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HOSPITAL SURGERY
Edited by:
L, Kovalchuk
V. Sayenko
G. Knyshov
M. Nychytailo
Ternopil
"Ukrmedknyha"
2004
ВВК 54.54
Н87
UDK 617(075.8)
Н 87 Hospital surgery / Edited by L. Kovalchuk, V. Sayenko, G. Knyshov,
M. Nychytailo. - Temopil: Ukrmedknyha, 2004. - 472 p., ill. 353, tabl. 6.
ISBN 966-7364-02-X
The modern requirements of doctor's training need the mastering of
many medical subjects, among which surgery is one of the leading ones.
The textbook represents the knowledge of the leading surgeons and scien­
tists from prestigeous medical schools of Ukraine. It has been tried to present
modern concepts of the clinical course, diagnostics and treatment of surgi­
cal diseases. Special attention has been paid to new technologies, which are
being used in diagnostics and treatment of the patients.
The content of the textbook fulfills the educational programme of hos­
pital surgery. The structure of material is presented with attention on the
basic parts, signs, methods of diagnostics, differential diagnostics, compli­
cations, tactics and methods of surgical treatment. In opinion of the au­
thors, such structure of the textbook is beneficial for mastering the subject.
For the students of senior courses of the medical schools of III-
IV accrediting level.
BBK 54.54
UDK 616(075/8)
ISBN 966-7364-02-X
© Видавництво "Укрмедкнига", 2002
© Переклад на англійську мову "Ukrmedknyha" 2004
A u t h o r s
Bagirov M.M. Doctor of Medical Sciences, Professor of Pulmomary Chair of Kyiv
Institute of Post-Diploma Education;
Bedeniuk A.D. Candidate of Medical Sciences, Associate Professor of Abdominal
Surgery Course of Hospital Surgery Clinics of Ternopil Medical Academy;
Vardynets I.S. Candidate of Medical Sciences, Chief Physician of Ternopil District
Hospital;
ч-Veligotsky M.M. Doctor of Medical Sciences, Professor, Head of Thoracoabdominal
Surgery Clinics of Kharkiv Post-Diploma Physician Institute, Laureate of State
prize of Ukraine;
Venger I.K. Doctor of Medical Sciences, Professor of Vascular Surgery Course of
Hospital Surgery Clinics of Ternopil Medical Academy;
Grubnyk V.V. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clin-
• ics of Odessa Medical University, Laureate of State prize of Ukraine;
Gusak O.M. Assistant Professor of Proctology Course of Hospital Surgery Clinics of
Ternopil Medical Academy;
Deykalo I.M. Doctor of Medical Sciences, Associate Professor of General Surgery
Clinics of Ternopil Medical Academy;
Dziubanovsky I.Y. Doctor of Medical Sciences, Professor, Head of Surgery Clinics of
Post-Diploma Education Faculty of Ternopil Medical Academy;
Dryzhak V.I. Doctor of Medical Sciences, Professor, Head of Oncology Clinics of
Ternopil Medical Academy;
Driuk M.F. Doctor of Medical Sciences, Professor, Head of Microvascular Surgery
Department of Kyiv SRI of Clinical and Exprimental Surgery, Honored Scientist
and Technician of Ukraine, Laureate of State prize of Ukraine;
Zakharash M.P. Doctor of Medical Sciences, Professor of National Medical Univer­
sity, Chief of Military-Medical Board of Ukrainian Security Service, Major-
General of Medical Service;
Zakharov V.P. Candidate of Medical Sciences, Associate Professor of Ternopil Medi­
cal Academy;
Zinkovsky M.F. Doctor of Medical Sciences, Professor, Corresponding Member of
AMS of Ukraine, Head of Congenital Heart Defects Department of Kyiv Insti­
tute of Cardiovascular Surgery, Laureate of State prize of Ukraine;
Kimakovych V.Y. Doctor of Medical Sciences, Associate Professor, Chief Physician
of Lviv Regional Diagnostic Centre;
Kit O.M. Doctor of Medical Sciences, Professor of Ternopil Medical Academy;
Knyshov G.V. Doctor of Medical Sciences, Professor, Academician of AMS of Ukraine,
Director of Kyiv Institute of Cardiovascular Surgery, Laureate of State prize of
Ukraine;
Kovalchuk L.Y. Doctor of Medical Sciences, Professor, Corresponding Member of
AMS of Ukraine, Rector of Ternopil Medical Academy, Head of Hospital Sur­
gery Clinics of Ternopil Medical Academy, Honored Scientist and Technician of
Ukraine;
Kovalchuk O.L. Candidate of Medical Sciences, Head of Laparoscopic Surgery De­
partment of Ternopil Central District Hospital;
Komorovsky Y.T. Doctor of Medical Sciences, Professor of Hospital Surgery Clinics
of Ternopil Medical Academy;
Authors
Bagirov M.M. Doctor of Medical Sciences, Professor of Pulmomary Chair of Kyiv
Institute of Post-Diploma Education;
Bedeniuk A.D. Candidate of Medical Sciences, Associate Professor of Abdominal
Surgery Course of Hospital Surgery Clinics of Ternopil Medical Academy;
Vardynets I.S. Candidate of Medical Sciences, Chief Physician of Ternopil District
Hospital;
ч-Veligotsky M.M. Doctor of Medical Sciences, Professor, Head of Thoracoabdominal
Surgery Clinics of Kharkiv Post-Diploma Physician Institute, Laureate of State
Venger I.K. Doctor of Medical Sciences, Professor of Vascular Surgery Course of
Hospital Surgery Clinics of Ternopil Medical Academy;
Grubnyk V.V. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clin-
> ics of Odessa Medical University, Laureate of State prize of Ukraine;
Gusak O.M. Assistant Professor of Proctology Course of Hospital Surgery Clinics of
Ternopil Medical Academy",
Deykalo I.M. Doctor of Medical Sciences, Associate Professor of General Surgery
Clinics of Ternopil Medical Academy;
Dziubanovsky I.Y. Doctor of Medical Sciences, Professor, Head of Surgery Clinics of
Post-Diploma Education Faculty of Ternopil Medical Academy;
Dryzhak V.I. Doctor of Medical Sciences, Professor, Head of Oncology Clinics of
Ternopil Medical Academy;
Driuk M.F. Doctor of Medical Sciences, Professor, Head of Microvascular Surgery
Department of Kyiv SRI of Clinical and Exprimental Surgery, Honored Scientist
and Technician of Ukraine, Laureate of State prize of Ukraine;
Zakharash M.P. Doctor of Medical Sciences, Professor of National Medical Univer­
sity, Chief of Military-Medical Board of Ukrainian Security Service, Major-
General of Medical Service;
Zakharov V.P. Candidate of Medical Sciences, Associate Professor of Ternopil Medi­
cal Academy;
Zinkovsky M.F. Doctor of Medical Sciences, Professor, Corresponding Member of
AMS of Ukraine, Head of Congenital Heart Defects Department of Kyiv Insti­
tute of Cardiovascular Surgery, Laureate of State prize of Ukraine;
Kimakovych V.Y. Doctor of Medical Sciences, Associate Professor, Chief Physician
of Lviv Regional Diagnostic Centre;
Kit O.M. Doctor of Medical Sciences, Professor of Ternopil Medical Academy;
Knyshov G.V. Doctor of Medical Sciences, Professor, Academician of AMS of Ukraine,
Director of Kyiv Institute of Cardiovascular Surgery, Laureate of State prize of
Ukraine;
Kovalchuk L.Y. Doctor of Medical Sciences, Professor, Corresponding Member of
AMS of Ukraine, Rector of Ternopil Medical Academy, Head of Hospital Sur­
gery Clinics of Ternopil Medical Academy, Honored Scientist and Technician of
Ukraine;
Kovalchuk O.L. Candidate of Medical Sciences, Head of Laparoscopic Surgery De­
partment of Ternopil Central District Hospital;
Komorovsky Y.T. Doctor of Medical Sciences, Professor of Hospital Surgery Clinics
of Ternopil Medical Academy;
Kontsevy O.O. Head of Abdominal Surgery Department of Ternopil Regional Clinical
Hospital;
Korchynsky Y.Y. Candidate of Medical Sciences, Assistant Professor of Proctology
Course of Hospital Surgery Clinics of Ternopil Medical Academy;
[Kurko V.S.[Doctor of Medical Sciences, Professor of Surgery Clinics of Post-Diploma
Education Faculty of Ternopil Medical Academy;
Maksymliuk V.I. Doctor of Medical Sciences, Associate Professor of Surgery Clinics
of Post-Diploma Education Faculty of Ternopil Medical Academy;
Malyovany V.V. Candidate of Medical Sciences, Associate Professor of Thoracic Sur-
gery Course of Hospital Surgery Clinics of Ternopil Medical Academy;
Mitiuk LI. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clinics
of Vinnytsia Medical University;
Moroz G.S. Doctor of Medical Sciences, Professor of Oncology Clinics of Ternopil
Medical Academy;
Nychytailo M.Y. Doctor of Medical Sciences, Professor, Head of Department of
Liver and Biliary Tract Surgery of Institute of Clinical and Experimental Sur-
gery of AMS of Ukraine;
[Polischuk V.Mj Doctor of Medical Sciences, Professor, Superior of Public Health
Board of Rivne Regional State Administration;
Sagenko V.F. Doctor of Medical Sciences, Professor, Corresponding Member of NAS
and AMS of Ukraine, Director of Kyiv SRI of Clinical and Experimental Sur-
gery, Honored Scientist and Technician of Ukraine, Laureate of State prize of
Ukraine;
Serdiuk A.M. Doctor of Medical Sciences, Professor, Corresponding Member of AMS
of Ukraine;
Sytar L.L. Doctor of Medical Sciences, Professor, Head of Department of Acquired
Heart Defects of Kyiv Institute of Cardiovascular Surgery, Laureate of State
prize of Ukraine;
Spizhenko Y.P. Doctor of Medical Sciences, Academician of AMS of Ukraine, Presi-
dent of Association of Pharmacologists of Ukraine;
Sukhariev I.I. Doctor of Medical Sciences, Professor, Honored Scientist and Techni-
cian of Ukraine, Laureate of State prize of Ukraine;
Ursulenko V.I. Doctor of Medical Sciences, Head of Department of Surgical Treat-
ment of Coronary Insufficiency, Laureate of State prize of Ukraine;
Shevchenko S.I. Doctor of Medical Sciences, Professor, Head of Faculty Surgery
Clinics of Kharkiv Medical Academy;
Shevchuk M.G. Doctor of Medical Sciences, Professor, Head of Hospital Surgery
Clinics of Ivano-Frankivsk Medical Academy;
Shidlovsky V.O. Doctor of Medical Sciences, Head of Faculty Surgery Clinics of
Ternopil Medical Academy;
Shkrobot V.V. Candidate of Medical Sciences, Assistant of Chief Physician on Sur-
gery of Ternopil Regional Clinical Hospital;
Yarema I.V. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clinics
of Moscow Medical Stomatological Institute, Chief Lymphologist of Russian Fed-
eration.
Data on pathological morphology are stated by Bodnar Y.Y., Doctor of Medical Sciences,
Professor, Head of Pathologic Morphology Chair of Ternopil Medical Academy;
Conservative therapy to the section "Abdominal Surgery" is described by Starodub Y.M.,
Doctor of Medical Sciences, Professor, Head of Therapy Clinics of Post-Diploma
Education Faculty of Ternopil Medical Academy.
CONTENS
1. THORACIC S U R G E R Y 7
1.1. LUNGS AND PLEURA 9
1.1.1. Acute suppurative diseases of lungs 9
1.1.2. Lung Cysts 18
1.1.3. Pleural empyema^. 22
1.1.4. Pyopneumothorax 27
1.1.5. Spontaneous pneumothorax 31
1.1.6. Lung Cancer 34
1.2<TRAUMA OF THE CHEST 42
1.2.1. Rib fracture 43
1.2.2. Sternal Fracture - 45
1.2.3. Posttraumatic pneumothorax 46
1.2.4. Hemothorax 48
1.2.5. Subcutaneous emphysema 51
1.2.6. Traumatic injury of trachea and main bronchi 52
1.2.7. Mediastinal emphysema 56
1.3/ESOPHAGUS 58
1.3.1. Esophageal diverticula 58
1.3.2. Achalasia of the cardia 63
1.3.3. Esophageal sticture 67
1.3.4. Esophageal cancer 72
1.4. MEDIASTINUM 78
1.4.1. Acute mediastinitis 78
1.4.2. Mediastinal tumors 81
1.5. DIAPHRAGMA 89
1.5.1. Diaphragmatic hernias 89
1.5.2. Diaphragmatic relaxation 94
2. CARDIO-VASCULAR S U R G E R Y 99
2.1. HEART '. 101
2.1.1. Mitral stenosis 101
2.1.2. Sick sinus syndrome and sinoauricular block 104
2.1.3. Penetrating cardiac injuries I l l
2-2TARTERIES 114
2.2.1. Endarteritis obliterans 114
2.2.2. Atherosclerosis obliterans of the inferior extremities 120
2.2.3. Abdominal ischemic syndrome 126
2.2.4. Acute arterial occlusion 132
4 Contens
2.2.5. Pulmonary embolism 137
2.2^6. Injuries of vessels 143
2.3^VEINS : 153
2.3.1. Varicosity 153
2.3.2. venous thromboses 161
2.3.3. Postflebitic syndrome (postthrombotic disease) 172
2.4. LYMPH SYSTEM 181
2.4.1. Clinical anatomy and physiology 181
2.4.2. Surgery of thoracic lymph duct 184
2.4.3. Lymphangioma 187
2.4.4. Lymph fistula 189
2.4.5. Lymphangitis and lymphadenitis 190
2.4.6. Lymphedema of extremities 192
3. ABDOMINAL S U R G E R Y 195
3.1. ABDOMINAL WALL 197
3.1.1. Abdominal wall hernia 197
3.1.2. Incarcerated hernia 205
3.2. STOMACH AND DUODENUM 212
3.2.1. Gastric ulcer 212
3.2.2. Duodenal ulcer 220
3.2.3. Ulcer stenosis 227
3.2.4. Perforated ulcer gastroduodenal ulcers 231
3.2.5. Bleeding gastroduodenal ulcers 236
3.2.6. Gastrointestinal bleeding of unulcer etiology 242
—3.2.7. Diseases of the operated stomach 249
3.2.8. Cancer of stomach 268
3.3. SMALL AND LARGE INTESTINE 277
3.3.1. Acute appendicitis 277
3.3.2. Acute intestinal obstruction 287
3.3.3. Crohn's disease 295
3.3.4. Nonspecific ulcerative colitis 300
3.3.5. Cancer of colon 306
3.4. LIVER AND HEPATIC DUCTS 311
3.4.1. Abscesses of liver 311
3.4.2. Cysts of liver 315
3.4.3. Syndrome of portal hypertension 319
3.4.4. Acute cholecystitis 332
3.4.5. Chronic cholecystitis 344
3.4.6. Obstructive jaundice 348
3.4.7. Postcholecystectomy syndrome 354
3.4.8. Cancer of liver 360
Contens 5
3.4.9. Cancer of gall-bladder 364
3.5. PANCREAS 370
3.5.1. Acute pancreatitis 370
3.5.2. Chronic pancreatitis 377
3.5.3. Cysts of pancreas 386
3.5.4. Cancer of pancreas 393
3.6. PERITONITIS 398
4. P R O C T O L O G Y 407
4.1. RECTUM AND PARARECTAL SPACE 409
4.1.1. Hemorrhoids 409
4.1.2. Rectal Fissures 412
4.1.3. Polyps of colon and rectum 416
4.1.4. Paraproctitis 420
4.1.5. Rectal fistulas (chronic paraproctitis) 424
4.1.6. Epithelial paracoccidioidal canals 429
4.1.7. Cancer of rectum 433
5. ENDOCRINOLOGIC S U R G E R Y 439
5.1. THYROID GLAND 441
5.1.1. Endemic and sporadic goiter 441
5.1.2. Diffuse goiter with hyperthyroidism 446
5.1.3. Inflammatory diseases of thyroid gland 459
5.1.4. Thyroid cancer 465
ЛІТЕРАТУРА 468
1. THORACIC SURGERY
1.1. LUNGS AND PLEURA
1.1.1. Acute suppurative diseases of lungs
Acute suppurative diseases of lungs include abscessing pneumonia,
acute and gangrenous abscesses, focal and extensive lung gangrene.
Abscessing pneumonia is characterized by the multiple destructive
foci 0,3-0,5 cm in size, within 1-2 segments of lungs, which is not disposed
to progression. The destruction is accompanied by expressed perifocal infil-
tration of a pulmonary tissue.
Lung abscess - a purulent or ichorous destruction of pulmonary
tissue within one segment with formation of one or several cavities, filled
by pus, and detached from adjacent parenchyma by a pyogenic capsule
and expressed perifocal infiltration of surrounding pulmonary tissue. It
arises at the persons with a maintained reactivity of the organism.
Gangrenous abscess is a purulent, ichorous necrosis of a pulmonary
tissue within 2-3 segments, detached from adjacent pulmonary paren-
chyma, with the liability to sequesters formation. Depending on reactivity
of the organism it can transform into purulent abscess (after the lysis of
sequesters) or gangrene.
Lung gangrene - a diffuse purulent, ichorous necrosis of the tissue
without the tendency to defined demarcation with prompt dynamics of
spreading of necrotic zone and destruction of the parenchyma. It is char-
acterized by a grave intoxication, liability to a pleural complications and
pulmonary bleeding. If only the one lobe is affected the gangrene is con-
sidered to be limited, if extensive area of lungs isaffected - the gangrene
is a wide-spread.
Etiology and pathogenesis
The agents of purulent pulmonary destruction are anaerobic
nonclostridial microorganisms, staphylococci, Gram-negative bacteria, and
mixed infection.
The predominant factors which cause the disease:
• disturbances of bronchial patency with the development of atelectasis;
• infectious inflammatory process in a pulmonary tissue;
• regional disturbances of blood supply with a further necrosis of areas of
pulmonary parenchyma.
The embodiment of these factors occurs in condition of the changed
reactivity of the organism.
10 1. Thoracic surgery
The states which result in the aspiration of contents of the upper
parts of alimentary tract (traumas of head, craniovascular disturbances,
alcoholism, narcomania, narcoses, epilepsy etc.) contribute to the pulmo-
nary abscessing. And also factors, which are capable to provoke secondary
immunodeficiency and suppression of reactive processes: diabetes melli-
tus, irradiation, long application of corticosteroids, antineoplastic therapy,
some hematological disease, AIDS favor the purulent processes.
Pathology
The abscesses mainly develop in II and VI segments of lungs. They
may be single and multiple. The abscess is confined from adjacent pulmo-
nary tissue by a capsule, which represents a granulating tissue and dense
leukocytic rampart. Usually it is possible to find out a draining bronchus.
Later on in the wall of the abscess the amount of connective tissue fibers
is enlarged.
In gangrene the pulmonary tissue is black in color, swollen, with
cavities, and in some places transfers into the sites with dark green color-
ing. The macropreparatus is characteristically fetid.
Classification
According to pathogenesis:
- postpneumonic;
- aspirative;
- obturative;
- posttraumatic;
- hematogenous or septic;
- lymphogenous;
- thromboembolic.
According to the character of purulent process:
- single purulent abscesses;
- multiple purulent abscesses;
- bilateral purulent abscesses;
- gangrenous abscesses (single, multiple, uni- and bilateral);
- limited gangrene;
- wide-spread gangrene.
According to localization (with the indication of affected segment or
lobe).
According to the stage:
- 1 stage - necrotic pneumonia;
- 2 stage - destruction and rejection;
- 3 stage - cleaning and cicatrization.
1.1. Lungs and pleura II
According to the term of existence:
- acute;
- chronic.
Complications:
- pulmonary bleeding;
- pyopneumothorax;
- pleural empyema;
- sepsis;
- bronchogenic dissemination.
Symptomatology and clinical course
The clinical manifestation of acute purulent destruction of lungs de-
pend on the size of the focus and character of destruction, reactivity of
the organism and stage of the disease, peculiarities of the drainage of
purulent cavities and complications.
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 39-40°C and has a hectic character. At the same time the chest pain
increases, which associates with a troubling cough and dyspnea. The con-
dition 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 destruc-
tive cavities through bronchus the daily quantity of the sputum reaches
500 ml and more. At this time also possible hemoptysis. The sputum is foul-
smelling. At sedimentation it divides into three layers:
- inferior - resembling a grey mass with detrites and flaps of a pulmoary
tissue;
- medial - purulent, turbid, liquid;
- 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 are well revealed at peripheral localization of the
process. On palpation - weakened vocal fremitus. By percussion - a blunted
sound over the site of the purulent focus and perifocal infiltration (at
subpleural location of the abscess). On auscultation - tubular sound with a
moist rales in the zone of purulent focus. Well-generated subpleural cavi-
ties of major sizes can be revealed by percussion as a bandbox sound, on
12 1. Thoracic surgery
Fig 1.1.1. Acute abscess of the lower lobe
of the right lung in the stage of necrotic
pneumonia.
auscultation - as moist rales on the
background of amphoric respiration.
X-ray of the chest in the stage of
necrotic pneumonia shows a rounded
lesion with irregular contour (fig. 1.1.1).
For the second stage is characteristic
the enlightenment of the shadow with
a further developing of the rounded
cavity with air-fluid level (Kordin's
symptom), gentle pyogenic sheath and
the perifocal infiltration (fig. 1.1.2). In the
third stage on the place of suppuration
observed expressed fibrosis, sometimes
as a thin-walled annular formation.
Gangrenous abscess is character-
ized by a grave state of the patient,
expressed purulent intoxication, cough
with expectoration of a great amount
(500 ml and more) of grey-green, foul-
smelling sputum with hectic body tem-
perature. Roentgenologically the inline of
the cavity is poorly defined, it contains
a visible sequesters that look as a poly-
morphous shadow. The adjacent pulmo-
nary tissue is infiltrated (fig. 1.1.3).
The clinics of a pulmonary gan-
grene differs by terminal expression of
signs. The state of the patients is critical.
The patient is adynamic, exhausted, with
edemas on legs. Dyspnea in rest, hemo-
dynamic disturbances are evident. Dirty-
grey or brown sputum with detrites,
pieces of necrotic parenchyma and
threads of blood excretes out with the
cough up to 1 littre. Early pleural com-
plication, such as pulmonary bleeding,
is usual and may be profuse. Often it is
associated with vital organ dysfunction
and loss of consciousness.
The intensive shadow which occupies a considerable area of lungs
with a visible cavities, that contain sequesters, fluid levels, is roentgeno-
logically revealed. The shadow outline is irregular, but could be well de-
fined if the process is within interlobar sulcus (fig. 1.1.4).
Fig. 1.1.2. Acute abscess of the lower lobe
of the right lung.
