Download CHAPTER TWO. CLINICAL FORMS OF TUBERCULOSIS PRIMARY

CHAPTER TWO.
CLINICAL FORMS OF TUBERCULOSIS
PRIMARY TUBERCULOSIS
Primary tuberculosis starts due to contact of the uninfected host with Mycobacteria
tuberculosis. This type of tuberculosis is characteristic for children, teenagers, and young adults.
90-95% of infected with MBT never develop clinical tuberculosis.
Pathogenesis. Most often tuberculosis is air-borne, rarely alimentary or contact.
Reaching alveoli, MBT stay and multiply there. Some of bacilli enter intercellular space, lymph
(baceteriolymphia) and blood (bacteriemia), staying in organs rich with macrophages (lymph
nodes, bone marrow, spleen, liver, and lungs).
Bacteriemia leads to sensitization of the host and virage of tuberculin skin test.
Paraspecific reactions may occur during this allergic period. Such functional signs as sleep
disorders, loss of appetite, fatigue, irritation, disorders of thermal regulation and cardiac
arrhythmias characterize this period of early tuberculosis infection. Degree of functional
disorders can be different because infection does not always cause clinical disease.
Paraspecific reactions are caused by Mycobacteria tuberculosis, but their histological
structure is different from tubercular granuloma. Paraspecific reactions include erythema
nodosum (subcutaneous hystiolymphocyte infiltrates), rheumatoid granulomas in lungs, liver,
kidneys, phlyctena conjunctivitis, upper respiratory tract infection.
Paraspecific reactions may take different course: in case of dissolution tubercular
infection may result in formation of primary foci and primary tubercular complex. Cases when
paraspecific reaction causes clinical symptoms are said to have tuberculosis of unknown primary
site usually resulting into recovery.
Inflammation may progress in:
-
intrathoracic lymph nodes resulting in minimal or significant (total) alteration.
This form of primary tuberculosis is called tuberculosis of intrathoracic lymph
nodes.
-
Primary Tuberculosis Complex which is formed as follows:
A. Tubercular granulomas are formed at the site of infection in lung, converging into
pneumonic focus (primary focus), followed by involvement of lymphatic vessels
passing to lung root and infecting the regional lymph nodes. Thus forms primary
tuberculosis complex.
B. Tubercular inflammation may also spread in retrograde fashion, from affected
lymph nodes through lymphatics to pulmonary parenchyma resulting into
formation of primary focus.
Primary tuberculosis has the following features different from secondary tuberculosis:
-
acute onset; seeding of infection with lymphatics and blood flow; MBT in blood
(bacteriemia) and lymph (baceteriolymphia);
-
ІІІ, V, VІ, VІІ, VІІІ, ІХ segments are affected primarily;
-
Uniform involvement of lymphatic vessels and nodes;
-
High sensitization of the host causing more pronounced tuberculin skin tests.
Propensity to exudative reactions is result of this, leading to pleuritis.
-
Inclination to benign course, sometimes infection is self-contained.
There are following types of primary tuberculosis: tuberculosis of unknown primary site ,
primary tuberculosis complex, tuberculosis of intrathoracic and mesenteric lymph nodes,
primary soft focal and miliary tuberculosis. Extra-pulmonary primary forms of tuberculosis may
also develop.
Tuberculosis of unknown primary site
Another name of tuberculosis of unknown primary site is “tubercular intoxication”, a
complex of symptoms resulting from primary MBT infection in children. This earliest form of
clinical tuberculosis has minimal specific symptoms and is not diagnosed with either radiological
or instrument-aided methods of examination.
Pathology. In tuberculosis of unknown primary site , lymph nodes develop single
tubercular granulomas with caseous necrosis in the middle.
Clinical signs. Chief sign of tuberculosis of unknown primary site is syndrome of
intoxication found right after or during tuberculin skin test virage. Characteristic signs include
irritability or slow reaction, easy fatigability, subfebrile fever, headache, loss of appetite and
sleep, enlargement of peripheral lymph nodes (micropolyadenitis). Fever is not constant but may
change during the day. Common blood count has lymphocytosis, increase in band forms.
