogenic shock and or persistent
hypotension):
• streptokinase 250000IU loading dose over 30minutes, urokinase 175U/kg once
daily, alteplase 100mg
• Heparin should not be infused concurrently with streptokinase or urokinase but
it can be infused during alteplase
Surgery: pulmonary embolectomy, percutaneous catheter embolectomy or
fragmentation, venous filters.

72. Indications and methods of surgical treatment of pulmonary

embolism.
• cases whose hemodynamics are extremely unstable and who do not respond to
medication,
• cases with angiogram or CT scan findings of obstructions over a wide area of
the pulmonary arteries,
• cases showing rapid progression of heart failure or respiratory failure,
• cases in which thrombolytic therapy is contraindicated, and
• cases with thrombi suspended from the right atrium to the right ventricle.
Surgery: pulmonary embolectomy, percutaneous catheter embolectomy or
fragmentation, venous filters.

73. Prophylaxis of pulmonary embolism

Preventing idiopathic outpatient pulmonary embolism is difficult, if not impossible.
That said, the majority of pulmonary embolisms occur in hospitalized patients. The
incidence in these cases can be reduced through appropriate prophylaxis, achieved
mechanically or via the administration of heparin, LMWH (enoxaparin, dalteparin,
ardeparin), or warfarin.

Classification of post-thrombotic syndrome

Post-thrombotic syndrome (PTS), also called postphlebitic syndrome and venous
stress disorder is a medical condition that may occur as a long-term complication of
deep vein thrombosis
Classification
According to the form of disease:
• Sclerotic;
• Varicose;
• Edematous;
• Ulcerative.
According to localization of the lesion:
• Inferior vena cava;
• Iliac vein;
• Femoral vein;
• Popliteal vein;
• Tibial veins.
According to spreading of the lesion:
• Isolated;
• Combined;
• Wide-spread.
According to the character of the lesion:
• Occlusion;
• Partial recanalization;
• Complete recanalization.
According to the degree of a venous insufficiency:
• Compensation;
• Subcompensation;
• Decompensation.

Etiology and pathogenesis of post-thrombotic syndrome

• The cause of a postflebitic syndrome is the acute thrombosis of major veins of
the system of inferior vena cava.
• At once after formation of a thrombus under the influence of the factors of a
blood coagulating system there comes its retraction.
• Simultaneously under the influence of fibrinolysis a spontaneous lysis occurs.
• Depending on activity of these systems there could be such further course of
the disease: in one cases a complete recanalization of the thrombus take place;
and in others – complete obliteration or partial patency of the vessel could be
restored.
• Nevertheless, despite the character, in this or that degree it always leads to
incompetence of a valvular system of affected veins.
• It also causes a venous hypertension more distal to pathological process.

Clinical manifestation of post-thrombotic syndrome

• The postflebitic syndrome clinically manifests by a dull ache in the affected
extremity, expressed edema and secondary varicosity.
• In the course of the disease with the change of stages a lot of new signs may
occur, such as induration of tissues, hyperpigmentation of the skin, cyanotic
stasis dermatitis. Recurrent trophic ulcers they are formed most frequently in
the lower third of the leg, on its interior surface. The general state of the patient
usually remains satisfactory.
• It also causes the edemas on legs, which are mostly expressed after prolonged
standing of the patient or during the latter part of the day.
• Some manifestations of postflebitic syndrome caused by venous insufficiency
(arching pain, heaviness in legs) after recumbence or elevation of legs may
considerably decrease or disappear.
Postflebitic syndrome is characterized by a stage course of the disease.
• I stage manifests by edema of legs without the phenomena of skin
hyperpigmentation and induration of a subcutaneous fat. In these patients it is
possible to note a cyanosis of the skin. After recumbence or night rest the
edema completely disappears.
• II stage of the disease is characterized by the edema, which decreases after 24
hours staying in bed. It might be connected with initial disturbances of a lymph
flow. Further there may be a slight hyperpigmentation of the skin and
indurative changes of a subcutaneous fat.
• III stage is accompanied by decompensation of a lymph outflow from the
extremity and transformation of a venous edema in lymphovenous. It results in
the development of a testaceous fibrosis, which extends around inferior
 Indications and contraindications for surgical treatment of post-
thrombotic syndrome
• I stage varicose form: bypass grafting
• The II stage of the development of postflebitic disease usually requires the
removing of dilated veins, and ligating of perforating veins. plastic and
reconstructive operations
• In III stage of the disease the surgical treatment is indicated even more often,
o The Palma’s operation is performed in segmental lesion of iliofemoral
segment of the venous system. The bypass, from a great saphenous vein
of a healthy extremity is formed, which connects the distal end of the
occluded segment.
o In restricted occlusion of the iliofemoral segment the anastomosis of the
popliteal vein with a great saphenous vein of the thigh is formed.
o The operations, which improve the blood flow in deep veins include a
thrombintimectomy, bougienage of the occluded part of the vein,
plastics of a deep fascia of the leg (Ascor operation).
o Operations, which reduce hydrostatic pressure in different levels of a
venous system of inferior extremity:
• resection of popliteal vein;
• resection of femoral vein;
• resection of posterior tibial vein;
o Operations, which prevent the pathologic reflux of a blood in varicose
superficial veins: removing, electrocoagulation and sclerotherapy of
varicose veins and the ligating of perforating veins by Kocket-Linton
method.

Clinic tumour of anterior mediastinum

ANTERIOR MEDIASTINAL TUMORS
• Thyroid mass
• Teratoma and associated germinal cell tumors
• Thymic tumor
• Tissue tumor - bronchogenic cyst: enteric cyst, fibroma, hemangioma, lipoma
or lipomatosis, lymphadenopathy or lymphoma, lymphangioma, neurogenic,
pericardial lesion
• T cell lymphoma: Hodgkin, non hodgkin
• Parathyroid tumor
Signs
• On early stages of the development the tumours are almost asymptomatic, and
40 % of mediastinal neoplasms are revealed at preventive chest X-ray
examination. The patients most often complain of chest pain. The intensity of
pain depends on degree of tumour compression or growth into nervous
structures. In malignant growth the pain has more intensive character, than in
benign. Frequently the pain precedes by feeling of heaviness, discomfort and
foreign body in chest. Sometimes observed dyspnea caused by compression
of airways, and major vessels both of anterior, and posterior mediastinum.
 • Owing to compression of the lumen of superior vena cava the syndrome of
superior vena cava develops, which manifest by cyanosis of face, neck and
upper half of chest, distend cervical veins, edema and dyspnea. Resulting
from the rise of blood pressure and disrupture of venous walls, the nasal,
esophageal and pulmonary bleedings develop. As the characteristic features
considered headache, loss of consciousness and hallucinations. In
overwhelming cases superior vena cava syndrome results from malignant
tumours of lungs and mediastinum. Only in 5-7 % of patients they are benign.
• Hodgkins lymphomas may have concomitant cervical or supraclavicular nodes
as well as fever, night sweats and weight loss ('B' symptoms) in one-third of
patients

Clinic of tumour of posterior mediastinum

1. Neurogenic tumors are the most common cause of a posterior mediastinal mass
and constitute 75% of neoplasms in the posterior mediastinum.
2. Mesenchymal tumors
3. Other posterior mediastinal masses
a. Lymphomas
b. Goiter
Signs
• cough
• shortness of breath
• chest pain
• fever/chills
• night sweats
• coughing up blood
• unexplained weight loss
• swollen lymph nodes
• respiratory blockage
• hoarseness
 PEDIATRIC SURGERY
74. Relevant anatomy of the appendix and abdominal cavity in children.
The appendix is a wormlike extension of the cecum, and its average length is 8-10 cm
(ranging from 2-20 cm). This organ appears during the fifth month of gestation,
Layers of appendix
• 1-mucosal layer (lymphoid follicles are scattered in its mucosa. Its number
increases when individuals are aged 8-20 years
• 2a - inner muscular layer (circular )
• 2b - outer muscular layer (longitudinal, derives from the taenia coli)
• 3 – serosa
• 4 – mesoappendix
Location of appendix in abdominal cavity
• Typical position: McBurney point (two thirds of the way between the
umbilicus and the anterior superior iliac spine)
• Inconstancy of position:
o Retrocecal – 74 %
o Pelvic – 21 %
o Subcaecal – 1 – 5 %;
o Postileal – 5%;
o Preileal – 1%;
o Paracecal – 2%;
o In left iliac fossa or in the hypochondrium – very occasionally

75. The classic clinical manifestation of the acute appendicitis.

• Gradual onset of generalized, periumbilical pain
• After few hours Gradual location of pain to right lower quadrant
• Anterior abdominal tenderness
• Peritoneal signs, guarding, rebound tenderness
• Gradual worsening of pain
• Fever
• Leucocytosis
Signs
• cough sign (sharp pain in the right lower quadrant after a voluntary cough, ie,
Dunphy sign)
• rebound tenderness related to peritoneal irritation elicited by deep palpation
with quick release (Blumberg sign)
• pain in the right lower quadrant in response to left-sided palpation (Rovsing
sign

76. Features of clinical presentations of acute appendicitis in

newborn and toddlers.
Clinical signs
• In neonates, the clinical features of appendicitis are nonspecific and include
irritability or lethargy, abdominal distention, vomiting, a palpable abdominal
mass and cellulitis or hyperemia of the abdominal wall.
 • In infants and children up to two years of age, symptoms include vomiting,
pain, diarrhea and fever. Diagnosis is more difficult in this age group because
the symptoms are nonspecific.
• In children two to five years of age, symptoms include vomiting, abdominal
pain, fever and anorexia. Tenderness of the right lower quadrant is more
common in this age group than it is in younger children, who usually have
diffuse tenderness.
Physical exam
• A child with acute appendicitis walks slowly, often humped forward protecting
the right side. The facial expression reflects discomfort and apprechension.
• The right hip frequently is held in slight flexion. Fever, tachycardia, and signs
of dehydration usually are minimal in the first 12 to 24 hours but quickly
increase in the later stages.

77. Lab studies and imaging studies in children with acute appendicitis.
Lab St1udies. Laboratory findings may increase the suspicion for appendicitis but are
not diagnostic.
• The White blood cell (WBC) count is elevated in approximately 70-90% of
patients with acute appendicitis but also is elevated in many other abdominal
conditions. If the WBC count exceeds 15,000 cells/mm3, the patient is more
likely to have a perforation. However, one study found no difference in the
WBC count between children with simple appendicitis and those with a
perforated appendicitis.
• Urinalysis is useful for detecting urinary tract disease, such as infection or
renal stones. Irritation of the bladder or ureter by an inflamed appendix may
result in a few WBCs in the urine, but the presence of over 20 WBCs suggests
a urinary tract infection
• Electrolytes and renal function tests are more helpful in the management than
in the diagnosis of appendicitis. Indications for assessing electrolytes include a
significant history of vomiting or clinical suspicion of dehydration.
Additional studies:
• Liver function tests, serum amylase, and serum lipase may be helpful when the
etiology of the abdominal pain is unclear.
• Urinary levels of human chorionic gonadotropin-beta subunit (hCG-beta) are
useful in sexually active adolescent females to exclude ectopic pregnancy.
• Computed tomography (CT).
• Ultrasonography: An outer diameter of greater than 6 mm, noncompressibility,
lack of peristalsis, or presence of a periappendiceal fluid collection
characterizes an inflamed appendix.
• Abdominal radiography.
• Barium enema.
• Diagnostic laparoscopy may be useful in selected cases (eg, infants, elderly
patients, female patients) to confirm the diagnosis. If findings are positive,
such procedures should be followed by definitive surgical treatment at the time
of laparoscopy.
 78. Differential diagnosis of acute appendicitis and gastroenteritis.
Gastroenteritis - usually causes pain, diarrhoea and vomiting. The pain does not
usually shift from centrally to the right lower part of the abdomen.