Fig. 1.1.3. Gangrenous abscess of the
lower lobe of the left lung.
1.1. Lungs and pleura 13
A
Fig. 1.1.4. Right-side pulmonary gangrene.
Plain roentgenogram, direct view (A).
Tomogram (B). В
Chronic lung abscess 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 out
of 250-500 ml of a purulent foul sputum, chest pain, dyspnea, hectic
temperature with the difference in 1,5-2°C. Dizziness, suppression of ap­
petite, general weakness increases according to intoxication. The skin is
pale with moderate cyanosis. The respiratory rate rises to 28-30 per min. In
6-8 months 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). Percussion reveals a
short sound in projection of pathological process, auscultation - a lot of
moist rales on the background of amphoric respiration.
Roentgenologically chronic abscess is shown by one or several cavities
of a spherical shape with a thick, dense pyogenic sheath. Exacerbation of
the process manifests by a cavity with horizontal air-fluid level. The size of
surrounding perifocal infiltration depends on the phase of the process
The blood analysis in pulmonary destruction is characterized by leu­
kocytosis with deviation of the differential count to the left, lymphocy­
topenia, elevation of the erythrocyte sedimentation rate. Gangrenous change
of the process is accompanied by a progressing anemia, sometimes by
leukopenia. The hypoproteinemia arises from major losses of protein with
purulent sputum. Intoxication and toxic lesion of liver leads to disproteinemia.
It is associated with the enlarged concentration of mucoprotein, sialine
acids, seromucoid, and fibrinogen.
(fig. 1.1.5).
14 1. Thoracic surgery
Fig. 1.1.5. Chronic abscess of the right lung. Plain roentgenogram, direct view (A). Fragment
of the computer tomogram (B).
The immunogram reveals the suppression of cellular and humoral
immunity with a liability to hyperergy and autoaggression, depression of
nonspecific protection mechanisms.
The cytological bronchial water lavage is characterized by expressed
neutrocytosis, noncellular postdestructive insertions at lack or absence of
alveolar macrophages.
Variants of clinical course and complications
According to the clinical course, there are such variants of the devel-
opment of purulent diseases of lungs:
1. Favorable course. The adequate treatment results in prompt positive clini-
cal, roentgenological and laboratory dynamics, and ends by recovery.
2. Non-progressive course. A poor drainage of the suppurative focus and
permanent purulent intoxication results in transferring of the process
in chronic form.
3. Progressing course. Is predetermined by combination of a series of un-
favorable factors (low resistance of the organism, autoimmune ag-
gression, high virulence of the infecting agent etc.). Characterized by
diffusion of the zone of necrosis and destruction with transferring in
gangrene.
4. Incapsulated process. Caused by the absence or complete obstruction of
the draining bronchus under condition of satisfactory resistance of the
organism.
5. Complicated course. Mostly is the result of progressive development of
the pathological process.
1.1. Lungs and pleura 15
Pulmonary bleeding arises suddenly, and associated with coughing
out of a foamy, bright-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 manifestation of a pulmo-
nary suppuration is accompanied by dizziness, weakness, dyspnea, chest
pain. The hemodynamic disturbances depend on intensity of the bleeding.
The auscultation of lungs reveals the moist rales (aspiration) on both sides.
If the pulmonary destruction is present the plain film of the chest shows
the localization of the source of bleeding. After hospitalization of the
patient with this complication the exclusive information is obtained with a
fibrobronchoscopy.
According to the degree, the pulmonary bleedings are classified
(V.Struchkov, 1985):
I degree - hemorrhage to 300 ml.
1. Single hemoptysis.
2. Multiple hemoptysis.
II degree - hemorrhage to 700 ml.
1. Single bleeding:
a) with falling of arterial pressure and decreasing of hemoglobin;
b) without falling of arterial pressure and decreasing of hemoglobin.
2. Multiple bleeding:
a) with falling of arterial pressure and decreasing of hemoglobin;
b) without falling of arterial pressure and decreasing of hemoglobin.
III degree - hemorrhage exceeds 700 ml.
1. Massive bleeding.
2. Fulminant, lethal bleeding.
The I degree of a pulmonary bleeding manifests by coughing out the
sputum tinged with blood, the hemodynamic disturbance usually absent.
The bleeding of II degree is characterized by decreasing of arterial pres-
sure on 20-30 mm Hg, tachycardia to 100 beats/min, contents of hemo-
globin within 60-80 g/1. The bleeding of III degree are accompanied with
sharp decreasing of arterial pressure, rapid (more than 100-120 beats/
min), small, sometimes thread pulse, and even its disappearance on pe-
ripheral arteries, tachypnea to 40 per 1 min, hemoglobin to 50-60 g/1.
Possible the fulminant course up to the terminal state with prompt failure
of cardiac activity and asphyxia by blood.
Sepsis manifests by multisystem lesion with progression of the syn-
drome of polyorganous failure, hematosepsis, purulent metastasizing (fre-
quently in brain).
Characteristic complications for lung suppurative diseases such as pleu-
ral empyema and pyopneumothorax are described in separate parts.
16 1. Thoracic surgery
The diagnostic program
Complaints and anamnesis.
Physical findings.
X-ray examination of chest in two planes (direct and lateral).
Tomogram of lungs.
Examination of the sputum (bacteriological, cytological).
General blood and urine analyses.
Biochemical blood analysis (protein and its fractions).
Immunogram.
Fibrobronchoscopy.
Differential diagnostics
The central lung cancer due to the bronchial obturation results in
atelectasis of a lung segment or lobe, with probable further abscessing.
For the differentiation used tomography, which reveals the bronchial ob-
turation by tumour, lesion of central lymph nodes), cytological examina-
tion of sputum and bronchial outwashes. The determinant role belongs to
fibrobronchoscopy with a biopsy and verification of the diagnosis.
The peripheral lung cancer with destruction on tomograms is charac-
terized by cavity with irregular inner surface, which external outline con-
nects with root of the lung because of lymphatic metastatic spreading.
The central lymph nodes frequently enlarged. The diagnosis is improved
by results of transthoracic puncture or catheterizing biopsy with cytologi-
cal investigation, fibrobronchoscopy. If it is impossible to confirm the di-
agnosis the thoracotomy is indicated.
The tubercular cavern is mainly located in the upper lobes of lungs,
roentgenologically revealed on the background of characteristic changes
of adjacent pulmonary tissue (calcification, dissemination), sometimes a
draining bronchus is detected. In the sputum mycobacteria of tuberculosis
are frequently found.
The suppurative cyst of lungs differs by a gradual onset, slow course
of the suppuration, less expressed intoxication. Roentgenologically its cav-
ity has the oval or rounded shape with a thin sheath and regular contour.
Perifocal infiltration is not characteristic.
Tactics and choice of treatment
The tactics in acute pulmonary destruction should be mainly conser-
vative.
1. The adequate antibacterial, antiinflammatory therapy consists of
intravenous introduction of antibiotics of a wide spectrum activity.
1.1. Lungs and pleura 17
With the purpose of maximal concentration of drugs in the patho-
logical focus applied:
- Injection of antibiotics in the vessels of a pulmonary circulation by
means of catheterization of central veins, pulmonary artery;
- Introduction of medicines into respiratory tracts (in the second stage) - through
the endotracheal microirrigator, nasogastric tube, during bronchoscopy, en-
doscopic catheterization of the abscess cavity through the draining bronchus,
during aerosolic inhalations. The composition of medical admixtures includes:
antibiotics, antiseptics (10 % dimexid, dioxydin, microcid etc.), enzymes;
- Transcutaneously in the focus of destruction by means of puncture
or draining with the usage of physical antiseptics.
- Intrapleural injections;
- By means of electrophoresis.
2. 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.
3. Detoxycation therapy (intra- and extracorporal).
4. Immune correction (under the control of immunogram):
- Active - staphylococcal anatoxin;
- Passive - specific gamma-globulins, hyperimmune plasma;
- Non-specific (pirimidine and purine derivates, drugs of thymus gland,
splenin, levamisol,).
5. Homeostatic correction (oxygenotherapy, correction of anemia,
hypoproteinemia, acidosis, microcirculatory disturbance).
6. Desensitizing, antiinflammatory therapy, regulation of proteases
activity: antihistamine, nonsteroid antiinflammatory agents, inhibitors of
proteases, antioxidants.
7. Correction of the organ and system dysfunction, prevention of
complications, symptomatic therapy.
Indications for operative management in acute destructive processes
of lungs:
- Pulmonary bleeding of II-III degree;
- Progression of the process despite active and appropriate therapy;
- Tension 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 systemic functions in
the terminal stage, bilateral purulent destruction of lungs, concomitant
incurable malignant tumours.
18 1. Thoracic surgery
Operational incisions - anterolateral (fig. 1.2.16), lateral (fig. 1.2.17)
and posterolateral (fig. 1.2.18) thoracotomy. The operation suggests seg-
mental, polysegmental resection, lobectomy, bilobectomy, combined in-
tervention (with the decortication, pleurectomy).
The patients with chronic abscesses should undergo the operative
treatment after complete liquidation of exacerbation.
In a pulmonary gangrene the stabilization of the process on the back-
ground of active conservative treatment allows in future to apply conserva-
tive tactics up to recovery or making optimal conditions for operation (liqui-
dation of intoxication, aggressive panbronchitis, diffuse infiltration of the
parenchyma, pleural complications). The headlong progression of the gan-
grene during first days, despite the active correction, occurrence of pulmo-
nary bleeding requires urgent performance of operative management. Vol-
ume of the operation - pneumonectomy, bilobectomy, lobectomy.
1.1.2. Lung Cysts
The cysts of lungs are the thin-walled cavitary formations, filled
with air or liquid contents.
Inherent and acquired cyst are distinguished.
Etiology and pathogenesis
Inherent cysts arise from the abnormalities of the development of
lungs under the influence of multiple chemical, physical and biological
factors. They can develop from a bronchial tree (bronchial) or from alveolar
tissue (alveolar). Their occurrence resulting from the delay of the develop-
ment of peripheral parts of bronchus with its expansion or agenesia of
alveoli with dilatation of terminal bronchioles. Congenital cysts at first
develop and grow as secretory formations. After communication with bron-
chus they finally form as air or hydroair cavities.
Acquired cysts are represented by fibrous cavities, which remain
after abscesses, tubercular caverns, echinococci, posttraumatic intrapul-
monary hematomas. The degenerative changes in the wall of bronchus
with obliteration of its lumen by a cloggy secret as athe result of repeated
inflammatory processes lead to occurrence of acquired retentional cysts.
Pathology
Congenital cyst can be located in any part of lungs. The walls of
bronchogenic cavities contain chaotically disposed elements of bronchus
(cartilagous plates, muscle fibers, mucous glands), they are lined from
1.1. Lungs and pleura 19
inside by cylindrical or cubic epithelium. Squeezed alveolar cells line the
walls of alveolar formations.
The acquired cyst revealed in the site of previous diseases. Its walls
mainly consist of connective tissue. Epithelization is possible due to trans-
ferring of the epithelium from a draining bronchus at long existence.
The cysts could be uni- or multichamber, closed and open (depend-
ing on the presence of communication with bronchus).
Classification
According to the etiology:
- congenital;
- acquired.
According to displacement:
- single, multiple;
- unilateral, bilateral.
Complications:
- Suppuration;
- Appearance of the valvular mechanism;
- Bleeding;
- Burst into pleural space (pneumothorax, pyopneumothorax, pleu-
ral empyema);
- Malignancy.
Symptomatology and clinical course
Clinical manifestations of uncomplicated pulmonary cysts are vague.
Sometimes patients complain of a chest pain, periodic cough, and inflam-
matory diseases of respiratory tract in history. In children the signs are
rather expressed, the dyspnea associates with the compression of airways.
In great, superficially disposed cysts revealed delayed respiratory
movements on affected side during breathing.
On palpation - weakened vocal fremitus.
On percussion - short or bandbox sound, depending on contents.
On auscultation - weakened respiration, over the huge open cavi-
ties — amphoric.
On plain chest films the closed congenital cyst forms a homoge-
neous shadow of the spherical or oval shape of average intensity with
rather regular edge on the background of an intact pulmonary tissue.
During roentgenoscopy sometimes observed the change of its shape
depending on the phase of breathing - elongation during inspiration
(Escudero's syndrome). The character of the shadow is better to study
on tomograms.
20 1. Thoracic surgery
Acquired retentional cyst is
roentgenologically shown by a shadow
of irregular shape (piriform, spindle-
shaped etc.), that displays the shape
of the distended bronchus. The adja-
cent tissue, as a rule, changed due to
bronchiectases, pneumosclerosis, etc.
Open cysts are observed as thin-
walled, good defined cavities of an-
nular or oval shape (fig. 1.1.6).
The bronchogram in congenital
cysts reveals hypoplasia of segmental
or lobar bronchus, lack of bronchial
bifurcations, which tends to bone.
Sometimes observed bronchiectases in
the neighboring parts of lungs. A cys-
tic cavity is infrequently defined.
The angiopulmonography reveals deformation of vascular branches,
which circumflex the cyst.
Fig. 1.1.6. Cyst of the right lung.
Variants of clinical course and complications
The suppuration of the closed cysts resembles the development of a
lung abscess with lesser expression of signs of intoxication (protective role
of epithelial wall).
Infection of the open cysts is characterized by a gradual long course,
moderate manifestation of suppuration and late intoxication.
The tension (valvular) cysts occur more often in children. They are
characterized by severe respiratory and hemodynamic disturbances, up to
terminal, as the result of inflexion of venous trunks, shift of mediasti-
num and compression of lungs. The predominant signs are increased dys-
pnea, cyanosis, chest pain, respiratory lag on affected side, absence or
weakening of respiration on auscultation, bandbox percussion sound over
the cavity.
Pleural complications of pulmonary cysts, and also bleeding de-
scribed in the relevant parts.
The malignant degeneration of pulmonary cysts occurs very rarely.
The diagnostic program
1. Complaints and history of the disease.
2. Physical methods of examination.
3. Chest X-ray film in two planes.
1.1. Lungs and pleura 21
4. Lung tomography.
5. Bronchography.
6. Angiopulmonography.
7. General blood and urine analyses.
Differential diagnostics
Lung abscess, in contrast to a suppurative cyst, is characterized by
prompt course, expressed purulent intoxication, roentgenologically its wall
is irregular, with proper considerable perifocal infiltration.
Lung cancer with destruction differs by a thick wall with a tuberous
inner surface, phenomena of lymphangitis in adjacent tissue. The deter-
minant value has endoscopic examination or puncture with a biopsy and
following morphological investigation.
Tubercular cavern is commonly located in the upper lobes, in adja-
cent tissue revealed fibrosis, petrifactions, dissemination, peribronchial
lymphadenitis. In the sputum - mycobacterium of tuberculosis.
Opposite to cyst, in termed diseases, the circumflex deformation of
vascular branches are never observed on angiopulmonography.
The considerable difficulties can arise during differentiation of the
closed congenital cysts.
Tuberculoma differs from them by characteristic localization. On X -
ray examination the heterogenity of the shadow with calcifications, early
excentric destruction, "tubercular" background is observed.
Benign tumours sometimes possible to differentiate only after the
results of cytological investigation of punctate or after the operation.
Echinococcal cyst on tomogram has a double contour of chitinous
and fibrous sheaths. In blood analyses observed eosinophilia. The final de-
cision is taken out after the results of immunological (indirect
microagglutination test) and allergic (Cacconi's reaction) tests.
Huge cysts, in contrast to open air cysts, are characterized by a
subpleural location.
The diagnostic doubts at suspicion on a diaphragmatic hernia are
solved by radiopaque examination of a gastrointestinal tract.
The acquired cysts differ from congenital by roentgenological signs
of the lesion of surrounding tissues (pneumofibrosis, deforming bronchi-
tis, secondary bronchiectases, and calcifications). Postpneumonic cavities
are of irregular shape, with grooves and pockets, their walls of different
thick. During bronchography they filled through some small bronchi. Some-
times the verification is possible only after postoperative morphological
investigation.
22 1. Thoracic surgery
Tactics and choice of treatment
The pulmonary cysts require the surgical treatment. In case of com-
plications the indication for operation becomes absolute. Contraindications:
the severe respiratory disturbance, concomitant malignant nonresectable
tumors, vital organs dysfunction in the stage of permanent decompensa-
tion, elderly age of the patients.
The volume of the operation: if adjacent pulmonary tissue is in-
tact - cystectomy, otherwise - segmental or wedged resection, lobec-
tomy.
The conservative therapy is applied in suppuration of cysts with the
purpose of preoperative preparation. It is the similar, which applied for
lung abscesses.
1.1.3. Pleural empyema
The pleural empyema is a purulent inflammation of its visceral and
parietal membranes, which associated with accumulation of pus in a pleu-
ral space.
Etiology and pathogenesis
The causes of acute pleural empyema are inflammatory, or puru-
lent, destructive processes of lungs, abscesses of abdominal cavity (sec-
ondary pleural empyema), open and closed damages of chest, and also, in
some cases, surgical operations on thoracic organs (primary pleural empy-
ema).
A secondary pleural empyema occurs in 88 % of the patients. Thus
develops fibrinous, exsudative, and then purulent pleurisy.
If empyema is caused by pulmonary gangrene, purulent mediastini-
tis, subphrenic abscess, the stage of exsudative pleurisy is extremely
short. The progression of the process results in transferring of focal pleu-
ral empyema into wide-spread.
Pathology
Macroscopically pleura is thickened, covered by pus with punctate
hemorrhages. Microscopically it is diffusely oozed with neutrophils. In cases,
when the empyema overcome into chronic course, the pleura deposits the
calcareous salts, thick pus encapsulates, sometimes with the development
of fistula.
1.1. Lungs and pleura 23
Classification
I. According to the etiological factor:
1. Specific.
2. Nonspecific.
II. According to the pathogenic factor:
1. Primary.
2. Secondary.
III. According to the clinical course:
1. Acute.
2. Chronic.
IV. According to extension of the process:
1. Focal.
2. Wide-spread.
V. According to the presence of lung destruction:
1. Empyema with destruction of pulmonary tissue.
2. Empyema without destruction of pulmonary tissue.
3. Pyopneumothorax.
VI. According to communication with environment:
1. Closed pleural empyema;
2. Open pleural empyema:
• bronchopleural fistula;
• thoracopleural fistula;
• thoracopleurobronchial fistula;
• cribrate lung.
Symptomatology and clinical course
The clinics of acute pleural empyema depends on extension of the
process, reactivity of the organism and presence of complications.
The pain is the sign, which denote the involvement of pleural mem-
branes in the process. Its intensity increases depending on depth of respi-
ration and body position.
The dyspnea arises from accumulation of a purulent content in a pleu-
ral space and exception of particular volume of 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 destruc-
tive process in a pulmonary tissue.
Fever to 39-40°C, headache, sleeplessness, general malaise, and an-
orexia - all these are the manifestation of intoxication.
The forced patient's position and restriction of breathing should be
considered as outcomes of a pain syndrome. The extension of pleural em-
pyema causes the swelling of thoracic wall, smoothing of intercostal spaces.
24 1. Thoracic surgery
On 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. By percussion over the
exudate it is possible to reveal short sound with oblique upper contour.
Above the exudate - tympanic sound resulting from consolidation of pul­
monary tissue. On auscultation - diminished or absent sound in a great
amount of exudate.
The predominant roentgenological sign of a focal or wide-spread
empyema - the presence of exudate. In localized acute pleural empyema
observed a local intensive homogeneous shadow. Roentgenologically ac­
cording to localization distinguished such types of a focal empyema:
1) apical;
2) paramediastinal;
3) parietal;
4) interlobar;
5) ері phrenic.
The wide-spread pleural empyema manifests by intensive homoge­
neous shadow in a basal parts with oblique upper contour (Damuaso' line).
The diaphragmatic dome is failed to observe. The more pus is in pleural
space, the higher upper border of the exudate (fig. 1.1.7).
А В
Fig. 1.1.7. Left-side pleural empyema.
Variants of clinical course and complications
The clinic of a focal pleural empyema depends on the site of the
process. The apical empyema, due to involvement of a vascular-nervous
fascicle in the process, manifests by intensive pain. The soft tissues of
supraclavicular region are swelled. The percussion and auscultation has no
information.
1.1. Lungs and pleura 25
The pain syndrome in parietal (paracostal) empyema is more expressed.
Thoracic excursion is restricted. The diminishing of respiratory sound can
be detected over the exudate.
The chief complaint in paramediastinal empyema is the heart pain.
The location of the process in the upper mediastinum can cause the supe­
rior vena cava syndrome. The physical findings are vague.
In case of basal (ері phrenic) empyema the patients complain of pain
in subcostal area, which increases at respiration and irradiates in supra­
clavicular region. In some cases the pain irradiates in epigastric region. The
palpation of intercostal spaces and hypochondrium is painful.
The clinical course of postoperative empyema depends on the char­
acter of operative approach (marginal resection of lung, lobectomy,
pneumonectomy, operation on esophagus) and infection of the pleural
space.
The clinical manifestation of posttraumatic empyema depends on the
size of the damage of chest, lungs, mediastinal organs and complications
(suppuration, hemothorax).
The involvement in the purulent process of a pulmonary tissue re­
sults in fusion of a pleural membranes with formation of a bronchial or
thoracopleural fistula (discharge of abscess through thoracic wall).
The inappropriate elimination of empyema results in chronic course,
cribrate lung and pleurogenic cirrhosis of lungs.
The diagnostic program
Complaints and history of the disease.
Physical findings.
Data of chest X-ray (in two planes, if necessary - laterography).
Pleural puncture.
The microbiological investigation of the exudate for its sensivity
to antibiotics.
General blood and urine analyses.
Biochemical blood analysis.
Pleurography (in transferring of the process into chronic form).
Differential diagnostics
Pleuropneumonia complicated with exsudative pleurisy in some cases
resembles acute pleural empyema: a chest pain, fever, dyspnea, cough,
and general weakness. The chest roentgenogram reveals hydrothorax
(exsudative pleurisy, pleural empyema, hemothorax). The chief diagnos­
tic method for differentiation is the thoracentesis. The presence of a serous
(lucent, bright-yellow) exudate testifies about the pleuropneumonia, com-
1.
2.
3.
4.
5.
6.
7.
8.
26 1. Thoracic surgery
plicated with pleural effusion, and cloudy, foul-smelling exudate of white
or greenish color - about acute empyema.
The major difficulties in differential diagnostics are caused in case of
limited forms of empyema.
Pancoast cancer clinically and roentgenologically in most cases has
almost the similar course to apical form of empyema. The transthoracic
biopsy allows to confirm the diagnosis.
Acute cholecystitis is necessary to differentiate with the ері phrenic
empyema. The pain in the right hypochondrium, fever, phrenic symptom
are common for both diseases. However the objective findings, X-radiog-
raphy of chest and the thoracentesis allow to differentiate these patho­
logical processes.