Diagnosis of tuberculosis of unknown primary site is based on the following data:
-
Presence of syndrome of intoxication;
-
Virage of tuberculin skin test with diameter of infiltrate over 12 mm;
-
Micropolyadenitis most often in posterior neck triangle area;
-
Tuberculosis in parents;
-
Contact with tuberculosis patient, especially with bacterial seeder;
-
Presence of and marked post-vaccination scar;
-
Negative differential diagnosis with other diseases leading to similar symptoms
of intoxication.
Test therapy with anti-mycobacterial antibiotics may also be used: improvement of
symptoms suggests tuberculosis of unknown primary site.
Treatment of children and teenagers with tuberculosis of unknown primary site is done
on an in-patient basis. First line therapy (isoniazid and ethambutol or pyrasinamide) is usually
prescribed until full recovery from symptoms of intoxication.
Outcome. Favorable outcome is full recovery. Spontaneous recovery is also documented.
Unfavorable outcome is turn of tuberculosis of unknown primary site to local form of
primary tuberculosis.
Differential diagnosis of tuberculosis of unknown primary site is sometimes difficult
and should include chronic tonsillitis, rheumatic fever, sinusitis, pyelonephritis, hyperthyroidism,
hepatitis, cholecystitis, worm infestation, chronic inflammatory non-specific pulmonary disease.
Thus history of disease should include detailed anamnesis of contacts with tuberculosis patient,
terms of the last BCG vaccination and re-vaccination, previous and current results of tuberculin
skin test.
-
Chronic tonsillitis. Frequent tonsillitis in anamnesis can result in intoxication and lead to
weakness and easy fatigability. In tonsillitis there are periods of remission while tubercular
intoxication is constantly present. Tonsils are enlarged; regional submandibular and neck
lymph nodes are enlarged and painful; foul smelling is sometimes present in the mouth.
-
Rheumatic fever. There should be indication of rheumatic attack in the past. Subfebrile fever
and nodular erythema are seen in rheumatic fever as well as in tuberculosis of unknown
primary site . But rheumatism also manifests as chest and joint pain, dull heart beat on
auscultation, apical systolic murmur; common blood count in rheumatism will have
leucocytosis, monocytosis, increase in ESR; serology tests for rheumatism will be positive.
-
Sinusitis. Anamnesis includes acute maxillary or frontal sinusitis; present pain on typical
location, discharge from the nose. X-ray finds include opacity of maxillary or frontal sinuses.
CBC includes leucocytosis with prevalent band forms, increased ESR.
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Pyelonephritis. Diagnosis is laboratory and instrumental aided: urine analysis will have
significant leucocyte numbers and urine culture will identify responsible agent.
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Hyperthyroidism has to be ruled out in older children and teenagers. Increase of thyroid glad
sizes, exophthalmia, tachicardia, trembling fingers, weight loss while preserved good
appetite are all symptoms of hyperthyroidism. Subfebrile temperature in hyperthyroidism is
constant; basal metabolism in hyperthyroidism is high.
-
Hepatitis, cholecystitis may manifest with intoxication but also with right upper quadrant
pain (when fasting or after meals), dyspepsia. Liver area is painful on palpation. Duodenal
juice sampling, cholecystogrpahy and abdominal ultrasound examination will help diagnosis.
-
Worm infestation. Symptoms include abdominal pain, nausea, vomiting, itching, and
irritability. Body temperature is normal; there is no lymph node enlargement. Eosinophilia
may be found in CBC. Repeated feces examination should find worm eggs.
-
Chronic non-specific inflammation of lungs may be reason for long-term intoxication
syndrome. Frequent respiratory infections with sputum, dry and wet rales on auscultation and
positive result of test treatment with wide-spectrum antibiotics and non-specific antiinflammatory therapy will help correct diagnosis.
Study questions.
1. What are paraspecific reactions and why are they called so?
2. What are signs of primary tuberculosis?
3. What system is affected is characteristic for primary tuberculosis?
4. What is tuberculosis of unknown primary site ?
5. How often tuberculosis of unknown primary site in children is found on
X-ray?
6. What are typical complaints in tuberculosis of unknown primary site ?
7. What complaints are typical for syndrome of intoxication?
8. What objective symptom is found in tubercular intoxication?
9. What therapy should be administered for treatment of tubercular
intoxication?
10. What is outcome of tubercular intoxication?
Primary tubercular complex.