79. Differential diagnosis of acute appendicitis and infection diseases.

Urinary tract infection - there is often pain on passing water (urination) and the
doctor can test the urine to look for signs of infection to exclude this. Increased
leukocyte in urine

80. Meckel's diverticulitis: causes, clinical presentation, diagnostic

procedures, treatment.
Meckel diverticulum (also referred to as Meckel's diverticulum) is the most common
congenital abnormality of the small intestine; it is caused by an incomplete
obliteration of the vitelline duct (ie, omphalomesenteric duct).
Clinical presentation
• Most patients live their entire lives without any symptoms. Meckel
diverticulum is most frequently diagnosed as an incidental finding when a
barium study or laparotomy is performed for other abdominal conditions
• When patients develop symptoms, presence of complications is almost always
indicated. Development of complications is usually rare but can occur in up to
4% of patients. Complications of Meckel diverticulum included bowel
obstruction (35%), hemorrhage (32%), diverticulitis (22%), umbilical fistula
(10%), and other umbilical lesions (1%).
• In children, bleeding is the most common presenting sign. Painless
hematochezia (rectal bleeding).
• Abdominal pain may be reported when the presentation is related to an
obstruction or inflammation.
• Like other diverticula in the body, Meckel diverticulum can become inflamed.
Diverticulitis is usually seen in older patients but has been seen in children:
includes abdominal pain in the periumbilical area that radiates to the right
lower quadrant. Abdominal pain is present more in the periumbilical region
than the pain of appendicitis.
Diagnosis: CBC, abdominal Tc-99m pertechnetate scintigraphy, barium enema,
ultrasound
Treatment
• Nasogastric decompression
• Gastric lavage
• excision of the diverticulum along with the adjacent ileal segment

81. Complications of appendicitis. Clinical presentations of the

appendicular abscess.
Complications of appendicitis:
• Perforation
• Periappendicular abscess
• Peritonitis
• Wound infection
 • Intraabdominal abscesses
• Small bowel obstruction
Appendicular abscess is defined as a collection of pus resulting from necrosis of the
tissue superimposed with infection in an inflamed appendix. It is unusual and rare
entity; appendicular abscess is a life-threatening complication of acute appendicitis
(preoperatively) or appendectomy (postoperatively).
• Symptoms of appendicular abscess are mostly atypical compared to
appendicitis and include include high grade fever, constant pain in the right
iliac fossa, prolonged diarrhea associated with nausea and vomiting and
increased micturition The patient may appear toxic with diffuse abdominal
pain and high grade fever and tachycardia. Even minimal pressure on the
abdomen can elicit a marked response from the patient due to pain and
tenesmus.
• leukocytosis, anemia, abnormal platelet counts, and abnormal liver function
frequently are present in patients with appendicular abscess
• Ultrasound: Findings include fluid collection (hypoechoic) in the appendicular
region which may be well circumscribed with dilated appendicular wall.

82. Treatment of acute appendicitis.

• Antibiotics: Cefotetan and cefoxitin seem to be the best choices of antibiotics
• Surgical: open or laparoscopic appendectomy

83. Preoperative management in children with acute appendicitis.

Preparation of patients undergoing appendectomy is similar for both open and
laparoscopic procedures.
• Because they may mask the underlying disease, do not administer analgesics
and antipyretics to patients with suspected appendicitis who have not been
evaluated by the surgeon.
• Perform complete routine laboratory and radiologic studies before intervention.
• Venous access must be obtained in all patients diagnosed with appendicitis.
Venous access allows administration of isotonic fluids and broad-spectrum
intravenous antibiotics prior to the operation.
• Patients presenting with perforated appendicitis may be volume depleted and
require aggressive fluid resuscitation. The combination of cefotaxim,
clindamycin, and amycacin is administered to treat infection from aerobic and
anaerobic organisms. Alternative regimens include ampicillin and sulbactam,
cefoxitin, cefotetan, piperacillin and tazobactam, ticarcillin and clavulanate,
and imipenem and cilastatin.
• Prior to the start of the surgical procedure, the anesthesiologist performs
endotracheal intubation to administer volatile anesthetics and to assist
respiration.
• The abdomen is washed, antiseptically prepared, and then draped.

84. Advantages and disadvantages of laparoscopic appendectomy.

Laparoscopy has some advantages, including decreased postoperative pain, better
aesthetic result, a shorter time to return to usual activities, and lower incidence of
wound infections or dehiscence. This procedure is cost effective but may require
more operative time compared with open appendectomy.

85. Postoperative complications after appendectomy (open and

laparoscopic).
• After an appendectomy there is a 10% risk of infection in the wound, which
can usually be treated by the GP prescribing antibiotics. Occasionally it will
require a small operation in hospital.
• A small number of patients can get an abscess in the abdomen, especially if the
appendix had perforated. These cause diarrhoea and make the patient unwell
often a few days after the operation. It may be necessary to have another
operation but they can usually be treated with a drain placed into the abdomen
using a scanner to guide the placement and the prescription of antibiotics.
• Fifteen to 20% of appendectomies are performed in cases for which test results
are later determined to be falsely positive, as appendicitis is difficult to
diagnose in infants and toddlers

86. Postoperative management after appendectomy.

• Length of stay. Hospital stay averages two to three days after the operation if
the appendix was not perforated and there were no complications. A longer
stay of five to seven days is required for treatment of a perforated appendix.
Bowel function normally returns after two to four days, but intravenous
antibiotics are required for at least four to five days and sometimes longer,
depending upon the child's fever and white blood cell count.
• Diet. If the appendix did not rupture and a nasogastric tube is not needed, clear
liquids by mouth are usually started the first day after the operation. The diet is
then advanced to normal if the child tolerates the clear liquids (no vomiting or
nausea). Children with perforation of the appendix are started on clear liquids
once the child has passed gas or stool from the rectum. Again, as long as the
child is tolerating the clear liquids, diet is advanced.
• Activity. After appendectomy, children may usually return to school within a
week of discharge from the hospital, although they may find that they tire
quickly. Vigorous activities and contact sports should be limited for at least
three weeks. When the appendectomy is done using a laparoscope, children
may resume their usual physical activities as soon as they feel ready- there are
no activity constraints

87. Classification of peritonitis.

Classification. Depending on the underlying pathology, the resultant peritonitis may
be infectious or sterile (ie, chemical or mechanical).
❖ Peritoneal infections are classified as primary (ie, spontaneous), secondary (ie,
related to a pathologic process in a visceral organ), or tertiary.
❖ According to character of exudate: serous, fibrinous, fibrinopurulent,
purulent, hemorrhagic, peritonitis sicca.
❖ According to extension of inflammatory process: local, diffuse and
generalized
 ❖ According to clinical course: acute and chronic

88. Causes of peritonitis in newborn.

The majority of cases of bacterial peritonitis are due to intestinal perforations,
ruptured omphaloceles, or ischemic intestinal necrosis. Seventy-three babies had
peritonitis secondary to intestinal perforation. Although the majority of neonatal
perforations are subsequent to intestinal obstruction, many instances of unexplained
perforation, possibly secondary to defects in the intestinal musculature or visceral
ischemia, were found. The less common chemical peritonitis is due to prenatal
intestinal perforation with extrusion of sterile meconium into the peritoneal cavity.
• Spontaneous peritonitis is caused by an infection in the blood that occurs when
irritant fluid accumulates in the space between the layers of the peritoneum.
This is most commonly one of the complications of cirrhosis. However, it is
also sometimes related to peptic ulcer disease, appendicitis or diverticulitis.
• Secondary peritonitis is a chronic or acute inflammation caused by bacteria
entering the peritoneum following perforation of the gastrointestinal tract (for
example, ruptured appendix). The irritant can be gastric juice, small bowel
contents or faeces from the colon.
• Tertiary peritonitis is persistent or recurrent infection after adequate initial
therapy. The intra-abdominal infection may be localized or generalized, with or
without abscess formation.

89. Etiology and patophysiology of necrotizing enterocolitis in

newborn.
Necrosis of the bowel wall may complicate bowel ischaemia after asphyxia, infection
or shock in newborn infants.
Ukrainian classification
Stage Clinical signs X-ray
І - Incidence Bad thermoregulation, poor sucking, loss of bowel wall
appetite, vomiting; Local signs: meteorism, thickening and
defecation up to 10 per day with large bubbles of air in
amount of mucus. bowel
ІІ - height General status is hard, often apneas, Enlargement
bradicardia, hypotonia, lethargy; blood in bubbles of air in
stools; Local signs: vomiting is often, edema bowel, levels of
of the anterior abdominal wall, sex organs. the fluid, bubbles
Abdomen is enlarged, lustering, peristalsis is of air in bowel
depressed or absent wall
ІІІ - The same + increasing of the brease and Fluid
progressive cardiac defficiency, hypothermia, jaundice, sequestration in
DIC-syndrome; peritonitis, bowel inpassage, the abdominal
ascites cavity, bowel wall
necrosis
ІV - Perforation, peritonitis, anuria, DIC-syndrom, The same +
complication septic shock. pneumoperitoneu
 s m
Bells classification

90. Main principles of necrotizing enterocolitis treatment.

TREATMENT:
• stop the feeding
• parenteral antibiotics: ampicillin, gentamicin, and clindamycin or
metronidazole)
• nasogastric decompression
• parenteral nutrition
• fluid replacement
• insure adequate oxygen delivery
• cardiovascular support ( dopamine or dobutamine)
Treatment according to stages
• Bell stages IA and IB: The patient is kept on an NPO diet with antibiotics for 3
days. IV fluids are provided, including total parenteral nutrition (TPN).
• Bell stages IIA and IIB: Treatment includes support for respiratory and
cardiovascular failure, including fluid resuscitation, NPO, and antibiotics for
14 days. Surgical consultation should be considered. After stabilization, TPN
should be provided during the period that the infant is NPO.
• Bell stage IIIA: Treatment involves NPO for 14 days, fluid resuscitation,
inotropic support, and ventilator support. Surgical consultation should be
obtained. TPN should be provided during the period of NPO.
 • Bell stage IIIB: Surgical intervention: to remove only the dead or perforated
segment and to leave as much as possible. Even if some of the intestine that’s
left is inflamed or infected, it might heal.