Tumour of anterior mediastinum complicated by superior vena cava
syndrome is necessary to differentiate with paramediastinal empyema. Nev­
ertheless the body temperature in such patients, as a rule, is normal. The
upper cavography is possible to find out the shift of cava vein and its
irregular contours (filling defect) due to growth of the mediastinal tumour.
There are some difficulties in differential diagnostics of empyema
with a posttraumatic diaphragmatic hernia. Such X-ray findings as defor­
mation of diaphragm, additional shadows with a fluid level, intestinal
loop suggest a diaphragmatic hernia. A laterography and contrast study of
gastrointestinal tract is basic in differential diagnostics of this disease.
Atelectasis of a lung segment, or lobe in some cases can cause
misdiagnostics. Except X-ray chest examination (in two planes and tomog­
raphy), these situations require necessity of diagnostic bronchoscopy, which
reveals the cause of bronchial obturation (foreign body, endobronchial
cancer etc.).
Tactics and choice of treatment
The presence of pus in a pleural space is the indication for its elimi­
nation. In the site of diagnostic thoracentesis performed the draining of
empyema's cavity, its sanation by means of antiseptic solutions. In a focal
empyema the aspiration of pus is carried out by thoracentesis and only in
its inefficiency performed a draining of pleural space.
Intensive antibacterial and antiinflammatory therapy should be im­
mediately instituted. For general improving used detoxication therapy (in­
fusion of saline solutions, hemotransfusion, transfusion of proteins, solu­
tions of dextran, forced diuresis, hemosorption if necessary), therapy for
increasing of immunological resistance of the organism.
The empyema's sanation decreases the amount of pus, which dis­
charged out through the drainage. The optimal variant of such course is
the liquidation of empyema's cavity, then the drainage must be removed.
1.1. Lungs and pleura 27
Transition of the process into the chronic form (10-12 weeks) results
in formation of a residual empyema's cavity, which is possible is to reveal
by means of pleurography - introduction through the drainage of water-
soluble contrast with the further X-radiography in two planes.
Operative approach is applied when the process has transited into the
chronic form, that is in the case of residual empyema cavity. The volume
of the operation - pleurectomy, decortication of lung.
A bronchial fistula and great empyema cavity requires the perfor-
mance of lung resection and corrective thoracoplasty.
1.1.4. Pyopneumothorax
Pyopneumothorax is the burst of lung abscess into pleural space,
which is accompanied by purulent inflammation of pleural membranes
with a collapse of lung.
Etiology and pathogenesis
Peripheral location of the purulent focus in a pulmonary tissue re-
sults in destruction (fusion) of visceral membrane. As a result of, the pus
and air penetrate into a pleural space that leads to a purulent inflammation
of parietal and visceral membranes of pleura. The disorder of a pleural
continuity results in a lung collapse.
Among other causes of pyopneumothorax are the chest trauma, which
results in collapse of lung, infection and purulent inflammation of pleural
membranes.
As the basic causes of pyopneumothorax are considered:
- acute abscess of lung;
- gangrenous abscess of lung;
- lung gangrene;
- purulent lung cyst;
- abscessing pneumonia;
- bronchiectatic disease;
- subphrenic abscess, which has effluencedinto pleural space;
- injury of esophagus;
- mediastinitis;
- chest trauma;
- operation and diagnostic manipulations on chest organs.
28
Pathology
1. Thoracic surgery
Morphologically pus and air are present in pleural space in pyopneumothorax.
In lungs revealed subpleural purulent or necrotic foci, which connected with a
pleural space through a pleuro-pulmonary fistula. From the outside the zone of
disrupture is restricted by perifocal inflammation. In the draining bronchus it is
possible to see manifestations of deforming, frequently polypous bronchitis.
Classification
I. According to the etiological factor:
1. Specific.
2. Nonspecific.
II. According to the pathogenic factor:
1. Primary.
2. Secondary.
III. According to the clinical course:
1. Asymptomatic form.
2. Mild form.
3. Acute form.
IV. According to extension of the process:
1. Localized pyopneumothorax:
a) parietal;
b) apical;
c) ері phrenic;
d) paramediastinal;
e) polychamber.
2. Subtotal pyopneumothorax.
3. Total pyopneumothorax.
4. Tension pyopneumothorax.
Manifestation and clinical course
The manifestation of pyopneumothorax depends on the size of the
focus of destruction, which influences on the degree of lung collapse, and
on amount of purulent content in a pleural space.
The pain owing to the burst of destructive focus into pleural space
often arises suddenly.
The dyspnea occurs as a result of lung collapse owing to leakage of
pus and air into pleural space. Its expression is in direct ratio to lung col­
lapse. Therefore a dyspnea in rest observed in a subtotal and total pyop­
neumothorax. It sharply amplifies even at minor physical activity. Auxil­
iary muscles take part in order to force respiration.
1.1. Lungs and pleura 29
The expectoration of sputum with ichorous smell is the outcome of
destructive process in a pulmonary tissue. Its amount decreases after effu-
sion of pus into pleural space.
Hectic fever is caused by enlargement of the area of resorption. The
patients are adynamic, flaccid. Some of them are unconsciousness.
On objective examination the position of patients is forced, they sit
leaning upon the bed (subtotal, total pyopneumothorax). The affected
hemithorax takes no part in respiration.
On palpation - diminished vocal fremitus on the side of lesion.
Percussion reveals a sharp shortening of sound over the zone of
exudate and bandbox sound above the region of collapsed lung.
On auscultation there are no breathing sounds on the affected side.
In case of localized pyopneumothorax - weakened or sharply weakened
sound with a bronchial or amphoric tone.
The X-ray picture of pyopneumothorax depends on its form, but
the obligatory sign is the air-fluid level in a pleural space with well-de-
fined edge of collapsed lung on its background (fig. 1.1.8).
Fig. 1.1.8. Left-side total pneumothorax, represented by air-fluid level in the pleural space
and well-defined edge of the collapsed lung.
Variants of clinical course and complications
The clinical course of pyopneumothorax depends on adhesions be-
tween pleural membranes. It sometimes changes typical clinical course of a
total lung collapse. The manifestation of the disease depends also on amount
of a purulent exudate. Therefore, according to extension of the process and
size of lung destruction, distinguished acute, mild and asymptomatic forms
of pyopneumothorax. Especially difficult for diagnostics is the asymptomatic
form of localized pyopneumothorax. Dyspnea for such pathology is not char-
acteristic, as the adhesion of membranes prevents complete collapse of
lung. Dyspnea is vague or absent at all in partial collapse. A diminished vocal
ЗО 1. Thoracic surgery
fremitus on the side of pathological process, shortening of percussion sound
and weakened or sharply weakened breathing sounds over the collapsed
lung and exudate are revealed. Roentgenological manifestation in localized
pyopneumothorax not expressed and include horizontal fluid level, margin
of partially collapsed lung and minor air in the pleural space.
In most cases after the effkuence of the destructive focus into a
pleural space and lung collapse observed the closure of bronchopleural
fistula. Nevertheless the inflammatory process in a pulmonary tissue and
pleural space is going on.
The diagnostic program
1. Complaints and history of the disease.
2. Physical findings.
3. Chest X-radiography examination.
4. Thoracentesis.
5. Pleurography.
6. Bacterial culture and antibiotic sensitivity.
7. General blood, and urine analyses.
8. Biochemical blood analysis.
Differential diagnostics
They're no special necessity for differential diagnostics of pyopneu­
mothorax in the majority of patients. History (presence of the purulent
focus in a pulmonary tissue), clinical course (acute pain and dyspnea in
abscess burst into pleural space), and also chest X-ray findings and thora­
centesis frequently reliably permit to make the diagnosis.
In some cases a localized pyopneumothorax according to clinical course
resembles a huge acute abscess of lungs. But the differences of roent­
genological symptomatology allow to verify these pathological processes. In
acute lung abscess the cavity of destruction localized in a pulmonary pa­
renchyma, it is round in form with horizontal fluid level and expressed
perifocal infiltration.
Tactics and choice of treatment
The purpose of treatment should include sanation of the destructive
focus in pulmon ary tissue and liquidation of complications; that means elimi-
nation of pus and air from a pleural space and prompt expanding of lung.
1. Active sanation of tracheobronchial tree by means of tracheocentesis.
2. Draining of pleural space, active aspiration of its content (air, pus) to
expand the lung.
1.1. Lungs and pleura 31
3. Lavage of pleural space by antiseptic solutions.
4. Appropriate antibacterial, antiinflammatory and infusion therapy.
5. The therapy for increasing of immunological resistance of the organism
(staphylococcal anatoxin , antistaphylococcal gamma-globulin,
antistaphylococcal plasma).
6. Endolymphatic introduction of immunity stimulators (thymalin,
thymogen, T-activin).
The indications for operative management are the same, as in pleural
empyema.
1.1.5. Spontaneous pneumothorax
Spontaneous pneumothorax is the entry of air in a pleural space with
the further lung collapse, which not associated with traumatic damage of
chest or pulmonary tissue.
Etiology and pathogenesis
As a result of spontaneous disrupture of lung blebs and subpleural
air cysts the damage of pleural visceral membrane occurs. It causes entry
of air in pleural space. Owing to its leakage the elastic pulmonary tissue
collapses. The degree of the collapse depends on amount of air, that has
penetrated a pleural space.
Pathology
Morphologically in spontaneous pneumothorax found out a focal bullous
emphysema with disrupture of blebs, subpleural air cyst, and also disor-
ders, which have caused disturbances of ventilating ability of bronchi. It
can be bronchitis, pneumosclerosis, tuberculosis and fibrous alveolitis.
Classification
The pneumothorax can be:
1. Unilateral or bilateral.
2. Partial (lung collapse less 1/3 of its volume).
3. Subtotal (lung collapse less 2/3 of its volume).
4. Total (lung collapse exceeds 2/3 of its volume).
5. Tension or valvular (complete collapse of lungs and shift of mediasti-
num to the opposite side).
6. Rigid (neglected pneumothorax with thickened visceral pleura).
32
Manifestation and clinical course
1. Thoracic surgery
The onset of the disease is sudden. The patient's state and expression
of clinical manifestation depends on amount of air, which has entered the
pleural space. Usually in normal conditions, and sometimes after physical
activity, the patients suddenly feel sharp pain on the side of lesion, dys-
pnea, pain in the heart region and heartbeating. Acrocyanosis or total c y -
anosis of skin is observed. The circulatory disturbance depends on the
degree of hypoxia. Intensity of pain and dyspnea gradually decreases, but
a dry troubling cough appears.
Examination of the chest allows to observe expansion of intercostal
spaces and restriction of respiratory excursion. On palpation - diminishing
of vocal fremitus on the affected side. On percussion a chief sign of pneu-
mothorax is the tympanic sound. Auscultation reveals weakened or sharply
weakened breathing sounds. The cardiac tones are muffled, tachycardia.
Fig. 1.1.9. Pneumothorax. Right-side partial
pneumothorax (A), right-side subtotal
pneumothorax (B), right-side total
pneumothorax (C).
1.1. Lungs and pleura 33
The diagnosis of spontaneous pneumothorax is confirmed by X-ray
examination. On the plain roentgenogram the air is present in pleural space,
and the margins of collapsed lung are found out on its background (fig. 1.1.9).
Thoracoscopy in pneumothorax possible to find out subpleural blebs of
different sizes (0,5-3 cm), which are mainly disposed on the apex of lung.
Variants of clinical course and complications
The atypical (asymptomatic) spontaneous pneumothorax occurs in 20 %
of the patients, and mainly revealed by X-ray examination. In most cases
it is the partial pneumothorax.
The expressed pain syndrome and dyspnea, resulting from collapse
of lung, characterizes subtotal and total pneumothorax.
The tension spontaneous pneumothorax is the most severe form of
pneumothorax. It manifests by sudden onset, progressive increase of dys-
pnea, expressed cyanosis. The breathing is superficial, rapid, with active
participation of auxiliary muscles. Mediastinal shift and flexion of vessels
results in disturbance of cardiac activity up to the cardiac arrest, and
requires urgent management.
Rigid pneumothorax (rigid lung). The neglected pneumothorax causes
fibrinous exsudative pleurisy. On the surface of lung (visceral pleura) com-
missures are formed, that give no opportunity for lung expansion. The
presence of residual pleural cavity and progressive development of a pu-
rulent infection results in occurrence of acute pleural empyema. In such
cases the patients complain of the fever to 38-38,5°C, general weakness
and increasing dyspnea. The phenomena of intoxication are evident. Thus
such patients require the treatment of pleural empyema.
The diagnostic program
1. Complaint and anamnesis of disease.
2. Physical findings.
3. Plain chest film (direct and lateral projection).
4. Thoracentesis.
5. Thoracoscopy.
6. Tomography of lungs.
Differential diagnostics
Pleural effusion. This pathology manifests by more gradual onset. As
opposite to pneumothorax, the complaints of chest pain predominate above
the complaints of dyspnea. Frequently such patients specify on previous
undercooling.
34 1. Thoracic surgery
As well as the spontaneous pneumothorax, the pleural effusion is char-
acterized by diminishing of vocal fremitus, dullness of percussion sound,
weakened or absent breathing sounds over the exudate. Nevertheless in the
plain roentgenogram in such cases observed a homogeneous intensive shadow
of a pleural space with oblique upper contour. The puncture of pleural
space enables finally to confirm the diagnosis of pleural effusion.
Intercostal neuralgia. A predominant sign in clinical pattern is acute
pain, which intensifies at physical activity, changes of body position and
body movements, at deep breathing. The localization of pain coincides
with zone of innervation of intercostal nerves.
Examination and chest X-radiography reveals no pathological changes.
Tactics and choice of treatment
Conservative treatment is applied in the patients with a partial pneu-
mothorax. Thus thoracentesis in II intercostal space in the midclavicular
line with aspiration of air is performed. The cases of its inefficiency, and
also subtotal, total and tension pneumothorax require the draining of a
pleural space with active aspiration of air.
The operative management is necessary, if there is no efficiency
from active aspiration (in incomplete expansion of lung), recurrent of
course of the process, presence of great subpleural blebs and rigid pneu-
mothorax. The volume of operation depends on extension of the process:
liquidation of alveolar fistula, wedged resection of lung or lobectomy.
1.1.6. Lung Cancer
The tumour arises from epithelium of bronchi, bronchial mucous
glands, and also terminal bronchioles.
Etiology and pathogenesis
It is well established that the dominant risk factor for lung cancer is
cigarette smoking.
The risk increases with the number of cigarettes smoked daily, the
duration of smoking, young age at onset of smoking, degree of inhala-
tion, the tar and nicotine content and the use of unfiltered cigarettes. Also
other types of smoking including passive smoking, and occupational ex-
posures to carcinogenic agents such as asbestos fibers, arsenic compounds,
chromium compounds, mustard gas, nickel compounds, ionizing radia-
tion, tars and some mineral oils, are associated with the risk of developing
lung cancer. A synergistic interaction has been observed for asbestos, ion-
1.1. Lungs and pleura 35
izing radiation, and arsenic compounds in combination with tobacco smok-
ing, in such a way that the combined exposure is associated with a lung
cancer risk that for exceeds that expected from the separate exposure to
each of the agents.
The contributing factors:
a) Chronic obstructive diseases of lungs;
b) Other chronic diseases of lungs (chronic fibrosis);
c) Lung scars.
Histopatology
More than 95% of bronchial tumors can be classified into four major
cell types: small cell carcinoma squamous cell carcinoma, adenocarcinoma
and large cell carcinoma. The remaining 5% include mesothelional and
carcinids. The frequency of small cell carcinoma seems rather constant
(20-30%), whereas the variations in frequency for the rest types are differ-
ent. For practical and therapeutic purposes these tree types are commonly
referred to as non-small cell lung cancer.
Classification
Lung cancer is divided into central, peripheral and atypical cancer.
Central cancer includes the tumours of the first-third order bronchi. Ac-
cording to the loco-regional spread it is divided into endobronchial and
peribronchial cancer making a great influence on the roentgenological pic-
ture. On early stages vicar emphysema develops, caused by difficulties in
breathing out. Then it overcomes into hypoventilation, caused by difficul-
ties in breathing in. Later an obturative atelectasis develops.
Peripheral cancer include rounded tumour, pneumonielike tumour
and Pancoast's cancer. Atypical form include miliary carcinomatosis, me-
diastinal form, etc.
TNM - classification of non-small lung cancer
TQ - no evidence of primary tumour
T. - carcinoma in situ
is
Tj - tumour less than 3 cm in greatest dimension, surrounded with
lung tissue.
T2 - tumour more than 3 cm in greatest dimension or tumour result-
ing in lobar atelectasis, or tumour located more than 2 cm from carina.
T3 - tumour resulting in total atelectasis, or tumour located less than
2 cm from carina, or tumour extending through diaphragm, pleura, peri-
cardium.
36 1. Thoracic surgery
T4 - tumour extending through the vital organs (heart, esophagus,
aorta).
N0 - no regional lymph node metastasis.
N - metastasis in lymph node of the root of the lung.
N2 - metastasis in lymph node of carina or mediastinal lymph node
on the side of lesion.
N3 - metastasis in lymph node of the root of the opposite lung or
mediastinal lymph node of the opposite side.
Ml - distant metastasis.
Grouping according to stages
fig. 1.1.10.
fig. 1.1.11.
fig. 1.1.12.
fig. 1.1.13.
Occult carcinoma T x
N0
M
o
Stage 0 N
o M
o
Stage 1 T
. N
o M
o
T2 N
o M0
Stage 2 », м 0
N:
Stage ЗА T
. N
2 M
oT
.
N
2 4N0 ,Ni ; N2 M
o
Stage ЗА T T T T
J
' 1' -1
2' 3' A
4
м 0
T T T T
J
' 1' -1
2' 3' A
4
N
3 M
o
Stage 4 T T T T
•l
l>-l
2> 3 ' A
4
NpN2 ,N3
1.1. Lungs and pleura 37
Fig. 1.1.12. Stage ЗА. Fig. 1.1.13. Stage 3B.
Small cell lung cancer is classified as "limited" or "wide-spread" process.
Under the meaning "limited" process we consider a tumour disposed in one
side of the chest, including mediastinum and supraclavicular lymph nodes.
"Wide-spread" process is the lesion, which exceeds above-stated limits.
Manifestation and clinical course
The basic complaints and signs of a central lung cancer are:
1) The constant cough which has appeared recently or changed its
character in smokers. The cough increases in dynamics, dry in initial stages,
troublesome, with further occurrence of dirty, rusty sputum);
2) Hemoptysis;
3) Dyspnea, which depends on body position (upright, supine etc);
4) The dyspnea of exertion (can appear, if the bronchus completely
obstructed);
5) Rales;
6) The prolonged pneumonia, which is not responsible to treatment;
7) Obstructive pneumonia.
The complaints and signs in peri pheral lung cancer depend on the size
of a tumour. There are no complaints in case of small dimension, when it is
completely surrounded by a normal pulmonary tissue. If the tumour reaches
the considerable sizes, it can manifest by permanent cough, dyspnea owing
to pleural exudate and pain, which arises from the growth into pleura.
The peripheral cancer can manifest by general signs: general malaise
and loss of weight. The complaints and signs, as outcomes of local exten­
sion of the process or presence of the distant metastases, result from:
• growth of tumour into nervous fibers;
• growth into or compression of adjacent structures;
• distant metastasizing.
38 1. Thoracic surgery
The growth of tumour into nervous fibers manifests by:
• Severe chest pain (in lesion of intercostal nerves);
• Hoarseness (growth into recurrent nerve);
• Dyspnea (growth into diaphragmatic nerve and phrenoplegia);
• Brachial pain or weakness in arm (lesion of brachial plexus);
• Horner's Syndrome (caused by lesion of cervical sympathetic trunk).
The growth or pressure of the tumour on adjacent structures mani­
fests by:
1) superior vena cava syndrome;
2) cardiac arrhythmia, cardiac failure;
3) signs of esophageal obstruction;
4) dyspnea caused by carcinomatous pleurisy;
5) permanent hiccup;
Physical findings on initial stages of the disease are within norm. In
advanced stages on examination of the chest observed its asymmetry and
delayed breathing movements of affected side during respiration.
On palpation in advanced stages on the side of lesion it is possible to
find out diminished vocal fremitus and enlarged supraclavicular lymph
nodes.
On percussion over atelectasis or pleurisy revealed dull sound on the
side of lesion.
Fig. 1.1.14. Peripheral cancer of the right lung.
A - Plain chest X-ray film;
В - Direct tomogram;
С - cancer that caused atelectasis of the
lower lobe.
1.1. Lungs and pleura 39
On auscultation revealed bron-
chial breathing or moist rales.
The diagnosis of lung cancer es-
tablished on the base of clinical, roent-
genological, bronchoscopic, cytologi-
cal and histological findings.
Roentgenological diagnostics in
80 % of cases allows in time to find
out lung cancer. On plain roentgeno-
grams in central form of cancer ob-
served a small additional shadow su-
perimposed on the root of lung, in Fig. 1.1.15. Peripheral cancer of the right
peripheral - well-defined rounded !ung.
shadow (fig. 1.2.14-15). On tomograms
it is possible detect the additional shadow, which narrows, compresses or
charges a lumen of the bronchus. Complete obstruction results in segmen-
tal or lobar atelectasis or atelectasis of entire lung. The improvement of
the diagnosis is achieved by computer tomography (fig. 1.1.16) or scanning
of lungs (fig. 1.1.17).
А В
Fig. 1.1.17. Scanning of lungs. Central cancer of the right lung with lower lobe atelectasis
(A), normal lungs (B).
The bronchoscopic examination should be carried out for all patient
with suspicion on lung cancer. Such examination is suitable for central form
of the cancer and presence of malign ant tumour in the lumen of bronchus.
In peripheral localization performed a transthoracic puncture with
the further investigation of the material.
Variants of clinical course
Pancoast's cancer (cancer of the apex of lung). It is characterized by
the brachial pain, paresthesias, lesion of brachial plexus and Horner's
syndrome (ptosis, miosis, enophthalmus). In some cases the destruction of
I rib is revealed.
In peripheral cancer with destruction the patients complain of cough,
expectoration of purulent sputum, hemoptysis, pulmonary bleeding, fe­
ver to 38-39°C, dyspnea and chest pain.
The mediastinal form of cancer revealed in advanced stages of the
process. As a rule, it is failed to find the primary focus. The metastases in
lymph nodes of mediastinum result in compression of superior cava vein.
The primary carcinomatosis is characterized by multiple metastatic
lesion of lungs. In most cases it is impossible to find the primary tumor.
The patients complain of progressing dyspnea. A chest pain caused by
spreading of the process on a pleural membrane and thoracic wall. The
hemoptysis arises if major bronchus involved in carcinomatosis.