Primary tubercular complex is characterized by presence of primary tubercular focus
(affect) in lungs, lymphangitis and lymphadenitis. Most often it is localized in I and III segments
of the right lung. Timely diagnosis and treatment of primary tubercular complex is prerequisite
of recovery. Otherwise complications and residual alteration may develop.
Pathology. Mycobacteria tuberculosis enter alveoli and multiply, causing inflammatory
reaction, or alveolitis, and bronchiolitis due to extension of inflammation to bronchioles. Size of
pneumonic focus depends on number of affected alveoli.
At first inflammation is unspecific, followed by specific caseous necrosis. Area of
cheese-like necrosis with perifocal inflammation is called primary affect. Inflammation spreads
from primary affect to regional lymph nodes through peribronchial and perivascular lymph
vessels. Specific tubercles develop around lymph nodes, thus tubercular lymphangitis. This is
followed by inflammation of regional lymph nodes, where inflammation is not unlike in lungs, is
non-specific at first, followed by specific one. This is followed by necrosis of large area, which
includes often whole lymph node. Such is pathogenesis of lymphadenitis.
Along with this, it is suggested that another pathway of development of primary
tubercular complex exists: after primary infection of intrathoracic lymph nodes MBT spread in
retrograde fashion to pulmonary parenchyma through lymphatic vessels (retrograde lymphatic
pathway). Inflammation in lungs soon becomes specific.
Regress of primary tubercular complex starts with dissolution of perifocal inflammation,
appearance of epithelioid tubercles, which undergo sclerosis and capsule formation. Calcium
salts retain in focus of inflammation and petrify. Petrified primary focus is called focus of Gohn.
With time bone tissue may develop in focus of Gohn. It is noteworthy that inflammation in
lymph nodes is much slower then in pulmonary tissue, and often regress takes long time
resulting in petrifaction.
Clinical symptoms. Primary tubercular complex may have acute, imperceptible and
asymptomatic beginning. The beginning and clinical symptoms depend on morphological
alteration, such as size of cheese-like necrosis, zone of perifocal inflammation, and intrathoracic
lymphadenitis. In children age influences the clinical symptoms of primary tubercular complex.
Propensity to generalized inflammation is seen in children from 0 to 7 years of age due to their
peculiar pulmonary anatomy.
Acute onset manifests with intoxication; imperceptible beginning may not alter general
condition of a child, but there will be enlarged peripheral lymph nodes, hepatic-lien syndrome,
paraspecific reactions.
Percussion over primary tubercular complex produces short pulmonary sound, breath is
weakened or puerile on auscultation, rarely one may hear dry or fine bubbling rales.
Leucocytosis up to 10-12x109 / L with prevalence of band forms and increase in ESR to
20-30 mm/hour is seen in CBC.
Radiology symptoms also reflect on one of 4 stages of primary tubercular complex
(Fig.2.1):
I stage of infiltration is characterized by single homogeneous shadow. Perifocal area of
inflammation converges with widened lung root. This stage is difficult to differentiate from
pneumonia, so it is sometimes called “pneumonic” stage.
II stage is “bipolar” (resolving phase). Lymphangitis and clear two poles
(primary affect and altered intrathoracic lymph nodes, or symptom of Redecker) develop at this
stage.
On III stage (phase of consolidation) deposit calcium salts.
IV stage (phase of calcification) is seen by shadow of high intensity (Gohn focus) and
petrified intrathoracic lymph nodes.
Figure 2.1. Primary tubercular complex.
Reinfection primary complex. It is real reinfection, which leads to complete anatomical and
clinical picture of primary complex. There is primary affect, lymphangitis, and lymphadenitis
along with residues of healed primary tubercular complex.
Treatment. Patients with tuberculosis are treated according to their 1,2 or 3 category.
Outcome depends on spread of primary affect, degree of inflammation of intrathoracic
lymph nodes and timely diagnosis of infiltration phase and treatment.
Favorable outcome is when specific changes in lungs and lymph nodes resolve
completely; this is seen in local primary focus and insignificant alterations in lymph nodes, and
in adequate and timely anti-mycobacterial therapy.
Relatively favorable outcome is calcification of primary affect and in lymph node. This
happens in cases of late diagnosis of primary tubercular complex or with significant caseous
alteration in primary affect and in lymph nodes.