91. Complications of necrotizing enterocolitis

Complications may include:
❖ Peritonitis
❖ Sepsis
❖ Intestinal perforation
❖ Intestinal stricture
❖ Liver problems from prolonged inability to tolerate enteral feeds and need for
parenteral (IV) nutrition
❖ Short bowel syndrome if a large amount of intestine is lost

92. Causes of primary (idiopathic) and secondary (with pathologic

lead point) intussusception
Intussusception is a process in which a segment of intestine invaginates into the
adjoining intestinal lumen, causing a bowel obstruction.
Intussusception is most commonly idiopathic and no anatomic lead point can be
identified. Several viral gastrointestinal pathogens (rotavirus, reovirus, echovirus)
may cause hypertrophy of the Peyer’s patches of the terminal ileum which may
potentiate bowel intussusception.
Processes that result in a mechanical lead point
• Meckel diverticulum
• Intestinal polyp (eg, Peutz-Jeghers syndrome, familial polyposis coli, juvenile
polyposis)
• Intestinal lymphosarcoma
• Blunt abdominal trauma with intestinal or mesenteric hematomas
• Hemangioma
• Foreign body
• Henoch-Schönlein purpura (small bowel hematomas cause small bowel
intussusception)

93. Clinical presentation of intussusception

the classic triad of vomiting, abdominal pain, and passage of blood per rectum
(bloody mucus stools like red current jelly) occurs in only one third of patients.
• The patient is usually an infant presenting with vomiting, abdominal pain,
passage of blood and mucus, lethargy, and a palpable abdominal mass. These
symptoms often are preceded by an upper respiratory infection.
These patients are more likely to have a surgical lead point causing recurrent attacks
of intussusception with spontaneous reduction. Symptoms include the following:
• Pain is colicky, severe, and intermittent. The parents or caregivers describe the
child as drawing the legs up to the abdomen and kicking the legs in the air.
• Initially, vomiting is nonbilious and reflexive, but when the intestinal
obstruction occurs, vomiting becomes bilious. Any child with bilious vomiting
 is assumed to have a condition that must be treated surgically until proven
otherwise.
• Parents also report the passage of stools that look like currant jelly. This is a
mixture of mucus, sloughed mucosa, and shed blood.
• Lethargy is a relatively common presenting symptom with intussusception.
Lethargy can be the sole presenting symptom, which makes the diagnosis
challenging.
• Diarrhea also can be an early sign of intussusception.
Physical: The infant can be pale, diaphoretic, and hypotensive if shock has occurred.
The hallmark physical findings in intussusception are a right hypochondrium
sausage-shaped mass and emptiness in the right lower quadrant (Dance sign). This is
hard to detect and is palpated best when the infant is quiet between spasms of colic.
Abdominal distention frequently is found if obstruction is complete.

94. Complication of intussusception

• Intestinal hemorrhage
• Necrosis and bowel perforation
• Shock and sepsis

95. Imaging studies in patients with suspected intussusception

• Plain abdominal x-ray :On abdominal radiographs, the classical description of
an intussusception is a mass lesion seen indenting the colon with or without
signs of bowel obstruction. There is a paucity of right-sided colonic gas.
Intussusceptions may present anywhere along the colon and even present in the
rectum. The typical location is from the hepatic flexure to mid descending
colon. A normal abdominal radiograph does not exclude intussusception.
• Ultrasonography. Characteristic findings include a target sign visible on
transverse section and a pseudo kidney sign viewed on longitudinal section.
• Colour Doppler has been used to assess bowel viability and as a prognostic
sign that reduction will be successful, no colour signal of the intussusception
being regarded as having a poor prognosis.
• Computed tomography (CT) scan also has been proposed to be useful making
the diagnosis of intussusception; however, CT findings are unreliable, and use
of CT carries the risks associated with intravenous contrast administration,
radiation exposure, and sedation.
• Diagnostic and therapeutic enema

96. Nonoperative management of intussusceptions: indications

• All intussuceptions are first treated with non operative measures by barium
reduction
• The presence of peritonitis and any evidence of perforation revealed on plain
radiographs are the only 2 absolute contraindications to an attempt at
nonoperative reduction with a therapeutic enema.

97. Methods of nonoperative management of intussusception

 • Once the diagnosis of intussusception is entertained, surgical personnel should
be notified and an intravenous (IV) line for fluids and antibiotics. Nasogastric
tube should be placed.
• Therapeutic enemas can be hydrostatic, with either barium or water-soluble
contrast, or pneumatic, with air insufflation.
• Insert ungreased Foley catheter in rectum, distend ballon and pull down against
levator. Strap in place
• When performing a therapeutic enema, the recommended pressure of air
insufflation should not exceed 120 cm of water. When using barium or water-
soluble contrast, the column of contrast should not exceed 100 cm above the
level of the buttocks. An attempt is not considered successful until the reducing
agent, whether air, barium, or water-soluble contrast, is observed refluxing
back into the terminal ileum. Otherwise, the intussusception can remain at the
ileocecal region and can resume its progression.
Summary
• 1. Perform nasogastric suction: administer 4 fluids or blood and antibiotics
• 2. Insert ungreased Foley catheter in rectum, distend ballon and pull down
against levator. Strap in place
• 3. Wrap legs
• 4. Let barium run from height of 30 cm in above table
• 5. X-ray intermittently
• 6. Stop if barium column is stationary and its unchanging for 10 min
• 7. Reduction

98. Contraindications to nonoperative management of

intussusception
• The presence of peritonitis and any evidence of perforation revealed on plain
radiographs are the only 2 absolute contraindications to an attempt at
nonoperative reduction with a therapeutic enema.

99. Surgical treatment of intussusception

The intussusception is milked back by progressive compression of the bowel
In severe cases:
• Intestinal resection
• Placement of ileotransversal anastomosis
• Ileostoma and caecostoma placement

100. Recurrent intussusception: causes, treatment

Most of the recurrent intussusceptions present within 6 months of initial episode and
have been observed with almost all the treatment modalities. These are frequently
reported after non-operative reduction (hydrostatic/pneumatic), whereas their
incidence is negligible after operative management.
Occurs when there is presence of pathological lead points as q19
Treatment
 • Non operative: Repeat hydrostatic or pneumatic enema for reduction for 3
consecutive recurrence
• If not effective, surgical reduction is needed for any further intersucception

101. Causes and clinical presentations of paralytic ileus

Ileus is a condition in which there is neurogenic failure or loss of peristalsis in the
intestine in the absence of any mechanical obstruction. It is commonly seen in
hospitalized patients as a result of:
• intra-abdominal processes such as recent gastrointestinal or abdominal surgery
or peritoneal irritation (peritonitis, pancreatitis, ruptured viscus, hemorrhage);
• severe medical illness such as pneumonia, respiratoryfailure requiring
intubation, sepsis or severe infections, uremia, diabetic ketoacidosis, and
electrolyte abnormalities (hypokalemia, hypercalcemia, hypomagnesemia,
hypophosphatemia); and
• medications that affect intestinal motility (opioids, anticholinergics,
phenothiazines).
• Following surgery, small intestinal motility usually normalizes first (often
within hours), followed by the stomach (24-48 hours), and the colon (48-72
hours).
Clinical presentation
• Constant gnawing pain
• repeated vomiting
• symmetric abdominal distention
• reduced or absence of peristalsis
• increasing meteriorism
• constipation
• heavy intoxication

102. Treatment of paralytic ileus

• Para-nephral and pre-sacral novocaine nerve blocks
• Gastric lavage and intestinal intubation
• Stimulation of intestinal peristalsis: motilinum, metoclopramide
• IV fluids and electrolytes,
• a minimal amount of sedatives,
• adequate serum K level (> 4 mEq/L [> 4 mmol/L])
• Sometimes colonic ileus can be relieved by colonoscopic decompression;
rarely cecostomy is required. Ileus persisting > 1 wk probably has a
mechanical obstructive cause, and laparotomy should be considered.

103. Clinical and x-ray symptoms of small bowel obstruction

• Multiple air-fluid levels
• Stacked
• Centrally located loops of intestine
• Dilated small bowel greater than 3 cms visible with valvulae conniventes.
• String of pearl sign caused by slow resorption of intraluminal air leaving small
air bubbles trapped between valvulae conniventes
 • Absence or paucity of colon gas: Collapsed colon

104. Clinical and x-ray symptoms of large bowel obstruction

• Obstructed colon usually appears as a peripherally located distended bowel
with haustral markings.
• No air distal to site of obstruction.
• Sometimes the mass may be seen.

105. Preoperative management of children with mechanical bowel

obstruction
Conservative treatment is the appropriate first step for patients with no or minimal
abdominal tenderness, no fever, no leukocytosis, and a cecal diameter less than 12
cm. The underlying illness is treated appropriately.
A nasogastric tube and a rectal tube should be placed. Patients should be ambulated
or periodically rolled from side to side and to the knee-chest position in an effort to
promote expulsion of colonic gas.
All drugs that reduce intestinal motility, such as opioids, anticholinergics, and
calcium channel blockers, are discontinued if possible.
Enemas maybe administered judiciously if large amounts of stool are evident on
radiography. Oral laxatives are not helpful and may cause perforation, pain, or
electrolyte abnormalities.

106. Complications of postoperative bowel obstruction

• perforation or ischemia is increased with cecal diameter > 12 cm and when
distention has been present for more than 6 days
• Sepsis
• Intra-abdominal abscess
• Wound dehiscence
• Aspiration
• Short-bowel syndrome (as a result of multiple surgeries)
• Death (secondary to delayed treatment)

107. Surgical treatment of postoperative bowel obstruction

• Indications for operation include obstipation for 24 hours, continued abdominal
pain with fever and tachycardia, decreased blood pressure, increasing
abdominal tenderness, and leukocytosis despite adequate resuscitation and
medical treatment.
• The abdomen is opened through a previous incision, if present, and midline, if
not. The cecum is identified and the collapsed ileum is followed proximally
until dilated bowel and the point of obstruction is identified.
• The offending adhesive bands are disrupted and the abdomen is closed.
Laparoscopic lysis of adhesions is another option and may allow a shorter
postoperative recovery and hospital stay.
• Postoperatively, nasogastric decompression and intravenous fluids are
continued until return of bowel function and the volume of gastric aspirate
decreases.
 108. Clinical manifestation of upper and low gastrointestinal
bleeding
Probability of
Probability of
Clinical Indicator Lower GI
Upper GI Source
Source

Hematemesis: bright red blood

vomiting in esophagitits. Coffee Almost certain Rare
ground in peptic ulcer

Melena: mostly associated with

Probable Possible
duodenal ulcer

Hematochezia: Maroon stools, from

the right side of the colon.
Possible Probable
Bright red blood per rectum from
the left side of the colon

Blood-streaked stool Rare Almost certain

Occult blood in stool Possible Possible

109. Causes of bleeding in children with intussusception

The intestinal mucosa is extremely sensitive to ischemia because it is farthest away
from the arterial supply. Ischemic mucosa sloughs off, leading to the heme-positive
stools and subsequently to the classic "currant jelly stool" (a mixture of sloughed
mucosa, blood, and mucus).