The diagnostic program
1. Complaints of the patient and anamnesis.
2. Physical findings.
1.1. Lungs and pleura 41
• H 3. X-ray chest film in 2 planes.
4. Tomography of lungs.
5. Fibrobronchoscopy with a biopsy for cytological and histological
examinations.
6. Thoracentesis.
7. Computer tomography.
Tactics and choice of treatment
The primary curative treatment for non-small cell lung cancer is sur-
gery. In stages I or II a complete surgical resection is almost always possible.
Segmental resection will be selected for patients with small peripheral tumours
(less 2 cm in diameter), with no evidence of extension or metastases (Tj No
Mo). Lobectomy is performed for patients with a centrally located tumour
and free margins are required for this type of resection. Pneumonectomy is
the procedure of choice for patients with tumours extending to the orifice
of the lobar bronchus and tumours originating within or extending to the
main bronchus, with involvement of more than one lobe.
Non-small cell lung cancer patients with stage III disease other than
T3 lesions have an extent of disease which prohibits surgical resection.
Therefore preoperative chemotherapy or radiotherapy, either alone or in
combination, has been applied to minimize the extent of tumour before
surgery thereby increasing the possibility of radical resection. As more
than two-thirds of all resected patients relapse, great interest has been
given to adjuvant treatment, such as postoperative radiation therapy and
adjuvant chemotherapy.
The disseminated nature of small cell lung cancer, displaying a high
frequency of metastases at the time of diagnosis combined with a high
sensivity to cytostatic agents, has led to the use of chemotherapy as the
treatment of choice in all stages. Usually chemotherapy is combined with
radiotherapy because of the high radiosensitivity of small cell lung cancer.
1.2. TRAUMA OF THE CHEST
The modern traumatism represents the important social problem. Re-
cently observed the increase of major combined trauma, which complica-
tions often result in death. The trauma of the chest is usually accompanied
by dysfunction of the vital organs. Therefrom it is necessary constantly to
improve diagnostics and treatment of the patients who suffer from trauma.
Classification
The closed damages of the chest are divided:
I. According to the injury of other organs:
1. Isolated trauma.
2. Combined trauma (craniocerebral, with the damage of abdominal
organs, with the damage of bones).
II. According to the mechanism of trauma:
1. Contusion.
2. Compression.
3. Commotion.
4. Fracture.
III. According to the character of the damage of chest organs:
1. Without damage of organs.
2. With damage of organs (lungs, trachea, bronchi, esophagus, heart,
vessels, diaphragm etc.).
IV. According to the character of complications:
1. Uncomplicated.
2. Complicated:
1) Early (pneumothorax, hemothorax, subcutaneous, mediastinal em-
physema floatative rib fracture, traumatic shock, asphyxia);
2) Late (posttraumatic pneumonia, posttraumatic pleurisy, suppura-
tive diseases of lungs and pleura).
V. According to the state of cardiopulmonary system:
1. Without phenomena of respiratory failure.
2. Acute respiratory failure (of I, II, III degree).
3. Without phenomena of cardiovascular failure.
4. Acute cardiovascular failure (of I, II, III degree).
VI. According to the severity of trauma:
1. Mild.
2. Moderate.
3. Severe.
1.2. Trauma of the chest 43
1.2.1. Rib fracture
The direct force of traumatizing factor on the chest wall results in rib
fracture.
The pain localized in the zone of damage, is the chief clinical mani-
festation. The pain intensifies at respi-
ration, cough and change of a body
position of the patient. The overwhelm-
ing majority of the patients complain
of crepitation of ribs in the fracture
site.
On examination the respiratory
lag on affected side is observed.
Depending on number of injured
ribs, crepitating of osseous fragment
revealed by palpation, and diminished
breathing sounds on auscultation.
On chest roentgenograms the
break in continuity of bone fragments Fig. 1.2.1. Closed chest trauma, complicated
of ribs is observed (fig. 1.2.1). with left-side VI-VIII rib fracture.
Floatating rib fracture
This is one of the most severe complication of the closed trauma of
the chest. The floatation arises from fracture of three and more ribs along
two anatomic lines. The multiple rib fractures produce an unstable seg-
ment of chest wall that moves paradoxically inward at inspiration and
balloons outward during expiration (flail chest). Thereby the respiration
disturbed not only in the area of a floatating segment, but also in all lungs.
The permanent movements of floatating segment result in rocking shift
of mediastinum, which causes deviation of its organs. As a result the
respiratory failure is associated with cardiovascular.
Classification
1. Central floatative segment - a multiple rib fracture along parasternal or
midclavicular lines.
2. Anterolateral floatative segment - a multiple rib fracture along parasternal
and anteaxillary lines.
3. Lateral floatative segment - a multiple rib fracture along anterior and
posterior axillary lines.
4. Posterior floatative segment - a multiple rib fracture along postaxillary
and paravertebral lines.
Symptomatology and clinical course
The patients state is grave or extremely grave. The expressed pain
syndrome frequently results in traumatic shock. The patient is restless.
Observed the skin cyanosis, tachypnea, and tachycardia to 120-160 beat/
min of weak filling and tension. Arterial pressure at first elevated, then its
decrease is observed. On examination
characteristic paradoxical respiratory
movements of chest, inward at inspi-
ration and outward during expiration,
and also crepitus of bone fragments
by palpation are revealed. Breathing
sounds diminished on the side of dam-
age on auscultation.
In case of floatative rib fracture
the chest X-ray examination reveals
multiple (fig. 1.2.2), double rib fracture
with deformity of the chest.
In 75 % of cases the multiple rib
fracture is the cause of injury of
Fig. 1.2.2. Bilateral rib fracture. Right-side ,
pneumohemothorax. Subcutaneous l u n
S s
> pneumothorax or pneumohe-
emphysema. mothorax.
Treatment
Pain relief in closed trauma of the chest is achieved by means of
different blocks:
1. Vagosympathetic block;
2. Alcohol - novocaine block of the site of fracture;
3. Paravertebral block.
Except blocks, in some cases analgesics and opiates are instituted. On
2-3 day desirable the administration of electrophoresis with novocaine. For
the prophylaxis of congested phenomena in a pulmonary tissue used res-
piratory gymnastics, forced ventilation of lungs, inhalations.
The methods of renewal of the skeleton of the flail chest are divided
onto three groups:
1. External fixation of a movable segment by means of suturing for
intercostal muscles and traction during 2-3 weeks;
2. Intrmedullary costal osteosynthesis;
3. Mechanical ventilation (often with positive end-expiratory pres-
sure).
1.2. Trauma of the chest 45
1.2.2. Sternal Fracture
The fracture of breastbone is commonly caused by direct forces at
the site of the sternum. Usually it is the outcome of compression or result
of trauma to vehicle helm.
The fracture in most cases located in the upper and medial thirds of
sternum.
The patients complain of severe
pain in the site of fracture, which in-
tensifies at respiration and movements.
The pain behind the sternum and in
the heart area follows the contusion of
lungs and heart. Sometimes hemopty-
sis is observed.
Examination reveals the deformity
of breastbone in the site of fracture.
Displaced fragments are accompanied
by severe pain syndrome by palpation.
On auscultation, if there are no
intrapleural complications, the respi-
ration in the first 2-3 days is vesicular
on both sides. Then the fine bubbling
rales are auscultated, which are the
first objective manifestation of a post-
traumatic pneumonia.
The complete sternal fracture is
characterized by a break in continuity
of both cortical plates with a local dis-
location of fragments (fig. 1.2.3).
Fig. 1.2.3. Fracture of the breastbone
corpus with a local dislocation of
fragments.
The diagnostic program
1. Complaints and history of the disease.
2. Physical findings.
3. Chest roentgenograms in two planes.
Treatment
The sternal fracture without displacement of fragments requires only
conservative treatment. The fracture of the sternal corpus with disloca-
tion of fragments quite often requires operative treatment with perfor-
mance of osteosynthesis.
46 1. Thoracic surgery
1.2.3. 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.
Classification
I. According to extension of the process:
1. Unilateral.
2. Bilateral.
II. According to the degree of a lung collapse:
1. Partial (collapse of lung lessl/3 of its volume).
2. Subtotal (collapse of lung less 2/3 of its volume).
3. Total (collapse of lung exceeding 2/3 of its volume).
III. According to the mechanism of occurrence:
1. Closed.
2. Open.
3. Valvular.
The closed pneumothorax is the complication, which arises from the
damage of visceral pleural membrane, which results in entry of air into
pleural space and atelectasis of lung. In chest trauma the cause of occur-
rence of the closed pneumothorax is the perforation of visceral pleura
and pulmonary tissue by the fragment of fractured rib.
The open pneumothorax results from formation of hole in a chest
wall and free entry of air during inspiration into pleural space, and during
expiration - outward.
The valvular pneumothorax caused by the damage of a pulmonary
tissue or chest wall with formation of the valve, when the air during
inspiration enters a pleural space, and during expiration, due to valve
closure, does not exits outside. It is the most dangerous form of pneu-
mothorax, which results in a complete pulmonary collapse, shift of medi-
astinum, inflection of major vessels and cardiac arrest.
Symptomatology and clinical course
The predominant clinical manifestation of posttraumatic pneumothorax,
which results from a pulmonary collapse, is the rest dyspnea, which amplifies
at a minor exertion. This sign arises due to atelectasis of lung and its exclusion
from breathing. On the background of collapsed lung only the main and lobar
bronchi and pleural space are ventilated. The oxygenation of blood in collapsed
lungs does not occur, therefore the shunting of a venous blood observed.
The chest pain is more characteristic manifestation for trauma with
the damage of ribs, however pulmonary collapse also can associate
1.2. Trauma of the chest 47
with a pain syndrome. Nevertheless the patients promptly adapt to it
and the dyspnea finally remains the basic clinical manifestation of such
complication.
On the background of severe trauma of the chest the signs of dam-
age dominate in clinical manifestation on inappreciable entry of air in a
pleural space. Pneumothorax
mostly revealed during X-ray ex-
amination. Progressing of air en-
try in a pleural space and pulmo-
nary collapse cause the respira-
tory lag on affected side. By
palpation the vocal fremitus is ab-
sent. It indicates the origin of the
complication - rib fracture.
Percussion obtains bandbox
sound, or pulmonary sound with
tympanitis. On auscultation -
weak or absent breathing sounds,
sometimes - amphoric respiration.
The expressiveness of clinical pat-
tern depends on degree of a pul-
monary collapse.
Pulmonary atelectasis and presence of air in a pleural space are the
X-ray findings that enable to establish the final diagnosis (fig. 1.2.4).
Fig. 1.2.4. Closed chest trauma, complicated with
a right-side pneumohemothorax.
The diagnostic program
1. Complaints and history of the disease.
2. Physical examination.
3. Chest X-radiography in 2 planes.
4. Thoracentesis.
5. ECG.
Treatment
A chest trauma, complicated by pneumothorax with a partial pulmo-
nary collapse (lessl/3 of its volume) is the indication for aspiration of air
by means of thoracentesis. The cases, if the negative pressure in a pleural
space is not obtained, and also subtotal, or total pneumothorax require
closed drainage of a pleural space.
Under the local anesthesia by solution of novocaine in II intercostal
space in the midclavicular line through a trocar in pleural space inserted a
plastic tube, which fixed to skin. The drainage connects to aspirative sys-
48 1. Thoracic surgery
tern or Bulough's system. In the majority of patients the pneumothorax
liquidates in some hours, or 1-2 days.
The absence of effect (incomplete expansion of lung) of active aspi-
ration, and also valvular closed pneumothorax is the indication for opera-
tive management - suturing of the pulmonary wound. In some cases a
segmental resection of lung, or lobectomy is carried out.
1.2.4. Hemothorax
Hemothorax is the accumulation of blood in a pleural space. The
cause of occurrence of this complication is the damage of vessels of the
chest wall, pleura, lungs and mediastinum.
Classification
I. According to extent:
1. Unilateral.
2. Bilateral.
If. According to the degree of hemorrhage:
1. Small (the loss less 10 % of volume of circulating blood).
2. Moderate (loss of 10-20 % of volume of circulating blood).
3. Great (loss of 20-40 % of volume of circulating blood).
4. Total (exceeds 40 % of volume of circulating blood).
III. According to the duration of bleeding:
1. With continued hemorrhage.
2. With the stopped bleeding.
TV. According to the presence of clots in a pleural space:
1. Coagulated.
2. Non-coagulated.
V. According to the presence of infection:
1. Non-infected.
2. Infected (suppurative).
Symptomatology and clinical course
If hemothorax is the complication of blunt chest trauma, the clinical
manifestations depend on the severity of the trauma and degree of hem-
orrhage. Also hemothorax by itself results in pulmonary compression and
shift of mediastinum.
In case of small hemothorax the clinical manifestations of hemor-
rhage are slightly expressed or absent at all.
1.2. Trauma of the chest 49
Dyspnea, cough, general malaise
and dizziness are obvious in moderate
hemothorax. The skin is pale. The he-
modynamic disturbances: tachycardia
and decreased arterial pressure are ob-
served.
The great and total hemothorax
are associated with extremely grave
condition. The patients are troubled
with expressed general malaise, dizzi-
ness, dyspnea and difficult breathing.
In some cases they enter medical hos-
pitals in a terminal state. The skin is
sharply pale. The peripheral pulse im-
paired or absent. Tachycardia, weak
cardiac tones, low arterial pressure are
obvious.
On percussion the dullness is re-
vealed. On auscultation - the breath-
ing over the site of hemothorax is
sharply diminished or absent.
The X-ray picture of hemotho-
rax is rather specific. The intensive ho-
mogeneous shadow on the side of the
lesion with oblique upper contour
(Damuaso' line) is observed. The costal
sinus does not visualized. In small he-
mothorax, depending on the degree of
intrapleural bleeding, the shadow ob-
served only in the region of sinus
(fig. 1.2.5). In moderate hemothorax it
achieves a scapular angle (on the back
surface) or V rib on anterior surface of
the chest wall (fig. 1.2.6). In great hemothorax this shadow achieves III rib
(fig. 1.2.7), and total hemothorax characterized by complete shadow of a
pleural space, and in some cases - mediastinal shift to the healthy side
(fig. 1.2.8).
Fig. 1.2.5. Left-side small hemothorax.
Fig. 1.2.6. Left-side moderate hemothorax
The diagnostic program
1. Complaints and anamnesis of the disease.
2. Physical examination.
3. Chest roentgenograms in 2 planes.
Fig. 1.2.7. Right-side great hemothorax Fig. 1.2.8. Left-side total hemothorax.
4. Thoracentesis.
5. Investigation of a pleural content.
6. Revilour-Greguar's test.
7. General blood analysis.
8. Biochemical blood analysis.
9. Determining of the blood group and Rh factor.
Variants of clinical course and complications
The coagulated hemothorax. The late patient's apply for medical aid
or major bleeding results in formation of clots in a pleural space, and in
some cases all blood, which has accumulated in a pleural space, forms by
itself a major entire clot.
Depending on degree of bleeding and, consequently, size of clot,
the patients complain of chest pain, which intensifies at respiration, dys-
pnea, general malaise, and dizziness. As a rule, on 3-5 day the fever 37,5-
38°C is observed.
The physical findings (diminishing and absence of vocal fremitus by
palpation, dullness by percussion and sharply diminished or absent breathing
by auscultation) suggest the presence of pathological process in a pleural
space.
Chest roentgenogram reveals the intensive shadow, sometimes het-
erogeneous (with enlightenments and multiple levels).
The needle aspiration obtains small amount of a liquid hemolyzed
blood and small bloody thrombi (consequently to the inner diameter of the
needle).
Suppurative hemothorax. The coagulated hemothorax in overwhelm-
ing majority is infected, that results in pleural empyema (clinical manifes-
tations, diagnostics and treatment look in chapter " pleural empyema").
1.2. Trauma of the chest 51
Treatment
The treatment of small hemothorax requires needle aspiration or
drainage of pleural space and elimination of blood. The manipulation is
carried out in VI-VII intercostal spaces in the postaxillary or scapular lines.
Total, great or moderate hemothorax with persistent bleeding (posi-
tive Revilour-Greguar's test) 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.
1.2.5. Subcutaneous emphysema
The cause of this complication of blunt chest trauma is the damage
of parietal and visceral pleural membranes by the edge of broken rib with
the following entering of air from a pulmonary tissue into a pleural space
and through damaged chest wall (ruptured intercostal muscles) into sub-
cutaneous fat.
In overwhelming majority the subcutaneous emphysema is the out-
come of a valvular pneumothorax and pneumothorax in obliterated pleu-
ral space.
Classification
Subcutaneous emphysema is divided on:
1. Localized.
2. Widespread.
3. Total.
Symptomatology and clinical course
As the subcutaneous emphysema is the outcome of trauma compli-
cated by a rib fracture and posttraumatic pneumothorax, the chief com-
plaints are the chest pain and dyspnea, which intensify at respiration,
movements and minor physical activity.
In localized subcutaneous emphysema the manifestations of the chest
trauma are predominant in symptomatology. On examination observed a
swelling of a chest wall in the site of the damage. On palpation a subcuta-
neous crepitation is felt over this region. Percussion reveals a bandbox
sound or tympanitis. Auscultation of lungs over subcutaneous emphysema
is usually impossible.
52 1. Thoracic surgery
The widespread and total subcutaneous emphysema represents a
serious moral problem for the patient. Owing to extent of air all over the
chest, abdominal wall, neck (wide-spread emphysema), and also face,
arms and legs (total emphysema), the patients has a specific appearance:
swelled face, thick neck, enlarged chest, arms, and legs. Subcutaneous
emphysema by itself usually causes no respiratory and cardiovascular
disturbances. However the patients
note the change of the quality of
voice. By palpation the subcutaneous
emphysema is felt in whole body
("crisping snow").
It is necessary to note, that in
widespread and total emphysema the
auscultation is impossible. However the
presence of subcutaneous emphysema
in closed trauma of the chest enables
to suspect the presence of posttrau-
matic pneumothorax.
On the chest roentgenogram the
enlightenment of a subcutaneous fat
Fig. 1.2.9. Subcutaneous emphysema. (presence of air) is observed (fig. 1.2.9).
The diagnostic program
1. Complaints and history of the disease.
2. Physical findings.
3. Chest X-radiography.
Treatment
Widespread and total subcutaneous emphysema requires the draining
of subcutaneous space by plastic tubes in infra- and supraclavicular re-
gion, and also in the zone of the most expressed emphysema. Also per-
formed the drainage of a pleural space.
The subcutaneous emphysema resolves depending on its extent from
several days to 2-3,5 weeks.
1.2.6. Traumatic injury of trachea and main bronchi
The isolated injuries of trachea and bronchi as the result of blunt
trauma of the chest occur rarely and located mainly in a cervical part.
The main causes of tracheal and bronchial rupture are:
1.2. Trauma of the chest 53
1) shearing forces, which arises at the moment of trauma as a result of a
sudden rise of intraluminal pressure in airways when the glottis is closed;
2) compressing of a bronchial tree between a breastbone and vertebral
column;
3) in sudden and rapid deceleration or acceleration of the body a shift of
lungs occurs with more greater amplitude, than fixed bifurcation of
trachea.
Such disruptions most often occurs as a result of vehicular impacts,
falls from great heights, direct blows to the chest. In most cases disruption
of trachea and bronchi are accompanied with the other visceral damages:
lungs, skull and brain, heart, liver and flail chest.
Classification
I. According to the degree of disruption:
1. Partial:
• without damage of cartilaginous rings (I degree);
• with fracture of cartilaginous rings (II degree).
2. Partial disruption of all layers (III degree).
3. Complete transverse disruption of all walls without disjunction of the
of trachea, (bronchus) (IV degree).
4. Abruption with disjunction of the edges of trachea (bronchus) (V degree).
II. According to the rupture direction:
1. Longitudinal.
2. Oblique.
3. Transversal.
4. Mixed.
III. According to the localization of damage:
1. Tracheo-laryngeal.
2. Cervico-tracheal.
3. Mediastino-bronchial.
4. Bifurcation al.
5. Bronchial.
IV. According to the size of injury:
1. Combined damages of trachea (bronchi) and adjacent organs.
2. Damage of trachea (bronchi) and other segments of the body.
3. Damage of trachea (bronchi), adjacent organs and other segments of
the body.
Symptomatology and clinical course
The clinical manifestation of the tracheal injury depends on the type
of disruption, its degree and presence of concomitant damages.
54 1. Thoracic surgery
Incomplete isolated disruption of trachea commonly manifests by cough
and hemoptysis. Respiration, as a rule, is not disturbed.
The small disruptions are characterized by various clinics. If the hole
is occluded by clot and mediastinal tissues, the signs, which had appeared
earlier (cough, hemoptysis, mediastinal emphysema), can disappear. Nev-
ertheless the repeated occurrence of cough, as a rule, leads to severe
aggravation of the patient state.
Major and circular disruptions of trachea cause a grave state of the
patients. They manifest except difficult breathing by such signs:
1) mediastinal emphysema or pneumothorax;
2) compression syndrome - compression and inflection of major vessels
due to tension pneumothorax or mediastinal emphysema with trans-
ition into acute cardiopulmonary failure;
3) hemorrhage syndrome;
4) aspiration syndrome, which is the outcome of bleeding into airways or
aspiration of gastric content;
5) traumatic shock.
The injuries of bronchi occur in the way of abruption of main bron-
chi or their disruption in the zone of bifurcation. In the zone of a tracheal
bifurcation observed multiple (2-4) disruptions, which can be longitudi-
nal, transversal or oblique.
Depending on the character of trauma, it is necessary to distinguish
direct and secondary disruptions of bronchi. Direct injuries arise from the
gunshot and knife wounds, penetration of rib fragments or other subjects
in mediastinum or endoscopic manipulations.
The overwhelming majority of bronchial disruptions is the part of
blunt trauma of the chest. By the way, the damage of vessels of a lung
root occurs in 41,3 %.
The predominant clinical signs of a bronchial disruption are the res-
piratory disturbance, gas syndrome, hemoptysis and hemothorax. How-
ever these signs may observed only in isolated injuries of lungs.
The patients state is grave. Rest dyspnea and acute pain behind
sternum are the most troubling manifestations. The difficult swallowing,
hoarseness, swelling face and subcutaneous crepitation are observed. On
auscultation the breathing sounds are weak or absent at all on the side of
trauma.
The sequence of examination of the patients with injuries of tra-
chea and bronchi depends on the character and gravity of trauma, clinical
signs and concomitant damages, which threatening life.
If the state of the patient allows, a chest X-radiography is per-
formed. Commonly it is possible to find out mediastinal emphysema, some-
times the sign of discontinuing of trachea.
The injuries of bronchi manifest by distension of mediastinum and
presence of air strips along its borders, and in some cases total or tension
pneumothorax observed.