Unfavorable outcome is progress of specific inflammation. Primary tubercular complex
turns into fibrotic cavernal pulmonary tuberculosis. Big foci of caseation may follow.
Clinical course of primary tubercular complex can be smooth or complicated. Latter is
characteristic for children of young age, ineffective vaccinated children, close contacts with
bacterial seeder or children who often have respiratory infections.
Complications of primary tubercular complex can be early and late.
Early complications.
Tuberculosis of bronchus complicates primary tubercular complex most often. It
develops primarily when tuberculosis spreads from affected intrathoracic lymph nodes or
primary focus to bronchus. All layers of bronchus are affected. Tuberculosis of bronchus usually
manifests as dry or productive cough, dyspnea and pain at the affected side.
Microperforation of bronchus.
Atelectasis of bronchus develops due to compression of bronchus with affected lymph
node (compressive atelectasis) or due to specific bronchitis (obstructive bronchitis). Blunted
sound on percussion, voice fremitus and pulmonary sounds are decreased.
Pleuritis is complication of primary tubercular complex because latter precedes pleuritis.
Clinical signs of pleuritis include chest pain, dyspnea , fever as high as 38-390C. Dry pleuritis
will also manifest as plural friction rub; decreased voice fremitus, blunted sound on percussion
and weakened breath sounds on auscultation will suggest exudative pleuritis.
Lymphatic and hematogenous spread leads to new small sized foci in upper lung
segments. It rarely produces clinical symptoms. Dissolution will lead to intensification of
shadow, its contour become clearer. Such metastatic foci are called foci of Simon. These foci are
source of post-primary forms of tuberculosis.
Bronchogenic dissemination follows micro-perforation of bronchus and emptying
caseation masses from lymph node into bronchus. Such foci are found primarily in lower
segments of lungs. Fever and cough (or worsening of cough) are symptoms of this complication.
Primary pulmonary cavern (rare complication). Focus of primary tubercular complex
may melt and empty its caseation masses into the draining bronchus, forming cavern. These
caverns are usually situated peripherally.
Caseation pneumonia (very rare complication) results from progressing primary
tubercular complex. Clinical course is grave: fever, chills, rough cough with sputum and
sometimes hemoptysis ensue. Other symptoms include blunted sound on percussion, bronchial
breathing and different caliber wet rales.
Tubercular meningitis is most grave of complications.
Late complications.
Vascular sclerosis. In primary tubercular complex hyperplasia of vessels of lung root and
of mediastinal fat lead to formation of excessive connective tissue in their walls.
Bronchiectases develop due to failure of bronchial blood supply, especially in lung root.
Hemoptysis.
Differential diagnostics of primary tubercular complex is done with non-specific
pneumonia, lung cancer (central or peripheral), and with lung abscess in case of destruction.
Diagnostic criteria for non-specific pneumonia (acute or chronic).
-
history of respiratory diseases;
-
acute onset (in this case or indication in history);
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pronounced clinical symptoms;
-
grave general condition of a child; bronchial, pneumonic and pleural symptoms
are more pronounced then symptoms of intoxication (as opposed to symptoms
in primary tubercular complex)
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high fever, unchanged during the day;
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on auscultation there are multiple wet rales of different caliber and weakened
breathing sounds;
-
CBC will have leucocytosis up to 15x109 and higher with increased ESR;
-
X-ray will reveal low intensity foci with unclear contour, largely localized in
lower lung segments (sometimes bilateral), apical segments are usually not
affected;
-
bronchoscopy finds include wide-spread diffuse endobronchitis (mucosal
hyperemia and swelling);
-
quick positive effect from adequate antibiotic therapy.
One has to remember that when differential diagnostics is not possible physician has to
use wide-spectrum antibiotics not used for treatment of tuberculosis first (culture and sensitivity
test is mandatory).
Lung cancer. Peripheral lung cancer with metastases into intrathoracic lymph nodes, or
central cancer, complicated with atelectasis may remind clinical and radiological picture of
primary tubercular complex.