110. Causes of bleeding in children with Mekkel’s diverticulum.

Clinical symptoms, diagnostic procedures, treatment
Meckel diverticulum occurs on the antimesenteric border of the ileum, usually
60 cm proximal to the ileocecal valve. On average, the diverticulum is 2.99 cm long
and 1.92 cm wide. Meckel diverticulum is a true diverticulum because it contains all
layers of the intestinal wall.
The heterotopic mucosa is likely to be gastric in origin in 80% of cases of
Meckel diverticulum. This is important because peptic ulceration of this or adjacent
mucosa can lead to pain, bleeding, and/or perforation.
See Q7 for clinical, diagnosis and treatment

111. Causes of bleeding in children with solitary polyps and

polyposis
Isolated Juvenile polyps
• These are the most common polypoid lesion of infancy and childhood. The
peak age of incidence is between the ages of 3 and 10 years.
• As with most polyps, crampy abdominal pain and bleeding with bowel
movements are the presenting symptoms.
• Juvenile polyps are hamartomatous excrescencies of the intestinal mucosa.
They appear to lengthen from traction caused by peristalsis and the flow of
intestinal contents.
• There is no malignant potential, and juvenile polyps naturally auto-amputate if
given enough time.
• Seventy-five percent of juvenile polyps occur in the rectum and sigmoid colon,
but juvenile polyps may occur in the right colon as well.
Juvenile polyposis
• is an autosomal dominant disorder which causes polyps predominantly in the
large and small bowel.
• The lesions resemble adenomatous polyps individually but are actually
mucous-retention polyps.
• These polyps can occur anywhere along the gastrointestinal tract.
• It is considered a premalignant condition and 6% of these children will
eventually develop malignancy.
Familial adenomatous polyposis
• Is characterized by hundreds of adenomatous polyps in the rectum and colon
causing diarrhea and bleeding.
• It also shares an autosomal dominant pattern of inheritance.
• Malignant degeneration in one or more polyp is virtually certain before the age
of twenty years.
• the presence of at least one hundred individual polyps is required to make this
diagnosis

112. Causes and clinical manifestation of gastrointestinal polyposis

• Peutz-Jeghers Syndrome: This well-known syndrome causes polyps
predominantly in the small bowel. Its hallmark distinguishing feature is the
pigmented lesions observed on the buccal mucosa and lips of these patients.
Malignant degeneration can occur, and lifelong surveillance is necessary.
• Hemangiomatous polyps cause profuse bleeding and occur predominantly in
the distal small bowel. Profuse bleeding may require excision if it occurs
repeatedly. They tend to regress with time as do most hemangiomas after the
age of two years.
• Small bowel lymphoma is usually a non-Hodgkin’s B cell lymphoma. The two
most common gastrointestinal sites of non-Hodgkin’s lymphoma are the distal
small bowel and the stomach. Proximal gastric lesions may be visualized and
biopsied endoscopically although the lesion originates in the submucosa. In the
small bowel, CT scanning can usually image the lesion if it has attained
sufficient size to cause symptoms. Lymphoma of the bowel is rare in infancy,
but the incidence increases with advancing age peaking in adolescence.
Bleeding is the main symptom from gastric lesions. Small bowel lymphomas
 cause crampy abdominal pain, and may result in intussusception. Some may
erode and perforate into the free abdominal cavity presenting as
gastrointestinal perforation.

113. Classification of portal hypertension. Main causes of portal

hypertension in childhood

114. Clinical presentations of extrahepatic portal hypertension

• The most important are esophageal varices, striking dilation and prominence of
the collateral vessels on the anterior abdominal wall with centrifugal radiation
outward from the umbilicus, a pattern known as caput medusae.
• The latter results in large dilated, inferior rectal veins, often mistaken as gross
hemorrhoids. Rarely, collaterals can develop in atypical sites (eg, duodenum,
colon, or vagina).
Determining the presence of the complications of portal hypertension involves the
Following:
• Hematemesis or melena (gastroesophageal variceal bleeding or bleeding from
portal gastropathy),
• Mental status changes such as lethargy, increased irritability, and altered sleep
patterns (presence of portosystemic encephalopathy),
• Increasing abdominal girth (ascites formation),
• Abdominal pain and fever (spontaneous bacterial peritonitis [SBP], which also
presents without symptoms),
• Hematochezia (bleeding from portal colopathy)

115. Relevant anatomy of portal system. Tributary of portal vena.

Portortosystemic anastomosis: between v. cava surerior and
v.portae; between v. cava inferior and v.portae
 • The portal vein drains blood from the small and large intestines, stomach,
spleen, pancreas, and gallbladder.
• The superior mesenteric vein and the splenic vein unite behind the neck of the
pancreas to form the portal vein.
• The portal trunk divides into 2 lobar veins. The right branch drains the cystic
vein, and the left branch receives the umbilical and paraumbilical veins that
enlarge to form umbilical varices in portal hypertension.
• The left gastric vein (formerly, gastric coronary vein), which runs along the
lesser curvature of the stomach, receives distal esophageal veins, which also
enlarge in portal hypertension.

116. Diagnostic procedures in children with suspected portal

hypertension
Laboratory testing
• Complete blood count
• Liver disease–associated blood tests (eg, aspartate aminotransferase [AST],
alanine aminotransferase [ALT], bilirubin, alkaline phosphatase [ALP])
• Type and cross-match
• Coagulation studies (prothrombin time [PT], partial thromboplastin time
[PTT], international normalized ratio [INR]): Prolonged INR is suggestive of
impaired hepatic synthetic function
• Albumin: hypoalbuminemia is common. (impaired hepatic synthetic function)
• Blood urea nitrogen, creatinine, and electrolytes
• Arterial blood gas (ABG) and pH measurements
• Hepatic and viral hepatitis serologies, particularly hepatitis B and C serologies
Other laboratory tests may include the following:
• Antinuclear antibody, antimitochondrial antibody, antismooth muscle antibody
• Iron indices
• Alpha1-antitrypsin deficiency
• Ceruloplasmin, 24-hour urinary copper: Consider this test only in individuals
aged 3-40 years who have unexplained hepatic, neurologic, or psychiatric
disease
Imaging studies
• Duplex Doppler ultrasonography of the liver and upper abdomen
• Computed tomography (CT) scanning and/or magnetic resonance imaging
(MRI): Can be used when ultrasonographic findings are inconclusive
• Bleeding scan or angiography: Used when bleeding is obscure and the source
is unclear
Procedures
• Liver biopsy and histologic examination
• Hemodynamic measurement of the hepatic venous pressure gradient (HVPG):
A criterion standard for assessment of portal hypertension
• Upper GI endoscopy (or, esophagogastroduodenoscopy [EGD]): A criterion
standard for assessment of varices

117. Emergent treatment of acute variceal bleeding

• Airway, breathing, and circulation evaluation
• Nasogastric tube placement with hemodynamically significant upper GI
bleeding
• Nothing by mouth; establish 2 large-bore venous accesses
• Volume resuscitation, with or without blood product transfusion
• Portal pressure reduction (ie, anti-secretory agent infusion)
• Patient transfer to tertiary center with liver transplant service for uncontrolled
bleeding from portal hypertension
• Control and prevention of bleeding from esophageal varices
• Prevention of complications (eg, prophylactic antibiotics, combination
endoscopic/pharmacologic therapy)
• Administration of vasoconstrictors (eg, octreotide [agent of choice in acute
variceal bleeding], vasopressin)
• Endoscopic therapy (variceal ligation [EVL] [preferred], injection
sclerotherapy)
• Balloon-tube tamponade
• Percutaneous transhepatic embolization (PTE)
• Endoscopic administration of cyanoacrylate monomer
• Transjugular intrahepatic portosystemic shunt (TIPS)

118. Endoscopic treatment and prophylaxis of acute variceal

bleeding
• Endoscopic therapy (variceal ligation [EVL] [preferred], injection
sclerotherapy)
• Balloon-tube tamponade
• Endoscopic administration of cyanoacrylate monomer as hemostatic

119. Type of operation in children with portal hypertension. What

type of vascular shunts are you know?
• A transjugular intrahepatic portosystemic shunt (TIPS) is a viable option and is
less invasive for patients whose bleeding is not controlled.
• Portosystemic shunts:
o Total portal systemic shunts include any shunt larger than 10 mm in
diameter between the portal vein (or one of its main tributaries) and the
inferior vena cava (IVC) (or one of its tributaries).
o Partial portal systemic shunts reduce the size of the anastomosis of a
side-to-side shunt to 8 mm in diameter.
o Selective shunts provide selective decompression of gastroesophageal
varices to control bleeding while at the same time maintaining portal
hypertension to maintain portal flow to the liver. One example is the
distal splenorenal shunt, which is the most commonly used
decompressive operation for refractory variceal bleeding
• Devascularization procedures: eg, splenectomy, gastroesophageal
devascularization, and esophageal transection
• Orthotopic liver transplantation (OLT) - Treatment of choice in patients with
advanced liver disease
 120. Clinical signs, diagnostic evaluations and treatment of the
gastroesophageal reflux disease
Clinical features:
• heartburn, regurgitation, and dysphagia, belching air or food, hiccups,
hypersalivation, odynophagia
• In addition to these typical symptoms, abnormal reflux can cause atypical
(extraesophageal) symptoms, such as coughing, chest pain, and wheezing.
Diagnosis
• pH-metry shows decreased pH. Normal esophageal pH - 5,5-7,0.
• Internally esophageal manometry: motor function of LES decrease,
disorders of motility, achalasia
• Chromoscopy: intestine metaplasia
• Endoscopy: are reflux esophagitis: hyperemia and friability of mucose
(catarrhal oesophagitis), erosion (erosive reflux esophagitis varying degrees of
severity) and ulcerative reflux esophagitis.
o Gr.A – 1/> mucosal breaks<5mm
o Gr.B – 1/> mucosal breaks>5mm
o Gr.C – mucosal breaks>2 mucosal folds, <75% of esophageal
circumference
o Gr.D – mucosal breaks >2 mucosal folds, >75% of esophageal
circumference
Treatment
Diet
• exclusion of overeating. Weight loss
• avoidance horizontal body position for 3-4 hours after a meal; refusal of food
overnight.
• Stop smoking and drinking
• sleep with head elevated at least 15cm
• limit foods that reducing lower esophageal sphincter tone (coffee, strong tea,
chocolate, mint, milk, fatty meats, spices);
Proton pump inhibitors
• Omeprazole - 20 mg 2 / d
• Lansoprazole - 30 mg 2 / d
• Pantoprazole (Kontrolok) - 40 mg 1-2 / d
• Rabeprazole (Pariet) - 20 mg 1-2 / d
• Esomeprazole (Neksium) - 20 mg 1-2 / d
Prokinetics(to reinforce tone and reduce lower esophageal sphincter)
• Selective(domidon, motilium)
• Nonselective (metoclopramide
Antacids(to neutralize the hydrochloric acid and pepsin)
• almagel
• fosfalyugel
• Maalox
 121. Causes of anal fissure in children. Clinical presentation
An anal fissure is a tear in the mucosa and die anoderm lining the anal canal.
These lesions are common in infancy and are the most common cause of bright red
blood per rectum in that age group.
Etiology: Anal fissures occur in the setting of constipation and passage of large, hard
stools that cause a mechanical rear of the anal mucosa. Diarrhea can cause a chemical
irritation from stool alkalinity. Pain associated with anal fissures may potentiate
constipation and seems to be related to hyper tonicity of the anal sphincters.
Clinical Presentation
• Anal fissures in children most commonly occur during infancy. The usual
presenting symptom in that age group is bright red blood per rectum.
• Crying with bowel movements and hard stool streaked with bright-red blood
are the common findings observed by the parents.
• Gently spreading the anus (also having the older child bear down), exposes the
dentate line and the longitudinal tear comes into view.
• Fissures are most commonly located in the posterior midline and distal to the
dentate line. Fissures are sometime multiple and may occur anteriorly.
Fissures located laterally suggest Crohn's disease or immunodeficiency states.
Chronic anal fissures in older children may indicate inflammatory bowel
disease.
• An unhealed fissure may become infected and evolve into a chronic ulcer. If
this occurs a sentinel skin tag forms distal to the fissure, and the anal papilla
may hypertrophy.