Final and most informative diagnostic method is the tracheobroncho-
scopy, which can be also the therapeutic method. However it is necessary
to carry out decompression of a mediastinal emphysema and pneumotho-
rax before such investigation.
Before examination the clots and liquid blood are aspirated from
airways, then adjusted the localization and character of disruption. The
incomplete disruptions are usually longitudinal and oblique and located
on the line of membranous and cartilaginous part, circular - mainly in a
cervical part of trachea. Except disruption of the wall, observed the
absence of cartilaginous rings in this region and filled by blood
parabronchial fat.
The open damages of trachea take place mainly in cervical part and
rarely - in thoracic. In all cases of neck trauma it is necessary to suspect
the opportunity of the damage of trachea and esophagus.
Such variants of clinical course are distinguished:
- acute course (first 30 days after operation);
- chronic course (complication of trauma).
Acute course is divided onto three stages:
1. The initial stage (lasts during 2 days after the trauma with typical signs
of disruption; the urgent resuscitation measures are required).
2. The stage of temporary compensation (lasts during 2 weeks; at this time
it is possible to carry out diagnostic examination).
3. The stage of persistent compensation (lasts during 30 days; during this
time a stenosis and other persistent complications of disruption of tra-
chea and bronchi develops).
The diagnostic program
1. Complaints and history of the disease.
2. Physical findings.
3. Chest X-radiography.
4. Diagnostic thoracentesis.
5. General blood and urine analyses.
6. Biochemical blood analysis.
7. Tracheobronchoscopy.
8. Tomography.
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HOSPITAL SURGERY GUIDE

  • 1. HOSPITAL SURGERY Edited by: L, Kovalchuk V. Sayenko G. Knyshov M. Nychytailo Ternopil "Ukrmedknyha" 2004
  • 2. ВВК 54.54 Н87 UDK 617(075.8) Н 87 Hospital surgery / Edited by L. Kovalchuk, V. Sayenko, G. Knyshov, M. Nychytailo. - Temopil: Ukrmedknyha, 2004. - 472 p., ill. 353, tabl. 6. ISBN 966-7364-02-X The modern requirements of doctor's training need the mastering of many medical subjects, among which surgery is one of the leading ones. The textbook represents the knowledge of the leading surgeons and scien­ tists from prestigeous medical schools of Ukraine. It has been tried to present modern concepts of the clinical course, diagnostics and treatment of surgi­ cal diseases. Special attention has been paid to new technologies, which are being used in diagnostics and treatment of the patients. The content of the textbook fulfills the educational programme of hos­ pital surgery. The structure of material is presented with attention on the basic parts, signs, methods of diagnostics, differential diagnostics, compli­ cations, tactics and methods of surgical treatment. In opinion of the au­ thors, such structure of the textbook is beneficial for mastering the subject. For the students of senior courses of the medical schools of III- IV accrediting level. BBK 54.54 UDK 616(075/8) ISBN 966-7364-02-X © Видавництво "Укрмедкнига", 2002 © Переклад на англійську мову "Ukrmedknyha" 2004
  • 3. A u t h o r s Bagirov M.M. Doctor of Medical Sciences, Professor of Pulmomary Chair of Kyiv Institute of Post-Diploma Education; Bedeniuk A.D. Candidate of Medical Sciences, Associate Professor of Abdominal Surgery Course of Hospital Surgery Clinics of Ternopil Medical Academy; Vardynets I.S. Candidate of Medical Sciences, Chief Physician of Ternopil District Hospital; ч-Veligotsky M.M. Doctor of Medical Sciences, Professor, Head of Thoracoabdominal Surgery Clinics of Kharkiv Post-Diploma Physician Institute, Laureate of State prize of Ukraine; Venger I.K. Doctor of Medical Sciences, Professor of Vascular Surgery Course of Hospital Surgery Clinics of Ternopil Medical Academy; Grubnyk V.V. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clin- • ics of Odessa Medical University, Laureate of State prize of Ukraine; Gusak O.M. Assistant Professor of Proctology Course of Hospital Surgery Clinics of Ternopil Medical Academy; Deykalo I.M. Doctor of Medical Sciences, Associate Professor of General Surgery Clinics of Ternopil Medical Academy; Dziubanovsky I.Y. Doctor of Medical Sciences, Professor, Head of Surgery Clinics of Post-Diploma Education Faculty of Ternopil Medical Academy; Dryzhak V.I. Doctor of Medical Sciences, Professor, Head of Oncology Clinics of Ternopil Medical Academy; Driuk M.F. Doctor of Medical Sciences, Professor, Head of Microvascular Surgery Department of Kyiv SRI of Clinical and Exprimental Surgery, Honored Scientist and Technician of Ukraine, Laureate of State prize of Ukraine; Zakharash M.P. Doctor of Medical Sciences, Professor of National Medical Univer­ sity, Chief of Military-Medical Board of Ukrainian Security Service, Major- General of Medical Service; Zakharov V.P. Candidate of Medical Sciences, Associate Professor of Ternopil Medi­ cal Academy; Zinkovsky M.F. Doctor of Medical Sciences, Professor, Corresponding Member of AMS of Ukraine, Head of Congenital Heart Defects Department of Kyiv Insti­ tute of Cardiovascular Surgery, Laureate of State prize of Ukraine; Kimakovych V.Y. Doctor of Medical Sciences, Associate Professor, Chief Physician of Lviv Regional Diagnostic Centre; Kit O.M. Doctor of Medical Sciences, Professor of Ternopil Medical Academy; Knyshov G.V. Doctor of Medical Sciences, Professor, Academician of AMS of Ukraine, Director of Kyiv Institute of Cardiovascular Surgery, Laureate of State prize of Ukraine; Kovalchuk L.Y. Doctor of Medical Sciences, Professor, Corresponding Member of AMS of Ukraine, Rector of Ternopil Medical Academy, Head of Hospital Sur­ gery Clinics of Ternopil Medical Academy, Honored Scientist and Technician of Ukraine; Kovalchuk O.L. Candidate of Medical Sciences, Head of Laparoscopic Surgery De­ partment of Ternopil Central District Hospital; Komorovsky Y.T. Doctor of Medical Sciences, Professor of Hospital Surgery Clinics of Ternopil Medical Academy;
  • 4. Authors Bagirov M.M. Doctor of Medical Sciences, Professor of Pulmomary Chair of Kyiv Institute of Post-Diploma Education; Bedeniuk A.D. Candidate of Medical Sciences, Associate Professor of Abdominal Surgery Course of Hospital Surgery Clinics of Ternopil Medical Academy; Vardynets I.S. Candidate of Medical Sciences, Chief Physician of Ternopil District Hospital; ч-Veligotsky M.M. Doctor of Medical Sciences, Professor, Head of Thoracoabdominal Surgery Clinics of Kharkiv Post-Diploma Physician Institute, Laureate of State Venger I.K. Doctor of Medical Sciences, Professor of Vascular Surgery Course of Hospital Surgery Clinics of Ternopil Medical Academy; Grubnyk V.V. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clin- > ics of Odessa Medical University, Laureate of State prize of Ukraine; Gusak O.M. Assistant Professor of Proctology Course of Hospital Surgery Clinics of Ternopil Medical Academy", Deykalo I.M. Doctor of Medical Sciences, Associate Professor of General Surgery Clinics of Ternopil Medical Academy; Dziubanovsky I.Y. Doctor of Medical Sciences, Professor, Head of Surgery Clinics of Post-Diploma Education Faculty of Ternopil Medical Academy; Dryzhak V.I. Doctor of Medical Sciences, Professor, Head of Oncology Clinics of Ternopil Medical Academy; Driuk M.F. Doctor of Medical Sciences, Professor, Head of Microvascular Surgery Department of Kyiv SRI of Clinical and Exprimental Surgery, Honored Scientist and Technician of Ukraine, Laureate of State prize of Ukraine; Zakharash M.P. Doctor of Medical Sciences, Professor of National Medical Univer­ sity, Chief of Military-Medical Board of Ukrainian Security Service, Major- General of Medical Service; Zakharov V.P. Candidate of Medical Sciences, Associate Professor of Ternopil Medi­ cal Academy; Zinkovsky M.F. Doctor of Medical Sciences, Professor, Corresponding Member of AMS of Ukraine, Head of Congenital Heart Defects Department of Kyiv Insti­ tute of Cardiovascular Surgery, Laureate of State prize of Ukraine; Kimakovych V.Y. Doctor of Medical Sciences, Associate Professor, Chief Physician of Lviv Regional Diagnostic Centre; Kit O.M. Doctor of Medical Sciences, Professor of Ternopil Medical Academy; Knyshov G.V. Doctor of Medical Sciences, Professor, Academician of AMS of Ukraine, Director of Kyiv Institute of Cardiovascular Surgery, Laureate of State prize of Ukraine; Kovalchuk L.Y. Doctor of Medical Sciences, Professor, Corresponding Member of AMS of Ukraine, Rector of Ternopil Medical Academy, Head of Hospital Sur­ gery Clinics of Ternopil Medical Academy, Honored Scientist and Technician of Ukraine; Kovalchuk O.L. Candidate of Medical Sciences, Head of Laparoscopic Surgery De­ partment of Ternopil Central District Hospital; Komorovsky Y.T. Doctor of Medical Sciences, Professor of Hospital Surgery Clinics of Ternopil Medical Academy;
  • 5. Kontsevy O.O. Head of Abdominal Surgery Department of Ternopil Regional Clinical Hospital; Korchynsky Y.Y. Candidate of Medical Sciences, Assistant Professor of Proctology Course of Hospital Surgery Clinics of Ternopil Medical Academy; [Kurko V.S.[Doctor of Medical Sciences, Professor of Surgery Clinics of Post-Diploma Education Faculty of Ternopil Medical Academy; Maksymliuk V.I. Doctor of Medical Sciences, Associate Professor of Surgery Clinics of Post-Diploma Education Faculty of Ternopil Medical Academy; Malyovany V.V. Candidate of Medical Sciences, Associate Professor of Thoracic Sur- gery Course of Hospital Surgery Clinics of Ternopil Medical Academy; Mitiuk LI. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clinics of Vinnytsia Medical University; Moroz G.S. Doctor of Medical Sciences, Professor of Oncology Clinics of Ternopil Medical Academy; Nychytailo M.Y. Doctor of Medical Sciences, Professor, Head of Department of Liver and Biliary Tract Surgery of Institute of Clinical and Experimental Sur- gery of AMS of Ukraine; [Polischuk V.Mj Doctor of Medical Sciences, Professor, Superior of Public Health Board of Rivne Regional State Administration; Sagenko V.F. Doctor of Medical Sciences, Professor, Corresponding Member of NAS and AMS of Ukraine, Director of Kyiv SRI of Clinical and Experimental Sur- gery, Honored Scientist and Technician of Ukraine, Laureate of State prize of Ukraine; Serdiuk A.M. Doctor of Medical Sciences, Professor, Corresponding Member of AMS of Ukraine; Sytar L.L. Doctor of Medical Sciences, Professor, Head of Department of Acquired Heart Defects of Kyiv Institute of Cardiovascular Surgery, Laureate of State prize of Ukraine; Spizhenko Y.P. Doctor of Medical Sciences, Academician of AMS of Ukraine, Presi- dent of Association of Pharmacologists of Ukraine; Sukhariev I.I. Doctor of Medical Sciences, Professor, Honored Scientist and Techni- cian of Ukraine, Laureate of State prize of Ukraine; Ursulenko V.I. Doctor of Medical Sciences, Head of Department of Surgical Treat- ment of Coronary Insufficiency, Laureate of State prize of Ukraine; Shevchenko S.I. Doctor of Medical Sciences, Professor, Head of Faculty Surgery Clinics of Kharkiv Medical Academy; Shevchuk M.G. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clinics of Ivano-Frankivsk Medical Academy; Shidlovsky V.O. Doctor of Medical Sciences, Head of Faculty Surgery Clinics of Ternopil Medical Academy; Shkrobot V.V. Candidate of Medical Sciences, Assistant of Chief Physician on Sur- gery of Ternopil Regional Clinical Hospital; Yarema I.V. Doctor of Medical Sciences, Professor, Head of Hospital Surgery Clinics of Moscow Medical Stomatological Institute, Chief Lymphologist of Russian Fed- eration. Data on pathological morphology are stated by Bodnar Y.Y., Doctor of Medical Sciences, Professor, Head of Pathologic Morphology Chair of Ternopil Medical Academy; Conservative therapy to the section "Abdominal Surgery" is described by Starodub Y.M., Doctor of Medical Sciences, Professor, Head of Therapy Clinics of Post-Diploma Education Faculty of Ternopil Medical Academy.
  • 6. CONTENS 1. THORACIC S U R G E R Y 7 1.1. LUNGS AND PLEURA 9 1.1.1. Acute suppurative diseases of lungs 9 1.1.2. Lung Cysts 18 1.1.3. Pleural empyema^. 22 1.1.4. Pyopneumothorax 27 1.1.5. Spontaneous pneumothorax 31 1.1.6. Lung Cancer 34 1.2<TRAUMA OF THE CHEST 42 1.2.1. Rib fracture 43 1.2.2. Sternal Fracture - 45 1.2.3. Posttraumatic pneumothorax 46 1.2.4. Hemothorax 48 1.2.5. Subcutaneous emphysema 51 1.2.6. Traumatic injury of trachea and main bronchi 52 1.2.7. Mediastinal emphysema 56 1.3/ESOPHAGUS 58 1.3.1. Esophageal diverticula 58 1.3.2. Achalasia of the cardia 63 1.3.3. Esophageal sticture 67 1.3.4. Esophageal cancer 72 1.4. MEDIASTINUM 78 1.4.1. Acute mediastinitis 78 1.4.2. Mediastinal tumors 81 1.5. DIAPHRAGMA 89 1.5.1. Diaphragmatic hernias 89 1.5.2. Diaphragmatic relaxation 94 2. CARDIO-VASCULAR S U R G E R Y 99 2.1. HEART '. 101 2.1.1. Mitral stenosis 101 2.1.2. Sick sinus syndrome and sinoauricular block 104 2.1.3. Penetrating cardiac injuries I l l 2-2TARTERIES 114 2.2.1. Endarteritis obliterans 114 2.2.2. Atherosclerosis obliterans of the inferior extremities 120 2.2.3. Abdominal ischemic syndrome 126 2.2.4. Acute arterial occlusion 132
  • 7. 4 Contens 2.2.5. Pulmonary embolism 137 2.2^6. Injuries of vessels 143 2.3^VEINS : 153 2.3.1. Varicosity 153 2.3.2. venous thromboses 161 2.3.3. Postflebitic syndrome (postthrombotic disease) 172 2.4. LYMPH SYSTEM 181 2.4.1. Clinical anatomy and physiology 181 2.4.2. Surgery of thoracic lymph duct 184 2.4.3. Lymphangioma 187 2.4.4. Lymph fistula 189 2.4.5. Lymphangitis and lymphadenitis 190 2.4.6. Lymphedema of extremities 192 3. ABDOMINAL S U R G E R Y 195 3.1. ABDOMINAL WALL 197 3.1.1. Abdominal wall hernia 197 3.1.2. Incarcerated hernia 205 3.2. STOMACH AND DUODENUM 212 3.2.1. Gastric ulcer 212 3.2.2. Duodenal ulcer 220 3.2.3. Ulcer stenosis 227 3.2.4. Perforated ulcer gastroduodenal ulcers 231 3.2.5. Bleeding gastroduodenal ulcers 236 3.2.6. Gastrointestinal bleeding of unulcer etiology 242 —3.2.7. Diseases of the operated stomach 249 3.2.8. Cancer of stomach 268 3.3. SMALL AND LARGE INTESTINE 277 3.3.1. Acute appendicitis 277 3.3.2. Acute intestinal obstruction 287 3.3.3. Crohn's disease 295 3.3.4. Nonspecific ulcerative colitis 300 3.3.5. Cancer of colon 306 3.4. LIVER AND HEPATIC DUCTS 311 3.4.1. Abscesses of liver 311 3.4.2. Cysts of liver 315 3.4.3. Syndrome of portal hypertension 319 3.4.4. Acute cholecystitis 332 3.4.5. Chronic cholecystitis 344 3.4.6. Obstructive jaundice 348 3.4.7. Postcholecystectomy syndrome 354 3.4.8. Cancer of liver 360
  • 8. Contens 5 3.4.9. Cancer of gall-bladder 364 3.5. PANCREAS 370 3.5.1. Acute pancreatitis 370 3.5.2. Chronic pancreatitis 377 3.5.3. Cysts of pancreas 386 3.5.4. Cancer of pancreas 393 3.6. PERITONITIS 398 4. P R O C T O L O G Y 407 4.1. RECTUM AND PARARECTAL SPACE 409 4.1.1. Hemorrhoids 409 4.1.2. Rectal Fissures 412 4.1.3. Polyps of colon and rectum 416 4.1.4. Paraproctitis 420 4.1.5. Rectal fistulas (chronic paraproctitis) 424 4.1.6. Epithelial paracoccidioidal canals 429 4.1.7. Cancer of rectum 433 5. ENDOCRINOLOGIC S U R G E R Y 439 5.1. THYROID GLAND 441 5.1.1. Endemic and sporadic goiter 441 5.1.2. Diffuse goiter with hyperthyroidism 446 5.1.3. Inflammatory diseases of thyroid gland 459 5.1.4. Thyroid cancer 465 ЛІТЕРАТУРА 468
  • 10. 1.1. LUNGS AND PLEURA 1.1.1. Acute suppurative diseases of lungs Acute suppurative diseases of lungs include abscessing pneumonia, acute and gangrenous abscesses, focal and extensive lung gangrene. Abscessing pneumonia is characterized by the multiple destructive foci 0,3-0,5 cm in size, within 1-2 segments of lungs, which is not disposed to progression. The destruction is accompanied by expressed perifocal infil- tration of a pulmonary tissue. Lung abscess - a purulent or ichorous destruction of pulmonary tissue within one segment with formation of one or several cavities, filled by pus, and detached from adjacent parenchyma by a pyogenic capsule and expressed perifocal infiltration of surrounding pulmonary tissue. It arises at the persons with a maintained reactivity of the organism. Gangrenous abscess is a purulent, ichorous necrosis of a pulmonary tissue within 2-3 segments, detached from adjacent pulmonary paren- chyma, with the liability to sequesters formation. Depending on reactivity of the organism it can transform into purulent abscess (after the lysis of sequesters) or gangrene. Lung gangrene - a diffuse purulent, ichorous necrosis of the tissue without the tendency to defined demarcation with prompt dynamics of spreading of necrotic zone and destruction of the parenchyma. It is char- acterized by a grave intoxication, liability to a pleural complications and pulmonary bleeding. If only the one lobe is affected the gangrene is con- sidered to be limited, if extensive area of lungs isaffected - the gangrene is a wide-spread. Etiology and pathogenesis The agents of purulent pulmonary destruction are anaerobic nonclostridial microorganisms, staphylococci, Gram-negative bacteria, and mixed infection. The predominant factors which cause the disease: • disturbances of bronchial patency with the development of atelectasis; • infectious inflammatory process in a pulmonary tissue; • regional disturbances of blood supply with a further necrosis of areas of pulmonary parenchyma. The embodiment of these factors occurs in condition of the changed reactivity of the organism.
  • 11. 10 1. Thoracic surgery The states which result in the aspiration of contents of the upper parts of alimentary tract (traumas of head, craniovascular disturbances, alcoholism, narcomania, narcoses, epilepsy etc.) contribute to the pulmo- nary abscessing. And also factors, which are capable to provoke secondary immunodeficiency and suppression of reactive processes: diabetes melli- tus, irradiation, long application of corticosteroids, antineoplastic therapy, some hematological disease, AIDS favor the purulent processes. Pathology The abscesses mainly develop in II and VI segments of lungs. They may be single and multiple. The abscess is confined from adjacent pulmo- nary tissue by a capsule, which represents a granulating tissue and dense leukocytic rampart. Usually it is possible to find out a draining bronchus. Later on in the wall of the abscess the amount of connective tissue fibers is enlarged. In gangrene the pulmonary tissue is black in color, swollen, with cavities, and in some places transfers into the sites with dark green color- ing. The macropreparatus is characteristically fetid. Classification According to pathogenesis: - postpneumonic; - aspirative; - obturative; - posttraumatic; - hematogenous or septic; - lymphogenous; - thromboembolic. According to the character of purulent process: - single purulent abscesses; - multiple purulent abscesses; - bilateral purulent abscesses; - gangrenous abscesses (single, multiple, uni- and bilateral); - limited gangrene; - wide-spread gangrene. According to localization (with the indication of affected segment or lobe). According to the stage: - 1 stage - necrotic pneumonia; - 2 stage - destruction and rejection; - 3 stage - cleaning and cicatrization.
  • 12. 1.1. Lungs and pleura II According to the term of existence: - acute; - chronic. Complications: - pulmonary bleeding; - pyopneumothorax; - pleural empyema; - sepsis; - bronchogenic dissemination. Symptomatology and clinical course The clinical manifestation of acute purulent destruction of lungs de- pend on the size of the focus and character of destruction, reactivity of the organism and stage of the disease, peculiarities of the drainage of purulent cavities and complications. 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 39-40°C and has a hectic character. At the same time the chest pain increases, which associates with a troubling cough and dyspnea. The con- dition 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 destruc- tive cavities through bronchus the daily quantity of the sputum reaches 500 ml and more. At this time also possible hemoptysis. The sputum is foul- smelling. At sedimentation it divides into three layers: - inferior - resembling a grey mass with detrites and flaps of a pulmoary tissue; - medial - purulent, turbid, liquid; - 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 are well revealed at peripheral localization of the process. On palpation - weakened vocal fremitus. By percussion - a blunted sound over the site of the purulent focus and perifocal infiltration (at subpleural location of the abscess). On auscultation - tubular sound with a moist rales in the zone of purulent focus. Well-generated subpleural cavi- ties of major sizes can be revealed by percussion as a bandbox sound, on
  • 13. 12 1. Thoracic surgery Fig 1.1.1. Acute abscess of the lower lobe of the right lung in the stage of necrotic pneumonia. auscultation - as moist rales on the background of amphoric respiration. X-ray of the chest in the stage of necrotic pneumonia shows a rounded lesion with irregular contour (fig. 1.1.1). For the second stage is characteristic the enlightenment of the shadow with a further developing of the rounded cavity with air-fluid level (Kordin's symptom), gentle pyogenic sheath and the perifocal infiltration (fig. 1.1.2). In the third stage on the place of suppuration observed expressed fibrosis, sometimes as a thin-walled annular formation. Gangrenous abscess is character- ized by a grave state of the patient, expressed purulent intoxication, cough with expectoration of a great amount (500 ml and more) of grey-green, foul- smelling sputum with hectic body tem- perature. Roentgenologically the inline of the cavity is poorly defined, it contains a visible sequesters that look as a poly- morphous shadow. The adjacent pulmo- nary tissue is infiltrated (fig. 1.1.3). The clinics of a pulmonary gan- grene differs by terminal expression of signs. The state of the patients is critical. The patient is adynamic, exhausted, with edemas on legs. Dyspnea in rest, hemo- dynamic disturbances are evident. Dirty- grey or brown sputum with detrites, pieces of necrotic parenchyma and threads of blood excretes out with the cough up to 1 littre. Early pleural com- plication, such as pulmonary bleeding, is usual and may be profuse. Often it is associated with vital organ dysfunction and loss of consciousness. The intensive shadow which occupies a considerable area of lungs with a visible cavities, that contain sequesters, fluid levels, is roentgeno- logically revealed. The shadow outline is irregular, but could be well de- fined if the process is within interlobar sulcus (fig. 1.1.4). Fig. 1.1.2. Acute abscess of the lower lobe of the right lung. Fig. 1.1.3. Gangrenous abscess of the lower lobe of the left lung.