Diagnostic criteria for lung cancer:
-
cancer may have asymptomatic beginning;
-
cancer progress may manifest with “chest” symptoms (cough, becoming
troublesome with time, hemoptysis, growing chest pain on a side of cancer,
dyspnea )’
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“chest” symptoms are chief complaints;
-
CBC will have significant leucocytosis with prevalence of band forms and
increased ESR;
-
On X-ray peripheral cancer will localize at S3 or at the lower segments of lung.
Shadow of tumor is not homogenous, contours of peripheral cancer are unclear
and nodular. There are no small foci around tumor. In central cancer contours of
shadow are a bit diffuse, convex, the shadow is “palmate”
-
Bronchoscopy finds include sometimes visualization of tumor itself, or density
and bulging of involved bronchial wall or narrow or obstructed bronchus.
Study questions.
1. What is primary tubercular complex? What primary tubercular complex consists of?
2. In what segments primary tubercular complex takes place most often?
3. What are radiological stages of primary tubercular complex? What alterations there
are on each of the stages?
4. What is focus of Gohn?
5. What are foci of Simon and what way do they develop?
6. What is “reinfection primary complex”?
7. What are early and late complications of primary tubercular complex?
8. What causes atelectasis in primary tubercular complex?
9. What are diseases to be included in differential diagnosis with primary tubercular
complex?
Intrathoracic lymph nodes tuberculosis.
Intrathoracic lymph nodes tuberculosis is primary tuberculosis. Very rarely it can
develop due to endogenous reactivation of tubercular changes, which earlier took place in
intrathoracic lymph nodes.
Intrathoracic lymph nodes tuberculosis is found in 80% of cases of primary tuberculosis.
Pathogenesis. This form of tuberculosis develops as a result of infection of lymph nodes
with MBT by lymph or blood flow; MBT then multiply in lymph nodes leading to specific
symptoms.
Pathology. According to radiological exam, there are infiltration, tumor-like and petit
forms of intrathoracic lymph nodes tuberculosis. But infiltration form is not easily distinguished
from tumor-like form, so it has been suggested to also differentiate between hyperplastic,
caseation and induration forms depending on morphological changes in affected lymph nodes.
Hyperplastic form corresponds to infiltration form, and caseation form corresponds to tumor-like
one.
Infiltration form is characterized by lymphatic tissue hyperplasia and epithelioid
tubercles. Lymph node itself is not greatly enlarged with peri-nodular inflammation; thus
inflammation spreads beyond lymph node per se to pulmonary parenchyma.
In tumor-like form intrathoracic lymph nodes increase significantly, up to 5 cm in
diameter. Lymphoid tissue is replaced with caseation, but inflammation does not spread beyond
lymph node’ capsule.
Induration form is characterized by growth of fibrotic tissue with remnants of caseation
foci in lymph nodes.
Tumor-like (caseation) form of intrathoracic lymph nodes tuberculosis takes most grave
clinical course.
Clinical symptoms of intrathoracic lymph nodes tuberculosis is dependent on character,
localization and volume of tubercular inflammation, that is on what group of intrathoracic lymph
nodes are affected and how many groups of lymph nodes are involved.
According to classification of V.A.Sukennikov edited by Engel, there are following
groups of intrathoracic lymph nodes: paratracheal, tracheobronchial, bronchopulmonary,
bifurcation and para-aortic.
Clinical symptoms. Body temperature in tumor-like and infiltration forms may reach
38-390C and then remain subfebrile for a long time. Children will develop profuse sweating
“without apparent reason”, loss of appetite, young children will develop barking or bitonal
cough. Cough is usually nocturnal and dry at first, followed by production of sputum later on.
Clinical symptoms of intrathoracic lymph nodes tuberculosis lately became less
prominent due to vaccination and chemoprophylaxis. Body temperature may be subfebrile,
cough is not constant, and children may develop loss of appetite and moderate sweating.
Only physical exam will not be able to reveal intrathoracic lymph nodes tuberculosis
because lymph nodes are located inside of the chest. The following symptoms are found most
often:
Visual symptoms:
Wiederhoffer symptom is unilateral or bilateral dilation of peripheral vein collaterals in
I-II intercostal spaces due to compression of vena azygos.
Franck’ symptom is dilation of small superficial vessels in upper interscapular area.
Palpation symptoms:
Petrushka’ symptom is pain on pressure on spinous processes of III-VII chest vertebra.