122. Treatment of acute anal fissure in children

• Acute fissures respond to gentle anal dilation, stool softeners, laxatives, and
Sitz baths.
• If fissures are secondary to underlying conditions, treatment is directed to these
conditions as well.
• Fissures associated with inflammatory bowel disease may be treated with
metronidazole.
• Topical anesthetic ointments alter each bowel movement reduce sphincter
spasm and pain.
• A hypertonic anal sphincter may be treated with botulinum toxin and topical
nitroglycerine or a lateral subcutaneous internal sphincterotomy.

123. Etiology, clinical signs, diagnosis and treatment of acute

lymphadenitis in children
Lymphadenitis is the inflammation of a lymph node. Lymphadenitis is often a
complication of a bacterial infection (Streptococcal and staphylococcal bacteria are
the most common causes of lymphadenitis) of a wound, although it can also be
caused by viruses or other disease agents. Lymphadenitis may be either generalized,
involving a number of lymph nodes (infectious mononucleosis); or limited to a few
nodes in the area of a localized infection
The diagnosis of lymphadenitis is usually based on a combination of the patient's
history, the external symptoms, and laboratory cultures.
The doctor will press (palpate) the affected lymph nodes to see if they are sore or
tender. Swollen nodes without soreness are often caused by cat-scratch disease.
Lymphadenitis is marked by swollen lymph nodes that are painful, in most cases,
when the doctor touches them. If the lymphadenitis is related to an infected wound,
the skin over the nodes may be red and warm to the touch. Enlarged lymph nodes
can be asymptomatic, or they can cause local pain and tenderness. Overlying skin
may be unaffected or erythematous.
• Cervical lymphadenitis can lead to neck stiffness and torticollis.
• Preauricular adenopathy is associated with several forms of conjunctivitis,
including unilocular granulomatous conjunctivitis (catscratch disease,
chlamydial conjunctivitis, listeriosis, tularemia, or tuberculosis), pharyngeal
conjunctival fever (adenovirus type 3 infection) and keratoconjunctivitis
(adenovirus type 8 infection).
• Retropharyngeal node inflammation can cause dysphagia or dyspnea.
• Mediastinal lymphadenitis may cause cough, dyspnea, stridor, dysphagia,
pleural effusion, or venous congestion.
• Intra-abdominal (mesenteric and retroperitoneal) adenopathy can manifest as
abdominal pain.
• Iliac lymph node involvement may cause abdominal pain and limping.
Treatment
In patients with lymphadenitis, treatment depends on the causative agent and may
include expectant management, antimicrobial therapy (ampicillin and gentamycin or
cefotaxim, or chemotherapy and radiation (for malignancy).

124. Causes, clinical signs, diagnosis and treatment of mycobacterial

lymphadenitis
Causes and signs
• Subacute or chronic cervical lymphadenitis is usually caused by
nontuberculous mycobacterium (NTM - Mycobacterium avium-intracellulare
and Mycobacterium scrofulaceum most commonly). Most NTM infections
occur in immunocompetent children younger than 5 years of age.
• Mycobacterium tuberculous (TB) should also be considered in a patient with a
persistent unilateral lymphadenitis that fails to respond to appropriate
antimicrobial therapy or historically has risk factors for TB exposure or clinical
symptoms compatible with TB. Infection of the cervical nodes is usually
caused by extension from the paratracheal nodes to the tonsillar and
submandibular nodes. It also can occur by direct spread from the apical pleura
to the supraclavicular nodes.
Diagnosis: Mantoux testing with human purified protein derivative and an avium-
intracellular antigen may be more useful.
Treatment: Antituberculous drugs are ineffective. The organism was usually highly
resistant. Total excision is the treatment of choice
 125. Pathogenesis, clinical signs and treatment of perianal or
perirectal abscesses in children
Infants are commonly affected with infections and abscesses in the perianal area.
Infected diaper rash is the most common cause of superficial abscesses.
Staphylococcal or gram negative enteric organisms are the most common organisms
involved. Deeper abscesses of the anal canal or perirectal tissues arise from crypt
infections. These infections are usually caused by enteric and anaerobic organisms.
Clinical Presentation
• perianal mass and sitting intolerance. tender, erythematous mass lateral to the
anus. fever and malaise
Treatment
• Superficial perianal abscesses can be treated with Sitz baths. Typically
antibiotics are not required.
• If the area becomes fluctuant, incision and drainage may be offered. Deeper
infections require immediate drainage under general anesthesia along with
intravenous antibiotics.

126. Mastitis of the newborn: causes, clinical signs, diagnosis and

treatment
Neonatal mastitis typically occurs in full-term infants who are younger than two
months. It is usually unilateral and local in nature. Usually caused by staphylococcus
Clinical manifestation:
• general symptoms: restlessness, appetite and sleep disturbances
• local symptoms: tenderness, swelling, unilateral enlarged breast bud,
hyperemia, local rise in temperature, fluctuation, purulent nipple discharge
with “witch’s milk”, enlarged and tender axillary nodes
Treatment:
• conservative treatment: antibiotics(clindamycin and vancomycin for mrsa,
oxacillin 100-200mg/kg/day in 4 doses, acetaminophen 10-15mg/kg every 4-
6hours not to exceed 5doses i.e. 50-75mg/kg/day), antiseptic compresses,
ointment dressings, physiotherapy)
• Surgical: incision and drainage.

127. Omphalitis: causes, clinical signs, diagnosis and treatment.

Omphalitis as a complication of the umbilical fistulas
Omphalitis is a polymicrobial infection typically caused by a mixture of aerobic and
anaerobic organisms. Associated risk factors include the following:
• Low birthweight (<2500 g)
• Prior umbilical catheterization
• Septic delivery (as suggested by premature rupture of membranes, nonsterile
delivery, or maternal infection)
• Prolonged rupture of membranes
• Omphalitis occasionally manifests from an underlying immunologic disorder.
Serous omphalitis: serous discharge from the umbilical stump, prolonged
epithelization; symptoms from organs and systems, intoxication are absent.
Purulent omphalitis Local disease: Physical signs vary with the extent of disease.
Signs of localized infection include the following:
• Purulent or malodorous discharge from the umbilical stump
• Periumbilical erythema
• Edema
• Tenderness
Extensive local disease: The following signs indicate more extensive local disease,
such as fasciitis or myonecrosis. These signs also may suggest infection by both
aerobic and anaerobic organisms and include the following:
• Periumbilical ecchymoses
• Crepitus
• Bullae
• Progression of cellulitis despite antimicrobial therapy
Lab Studies:
• Obtain specimens from umbilical infection routinely, and submit specimens for
Gram stain and culture for aerobic and anaerobic organisms.
• Obtain a blood culture for aerobic and anaerobic organisms.
• Obtain a complete blood count with manual differential. Neutrophilia or
neutropenia may be present in acute infection. Thrombocytopenia may be
present.
Treatment of omphalitis (periumbilical edema, erythema, and tenderness) in the
newborn includes antimicrobial therapy and supportive care.
• Parenteral nutrition
• Give topical and systemic antibiotics
• Vancomycin and aminoglycoside (gentamycin). Metronidazole or clindamycin.
• Administration of platelets, fresh frozen plasma, or cryoprecipitate for DIC and
clinical bleeding is suggested.
• Oxygen, vasoactive drugs for hypotension,
• Management of necrotizing fasciitis and myonecrosis involves early and
complete surgical debridement of the affected tissue and muscle.

128. Hematogenes osteomyelitis in children: pathogenesis and

clinical manifestations
Pathogenetic stages
• Bone marrow phlegmon
• Periosteal abscess
• Soft tissue phlegmone
• Dermal fistula
Clinical manifestations.
• Acute hematogenous osteomyelitis is often preceded by the signs and
symptoms of bacteremia: fever, inflammation, malaise, cephalgia, myalgia,
anorexia. This phase of the illness may last for several days.
• The second phase of the disease is the clinical onset of involvement of bone.
This gives rise to: restricted motion, pseudoparalysis, soft tissue around the
inflamed bone which is, hyperemic, warm, edematous, tender, bone tenderness
.
 129. Hematogenes osteomyelitis in children: diagnostic procedures
and treatment
The WBC count may be elevated, but it frequently is normal. A leftward shift is
common with increased polymorphonuclear leukocyte counts. The C-reactive protein
level usually is elevated and nonspecific; it may be more useful than the erythrocyte
sedimentation rate.
Diagnosis of osteomyelitis needs at least 2 out of these 4 criteria
• Pus on aspiration
• Positive bacterial culture from bone or blood
• Presence of classic signs and symptoms of acute osteomyelitis
• Radiographic changes typical of osteomyelitis
Treatment
• Antibiotic: Nafcillin, clindamycin, vancomycin, cefotaxime, ciprofloxacin
• Drainage: If there is an open wound or abscess, it may be drained through a
procedure called needle aspiration. In this procedure, a needle is inserted into
the infected area and the fluid is withdrawn. Deep aspirations or biopsy is
much preferred in contrast to often-unreliable surface swabs.
• Splinting or cast immobilization: This may be necessary to immobilize the
affected bone and nearby joints in order to avoid further trauma and to help the
area heal adequately and as quickly as possible. Splinting and cast
immobilization are frequently done in children. However, eventually early
motion of joints after initial control is important to prevent stiffness and
atrophy.

130. Clinical peculiarities of the hematogenes osteomyelitis in

newborn
Neonatal osteomyelitis arises as a consequence of hematogenous spread of
microorganisms, which is the most common route of infection. In preterm infants,
neonatal osteomyelitis frequently results from directly inoculated bacteria (secondary
to heel or venipuncture, umbilical catheterization, infected cephalhematoma, etc.).
Newborns (younger than 4 mo): S aureus, Enterobacter species, and group A and B
Streptococcus species
Diagnostic criteria
• Infants can appear well except for failure to move an extremity or pain on
movement. Redness or swelling indicates that infection has spread into the
subperiosteal space. Rupture of a focus of osteomyelitis into a joint space can
result in septic arthritis. This is often observed in neonates.
• Laboratory studies: Blood cultures are positive only in 50% of pediatric
patients. Therefore, cultures of bone aspirate are useful in obtaining the
organism and planning for long-term therapy. In addition, C-reactive protein or
erythrocyte sedimentation rate are generally elevated in acute disease.
• Plain radiography can show soft tissue swelling and destroyed fascial planes
within days after onset of infection,
 • Computed tomography, magnetic resonance imaging, ultrasound, radiography
and bone scintigraphy scanning have been reported to be useful in detecting
osteomyelitis
• Magnetic resonance imaging (MRI) has high specificity (94%) and sensitivity
(97%) for the diagnosis of acute osteomyelitis, showing changes as early as
day 3 to 5 after the onset of infection.