  • 14. 1.1. Lungs and pleura 13 A Fig. 1.1.4. Right-side pulmonary gangrene. Plain roentgenogram, direct view (A). Tomogram (B). В Chronic lung abscess 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 out of 250-500 ml of a purulent foul sputum, chest pain, dyspnea, hectic temperature with the difference in 1,5-2°C. Dizziness, suppression of ap­ petite, general weakness increases according to intoxication. The skin is pale with moderate cyanosis. The respiratory rate rises to 28-30 per min. In 6-8 months 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). Percussion reveals a short sound in projection of pathological process, auscultation - a lot of moist rales on the background of amphoric respiration. Roentgenologically chronic abscess is shown by one or several cavities of a spherical shape with a thick, dense pyogenic sheath. Exacerbation of the process manifests by a cavity with horizontal air-fluid level. The size of surrounding perifocal infiltration depends on the phase of the process The blood analysis in pulmonary destruction is characterized by leu­ kocytosis with deviation of the differential count to the left, lymphocy­ topenia, elevation of the erythrocyte sedimentation rate. Gangrenous change of the process is accompanied by a progressing anemia, sometimes by leukopenia. The hypoproteinemia arises from major losses of protein with purulent sputum. Intoxication and toxic lesion of liver leads to disproteinemia. It is associated with the enlarged concentration of mucoprotein, sialine acids, seromucoid, and fibrinogen. (fig. 1.1.5).
  • 15. 14 1. Thoracic surgery Fig. 1.1.5. Chronic abscess of the right lung. Plain roentgenogram, direct view (A). Fragment of the computer tomogram (B). The immunogram reveals the suppression of cellular and humoral immunity with a liability to hyperergy and autoaggression, depression of nonspecific protection mechanisms. The cytological bronchial water lavage is characterized by expressed neutrocytosis, noncellular postdestructive insertions at lack or absence of alveolar macrophages. Variants of clinical course and complications According to the clinical course, there are such variants of the devel- opment of purulent diseases of lungs: 1. Favorable course. The adequate treatment results in prompt positive clini- cal, roentgenological and laboratory dynamics, and ends by recovery. 2. Non-progressive course. A poor drainage of the suppurative focus and permanent purulent intoxication results in transferring of the process in chronic form. 3. Progressing course. Is predetermined by combination of a series of un- favorable factors (low resistance of the organism, autoimmune ag- gression, high virulence of the infecting agent etc.). Characterized by diffusion of the zone of necrosis and destruction with transferring in gangrene. 4. Incapsulated process. Caused by the absence or complete obstruction of the draining bronchus under condition of satisfactory resistance of the organism. 5. Complicated course. Mostly is the result of progressive development of the pathological process.
  • 16. 1.1. Lungs and pleura 15 Pulmonary bleeding arises suddenly, and associated with coughing out of a foamy, bright-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 manifestation of a pulmo- nary suppuration is accompanied by dizziness, weakness, dyspnea, chest pain. The hemodynamic disturbances depend on intensity of the bleeding. The auscultation of lungs reveals the moist rales (aspiration) on both sides. If the pulmonary destruction is present the plain film of the chest shows the localization of the source of bleeding. After hospitalization of the patient with this complication the exclusive information is obtained with a fibrobronchoscopy. According to the degree, the pulmonary bleedings are classified (V.Struchkov, 1985): I degree - hemorrhage to 300 ml. 1. Single hemoptysis. 2. Multiple hemoptysis. II degree - hemorrhage to 700 ml. 1. Single bleeding: a) with falling of arterial pressure and decreasing of hemoglobin; b) without falling of arterial pressure and decreasing of hemoglobin. 2. Multiple bleeding: a) with falling of arterial pressure and decreasing of hemoglobin; b) without falling of arterial pressure and decreasing of hemoglobin. III degree - hemorrhage exceeds 700 ml. 1. Massive bleeding. 2. Fulminant, lethal bleeding. The I degree of a pulmonary bleeding manifests by coughing out the sputum tinged with blood, the hemodynamic disturbance usually absent. The bleeding of II degree is characterized by decreasing of arterial pres- sure on 20-30 mm Hg, tachycardia to 100 beats/min, contents of hemo- globin within 60-80 g/1. The bleeding of III degree are accompanied with sharp decreasing of arterial pressure, rapid (more than 100-120 beats/ min), small, sometimes thread pulse, and even its disappearance on pe- ripheral arteries, tachypnea to 40 per 1 min, hemoglobin to 50-60 g/1. Possible the fulminant course up to the terminal state with prompt failure of cardiac activity and asphyxia by blood. Sepsis manifests by multisystem lesion with progression of the syn- drome of polyorganous failure, hematosepsis, purulent metastasizing (fre- quently in brain). Characteristic complications for lung suppurative diseases such as pleu- ral empyema and pyopneumothorax are described in separate parts.
  • 17. 16 1. Thoracic surgery The diagnostic program Complaints and anamnesis. Physical findings. X-ray examination of chest in two planes (direct and lateral). Tomogram of lungs. Examination of the sputum (bacteriological, cytological). General blood and urine analyses. Biochemical blood analysis (protein and its fractions). Immunogram. Fibrobronchoscopy. Differential diagnostics The central lung cancer due to the bronchial obturation results in atelectasis of a lung segment or lobe, with probable further abscessing. For the differentiation used tomography, which reveals the bronchial ob- turation by tumour, lesion of central lymph nodes), cytological examina- tion of sputum and bronchial outwashes. The determinant role belongs to fibrobronchoscopy with a biopsy and verification of the diagnosis. The peripheral lung cancer with destruction on tomograms is charac- terized by cavity with irregular inner surface, which external outline con- nects with root of the lung because of lymphatic metastatic spreading. The central lymph nodes frequently enlarged. The diagnosis is improved by results of transthoracic puncture or catheterizing biopsy with cytologi- cal investigation, fibrobronchoscopy. If it is impossible to confirm the di- agnosis the thoracotomy is indicated. The tubercular cavern is mainly located in the upper lobes of lungs, roentgenologically revealed on the background of characteristic changes of adjacent pulmonary tissue (calcification, dissemination), sometimes a draining bronchus is detected. In the sputum mycobacteria of tuberculosis are frequently found. The suppurative cyst of lungs differs by a gradual onset, slow course of the suppuration, less expressed intoxication. Roentgenologically its cav- ity has the oval or rounded shape with a thin sheath and regular contour. Perifocal infiltration is not characteristic. Tactics and choice of treatment The tactics in acute pulmonary destruction should be mainly conser- vative. 1. The adequate antibacterial, antiinflammatory therapy consists of intravenous introduction of antibiotics of a wide spectrum activity.
  • 18. 1.1. Lungs and pleura 17 With the purpose of maximal concentration of drugs in the patho- logical focus applied: - Injection of antibiotics in the vessels of a pulmonary circulation by means of catheterization of central veins, pulmonary artery; - Introduction of medicines into respiratory tracts (in the second stage) - through the endotracheal microirrigator, nasogastric tube, during bronchoscopy, en- doscopic catheterization of the abscess cavity through the draining bronchus, during aerosolic inhalations. The composition of medical admixtures includes: antibiotics, antiseptics (10 % dimexid, dioxydin, microcid etc.), enzymes; - Transcutaneously in the focus of destruction by means of puncture or draining with the usage of physical antiseptics. - Intrapleural injections; - By means of electrophoresis. 2. 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. 3. Detoxycation therapy (intra- and extracorporal). 4. Immune correction (under the control of immunogram): - Active - staphylococcal anatoxin; - Passive - specific gamma-globulins, hyperimmune plasma; - Non-specific (pirimidine and purine derivates, drugs of thymus gland, splenin, levamisol,). 5. Homeostatic correction (oxygenotherapy, correction of anemia, hypoproteinemia, acidosis, microcirculatory disturbance). 6. Desensitizing, antiinflammatory therapy, regulation of proteases activity: antihistamine, nonsteroid antiinflammatory agents, inhibitors of proteases, antioxidants. 7. Correction of the organ and system dysfunction, prevention of complications, symptomatic therapy. Indications for operative management in acute destructive processes of lungs: - Pulmonary bleeding of II-III degree; - Progression of the process despite active and appropriate therapy; - Tension 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 systemic functions in the terminal stage, bilateral purulent destruction of lungs, concomitant incurable malignant tumours.
  • 19. 18 1. Thoracic surgery Operational incisions - anterolateral (fig. 1.2.16), lateral (fig. 1.2.17) and posterolateral (fig. 1.2.18) thoracotomy. The operation suggests seg- mental, polysegmental resection, lobectomy, bilobectomy, combined in- tervention (with the decortication, pleurectomy). The patients with chronic abscesses should undergo the operative treatment after complete liquidation of exacerbation. In a pulmonary gangrene the stabilization of the process on the back- ground of active conservative treatment allows in future to apply conserva- tive tactics up to recovery or making optimal conditions for operation (liqui- dation of intoxication, aggressive panbronchitis, diffuse infiltration of the parenchyma, pleural complications). The headlong progression of the gan- grene during first days, despite the active correction, occurrence of pulmo- nary bleeding requires urgent performance of operative management. Vol- ume of the operation - pneumonectomy, bilobectomy, lobectomy. 1.1.2. Lung Cysts The cysts of lungs are the thin-walled cavitary formations, filled with air or liquid contents. Inherent and acquired cyst are distinguished. Etiology and pathogenesis Inherent cysts arise from the abnormalities of the development of lungs under the influence of multiple chemical, physical and biological factors. They can develop from a bronchial tree (bronchial) or from alveolar tissue (alveolar). Their occurrence resulting from the delay of the develop- ment of peripheral parts of bronchus with its expansion or agenesia of alveoli with dilatation of terminal bronchioles. Congenital cysts at first develop and grow as secretory formations. After communication with bron- chus they finally form as air or hydroair cavities. Acquired cysts are represented by fibrous cavities, which remain after abscesses, tubercular caverns, echinococci, posttraumatic intrapul- monary hematomas. The degenerative changes in the wall of bronchus with obliteration of its lumen by a cloggy secret as athe result of repeated inflammatory processes lead to occurrence of acquired retentional cysts. Pathology Congenital cyst can be located in any part of lungs. The walls of bronchogenic cavities contain chaotically disposed elements of bronchus (cartilagous plates, muscle fibers, mucous glands), they are lined from
  • 20. 1.1. Lungs and pleura 19 inside by cylindrical or cubic epithelium. Squeezed alveolar cells line the walls of alveolar formations. The acquired cyst revealed in the site of previous diseases. Its walls mainly consist of connective tissue. Epithelization is possible due to trans- ferring of the epithelium from a draining bronchus at long existence. The cysts could be uni- or multichamber, closed and open (depend- ing on the presence of communication with bronchus). Classification According to the etiology: - congenital; - acquired. According to displacement: - single, multiple; - unilateral, bilateral. Complications: - Suppuration; - Appearance of the valvular mechanism; - Bleeding; - Burst into pleural space (pneumothorax, pyopneumothorax, pleu- ral empyema); - Malignancy. Symptomatology and clinical course Clinical manifestations of uncomplicated pulmonary cysts are vague. Sometimes patients complain of a chest pain, periodic cough, and inflam- matory diseases of respiratory tract in history. In children the signs are rather expressed, the dyspnea associates with the compression of airways. In great, superficially disposed cysts revealed delayed respiratory movements on affected side during breathing. On palpation - weakened vocal fremitus. On percussion - short or bandbox sound, depending on contents. On auscultation - weakened respiration, over the huge open cavi- ties — amphoric. On plain chest films the closed congenital cyst forms a homoge- neous shadow of the spherical or oval shape of average intensity with rather regular edge on the background of an intact pulmonary tissue. During roentgenoscopy sometimes observed the change of its shape depending on the phase of breathing - elongation during inspiration (Escudero's syndrome). The character of the shadow is better to study on tomograms.
  • 21. 20 1. Thoracic surgery Acquired retentional cyst is roentgenologically shown by a shadow of irregular shape (piriform, spindle- shaped etc.), that displays the shape of the distended bronchus. The adja- cent tissue, as a rule, changed due to bronchiectases, pneumosclerosis, etc. Open cysts are observed as thin- walled, good defined cavities of an- nular or oval shape (fig. 1.1.6). The bronchogram in congenital cysts reveals hypoplasia of segmental or lobar bronchus, lack of bronchial bifurcations, which tends to bone. Sometimes observed bronchiectases in the neighboring parts of lungs. A cys- tic cavity is infrequently defined. The angiopulmonography reveals deformation of vascular branches, which circumflex the cyst. Fig. 1.1.6. Cyst of the right lung. Variants of clinical course and complications The suppuration of the closed cysts resembles the development of a lung abscess with lesser expression of signs of intoxication (protective role of epithelial wall). Infection of the open cysts is characterized by a gradual long course, moderate manifestation of suppuration and late intoxication. The tension (valvular) cysts occur more often in children. They are characterized by severe respiratory and hemodynamic disturbances, up to terminal, as the result of inflexion of venous trunks, shift of mediasti- num and compression of lungs. The predominant signs are increased dys- pnea, cyanosis, chest pain, respiratory lag on affected side, absence or weakening of respiration on auscultation, bandbox percussion sound over the cavity. Pleural complications of pulmonary cysts, and also bleeding de- scribed in the relevant parts. The malignant degeneration of pulmonary cysts occurs very rarely. The diagnostic program 1. Complaints and history of the disease. 2. Physical methods of examination. 3. Chest X-ray film in two planes.
  • 22. 1.1. Lungs and pleura 21 4. Lung tomography. 5. Bronchography. 6. Angiopulmonography. 7. General blood and urine analyses. Differential diagnostics Lung abscess, in contrast to a suppurative cyst, is characterized by prompt course, expressed purulent intoxication, roentgenologically its wall is irregular, with proper considerable perifocal infiltration. Lung cancer with destruction differs by a thick wall with a tuberous inner surface, phenomena of lymphangitis in adjacent tissue. The deter- minant value has endoscopic examination or puncture with a biopsy and following morphological investigation. Tubercular cavern is commonly located in the upper lobes, in adja- cent tissue revealed fibrosis, petrifactions, dissemination, peribronchial lymphadenitis. In the sputum - mycobacterium of tuberculosis. Opposite to cyst, in termed diseases, the circumflex deformation of vascular branches are never observed on angiopulmonography. The considerable difficulties can arise during differentiation of the closed congenital cysts. Tuberculoma differs from them by characteristic localization. On X - ray examination the heterogenity of the shadow with calcifications, early excentric destruction, "tubercular" background is observed. Benign tumours sometimes possible to differentiate only after the results of cytological investigation of punctate or after the operation. Echinococcal cyst on tomogram has a double contour of chitinous and fibrous sheaths. In blood analyses observed eosinophilia. The final de- cision is taken out after the results of immunological (indirect microagglutination test) and allergic (Cacconi's reaction) tests. Huge cysts, in contrast to open air cysts, are characterized by a subpleural location. The diagnostic doubts at suspicion on a diaphragmatic hernia are solved by radiopaque examination of a gastrointestinal tract. The acquired cysts differ from congenital by roentgenological signs of the lesion of surrounding tissues (pneumofibrosis, deforming bronchi- tis, secondary bronchiectases, and calcifications). Postpneumonic cavities are of irregular shape, with grooves and pockets, their walls of different thick. During bronchography they filled through some small bronchi. Some- times the verification is possible only after postoperative morphological investigation.
  • 23. 22 1. Thoracic surgery Tactics and choice of treatment The pulmonary cysts require the surgical treatment. In case of com- plications the indication for operation becomes absolute. Contraindications: the severe respiratory disturbance, concomitant malignant nonresectable tumors, vital organs dysfunction in the stage of permanent decompensa- tion, elderly age of the patients. The volume of the operation: if adjacent pulmonary tissue is in- tact - cystectomy, otherwise - segmental or wedged resection, lobec- tomy. The conservative therapy is applied in suppuration of cysts with the purpose of preoperative preparation. It is the similar, which applied for lung abscesses. 1.1.3. Pleural empyema The pleural empyema is a purulent inflammation of its visceral and parietal membranes, which associated with accumulation of pus in a pleu- ral space. Etiology and pathogenesis The causes of acute pleural empyema are inflammatory, or puru- lent, destructive processes of lungs, abscesses of abdominal cavity (sec- ondary pleural empyema), open and closed damages of chest, and also, in some cases, surgical operations on thoracic organs (primary pleural empy- ema). A secondary pleural empyema occurs in 88 % of the patients. Thus develops fibrinous, exsudative, and then purulent pleurisy. If empyema is caused by pulmonary gangrene, purulent mediastini- tis, subphrenic abscess, the stage of exsudative pleurisy is extremely short. The progression of the process results in transferring of focal pleu- ral empyema into wide-spread. Pathology Macroscopically pleura is thickened, covered by pus with punctate hemorrhages. Microscopically it is diffusely oozed with neutrophils. In cases, when the empyema overcome into chronic course, the pleura deposits the calcareous salts, thick pus encapsulates, sometimes with the development of fistula.
  • 24. 1.1. Lungs and pleura 23 Classification I. According to the etiological factor: 1. Specific. 2. Nonspecific. II. According to the pathogenic factor: 1. Primary. 2. Secondary. III. According to the clinical course: 1. Acute. 2. Chronic. IV. According to extension of the process: 1. Focal. 2. Wide-spread. V. According to the presence of lung destruction: 1. Empyema with destruction of pulmonary tissue. 2. Empyema without destruction of pulmonary tissue. 3. Pyopneumothorax. VI. According to communication with environment: 1. Closed pleural empyema; 2. Open pleural empyema: • bronchopleural fistula; • thoracopleural fistula; • thoracopleurobronchial fistula; • cribrate lung. Symptomatology and clinical course The clinics of acute pleural empyema depends on extension of the process, reactivity of the organism and presence of complications. The pain is the sign, which denote the involvement of pleural mem- branes in the process. Its intensity increases depending on depth of respi- ration and body position. The dyspnea arises from accumulation of a purulent content in a pleu- ral space and exception of particular volume of 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 destruc- tive process in a pulmonary tissue. Fever to 39-40°C, headache, sleeplessness, general malaise, and an- orexia - all these are the manifestation of intoxication. The forced patient's position and restriction of breathing should be considered as outcomes of a pain syndrome. The extension of pleural em- pyema causes the swelling of thoracic wall, smoothing of intercostal spaces.
  • 25. 24 1. Thoracic surgery On 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. By percussion over the exudate it is possible to reveal short sound with oblique upper contour. Above the exudate - tympanic sound resulting from consolidation of pul­ monary tissue. On auscultation - diminished or absent sound in a great amount of exudate. The predominant roentgenological sign of a focal or wide-spread empyema - the presence of exudate. In localized acute pleural empyema observed a local intensive homogeneous shadow. Roentgenologically ac­ cording to localization distinguished such types of a focal empyema: 1) apical; 2) paramediastinal; 3) parietal; 4) interlobar; 5) ері phrenic. The wide-spread pleural empyema manifests by intensive homoge­ neous shadow in a basal parts with oblique upper contour (Damuaso' line). The diaphragmatic dome is failed to observe. The more pus is in pleural space, the higher upper border of the exudate (fig. 1.1.7). А В Fig. 1.1.7. Left-side pleural empyema. Variants of clinical course and complications The clinic of a focal pleural empyema depends on the site of the process. The apical empyema, due to involvement of a vascular-nervous fascicle in the process, manifests by intensive pain. The soft tissues of supraclavicular region are swelled. The percussion and auscultation has no information.
  • 26. 1.1. Lungs and pleura 25 The pain syndrome in parietal (paracostal) empyema is more expressed. Thoracic excursion is restricted. The diminishing of respiratory sound can be detected over the exudate. The chief complaint in paramediastinal empyema is the heart pain. The location of the process in the upper mediastinum can cause the supe­ rior vena cava syndrome. The physical findings are vague. In case of basal (ері phrenic) empyema the patients complain of pain in subcostal area, which increases at respiration and irradiates in supra­ clavicular region. In some cases the pain irradiates in epigastric region. The palpation of intercostal spaces and hypochondrium is painful. The clinical course of postoperative empyema depends on the char­ acter of operative approach (marginal resection of lung, lobectomy, pneumonectomy, operation on esophagus) and infection of the pleural space. The clinical manifestation of posttraumatic empyema depends on the size of the damage of chest, lungs, mediastinal organs and complications (suppuration, hemothorax). The involvement in the purulent process of a pulmonary tissue re­ sults in fusion of a pleural membranes with formation of a bronchial or thoracopleural fistula (discharge of abscess through thoracic wall). The inappropriate elimination of empyema results in chronic course, cribrate lung and pleurogenic cirrhosis of lungs. The diagnostic program Complaints and history of the disease. Physical findings. Data of chest X-ray (in two planes, if necessary - laterography). Pleural puncture. The microbiological investigation of the exudate for its sensivity to antibiotics. General blood and urine analyses. Biochemical blood analysis. Pleurography (in transferring of the process into chronic form). Differential diagnostics Pleuropneumonia complicated with exsudative pleurisy in some cases resembles acute pleural empyema: a chest pain, fever, dyspnea, cough, and general weakness. The chest roentgenogram reveals hydrothorax (exsudative pleurisy, pleural empyema, hemothorax). The chief diagnos­ tic method for differentiation is the thoracentesis. The presence of a serous (lucent, bright-yellow) exudate testifies about the pleuropneumonia, com- 1. 2. 3. 4. 5. 6. 7. 8.