Percussion symptoms:
Philosofov symptom (or ‘bowl’ symptom) is parasternal blunted sound on percussion in
I-II intercostal space, which narrows below that level due to infection of paratracheal lymph
nodes.
De la Camp symptom is blunted sound on percussion in interscapular area on the level of
II-IV vertebra due to infection of bronchopulmonary lymph nodes.
Koranyi symptom is blunted sound on percussion on spinous processes below I chest
vertebra (in children of 1-2 years of age), blunted sound below II chest vertebra in children from
2-10 years, and below III chest vertebra in children from older then 10 years. This symptom is
characteristic for enlarged bifurcation lymph nodes.
Auscultation symptoms:
D’Espine symptom is bronchophony on the spine below I chest vertebra.
Geibner symptom is tracheal breathing over the spine below I chest vertebra.
Radiological exam is important in diagnostics of intrathoracic lymph nodes tuberculosis.
This examination is done in anterior-posterior and lateral views as lymph node shadow may hide
behind the heart and other mediastinal organs. Infiltration form of intrathoracic lymph nodes
tuberculosis on X-ray (Fig. 2.2) may present as widened lung roots and unclear outer contour
due to infiltration of pulmonary tissue.
Figure 2.2. Infiltration form of intrathoracic lymph nodes tuberculosis.
Tumor-like intrathoracic lymph nodes tuberculosis will present on X-ray (Fig.2.3.) as
high intensity shadow in lung roots, which have clear convex wave-like appearance.
Figure 2.3. Tumor-like form of intrathoracic lymph nodes tuberculosis.
CBC finds will include insignificant leucocytosis and increased ESR; caseation form will
manifest as lymphopenia.
Treatment of patients with intrathoracic lymph nodes tuberculosis is administered
according to 1, 2 or 3 category.
Outcome. Favorable outcome is complete dissolution of specific alteration in
intrathoracic lymph nodes.
Relatively favorable can present as:
a. lung root sclerosis followed by bronchiectasis formation in this area; pathological
alteration is found on bronchoscopy only.
b. Calcinate formation in lung roots.
Outcome is said to be unfavorable with progress of inflammation.
Complications of intrathoracic lymph nodes tuberculosis will be the same as in primary
tuberculosis complex. Among late complications stone formation in bronchus (broncholithiasis)
is noteworthy.
Differential diagnostics of intrathoracic lymph nodes tuberculosis has to be done with nonspecific changes in lung root and mediastinum. Most often intrathoracic lymph nodes
tuberculosis is differentiated with non-specific adenopathy, lymphogranulomatosis (Hodgkin’
disease), lympholeucosis, lymphosarcoma, sarcoidosis, central lung cancer.
Chief diagnostic criteria for intrathoracic lymph nodes tuberculosis include:
-
childhood and teenage age; young adults are rarely affected;
-
history of contact with tuberculosis patient;
-
recent ‘virage’ of tuberculin skin test or hyperergic reactions on tuberculin;
-
weakly symptomatic course with insignificant intoxication; cough is rare; lack
of compression symptoms of adjacent organs;
-
normal CBC or slight leucocytosis with prevalence of band forms, lymphopenia
and increased ESR.
-
X-ray will reveal unilateral or bilateral asymmetric enlargement of lymph nodes
(most often tracheobronchial and bronchopulmonary) sometimes with
periadenitis. Late diagnostics my find calcifications.
-
Bronchoscopy finds will include tubercular alteration of bronchus and lymphobronchial fistulas;
-
Culture of MBT in sputum, bronchial wash and smears.
Non-specific adenopathy develop sometimes in viral infections, measles and pertussis.
These children will also have symptoms of respective infections, inflammation in ear, nose and
throat and may develop allergies.
Diagnostic criteria for non-specific adenopathy:
-
child with non-specific adenopathy has history of frequent upper respiratory
infections;
-
acute onset, pronounces intoxication, fever, productive cough;
-
bilateral infection on chest X-ray includes enlargement of bronchopulmonary
lymph nodes having clear contours and homogeneous structure. In acute period
there is diffuse infiltration of pulmonary vascular tree, most often in lower
segments, where pneumonic infiltration might be also found.
-
weak reaction on tuberculin;
-
diffuse non-specific endobronchitis on bronchoscopy;
-
non-specific therapy results in quick improving of symptoms.