131. Treatment of the osteomyelitis in newborn

Treatment
• Starting a semisynthetic penicillin, such as oxacillin (150 mg/kg/d),
empirically is a good choice for most cases of community-acquired
osteomyelitis. In patients with allergy to penicillin, a first-generation
cephalosporin and lyncomycin (40 mg/kg/d) are both excellent alternatives.
Cefuroxime (150 mg/kg/d), cefotaxime, vancomycin.
• Surgical Care: Surgery is usually indicated to drain purulent material from
the subperiosteal space or if infected foreign material is present.

132. Complications of the acute hematogenes osteomyelitis. Main

principles of complications’ prevention
Complications:
• Bone abscess
• Bacteremia
• Fracture
• Overlying soft-tissue cellulitis
• Draining soft-tissue sinus tracts
Complication can be prevented by adequate treatment, antibiotics for 2-3 weeks.

133. Clinical manifestation and diagnosis of the Tbc (mycobacterial)

osteitis
Osteomyelitis caused by nontuberculous mycobacteria (NTM) can have severe
consequences and a poor prognosis. Physicians therefore need to be alert to this
condition, especially in immunocompromised patients
• Osteomyelitis secondary to BCG vaccination is rare and usually involves
epiphysis of long tubular bones.
• BCG osteomyelitis and cold abscess, should be kept in mind when assessing a
child presenting chronic symptoms like pain, limping or local swelling of
extremities.
• Image guided tissue biopsy and PCR studies confirm diagnosis.
• Early use of a surgical curettage and debridement along with chemotherapy
soon afterwards, enabled these children to enjoy a satisfactory clinical
outcome.

134. Differential diagnosis of the acute hematogenes osteomyelitis

and BCG-osteitis
 135. Classification of sepsis (the Society of Critical Care Medicine,
1992)
• heart rate > 90 beats/minute
• temperature > 38°C or < 36°C
• respiration > 20/min or PaCO2 < 32mm Hg
• leukocyte count > 12,000/mm3, < 4,000/mm3 or > 10% immature (band) cells
According to SIRS, there were different levels of sepsis: sepsis, severe sepsis, and
septic shock. The definition of SIRS is shown below:
• SIRS is the presence of two or more of the following: abnormal body
temperature, heart rate, respiratory rate, or blood gas, and white blood cell
count.
• Sepsis is defined as SIRS in response to an infectious process.
• Severe sepsis is defined as sepsis with sepsis-induced organ dysfunction or
tissue hypoperfusion (manifesting as hypotension, elevated lactate, or
decreased urine output).
• Septic shock is severe sepsis plus persistently low blood pressure, despite the
administration of intravenous fluids.

136. SIRS-criteria’s in childhood

137. Definition of septic shock, severe sepsis and multiple organ

dysfunction
Severe sepsis is defined as sepsis with sepsis-induced organ dysfunction or tissue
hypoperfusion (manifesting as hypotension, elevated lactate, or decreased urine
output).
Septic shock is severe sepsis plus persistently low blood pressure, despite the
administration of intravenous fluids.
Multiple Organ dysfunction: More specific definitions of end-organ dysfunction exist
for SIRS in pediatrics.
 • Cardiovascular dysfunction (after fluid resuscitation with at least 40 ml/kg of
crystalloid)
• hypotension with blood pressure < 5th percentile for age or systolic
blood pressure < 2 standard deviations below normal for age, or
• vasopressor requirement, or
• two of the following criteria:
• unexplained metabolic acidosis with base deficit > 5 mEq/l
• lactic acidosis: serum lactate 2 times the upper limit of normal
• oliguria (urine output < 0.5 ml/kg/h)
• prolonged capillary refill > 5 seconds
• core to peripheral temperature difference > 3 °C
• Respiratory dysfunction (in the absence of cyanotic heart disease or known
chronic lung disease)
• the ratio of the arterial partial-pressure of oxygen to the fraction of
oxygen in the gases inspired (PaO2/FiO2) < 300 (the definition of acute
lung injury), or
• arterial partial-pressure of carbon dioxide (PaCO2) > 65 torr (20 mmHg)
over baseline PaCO2 (evidence of hypercapnic respiratory failure), or
• supplemental oxygen requirement of greater than FiO 2 0.5 to maintain
oxygen saturation ≥ 92%
• Neurologic dysfunction
• Glasgow Coma Score (GCS) ≤ 11, or
• altered mental status with drop in GCS of 3 or more points in a person
with developmental delay/intellectual disability
• Hematologic dysfunction
3
• platelet count < 80,000/mm or 50% drop from maximum in chronically
thrombocytopenic, or
• international normalized ratio (INR) > 2
• Disseminated intravascular coagulation
• Kidney dysfunction
• serum creatinine ≥ 2 times the upper limit of normal for age or 2-fold
increase in baseline creatinine in people with chronic kidney disease
• Liver dysfunction (only applicable to infants > 1 month)
• total serum bilirubin ≥ 4 mg/dl, or
• alanine aminotransferase (ALT) ≥ 2 times the upper limit of normal

138. Pneumothorax: classification, clinical symptoms, diagnostic

procedures, treatment
pneumothorax is an accumulation of air within the pleural space. It may occur
spontaneously or as the result of trauma, surgery, or a therapeutic intervention.
If the air accumulates under pressure, a tension pneumothorax ensues.
Classification
• Spontaneous pneumothorax may occur in children with no known underlying
disease or may result from or in fact, reveal an underlying condition, such as a
 congenital bleb, pneumonia with pneumatocele or abscess, tuberculosis, or
cystic adenomatoid malformation.
• Traumatic pneumothorax may result from a tear in the pleura,esophagus,
trachea, or bronchi
• Iatrogenic causes include mechanical ventilation, thoracentesis or central
venous catheter insertion, bronchoscopy, or cardiopulmonary resuscitation
Clinical signs and diagnosis
• The most common presenting symptoms of pneumothorax are ipsilateral chest
pain and dyspnea. Severe dyspnea should alert the surgeon to the presence of a
tension pneumothorax.
• Physical examination may reveal diminished breath sounds on one side of the
chest or a shift of the trachea from the suprasternal notch. Assymmetrical chest
movement
• A pneumothorax is usually detectable on a chest radiograph and is enhanced if
the radiograph is taken at end expiration. Visible air in upper part of lungs
Treatment
• Options for treatment of a small pneumothorax include thoracentesis,
placement of a unidirectional (Heimlich-type) valve, or placement of a small
pigtail catheter
• However, if air is continuously aspirated or if the pneumothorax recurs, a
standard chest tube should be inserted.
• A tension pneumothorax poses a surgical emergency and a chest tube should be
placed immediately. If a chest tube is not immediately available or if the
patient's condition deteriorates during preparation for placement, a large-bore
(14-gauge) needle should be placed in the second intercostal space anteriorly to
relieve the tension.

139. Hemothorax: causes, clinical signs, diagnosis, treatment

The blood volume of a pediatric patient is typically 7-8% of the total body weight.
Thus, a relative small blood volume loss can lead to hypovolemia and shock.
Hemothorax is usually a consequence of blunt or penetrating trauma. Much less
commonly, it may be a complication of disease, may be iatrogenically induced, or
may develop spontaneously. Diagnosis:
• When chest bleeding does occur, it can be insidious and life-threatening.
Bleeding is typically from an intercostal vessel or vessels, parenchyma, or
chest wall.
• Complaints:dyspnea, hypotension, shock.
• By percussion the dullness is revealed.
• By auscultation - the breathing over the site of hemothorax is sharply
diminished or is not heard.
• X-ray signs: On X-ray picture of hemothorax the intensive homogeneous
shadow on the side of the lesion with oblique upper contour is observed.
Treatment
• Treatment involves tube decompression. Thoracocentesis
• Video-assisted thoracic surgery (VATS) can be used as a diagnostic tool in an
acute or subacute hemodynamically stable patient with hemothorax.
 • Initial hemorrhage of more than 20 mL/kg or continued blood loss of more
than 2-3 mL/kg/hr for 3 consecutive hours may be an indication for open
thoracotomy.

140. Pulmonary contusion: causes, pathophysiology, clinical signs

• Pulmonary contusion is the most common thoracic injury in children and
represents a defining contrast between children and adults.
• In contrast to rib fractures in adults after blunt trauma, the kinetic energy of
blunt chest trauma is transmitted to the compliant chest wall in children. Thus,
both pulmonary contusion and hemorrhage are far more common than
pneumothorax.
• Pulmonary contusion from a car or truck rollover injury in children is a
common phenomenon.
• Typical chest radiographic findings include multiple opacifications
corresponding to intraparenchymal hemorrhage. Hypoxia from shunting and
ventilation perfusion mismatch, in addition to radiographic findings, is
characteristic of pulmonary contusion.
• Successful treatment involves aggressive pulmonary toilet and pain
management. Resolution of the contusion within a few days is not uncommon
• Pulmonary contusions are commonly identified by chest X-ray and confirmed
by CT .
• Due to the lack of comorbidities and excellent pulmonary reserve, these
injuries are seldom of clinical significance. Extensive or multilobar injuries,
however, can lead to respiratory compromise requiring aggressive support with
mechanical ventilation. Progression to respiratory distress syndrome has also
been observed with sign of dyspnea, tachycardia.
• Children with minimal symptoms but significant X-ray findings should
therefore be monitored closely. Excessive intravenous fluid resuscitation can
worsen pulmonary function in these patients.

141. Etiology and pathogenesis of plural empyema

Empyema refers to the accumulation of infected fluid in the pleural space.
In children, this is usually the result of severe pneumonia
However, empyema may also result from infection of the retropharyngeal,
mediastinal, or paravertebral spaces, thoracic trauma, or an immunocompromised
state
Etiology: Streptococcus pneumoniae, Streptococcus pyogenes. Staphylococcus
aureus, and Haemophilus influenzae.
Pathogenesis
• The first stage, or the exudative stage, is characterized by an accumulation of
thin pleural fluid with few cells. The pleura and lung are mobile, and the fluid
is amenable to drainage by thoracentesis. This stage may last only 24 to 72
hours.
• The second stage is the fibrinopurulent stage. Consolidation of infected pleural
fluid results in an accumulation of fibrinous material, formation of loculations.
and loss of lung mobility. This stage lasts 7 to 10 days.
 • The third stage is the organizing stage. A pleural peel forms secondary to
fibroblast proliferation and resorption of fibrin. The lung becomes entrapped,
and capillary proliferation extends from the fibrinous peel into the visceral
pleura itself. This usually occurs 2 to 4 weeks after the initial development of
the empyema.