  • 27. 26 1. Thoracic surgery plicated with pleural effusion, and cloudy, foul-smelling exudate of white or greenish color - about acute empyema. The major difficulties in differential diagnostics are caused in case of limited forms of empyema. Pancoast cancer clinically and roentgenologically in most cases has almost the similar course to apical form of empyema. The transthoracic biopsy allows to confirm the diagnosis. Acute cholecystitis is necessary to differentiate with the ері phrenic empyema. The pain in the right hypochondrium, fever, phrenic symptom are common for both diseases. However the objective findings, X-radiog- raphy of chest and the thoracentesis allow to differentiate these patho­ logical processes. Tumour of anterior mediastinum complicated by superior vena cava syndrome is necessary to differentiate with paramediastinal empyema. Nev­ ertheless the body temperature in such patients, as a rule, is normal. The upper cavography is possible to find out the shift of cava vein and its irregular contours (filling defect) due to growth of the mediastinal tumour. There are some difficulties in differential diagnostics of empyema with a posttraumatic diaphragmatic hernia. Such X-ray findings as defor­ mation of diaphragm, additional shadows with a fluid level, intestinal loop suggest a diaphragmatic hernia. A laterography and contrast study of gastrointestinal tract is basic in differential diagnostics of this disease. Atelectasis of a lung segment, or lobe in some cases can cause misdiagnostics. Except X-ray chest examination (in two planes and tomog­ raphy), these situations require necessity of diagnostic bronchoscopy, which reveals the cause of bronchial obturation (foreign body, endobronchial cancer etc.). Tactics and choice of treatment The presence of pus in a pleural space is the indication for its elimi­ nation. In the site of diagnostic thoracentesis performed the draining of empyema's cavity, its sanation by means of antiseptic solutions. In a focal empyema the aspiration of pus is carried out by thoracentesis and only in its inefficiency performed a draining of pleural space. Intensive antibacterial and antiinflammatory therapy should be im­ mediately instituted. For general improving used detoxication therapy (in­ fusion of saline solutions, hemotransfusion, transfusion of proteins, solu­ tions of dextran, forced diuresis, hemosorption if necessary), therapy for increasing of immunological resistance of the organism. The empyema's sanation decreases the amount of pus, which dis­ charged out through the drainage. The optimal variant of such course is the liquidation of empyema's cavity, then the drainage must be removed.
  • 28. 1.1. Lungs and pleura 27 Transition of the process into the chronic form (10-12 weeks) results in formation of a residual empyema's cavity, which is possible is to reveal by means of pleurography - introduction through the drainage of water- soluble contrast with the further X-radiography in two planes. Operative approach is applied when the process has transited into the chronic form, that is in the case of residual empyema cavity. The volume of the operation - pleurectomy, decortication of lung. A bronchial fistula and great empyema cavity requires the perfor- mance of lung resection and corrective thoracoplasty. 1.1.4. Pyopneumothorax Pyopneumothorax is the burst of lung abscess into pleural space, which is accompanied by purulent inflammation of pleural membranes with a collapse of lung. Etiology and pathogenesis Peripheral location of the purulent focus in a pulmonary tissue re- sults in destruction (fusion) of visceral membrane. As a result of, the pus and air penetrate into a pleural space that leads to a purulent inflammation of parietal and visceral membranes of pleura. The disorder of a pleural continuity results in a lung collapse. Among other causes of pyopneumothorax are the chest trauma, which results in collapse of lung, infection and purulent inflammation of pleural membranes. As the basic causes of pyopneumothorax are considered: - acute abscess of lung; - gangrenous abscess of lung; - lung gangrene; - purulent lung cyst; - abscessing pneumonia; - bronchiectatic disease; - subphrenic abscess, which has effluencedinto pleural space; - injury of esophagus; - mediastinitis; - chest trauma; - operation and diagnostic manipulations on chest organs.
  • 29. 28 Pathology 1. Thoracic surgery Morphologically pus and air are present in pleural space in pyopneumothorax. In lungs revealed subpleural purulent or necrotic foci, which connected with a pleural space through a pleuro-pulmonary fistula. From the outside the zone of disrupture is restricted by perifocal inflammation. In the draining bronchus it is possible to see manifestations of deforming, frequently polypous bronchitis. Classification I. According to the etiological factor: 1. Specific. 2. Nonspecific. II. According to the pathogenic factor: 1. Primary. 2. Secondary. III. According to the clinical course: 1. Asymptomatic form. 2. Mild form. 3. Acute form. IV. According to extension of the process: 1. Localized pyopneumothorax: a) parietal; b) apical; c) ері phrenic; d) paramediastinal; e) polychamber. 2. Subtotal pyopneumothorax. 3. Total pyopneumothorax. 4. Tension pyopneumothorax. Manifestation and clinical course The manifestation of pyopneumothorax depends on the size of the focus of destruction, which influences on the degree of lung collapse, and on amount of purulent content in a pleural space. The pain owing to the burst of destructive focus into pleural space often arises suddenly. The dyspnea occurs as a result of lung collapse owing to leakage of pus and air into pleural space. Its expression is in direct ratio to lung col­ lapse. Therefore a dyspnea in rest observed in a subtotal and total pyop­ neumothorax. It sharply amplifies even at minor physical activity. Auxil­ iary muscles take part in order to force respiration.
  • 30. 1.1. Lungs and pleura 29 The expectoration of sputum with ichorous smell is the outcome of destructive process in a pulmonary tissue. Its amount decreases after effu- sion of pus into pleural space. Hectic fever is caused by enlargement of the area of resorption. The patients are adynamic, flaccid. Some of them are unconsciousness. On objective examination the position of patients is forced, they sit leaning upon the bed (subtotal, total pyopneumothorax). The affected hemithorax takes no part in respiration. On palpation - diminished vocal fremitus on the side of lesion. Percussion reveals a sharp shortening of sound over the zone of exudate and bandbox sound above the region of collapsed lung. On auscultation there are no breathing sounds on the affected side. In case of localized pyopneumothorax - weakened or sharply weakened sound with a bronchial or amphoric tone. The X-ray picture of pyopneumothorax depends on its form, but the obligatory sign is the air-fluid level in a pleural space with well-de- fined edge of collapsed lung on its background (fig. 1.1.8). Fig. 1.1.8. Left-side total pneumothorax, represented by air-fluid level in the pleural space and well-defined edge of the collapsed lung. Variants of clinical course and complications The clinical course of pyopneumothorax depends on adhesions be- tween pleural membranes. It sometimes changes typical clinical course of a total lung collapse. The manifestation of the disease depends also on amount of a purulent exudate. Therefore, according to extension of the process and size of lung destruction, distinguished acute, mild and asymptomatic forms of pyopneumothorax. Especially difficult for diagnostics is the asymptomatic form of localized pyopneumothorax. Dyspnea for such pathology is not char- acteristic, as the adhesion of membranes prevents complete collapse of lung. Dyspnea is vague or absent at all in partial collapse. A diminished vocal
  • 31. ЗО 1. Thoracic surgery fremitus on the side of pathological process, shortening of percussion sound and weakened or sharply weakened breathing sounds over the collapsed lung and exudate are revealed. Roentgenological manifestation in localized pyopneumothorax not expressed and include horizontal fluid level, margin of partially collapsed lung and minor air in the pleural space. In most cases after the effkuence of the destructive focus into a pleural space and lung collapse observed the closure of bronchopleural fistula. Nevertheless the inflammatory process in a pulmonary tissue and pleural space is going on. The diagnostic program 1. Complaints and history of the disease. 2. Physical findings. 3. Chest X-radiography examination. 4. Thoracentesis. 5. Pleurography. 6. Bacterial culture and antibiotic sensitivity. 7. General blood, and urine analyses. 8. Biochemical blood analysis. Differential diagnostics They're no special necessity for differential diagnostics of pyopneu­ mothorax in the majority of patients. History (presence of the purulent focus in a pulmonary tissue), clinical course (acute pain and dyspnea in abscess burst into pleural space), and also chest X-ray findings and thora­ centesis frequently reliably permit to make the diagnosis. In some cases a localized pyopneumothorax according to clinical course resembles a huge acute abscess of lungs. But the differences of roent­ genological symptomatology allow to verify these pathological processes. In acute lung abscess the cavity of destruction localized in a pulmonary pa­ renchyma, it is round in form with horizontal fluid level and expressed perifocal infiltration. Tactics and choice of treatment The purpose of treatment should include sanation of the destructive focus in pulmon ary tissue and liquidation of complications; that means elimi- nation of pus and air from a pleural space and prompt expanding of lung. 1. Active sanation of tracheobronchial tree by means of tracheocentesis. 2. Draining of pleural space, active aspiration of its content (air, pus) to expand the lung.
  • 32. 1.1. Lungs and pleura 31 3. Lavage of pleural space by antiseptic solutions. 4. Appropriate antibacterial, antiinflammatory and infusion therapy. 5. The therapy for increasing of immunological resistance of the organism (staphylococcal anatoxin , antistaphylococcal gamma-globulin, antistaphylococcal plasma). 6. Endolymphatic introduction of immunity stimulators (thymalin, thymogen, T-activin). The indications for operative management are the same, as in pleural empyema. 1.1.5. Spontaneous pneumothorax Spontaneous pneumothorax is the entry of air in a pleural space with the further lung collapse, which not associated with traumatic damage of chest or pulmonary tissue. Etiology and pathogenesis As a result of spontaneous disrupture of lung blebs and subpleural air cysts the damage of pleural visceral membrane occurs. It causes entry of air in pleural space. Owing to its leakage the elastic pulmonary tissue collapses. The degree of the collapse depends on amount of air, that has penetrated a pleural space. Pathology Morphologically in spontaneous pneumothorax found out a focal bullous emphysema with disrupture of blebs, subpleural air cyst, and also disor- ders, which have caused disturbances of ventilating ability of bronchi. It can be bronchitis, pneumosclerosis, tuberculosis and fibrous alveolitis. Classification The pneumothorax can be: 1. Unilateral or bilateral. 2. Partial (lung collapse less 1/3 of its volume). 3. Subtotal (lung collapse less 2/3 of its volume). 4. Total (lung collapse exceeds 2/3 of its volume). 5. Tension or valvular (complete collapse of lungs and shift of mediasti- num to the opposite side). 6. Rigid (neglected pneumothorax with thickened visceral pleura).
  • 33. 32 Manifestation and clinical course 1. Thoracic surgery The onset of the disease is sudden. The patient's state and expression of clinical manifestation depends on amount of air, which has entered the pleural space. Usually in normal conditions, and sometimes after physical activity, the patients suddenly feel sharp pain on the side of lesion, dys- pnea, pain in the heart region and heartbeating. Acrocyanosis or total c y - anosis of skin is observed. The circulatory disturbance depends on the degree of hypoxia. Intensity of pain and dyspnea gradually decreases, but a dry troubling cough appears. Examination of the chest allows to observe expansion of intercostal spaces and restriction of respiratory excursion. On palpation - diminishing of vocal fremitus on the affected side. On percussion a chief sign of pneu- mothorax is the tympanic sound. Auscultation reveals weakened or sharply weakened breathing sounds. The cardiac tones are muffled, tachycardia. Fig. 1.1.9. Pneumothorax. Right-side partial pneumothorax (A), right-side subtotal pneumothorax (B), right-side total pneumothorax (C).
  • 34. 1.1. Lungs and pleura 33 The diagnosis of spontaneous pneumothorax is confirmed by X-ray examination. On the plain roentgenogram the air is present in pleural space, and the margins of collapsed lung are found out on its background (fig. 1.1.9). Thoracoscopy in pneumothorax possible to find out subpleural blebs of different sizes (0,5-3 cm), which are mainly disposed on the apex of lung. Variants of clinical course and complications The atypical (asymptomatic) spontaneous pneumothorax occurs in 20 % of the patients, and mainly revealed by X-ray examination. In most cases it is the partial pneumothorax. The expressed pain syndrome and dyspnea, resulting from collapse of lung, characterizes subtotal and total pneumothorax. The tension spontaneous pneumothorax is the most severe form of pneumothorax. It manifests by sudden onset, progressive increase of dys- pnea, expressed cyanosis. The breathing is superficial, rapid, with active participation of auxiliary muscles. Mediastinal shift and flexion of vessels results in disturbance of cardiac activity up to the cardiac arrest, and requires urgent management. Rigid pneumothorax (rigid lung). The neglected pneumothorax causes fibrinous exsudative pleurisy. On the surface of lung (visceral pleura) com- missures are formed, that give no opportunity for lung expansion. The presence of residual pleural cavity and progressive development of a pu- rulent infection results in occurrence of acute pleural empyema. In such cases the patients complain of the fever to 38-38,5°C, general weakness and increasing dyspnea. The phenomena of intoxication are evident. Thus such patients require the treatment of pleural empyema. The diagnostic program 1. Complaint and anamnesis of disease. 2. Physical findings. 3. Plain chest film (direct and lateral projection). 4. Thoracentesis. 5. Thoracoscopy. 6. Tomography of lungs. Differential diagnostics Pleural effusion. This pathology manifests by more gradual onset. As opposite to pneumothorax, the complaints of chest pain predominate above the complaints of dyspnea. Frequently such patients specify on previous undercooling.
  • 35. 34 1. Thoracic surgery As well as the spontaneous pneumothorax, the pleural effusion is char- acterized by diminishing of vocal fremitus, dullness of percussion sound, weakened or absent breathing sounds over the exudate. Nevertheless in the plain roentgenogram in such cases observed a homogeneous intensive shadow of a pleural space with oblique upper contour. The puncture of pleural space enables finally to confirm the diagnosis of pleural effusion. Intercostal neuralgia. A predominant sign in clinical pattern is acute pain, which intensifies at physical activity, changes of body position and body movements, at deep breathing. The localization of pain coincides with zone of innervation of intercostal nerves. Examination and chest X-radiography reveals no pathological changes. Tactics and choice of treatment Conservative treatment is applied in the patients with a partial pneu- mothorax. Thus thoracentesis in II intercostal space in the midclavicular line with aspiration of air is performed. The cases of its inefficiency, and also subtotal, total and tension pneumothorax require the draining of a pleural space with active aspiration of air. The operative management is necessary, if there is no efficiency from active aspiration (in incomplete expansion of lung), recurrent of course of the process, presence of great subpleural blebs and rigid pneu- mothorax. The volume of operation depends on extension of the process: liquidation of alveolar fistula, wedged resection of lung or lobectomy. 1.1.6. Lung Cancer The tumour arises from epithelium of bronchi, bronchial mucous glands, and also terminal bronchioles. Etiology and pathogenesis It is well established that the dominant risk factor for lung cancer is cigarette smoking. The risk increases with the number of cigarettes smoked daily, the duration of smoking, young age at onset of smoking, degree of inhala- tion, the tar and nicotine content and the use of unfiltered cigarettes. Also other types of smoking including passive smoking, and occupational ex- posures to carcinogenic agents such as asbestos fibers, arsenic compounds, chromium compounds, mustard gas, nickel compounds, ionizing radia- tion, tars and some mineral oils, are associated with the risk of developing lung cancer. A synergistic interaction has been observed for asbestos, ion-
  • 36. 1.1. Lungs and pleura 35 izing radiation, and arsenic compounds in combination with tobacco smok- ing, in such a way that the combined exposure is associated with a lung cancer risk that for exceeds that expected from the separate exposure to each of the agents. The contributing factors: a) Chronic obstructive diseases of lungs; b) Other chronic diseases of lungs (chronic fibrosis); c) Lung scars. Histopatology More than 95% of bronchial tumors can be classified into four major cell types: small cell carcinoma squamous cell carcinoma, adenocarcinoma and large cell carcinoma. The remaining 5% include mesothelional and carcinids. The frequency of small cell carcinoma seems rather constant (20-30%), whereas the variations in frequency for the rest types are differ- ent. For practical and therapeutic purposes these tree types are commonly referred to as non-small cell lung cancer. Classification Lung cancer is divided into central, peripheral and atypical cancer. Central cancer includes the tumours of the first-third order bronchi. Ac- cording to the loco-regional spread it is divided into endobronchial and peribronchial cancer making a great influence on the roentgenological pic- ture. On early stages vicar emphysema develops, caused by difficulties in breathing out. Then it overcomes into hypoventilation, caused by difficul- ties in breathing in. Later an obturative atelectasis develops. Peripheral cancer include rounded tumour, pneumonielike tumour and Pancoast's cancer. Atypical form include miliary carcinomatosis, me- diastinal form, etc. TNM - classification of non-small lung cancer TQ - no evidence of primary tumour T. - carcinoma in situ is Tj - tumour less than 3 cm in greatest dimension, surrounded with lung tissue. T2 - tumour more than 3 cm in greatest dimension or tumour result- ing in lobar atelectasis, or tumour located more than 2 cm from carina. T3 - tumour resulting in total atelectasis, or tumour located less than 2 cm from carina, or tumour extending through diaphragm, pleura, peri- cardium.
  • 37. 36 1. Thoracic surgery T4 - tumour extending through the vital organs (heart, esophagus, aorta). N0 - no regional lymph node metastasis. N - metastasis in lymph node of the root of the lung. N2 - metastasis in lymph node of carina or mediastinal lymph node on the side of lesion. N3 - metastasis in lymph node of the root of the opposite lung or mediastinal lymph node of the opposite side. Ml - distant metastasis. Grouping according to stages fig. 1.1.10. fig. 1.1.11. fig. 1.1.12. fig. 1.1.13. Occult carcinoma T x N0 M o Stage 0 N o M o Stage 1 T . N o M o T2 N o M0 Stage 2 », м 0 N: Stage ЗА T . N 2 M oT . N 2 4N0 ,Ni ; N2 M o Stage ЗА T T T T J ' 1' -1 2' 3' A 4 м 0 T T T T J ' 1' -1 2' 3' A 4 N 3 M o Stage 4 T T T T •l l>-l 2> 3 ' A 4 NpN2 ,N3
  • 38. 1.1. Lungs and pleura 37 Fig. 1.1.12. Stage ЗА. Fig. 1.1.13. Stage 3B. Small cell lung cancer is classified as "limited" or "wide-spread" process. Under the meaning "limited" process we consider a tumour disposed in one side of the chest, including mediastinum and supraclavicular lymph nodes. "Wide-spread" process is the lesion, which exceeds above-stated limits. Manifestation and clinical course The basic complaints and signs of a central lung cancer are: 1) The constant cough which has appeared recently or changed its character in smokers. The cough increases in dynamics, dry in initial stages, troublesome, with further occurrence of dirty, rusty sputum); 2) Hemoptysis; 3) Dyspnea, which depends on body position (upright, supine etc); 4) The dyspnea of exertion (can appear, if the bronchus completely obstructed); 5) Rales; 6) The prolonged pneumonia, which is not responsible to treatment; 7) Obstructive pneumonia. The complaints and signs in peri pheral lung cancer depend on the size of a tumour. There are no complaints in case of small dimension, when it is completely surrounded by a normal pulmonary tissue. If the tumour reaches the considerable sizes, it can manifest by permanent cough, dyspnea owing to pleural exudate and pain, which arises from the growth into pleura. The peripheral cancer can manifest by general signs: general malaise and loss of weight. The complaints and signs, as outcomes of local exten­ sion of the process or presence of the distant metastases, result from: • growth of tumour into nervous fibers; • growth into or compression of adjacent structures; • distant metastasizing.
  • 39. 38 1. Thoracic surgery The growth of tumour into nervous fibers manifests by: • Severe chest pain (in lesion of intercostal nerves); • Hoarseness (growth into recurrent nerve); • Dyspnea (growth into diaphragmatic nerve and phrenoplegia); • Brachial pain or weakness in arm (lesion of brachial plexus); • Horner's Syndrome (caused by lesion of cervical sympathetic trunk). The growth or pressure of the tumour on adjacent structures mani­ fests by: 1) superior vena cava syndrome; 2) cardiac arrhythmia, cardiac failure; 3) signs of esophageal obstruction; 4) dyspnea caused by carcinomatous pleurisy; 5) permanent hiccup; Physical findings on initial stages of the disease are within norm. In advanced stages on examination of the chest observed its asymmetry and delayed breathing movements of affected side during respiration. On palpation in advanced stages on the side of lesion it is possible to find out diminished vocal fremitus and enlarged supraclavicular lymph nodes. On percussion over atelectasis or pleurisy revealed dull sound on the side of lesion. Fig. 1.1.14. Peripheral cancer of the right lung. A - Plain chest X-ray film; В - Direct tomogram; С - cancer that caused atelectasis of the lower lobe.
  • 40. 1.1. Lungs and pleura 39 On auscultation revealed bron- chial breathing or moist rales. The diagnosis of lung cancer es- tablished on the base of clinical, roent- genological, bronchoscopic, cytologi- cal and histological findings. Roentgenological diagnostics in 80 % of cases allows in time to find out lung cancer. On plain roentgeno- grams in central form of cancer ob- served a small additional shadow su- perimposed on the root of lung, in Fig. 1.1.15. Peripheral cancer of the right peripheral - well-defined rounded !ung. shadow (fig. 1.2.14-15). On tomograms it is possible detect the additional shadow, which narrows, compresses or charges a lumen of the bronchus. Complete obstruction results in segmen- tal or lobar atelectasis or atelectasis of entire lung. The improvement of the diagnosis is achieved by computer tomography (fig. 1.1.16) or scanning of lungs (fig. 1.1.17).
  • 41. А В Fig. 1.1.17. Scanning of lungs. Central cancer of the right lung with lower lobe atelectasis (A), normal lungs (B). The bronchoscopic examination should be carried out for all patient with suspicion on lung cancer. Such examination is suitable for central form of the cancer and presence of malign ant tumour in the lumen of bronchus. In peripheral localization performed a transthoracic puncture with the further investigation of the material. Variants of clinical course Pancoast's cancer (cancer of the apex of lung). It is characterized by the brachial pain, paresthesias, lesion of brachial plexus and Horner's syndrome (ptosis, miosis, enophthalmus). In some cases the destruction of I rib is revealed. In peripheral cancer with destruction the patients complain of cough, expectoration of purulent sputum, hemoptysis, pulmonary bleeding, fe­ ver to 38-39°C, dyspnea and chest pain. The mediastinal form of cancer revealed in advanced stages of the process. As a rule, it is failed to find the primary focus. The metastases in lymph nodes of mediastinum result in compression of superior cava vein. The primary carcinomatosis is characterized by multiple metastatic lesion of lungs. In most cases it is impossible to find the primary tumor. The patients complain of progressing dyspnea. A chest pain caused by spreading of the process on a pleural membrane and thoracic wall. The hemoptysis arises if major bronchus involved in carcinomatosis. The diagnostic program 1. Complaints of the patient and anamnesis. 2. Physical findings.
  • 42. 1.1. Lungs and pleura 41 • H 3. X-ray chest film in 2 planes. 4. Tomography of lungs. 5. Fibrobronchoscopy with a biopsy for cytological and histological examinations. 6. Thoracentesis. 7. Computer tomography. Tactics and choice of treatment The primary curative treatment for non-small cell lung cancer is sur- gery. In stages I or II a complete surgical resection is almost always possible. Segmental resection will be selected for patients with small peripheral tumours (less 2 cm in diameter), with no evidence of extension or metastases (Tj No Mo). Lobectomy is performed for patients with a centrally located tumour and free margins are required for this type of resection. Pneumonectomy is the procedure of choice for patients with tumours extending to the orifice of the lobar bronchus and tumours originating within or extending to the main bronchus, with involvement of more than one lobe. Non-small cell lung cancer patients with stage III disease other than T3 lesions have an extent of disease which prohibits surgical resection. Therefore preoperative chemotherapy or radiotherapy, either alone or in combination, has been applied to minimize the extent of tumour before surgery thereby increasing the possibility of radical resection. As more than two-thirds of all resected patients relapse, great interest has been given to adjuvant treatment, such as postoperative radiation therapy and adjuvant chemotherapy. The disseminated nature of small cell lung cancer, displaying a high frequency of metastases at the time of diagnosis combined with a high sensivity to cytostatic agents, has led to the use of chemotherapy as the treatment of choice in all stages. Usually chemotherapy is combined with radiotherapy because of the high radiosensitivity of small cell lung cancer.
  • 43. 1.2. TRAUMA OF THE CHEST The modern traumatism represents the important social problem. Re- cently observed the increase of major combined trauma, which complica- tions often result in death. The trauma of the chest is usually accompanied by dysfunction of the vital organs. Therefrom it is necessary constantly to improve diagnostics and treatment of the patients who suffer from trauma. Classification The closed damages of the chest are divided: I. According to the injury of other organs: 1. Isolated trauma. 2. Combined trauma (craniocerebral, with the damage of abdominal organs, with the damage of bones). II. According to the mechanism of trauma: 1. Contusion. 2. Compression. 3. Commotion. 4. Fracture. III. According to the character of the damage of chest organs: 1. Without damage of organs. 2. With damage of organs (lungs, trachea, bronchi, esophagus, heart, vessels, diaphragm etc.). IV. According to the character of complications: 1. Uncomplicated. 2. Complicated: 1) Early (pneumothorax, hemothorax, subcutaneous, mediastinal em- physema floatative rib fracture, traumatic shock, asphyxia); 2) Late (posttraumatic pneumonia, posttraumatic pleurisy, suppura- tive diseases of lungs and pleura). V. According to the state of cardiopulmonary system: 1. Without phenomena of respiratory failure. 2. Acute respiratory failure (of I, II, III degree). 3. Without phenomena of cardiovascular failure. 4. Acute cardiovascular failure (of I, II, III degree). VI. According to the severity of trauma: 1. Mild. 2. Moderate. 3. Severe.
  • 44. 1.2. Trauma of the chest 43 1.2.1. Rib fracture The direct force of traumatizing factor on the chest wall results in rib fracture. The pain localized in the zone of damage, is the chief clinical mani- festation. The pain intensifies at respi- ration, cough and change of a body position of the patient. The overwhelm- ing majority of the patients complain of crepitation of ribs in the fracture site. On examination the respiratory lag on affected side is observed. Depending on number of injured ribs, crepitating of osseous fragment revealed by palpation, and diminished breathing sounds on auscultation. On chest roentgenograms the break in continuity of bone fragments Fig. 1.2.1. Closed chest trauma, complicated of ribs is observed (fig. 1.2.1). with left-side VI-VIII rib fracture. Floatating rib fracture This is one of the most severe complication of the closed trauma of the chest. The floatation arises from fracture of three and more ribs along two anatomic lines. The multiple rib fractures produce an unstable seg- ment of chest wall that moves paradoxically inward at inspiration and balloons outward during expiration (flail chest). Thereby the respiration disturbed not only in the area of a floatating segment, but also in all lungs. The permanent movements of floatating segment result in rocking shift of mediastinum, which causes deviation of its organs. As a result the respiratory failure is associated with cardiovascular. Classification 1. Central floatative segment - a multiple rib fracture along parasternal or midclavicular lines. 2. Anterolateral floatative segment - a multiple rib fracture along parasternal and anteaxillary lines. 3. Lateral floatative segment - a multiple rib fracture along anterior and posterior axillary lines. 4. Posterior floatative segment - a multiple rib fracture along postaxillary and paravertebral lines.
  • 45. Symptomatology and clinical course The patients state is grave or extremely grave. The expressed pain syndrome frequently results in traumatic shock. The patient is restless. Observed the skin cyanosis, tachypnea, and tachycardia to 120-160 beat/ min of weak filling and tension. Arterial pressure at first elevated, then its decrease is observed. On examination characteristic paradoxical respiratory movements of chest, inward at inspi- ration and outward during expiration, and also crepitus of bone fragments by palpation are revealed. Breathing sounds diminished on the side of dam- age on auscultation. In case of floatative rib fracture the chest X-ray examination reveals multiple (fig. 1.2.2), double rib fracture with deformity of the chest. In 75 % of cases the multiple rib fracture is the cause of injury of Fig. 1.2.2. Bilateral rib fracture. Right-side , pneumohemothorax. Subcutaneous l u n S s > pneumothorax or pneumohe- emphysema. mothorax. Treatment Pain relief in closed trauma of the chest is achieved by means of different blocks: 1. Vagosympathetic block; 2. Alcohol - novocaine block of the site of fracture; 3. Paravertebral block. Except blocks, in some cases analgesics and opiates are instituted. On 2-3 day desirable the administration of electrophoresis with novocaine. For the prophylaxis of congested phenomena in a pulmonary tissue used res- piratory gymnastics, forced ventilation of lungs, inhalations. The methods of renewal of the skeleton of the flail chest are divided onto three groups: 1. External fixation of a movable segment by means of suturing for intercostal muscles and traction during 2-3 weeks; 2. Intrmedullary costal osteosynthesis; 3. Mechanical ventilation (often with positive end-expiratory pres- sure).
  • 46. 1.2. Trauma of the chest 45 1.2.2. Sternal Fracture The fracture of breastbone is commonly caused by direct forces at the site of the sternum. Usually it is the outcome of compression or result of trauma to vehicle helm. The fracture in most cases located in the upper and medial thirds of sternum. The patients complain of severe pain in the site of fracture, which in- tensifies at respiration and movements. The pain behind the sternum and in the heart area follows the contusion of lungs and heart. Sometimes hemopty- sis is observed. Examination reveals the deformity of breastbone in the site of fracture. Displaced fragments are accompanied by severe pain syndrome by palpation. On auscultation, if there are no intrapleural complications, the respi- ration in the first 2-3 days is vesicular on both sides. Then the fine bubbling rales are auscultated, which are the first objective manifestation of a post- traumatic pneumonia. The complete sternal fracture is characterized by a break in continuity of both cortical plates with a local dis- location of fragments (fig. 1.2.3). Fig. 1.2.3. Fracture of the breastbone corpus with a local dislocation of fragments. The diagnostic program 1. Complaints and history of the disease. 2. Physical findings. 3. Chest roentgenograms in two planes. Treatment The sternal fracture without displacement of fragments requires only conservative treatment. The fracture of the sternal corpus with disloca- tion of fragments quite often requires operative treatment with perfor- mance of osteosynthesis.
  • 47. 46 1. Thoracic surgery 1.2.3. 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. Classification I. According to extension of the process: 1. Unilateral. 2. Bilateral. II. According to the degree of a lung collapse: 1. Partial (collapse of lung lessl/3 of its volume). 2. Subtotal (collapse of lung less 2/3 of its volume). 3. Total (collapse of lung exceeding 2/3 of its volume). III. According to the mechanism of occurrence: 1. Closed. 2. Open. 3. Valvular. The closed pneumothorax is the complication, which arises from the damage of visceral pleural membrane, which results in entry of air into pleural space and atelectasis of lung. In chest trauma the cause of occur- rence of the closed pneumothorax is the perforation of visceral pleura and pulmonary tissue by the fragment of fractured rib. The open pneumothorax results from formation of hole in a chest wall and free entry of air during inspiration into pleural space, and during expiration - outward. The valvular pneumothorax caused by the damage of a pulmonary tissue or chest wall with formation of the valve, when the air during inspiration enters a pleural space, and during expiration, due to valve closure, does not exits outside. It is the most dangerous form of pneu- mothorax, which results in a complete pulmonary collapse, shift of medi- astinum, inflection of major vessels and cardiac arrest. Symptomatology and clinical course The predominant clinical manifestation of posttraumatic pneumothorax, which results from a pulmonary collapse, is the rest dyspnea, which amplifies at a minor exertion. This sign arises due to atelectasis of lung and its exclusion from breathing. On the background of collapsed lung only the main and lobar bronchi and pleural space are ventilated. The oxygenation of blood in collapsed lungs does not occur, therefore the shunting of a venous blood observed. The chest pain is more characteristic manifestation for trauma with the damage of ribs, however pulmonary collapse also can associate
  • 48. 1.2. Trauma of the chest 47 with a pain syndrome. Nevertheless the patients promptly adapt to it and the dyspnea finally remains the basic clinical manifestation of such complication. On the background of severe trauma of the chest the signs of dam- age dominate in clinical manifestation on inappreciable entry of air in a pleural space. Pneumothorax mostly revealed during X-ray ex- amination. Progressing of air en- try in a pleural space and pulmo- nary collapse cause the respira- tory lag on affected side. By palpation the vocal fremitus is ab- sent. It indicates the origin of the complication - rib fracture. Percussion obtains bandbox sound, or pulmonary sound with tympanitis. On auscultation - weak or absent breathing sounds, sometimes - amphoric respiration. The expressiveness of clinical pat- tern depends on degree of a pul- monary collapse. Pulmonary atelectasis and presence of air in a pleural space are the X-ray findings that enable to establish the final diagnosis (fig. 1.2.4). Fig. 1.2.4. Closed chest trauma, complicated with a right-side pneumohemothorax. The diagnostic program 1. Complaints and history of the disease. 2. Physical examination. 3. Chest X-radiography in 2 planes. 4. Thoracentesis. 5. ECG. Treatment A chest trauma, complicated by pneumothorax with a partial pulmo- nary collapse (lessl/3 of its volume) is the indication for aspiration of air by means of thoracentesis. The cases, if the negative pressure in a pleural space is not obtained, and also subtotal, or total pneumothorax require closed drainage of a pleural space. Under the local anesthesia by solution of novocaine in II intercostal space in the midclavicular line through a trocar in pleural space inserted a plastic tube, which fixed to skin. The drainage connects to aspirative sys-
  • 49. 48 1. Thoracic surgery tern or Bulough's system. In the majority of patients the pneumothorax liquidates in some hours, or 1-2 days. The absence of effect (incomplete expansion of lung) of active aspi- ration, and also valvular closed pneumothorax is the indication for opera- tive management - suturing of the pulmonary wound. In some cases a segmental resection of lung, or lobectomy is carried out. 1.2.4. Hemothorax Hemothorax is the accumulation of blood in a pleural space. The cause of occurrence of this complication is the damage of vessels of the chest wall, pleura, lungs and mediastinum. Classification I. According to extent: 1. Unilateral. 2. Bilateral. If. According to the degree of hemorrhage: 1. Small (the loss less 10 % of volume of circulating blood). 2. Moderate (loss of 10-20 % of volume of circulating blood). 3. Great (loss of 20-40 % of volume of circulating blood). 4. Total (exceeds 40 % of volume of circulating blood). III. According to the duration of bleeding: 1. With continued hemorrhage. 2. With the stopped bleeding. TV. According to the presence of clots in a pleural space: 1. Coagulated. 2. Non-coagulated. V. According to the presence of infection: 1. Non-infected. 2. Infected (suppurative). Symptomatology and clinical course If hemothorax is the complication of blunt chest trauma, the clinical manifestations depend on the severity of the trauma and degree of hem- orrhage. Also hemothorax by itself results in pulmonary compression and shift of mediastinum. In case of small hemothorax the clinical manifestations of hemor- rhage are slightly expressed or absent at all.
  • 50. 1.2. Trauma of the chest 49 Dyspnea, cough, general malaise and dizziness are obvious in moderate hemothorax. The skin is pale. The he- modynamic disturbances: tachycardia and decreased arterial pressure are ob- served. The great and total hemothorax are associated with extremely grave condition. The patients are troubled with expressed general malaise, dizzi- ness, dyspnea and difficult breathing. In some cases they enter medical hos- pitals in a terminal state. The skin is sharply pale. The peripheral pulse im- paired or absent. Tachycardia, weak cardiac tones, low arterial pressure are obvious. On percussion the dullness is re- vealed. On auscultation - the breath- ing over the site of hemothorax is sharply diminished or absent. The X-ray picture of hemotho- rax is rather specific. The intensive ho- mogeneous shadow on the side of the lesion with oblique upper contour (Damuaso' line) is observed. The costal sinus does not visualized. In small he- mothorax, depending on the degree of intrapleural bleeding, the shadow ob- served only in the region of sinus (fig. 1.2.5). In moderate hemothorax it achieves a scapular angle (on the back surface) or V rib on anterior surface of the chest wall (fig. 1.2.6). In great hemothorax this shadow achieves III rib (fig. 1.2.7), and total hemothorax characterized by complete shadow of a pleural space, and in some cases - mediastinal shift to the healthy side (fig. 1.2.8). Fig. 1.2.5. Left-side small hemothorax. Fig. 1.2.6. Left-side moderate hemothorax The diagnostic program 1. Complaints and anamnesis of the disease. 2. Physical examination. 3. Chest roentgenograms in 2 planes.
  • 51. Fig. 1.2.7. Right-side great hemothorax Fig. 1.2.8. Left-side total hemothorax. 4. Thoracentesis. 5. Investigation of a pleural content. 6. Revilour-Greguar's test. 7. General blood analysis. 8. Biochemical blood analysis. 9. Determining of the blood group and Rh factor. Variants of clinical course and complications The coagulated hemothorax. The late patient's apply for medical aid or major bleeding results in formation of clots in a pleural space, and in some cases all blood, which has accumulated in a pleural space, forms by itself a major entire clot. Depending on degree of bleeding and, consequently, size of clot, the patients complain of chest pain, which intensifies at respiration, dys- pnea, general malaise, and dizziness. As a rule, on 3-5 day the fever 37,5- 38°C is observed. The physical findings (diminishing and absence of vocal fremitus by palpation, dullness by percussion and sharply diminished or absent breathing by auscultation) suggest the presence of pathological process in a pleural space. Chest roentgenogram reveals the intensive shadow, sometimes het- erogeneous (with enlightenments and multiple levels). The needle aspiration obtains small amount of a liquid hemolyzed blood and small bloody thrombi (consequently to the inner diameter of the needle). Suppurative hemothorax. The coagulated hemothorax in overwhelm- ing majority is infected, that results in pleural empyema (clinical manifes- tations, diagnostics and treatment look in chapter " pleural empyema").
  • 52. 1.2. Trauma of the chest 51 Treatment The treatment of small hemothorax requires needle aspiration or drainage of pleural space and elimination of blood. The manipulation is carried out in VI-VII intercostal spaces in the postaxillary or scapular lines. Total, great or moderate hemothorax with persistent bleeding (posi- tive Revilour-Greguar's test) 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. 1.2.5. Subcutaneous emphysema The cause of this complication of blunt chest trauma is the damage of parietal and visceral pleural membranes by the edge of broken rib with the following entering of air from a pulmonary tissue into a pleural space and through damaged chest wall (ruptured intercostal muscles) into sub- cutaneous fat. In overwhelming majority the subcutaneous emphysema is the out- come of a valvular pneumothorax and pneumothorax in obliterated pleu- ral space. Classification Subcutaneous emphysema is divided on: 1. Localized. 2. Widespread. 3. Total. Symptomatology and clinical course As the subcutaneous emphysema is the outcome of trauma compli- cated by a rib fracture and posttraumatic pneumothorax, the chief com- plaints are the chest pain and dyspnea, which intensify at respiration, movements and minor physical activity. In localized subcutaneous emphysema the manifestations of the chest trauma are predominant in symptomatology. On examination observed a swelling of a chest wall in the site of the damage. On palpation a subcuta- neous crepitation is felt over this region. Percussion reveals a bandbox sound or tympanitis. Auscultation of lungs over subcutaneous emphysema is usually impossible.
  • 53. 52 1. Thoracic surgery The widespread and total subcutaneous emphysema represents a serious moral problem for the patient. Owing to extent of air all over the chest, abdominal wall, neck (wide-spread emphysema), and also face, arms and legs (total emphysema), the patients has a specific appearance: swelled face, thick neck, enlarged chest, arms, and legs. Subcutaneous emphysema by itself usually causes no respiratory and cardiovascular disturbances. However the patients note the change of the quality of voice. By palpation the subcutaneous emphysema is felt in whole body ("crisping snow"). It is necessary to note, that in widespread and total emphysema the auscultation is impossible. However the presence of subcutaneous emphysema in closed trauma of the chest enables to suspect the presence of posttrau- matic pneumothorax. On the chest roentgenogram the enlightenment of a subcutaneous fat Fig. 1.2.9. Subcutaneous emphysema. (presence of air) is observed (fig. 1.2.9). The diagnostic program 1. Complaints and history of the disease. 2. Physical findings. 3. Chest X-radiography. Treatment Widespread and total subcutaneous emphysema requires the draining of subcutaneous space by plastic tubes in infra- and supraclavicular re- gion, and also in the zone of the most expressed emphysema. Also per- formed the drainage of a pleural space. The subcutaneous emphysema resolves depending on its extent from several days to 2-3,5 weeks. 1.2.6. Traumatic injury of trachea and main bronchi The isolated injuries of trachea and bronchi as the result of blunt trauma of the chest occur rarely and located mainly in a cervical part. The main causes of tracheal and bronchial rupture are:
  • 54. 1.2. Trauma of the chest 53 1) shearing forces, which arises at the moment of trauma as a result of a sudden rise of intraluminal pressure in airways when the glottis is closed; 2) compressing of a bronchial tree between a breastbone and vertebral column; 3) in sudden and rapid deceleration or acceleration of the body a shift of lungs occurs with more greater amplitude, than fixed bifurcation of trachea. Such disruptions most often occurs as a result of vehicular impacts, falls from great heights, direct blows to the chest. In most cases disruption of trachea and bronchi are accompanied with the other visceral damages: lungs, skull and brain, heart, liver and flail chest. Classification I. According to the degree of disruption: 1. Partial: • without damage of cartilaginous rings (I degree); • with fracture of cartilaginous rings (II degree). 2. Partial disruption of all layers (III degree). 3. Complete transverse disruption of all walls without disjunction of the of trachea, (bronchus) (IV degree). 4. Abruption with disjunction of the edges of trachea (bronchus) (V degree). II. According to the rupture direction: 1. Longitudinal. 2. Oblique. 3. Transversal. 4. Mixed. III. According to the localization of damage: 1. Tracheo-laryngeal. 2. Cervico-tracheal. 3. Mediastino-bronchial. 4. Bifurcation al. 5. Bronchial. IV. According to the size of injury: 1. Combined damages of trachea (bronchi) and adjacent organs. 2. Damage of trachea (bronchi) and other segments of the body. 3. Damage of trachea (bronchi), adjacent organs and other segments of the body. Symptomatology and clinical course The clinical manifestation of the tracheal injury depends on the type of disruption, its degree and presence of concomitant damages.
  • 55. 54 1. Thoracic surgery Incomplete isolated disruption of trachea commonly manifests by cough and hemoptysis. Respiration, as a rule, is not disturbed. The small disruptions are characterized by various clinics. If the hole is occluded by clot and mediastinal tissues, the signs, which had appeared earlier (cough, hemoptysis, mediastinal emphysema), can disappear. Nev- ertheless the repeated occurrence of cough, as a rule, leads to severe aggravation of the patient state. Major and circular disruptions of trachea cause a grave state of the patients. They manifest except difficult breathing by such signs: 1) mediastinal emphysema or pneumothorax; 2) compression syndrome - compression and inflection of major vessels due to tension pneumothorax or mediastinal emphysema with trans- ition into acute cardiopulmonary failure; 3) hemorrhage syndrome; 4) aspiration syndrome, which is the outcome of bleeding into airways or aspiration of gastric content; 5) traumatic shock. The injuries of bronchi occur in the way of abruption of main bron- chi or their disruption in the zone of bifurcation. In the zone of a tracheal bifurcation observed multiple (2-4) disruptions, which can be longitudi- nal, transversal or oblique. Depending on the character of trauma, it is necessary to distinguish direct and secondary disruptions of bronchi. Direct injuries arise from the gunshot and knife wounds, penetration of rib fragments or other subjects in mediastinum or endoscopic manipulations. The overwhelming majority of bronchial disruptions is the part of blunt trauma of the chest. By the way, the damage of vessels of a lung root occurs in 41,3 %. The predominant clinical signs of a bronchial disruption are the res- piratory disturbance, gas syndrome, hemoptysis and hemothorax. How- ever these signs may observed only in isolated injuries of lungs. The patients state is grave. Rest dyspnea and acute pain behind sternum are the most troubling manifestations. The difficult swallowing, hoarseness, swelling face and subcutaneous crepitation are observed. On auscultation the breathing sounds are weak or absent at all on the side of trauma. The sequence of examination of the patients with injuries of tra- chea and bronchi depends on the character and gravity of trauma, clinical signs and concomitant damages, which threatening life. If the state of the patient allows, a chest X-radiography is per- formed. Commonly it is possible to find out mediastinal emphysema, some- times the sign of discontinuing of trachea.
  • 56. The injuries of bronchi manifest by distension of mediastinum and presence of air strips along its borders, and in some cases total or tension pneumothorax observed. Final and most informative diagnostic method is the tracheobroncho- scopy, which can be also the therapeutic method. However it is necessary to carry out decompression of a mediastinal emphysema and pneumotho- rax before such investigation. Before examination the clots and liquid blood are aspirated from airways, then adjusted the localization and character of disruption. The incomplete disruptions are usually longitudinal and oblique and located on the line of membranous and cartilaginous part, circular - mainly in a cervical part of trachea. Except disruption of the wall, observed the absence of cartilaginous rings in this region and filled by blood parabronchial fat. The open damages of trachea take place mainly in cervical part and rarely - in thoracic. In all cases of neck trauma it is necessary to suspect the opportunity of the damage of trachea and esophagus. Such variants of clinical course are distinguished: - acute course (first 30 days after operation); - chronic course (complication of trauma). Acute course is divided onto three stages: 1. The initial stage (lasts during 2 days after the trauma with typical signs of disruption; the urgent resuscitation measures are required). 2. The stage of temporary compensation (lasts during 2 weeks; at this time it is possible to carry out diagnostic examination). 3. The stage of persistent compensation (lasts during 30 days; during this time a stenosis and other persistent complications of disruption of tra- chea and bronchi develops). The diagnostic program 1. Complaints and history of the disease. 2. Physical findings. 3. Chest X-radiography. 4. Diagnostic thoracentesis. 5. General blood and urine analyses. 6. Biochemical blood analysis. 7. Tracheobronchoscopy. 8. Tomography.