142. Clinical presentations and diagnosis of plural empyema

Clinical presentation
• Children with empyema generally present with fever, cough, respiratory
insufficiency, and chest pain.
• Physical signs may include dullness on chest percussion, tactile and vocal
fremitus, decreased breath sounds, rales, and a pleural friction rub.
Diagnosis
• A chest radiograph reveals a thickened pleura in addition to the primary
pneumonic process and pleural fluid.
• Transthoracic ultrasound or chest CT scan are beneficial in assessing the
degree of pleural thickening, fluid loculation, and lung consolidation.
• The diagnosis of empyema is confirmed by thoracentesis. The fluid is
characteristically turbid and may be thick during the later stages of the
infection.
• Laboratory analysis reveals a specific gravity greater than 1.016. protein
greater than 3 g per dL, lactate dehydrogenase (LDH) greater than 200 U per L.
pleural fluid protein/serum protein ratio greater than 0.5, pleural fluid
LDH/serum LDH ratio greater than 0.6. and white blood cell count higher than
15.000 per mm3.

143. Treatment of bacterial pneumonia with pleural effusion

• Once the diagnosis of empyema is made, appropriate antibiotics should be
administered based on Gram's stain and culture of the pleural fluid or sputum.
Main antibiotics are ampicillin and gentamycin or cefotaxime. Amoxicillin,
azithromycin
• Complete drainage of the empyema should be accomplished either by
thoracentesis or tube thoracostomy.
• Pleural cavity lavage with antibiotic solution

144. Pathogenesis, clinical signs and diagnosis of lung abscess

Generally, a lung abscess develops when at least one of two fundamental problems
exist: (1) a primary failure of host defenses is present, or (2) repeated aspiration of
oral or intestinal bacteria into the tracheobronchial tree occurs..
Clinical signs
• The clinical presentation of a patient with a lung abscess commonly includes
systemic complaints, such as fever, chills, night sweats, anorexia, and weight
loss.
• Nonspecific respiratory symptoms, such as coughing and wheezing, are also
frequent.
 • More specific and alarming symptoms, such as a productive cough, fetid
sputum, or hemoptysis, are later events associated with suppurative disease and
cavitation.
Diagnosis
• The most important examination is generally a plain chest radiograph. A single
cavity in a dependent location with an air fluid level is classic
Treatment
• Endoscopic drainage of a lung abscess into the tracheobronchial tree can be
achieved with a variety of needles, catheters, or other instruments passed
through rigid or flexible instruments
• Transpleural diagnostic aspiration and both open and closed external drainage
are all described and appropriate for selected patients.
• Antibiotics: Clindamycin, penicillin

145. Definition, causes and clinical manifestation of the acute

scrotum
Sudden pain in scrotum caused by:
• Torsion of testis and appendage
• Infection: epididymitis, epididymoorchitis, orchitis
• Trauma
• Hernia
• Idiopathic scrotal edema
Clinical manifestation
swollen, erythematous and tender scrotum. The symptom of ‘pain’ alone is not
characteristic of any specific etiology and in younger patients such as infants may be
completely absent at presentation. Some pediatric patients may present with a history
of appendicitis or acute loin pain when the actual cause of the patients symptoms is
secondary to an acute pediatric scrotum itself.

146. Pathogenesis of extravaginal and intravaginal testicular torsion

• Extravaginal torsion is more common in fetuses and neonates and denotes
torsion of the spermatic cord along its course but outside the tunica vaginalis.
Most babies born with an absent (Vanishing") testes are victims of this type of
prenatal torsion. Absence of testicular fixation is believed to predispose the
testicle to this type of torsion.
• The other variety, intravaginal torsion, is more common in childhood and
occurs within the tunica vaginalis. In these cases, fixation of the tunica
vaginalis is to the cord and not the testicle. Once the testicle is suspended
within the tunica vaginalis causing a "Bell-Clapper" deformity. Contraction of
the cremasteric muscle initiates testicular rotation in these predisposed
testicles.

147. Clinical signs of testicular torsion in newborns, toddlers and

teenagers
• Neonates with unilateral cryptorchidism may have had an in utero torsion.
Perinatal testicular torsion will present as a tender mass in the scrotum. Others
 may present with a red, firm, tender mass of the groin area which may not be
distinguishable from an incarcerated hernia.
• Older children and teenagers will present with a sudden onset of severe
testicular pain followed by local swelling and firmness with radiation of pain to
the ipsilateral groin and lower abdomen
• On examination, the child is restless and in obvious pain. On inspection, the
involved testicle is "high-riding". Later the scrotum becomes swollen, red and
tender. Careful and gentle palpation of the cord and scrotal contents may yield
a clue to the diagnosis.
• . In cases of torsion of the appendix testes, transillumination may demonstrate a
"blue dot" sign on the superior aspect of the testicle. This site will be tender,
but otherwise, the testicle and the cords are uninvolved.

148. Diagnostin evaluation, treatment and complications of

testicular torsion
Diagnosis
• Color doppler – decreased intratesticular flow
• Nuclear Technetium-99 radioisotope scan: Show testicular perfusion
Treatment: Never delay surgery on assumption of nonviability as prolonged
symptoms can represent periods of intermittent torsion
• Detorsion within 6hr = 100% viability
• Within 12-24 hrs = 20% viability
• After 24 hrs = 0% viability
Emergency surgery
• Manual detorsion in initial stages
• Surgical detorsion and orchiopexy if viable: Contralateral exploration and
fixation if bell-clapper deformity
• Orchiectomy if non-viable testicle

149. Pathogenesis, clinical symptoms and treatment of the torsion of

the appendix testis
Pathogenesis: Prepubertal estrogen may enlarge appendix and cause torsion
Clinical symptoms
• Peak age 3-13 yo (prepubertal)
• Sudden onset, pain less severe
• Classically, pain more often in abdomen or groin
• Non-tender testicle
• Tender mass at superior or inferior pole
• May be gangrenous, “blue-dot” (21% of cases)
• Normal cremasteric reflex, may have hydrocele
• Increased or normal flow by doppler U/S
Treatment
• Management supportive analgesics, scrotal support to relieve swelling
• Surgery for persistent pain
 150. Differential diagnosis of the testicular torsion and torsion of the
appendix testis

151. Differential diagnosis of the torsion of the appendix testis and

incarcerated inguinal hernia
Testicular torsion presents with sudden severe onset of pain associated with systemic
symptoms. High riding testicle and transverse lie of testical. Reduced ipsilateral
cremasteric reflex.
Hernia presents as unilateral inguinal/scrotal swelling and pain. On abdominal exam,
abdomen is tender. Bulging mass is palpable.

152. Differential diagnosis of the testicular torsion and idiopatic

scrotal edema
Idiopathic scrotal edema is typically unilaterall swelling and edema seen in children
<10years old. Presents with scrotal, perineal, inguinal erythema and edema.
Testicular torsion presents with sudden severe onset of pain associated with systemic
symptoms. High riding testicle and transverse lie of testical. Reduced ipsilateral
cremasteric reflex.

153. Peculiarities of pediatric tumors

Main tumours in children
Acute lymphoblastic leukemia 23.3 %
CNS tumors 20.7 %
Neuroblastoma 7.3 %
Non-Hodgkin's 6.3 %
Wilms' tumor 6.1 %
 Hodgkin's disease 5%
Acute myeloid leukemia 4.2 %
Rhabdomyosarcoma 3.4 %
Retinoblastoma 2.9 %
Osteosarcoma 2.6 %
Other 2.1 %
Common chief complaints given by parents that suggest a pediatric cancer
Chief complaints Suggested cancer

Chronic drainage from ear Rhabdomyosarcoma: Langerrhans cell

histiocytosis

Morning headache with vomiting Brain tumor

Lump in neck that that does not respond Hodgkin’s or non- Hodgkin’s lymphomas
to antibiotics

Swollen face and neck Non-Hodgkin’s lymphoma, leukemia

Mass in abdomen Wilm’s tumor, neuroblastoma, hepatoma

Bleeding from vagina Yolk sack tumor, rhabdomyosarcoma

Weight loss Hodgkin’s lymphoma

Bone pain Leukemia, neuroblastoma

154. Clinical presentations and diagnosis of mediastinal tumors

If symptoms develop, it’s often because the tumor is pushing on surrounding organs.
Symptoms can include:
• cough
• shortness of breath
• chest pain
• fever/chills
• night sweats
• coughing up blood
• unexplained weight loss
• swollen lymph nodes
 • respiratory blockage
• hoarseness
Diagnosis is made by chest x-ray, CT scan, MRI, biopsy
In the anterior of the mediastinum, tumors can be caused by:
• lymphoma, including Hodgkin’s disease and non-Hodgkin’s lymphoma
• thymoma and thymic cyst (a tumor of the thymus)
• thyroid mass mediastinal (generally a benign growth, but it can sometimes be
cancerous)
In the middle of the mediastinum, tumors can be caused by:
• bronchogenic cyst (a benign growth that starts in the respiratory system)
• lymphadenopathy mediastinal, or enlargement of the lymph nodes
• pericardial cyst (a benign growth on the heart lining)
• thyroid mass mediastinal
• tracheal tumors (usually benign growths)
• vascular complications, such as swelling of the aorta
In the posterior of the mediastinum, tumors can be caused by:
• extramedullary haematopoiesis (rare growths that start in the bone marrow and
are related to severe anemia)
• lymphadenopathy mediastinal (enlarged lymph nodes)
• neuroenteric cyst mediastinal (a rare growth involving both the nerves and the
gastrointestinal system)
• neurogenic neoplasm mediastinal (cancerous cells of the nerves)

155. Clinical presentations, diagnosis and treatment of the Wilms’

tumor
Also known as nephroblastoma
• The most common presentation is an asymptomatic abdominal mass
discovered by the parent or physician. Occasionally the child presents with
haematuria, but symptoms are often non-specific: abdominal fullness,
abdominal pain, gastrointestinal upset, fever, weight loss, malaise, and
anaemia. Hypertension is sometimes detectable.
• A small number of patients who have hemorrhaged into their tumor may
present with signs of hypotension, anemia, and fever
• syndromes (WAGR and BWS) associated with Wilms’ tumor, ie, aniridia,
genitourinary malformations, and signs of overgrowth.
Diagnosis: CT scan, abdominal ultrasound, biopsy,
Treatment
• The usual approach in most patients is nephrectomy followed by
• Chemotherapy: vincristine, dactinomycin, doxorubicin, cyclophosphamide,
etoposide
• with or without postoperative radiotherapy.

156. Pathology and clinical manifestation of the neuroblastoma due

to localization
Neuroblastoma is a tumour of neural crest origin which may occur in the adrenal
medulla or anywhere along the sympathetic ganglion chain, namely in the neck,
thorax, abdomen, and pelvis
The clinical presentation depends on the location of the primary. Often the symptoms
are few and general. The patients often appear ill and fail to thrive.
• Those with cervical tumors present with a mass in the neck or with Horner's
syndrome (meiosis, anhydrosis and ptosis).
• Those with thoracic primaries are diagnosed after a mass is found on a routine
chest radiograph.
• The parents often find abdominal tumors when they are bathing the child.
Abdominal tumors are more irregular than Wilms' tumors and more often cross
the midline.
• Pelvic tumors may result in obstructive symptoms (urethral or colonic). Rarely
they compress or infiltrate the iliac veins and/or arteries and present with lower
extremity edema.
• Tumors that extend intraspinal in any of these locations may present with
• neurologic symptoms. Two specific syndromes sometimes occur in patients
with neuroblastoma. Opsoclonus-myoclonus is a constellation of symptoms
including polymyoclonia, cerebellar ataxia with gait disturbance, and
opsoclonus ("dancing eyes").

157. Diagnostic evaluations and treatment of the neuroblastoma

The diagnosis of neuroblastoma is confirmed by:
• Biopsy with unequivocal diagnosis of neuroblastoma by light microscopyor
• Bone marrow biopsy or aspirate with unequivocal tumor cells and increased
serum or urine catecholamines.
• CT scan, chest radiograph, skeletal radiograph, ultrasound
Treatment
• Treatment for patients with neuroblastoma involves a combination of surgery
Complete excision should only be undertaken when there is not a concern for
undue morbidity to vital organs or the patient,
• radiation and
• chemotherapy: cyclophosphamide, cisplatin, doxirubicin and
epipodophyllotoxins, (teniposide-V'M-26 and etoposide-VP-16).

158. Embryology and pathology of the teratomas

Teratomas are tumors comprising more than a single cell type derived from more
than one germ layer.
Teratomas range from benign, well-differentiated (mature) cystic lesions to those that
are solid and malignant (immature). Besides being mature, with malignant
transformation, teratomas also may be monodermal and highly specialized.
Location
• sacrococcygeal (57%)
• gonads (29%)
• mediastinal (7%)
• retroperitoneal (4%)
 • cervical (3%)
• intracranial (3%)

159. Diagnosis, classification, management of the Sacrococcygeal

teratomas
Classification
• Type I tumors are predominantly external, attached to the coccyx, and may
have a small presacral component (45.8%). No metastases were associated
with this group.
• Type II tumors have both an external mass and significant presacral pelvic
extension (34%) and have a 6% metastases rate.
• Type III tumors are visible externally, but the predominant mass is pelvic and
intraabdominal (8.6%). A 20% rate of metastases was found in this group.
• Type IV lesions are not visible externally but are entirely presacral (9.6%) and
have an 8% metastases rate.
Clinical: Sacrococcygeal teratomas ( SCT ) are commonly very large ( average 8-10
cm ), well encapsulated and grossly lobulated. These masses possess both cystic and
solid components. SCT is nearly always arising from the tip of the coccyx.
Management
• Surgical, including removal of the coccyx
• Malignant = surgical excision + chemotherapy + radiation (metastases to lung,
bone, liver).

160. Pathology, diagnosis and treatment of the dermoid cysts

• Congenital dermoid inclusion cysts are superficial and located in proximity to
the hyoid bone.
• They are epithelial-lined cysts with variable skin appendages in a mesodermal
stroma.
• These masses do not move with swallowing or tongue protrusion. On occasion,
a dermoid cyst ruptures, resulting in an intense granulomatous inflammatory
reaction.
• Dermoid cysts are treated with simple excision and do not recur if the entire
cyst wall is excised. Excision of a midline cervical cleft is of cosmetic
importance only and is treated electively. Excision is done with a series of Z-
plasty incisions to prevent a linear contracture that interferes with extension of
the head.

161. Rhabdomyosarcoma: pathology, diagnosis, main principles of

treatment
Rhabdomyosarcoma (RMS), the most common soft tissue sarcoma in infants and
children, represents about 5-15% of all malignant solid lesions. RMS arises from a
primitive cell type and occurs in mesenchymal tissue at almost any body site
excluding brain and bone.
The Intergroup Rhabdomyosarcoma Study divides tumors into 5 types:
• embryonal (57 %),
• alveolar (19 %),
 • botryoid (6 %),
• undifferentiated (17 %),
• pleomorphic (1 %).
Clinical
• Tumors that develop in the nasopharynx or auditory canal present with bloody
or purulent drainage.
• If arising from the muscles of head and neck, an asymptomatic firm swelling is
apparent.
• Orbital tumors often cause pain and swelling about the eye with proptosis and
diplopia.
• Bloody vaginal discharge or the presence of a red polypoid friable lesion at the
introitus are highly suggestive of rhabdomyosarcoma of the vagina.
• Bladder tumors may mimic an infection with urinary frequency or other
difficulties with urination.
• Prostatic lesions can block the urinary flow necessitating catheterization.
• Rectal exam is usually diagnostic as the prostatic lesion bulges into the rectum.
• Lesions of the trunk or extremity present as a firm fixed mass beneath the
subcutanteous tissue.
Diagnosis: Ultrasound, CT, MRI, incisional biopsy

162. Classification and clinical features of the nevi

The term naevus refers to a hamartomatous malformation of the skin. Naevi may be
principally composed of dermal elements, such as connective tissue naevus,
melanocytes (naevocellular naevus), vascular elements, or epidermal elements
(epidermal naevi).
• Epidermal naevi are verrucous or wart-like and are frequently present at birth
although may develop later in childhood or (rarely) in adult life. They may be
small, resembling true viral warts, but more typically they form large linear
plaques or linear arrays of warty papules. Rarely, large areas of the body
surface may be covered by linear or swirling arrays of these lesions. Epidermal
naevi are typically asymptomatic, although large linear naevi may become
spontaneously inflamed, with the development of pruritus and erythema of the
lesions and surrounding skin. Histologically, epidermal naevi are characterized
by acanthosis and hyperkeratosis.. They are most commonly removed for
cosmetic reasons. Such treatment may involve excision with primary closure,
electrodesiccation, carbon dioxide laser ablation, or cryosurgery.
• Naevus sebaceus is a type of epidermal naevus that occurs exclusively on the
scalp or face. Histologically, naevus sebaceus is characterized by the same type
of epidermal proliferation seen in other epidermal naevi, but large mature
sebaceous glands and apocrine glands are also present. Before puberty, naevus
sebaceus is typically a smooth-surfaced flat plaque with slightly yellowish or
yellow-orange colour. When it occurs on the scalp, which is the most common
site, the absence of hair within the lesion may bring it to attention. At puberty,
the sebaceous element within the naevus begin to hypertrophy and the surface
becomes more verrucous.
 • Connective tissue naevi are generally present at birth. They consist of firm,
flesh-coloured papules and plaques and are usually solitary. The hair follicle
orifices may be prominent within lesions, giving them the appearance of pig
skin. Connective tissue naevi are usually idiopathic and are not associated with
any other disease, with the exception of the shagreen patch that occurs in
tuberous sclerosis. Histologically, connective tissue naevi are composed of
dense aggregations of dermal elements, usually collagen fibres or elastic fibres,
or both. Connective tissue naevi are harmless, although they may be excised
for cosmetic or functional reasons.

163. Predisposing factors, clinical signs and treatment of the

melanoma
The most dangerous form of skin cancer, these cancerous growths develop when
unrepaired DNA damage to skin cells (most often caused by ultraviolet radiation
from sunshine or tanning beds) triggers mutations (genetic defects) that lead the skin
cells to multiply rapidly and form malignant tumors.
Early signs of melanoma are summarized by the mnemonic "ABCDE":
• Asymmetry
• Borders (irregular with edges and corners)
• Color (variegated)
• Diameter (greater than 6 mm (0.24 in), about the size of a pencil eraser)
• Evolving over time
These classifications do not, however, apply to the most dangerous form of
melanoma, nodular melanoma, which has its own classifications:
• Elevated above the skin surface
• Firm to the touch
• Growing
Confirmation of the clinical diagnosis is done with a skin biopsy
Treatment
• wide local excision (WLE) with 1–2 cm (0.4–0.8 in) margins. Melanoma-in-
situ and lentigo malignas are treated with narrower surgical margins, usually
0.2–0.5 cm (0.1–0.2 in)
• Mohs surgery, or the double-bladed technique with margin control
• lymphadenectomy of sentinel lymph node
• Various chemotherapy agents, including temozolomide, dacarbazine (also
termed DTIC), immunotherapy (with interleukin-2 (IL-2) or interferon (IFN)),
as well as local perfusion, are used by different centers

164. Pathology and classification of the vascular anomalies

Vascular Hemangiomas
malformations (raised lesions)
(flat lesions)
 Salmon patch (also known Superficial hemangioma
as nevus simplex or nevus (Cherry, strawberry
telangiectaticus) hemangioma)
Port-wine stain (also known Deep hemangioma (also
as nevus flammeus) known as cavernous
hemangioma)

165. Pathology, clinical manifestations and imaging of the infantile

hemangioma
Infantile hemangiomas have a fairly predictable pattern of growth. Most appear
during the first weeks of life and grow rapidly (called the proliferative phase) for 6 to
12 months. Then they begin a much slower process of shrinking, or regressing (called
the involuting phase), which may take from one to about seven years. Finally, the
tumor enters its final, shrunken state (called the involuted phase), after which it will
never regrow.
Clinical manifestation
Frequency of cutaneous hemangiomas at particular sites is as follows:
• Head and neck - 60%
• Trunk - 25%
• Extremities - 15%
Sites of extracutaneous hemangiomas include the following:
• Liver
• Gastrointestinal tract
• Larynx
• Central nervous system
• Pancreas
• Gallbladder
• Thymus
• Spleen
• Lymph nodes
• Lung
• Urinary bladder
• Adrenal glands
Skin biopsy can be performed if the diagnosis is in question after a thorough history
and physical examination. Infantile hemangiomas uniformly stain positively for
glucose transporter 1 (GLUT-1) during both the proliferation and the involution
phases.
Ultrasonography: High vessel density (>5 vessels/cm2) and high peak arterial
Doppler shift (>2 kHz) are sensitive and specific for infantile hemangiomas, as
compared with other soft tissue masses
Magnetic resonance imaging (MRI) has the following uses: Delineate the location
and extent of cutaneous and visceral hemangiomas
 166. Treatment of the infantile hemangiomas
Treatment options for clinically significant hemangiomas include the following:
• Medication: propanolol, propanolol hydrochloride, corticosteroids
• Laser surgery: Lasers used especially on areas likely to result in significant
functional or psychological impact (eg, fingers, eyes, lips, nasal tip, ears, face)
• Surgical excision

167. Lymphatic malformations: clinical manifestations, imaging and

treatment
Lymphatic malformations are rare, non-malignant masses consisting of fluid-filled
channels or spaces thought to be caused by the abnormal development of the
lymphatic system. These malformations are usually apparent at birth or by two years
of age.
Symptoms may include:
• A mass or lump in the mouth, cheek, or tongue beneath the mucous membrane
that lines the area
• A large, fluid-filled mass to the lower side and back of the neck under the
platysma muscle (a thin, flat muscle that extends from the upper chest to the
jaw)
Imaging
• Ultrasound is a diagnostic tool used to evaluate organs and structures inside the
body with high-frequency sound waves. After birth, diagnosis of a lymphatic
malformation is generally determined by a physical examination. In addition to
a complete medical history and physical examination, diagnostic procedures
for a lymphatic malformation may include the following:
• Transillumination. A method of examination by the passage of light through
tissues to assist in diagnosis. The light transmission changes with different
tissues.
• Computed tomography scan (also called a CT or CAT scan). A CT scan is a
diagnostic imaging procedure that uses a combination of X-rays and computer
technology to produce horizontal, or axial, images (often called slices) of the
body.
Treatment may include:
• Observation of the malformation (to watch for growth or changes)
• Antibiotic medications (to treat infection)
• Incision and drainage of the lesion
• Surgery (to remove the lymphatic malformation)