Lymphogranulomatosis (Hodgkin’s disease) causes tumor-like enlargement of lymph
nodes. Most often found in men of 20-40 years of age, but children may also be affected. Spleen,
liver and bone marrow are often affected which makes Hodgkin’s a systemic disease.
Common
symptoms
for
intrathoracic
lymph
nodes
tuberculosis
and
lymphogranulomatosis are acute or gradual start, weight loss, weakness, easy fatigue, fever, dry
or productive cough with clear or suppurative sputum, sweating, enlargement of lymph nodes on
X-ray.
Diagnostic criteria for lymphogranulomatosis:
-
asymptomatic or gradual beginning, rarely acute;
-
sometimes pain in chest and extremities, cough, weigh loss;
-
characteristic triad of clinical symptoms: wave-like hectic fever, profuse
sweating, skin inching. Chest, extremities and joint pain , yellowish-gray skin
color, spleen enlargement ensue;
-
peripheral lymph nodes enlargement (mostly neck area); 90-95% will have also
intrathoracic and peripheral lymph nodes enlarged (often neck and
supraclavicular areas).As opposed to tuberculosis lymph nodes may enlarge
significantly, they are elastic, mobile, painless, do not undergo suppurative
destruction and loosely connected with skin (‘bag of potatoes’);
-
Upper vena cava may be compressed causing severe dyspnea , cyanosis, facial
and neck vein swelling;
-
often has negative reaction on tuberculin due to immune deficit, even following
positive tuberculin skin test;
-
CBC will reveal anemia, leucocytosis with increased neutrophils count,
progressing lymphopenia, hypereosinophylia. Tuberculosis does not usually
cause change in erythrocyte count, and there is lymphocytosis;
-
Lymphogranulomatosis affects most often paratracheal and tracheobronchial
lymph nodes of anterior and central mediastinum in symmetric and bilateral
fashion (‘symptom of plant pipe’) (Fig. 2.4). On X-ray these are shaped as
homogeneous conglomerate with coarse wave0like contours. Perifocal
inflammation around lymph nodes is absent;
Figure. 2.4. Lymphogranulomatosis.
-
chief method of diagnosis is puncture or biopsy of lymph node. Cytology of
enlarged peripheral lymph node will find cell polymorphism: lymphocytes,
neutrophils, plasmocytes, basophiles, eosinophils, giant multinuclear cells of
Berezovsky-Sternberg, which verify the diagnosis.
Lympholeukosis (lymphadenosis) is malignant tumor with bilateral symmetric
enlargement of intrathoracic lymph nodes. Disease manifests as hyperplasia and lymphatic
metaplasia of organs of erythropoesis (lymph nodes, spleen, liver, bone marrow).
Intrathoracic lymph nodes are enlarged and there are symptoms of intoxication, which
resembles tuberculosis of intrathoracic lymph nodes.
Diagnostic criteria of lympholeukosis:
-
typical patient is male of 40 years old and older;
-
in most cases lympholeukosis develops slowly and has long latent period;
-
gradually develops second period of disease with generalized enlargement of
lymph nodes, spleen and liver;
-
clinical symptoms depend on stage and variant of disease;
-
gradually symptoms of intoxication increase (fever, sweating, weakness,
anorexia) along with enlargement of peripheral lymph nodes; there is skin
itching (due to destruction of leucocytes and flooding of the host with products
of nucleic acids metabolism);
-
pale skin and visible mucosal surfaces due to anemia;
-
peripheral lymph nodes increase to significant sizes (up to the size of a walnut
or a chicken egg), elastic consistency, painless, movable, do not undergo
destruction, and do not cohere with each other or with the skin
-
important symptom is enlargement and density of the spleen and liver;
-
CBC reveals leucocytosis (from 30x109/L to 250x109/L), lymphocytosis (up to
95%), with young and band forms (lymphoblasts), thrombocytopenia,
worsening anemia (due to depressed erythropoesis and hidden hemolysis);
-
X-ray finds include enlargement of lymph nodes in lung roots and mediastinum,
which has clear contours; enlargement of all groups of intrathoracic lymph
nodes is characteristic for lympholeukosis; they form large symmetric
conglomerates with clear contours (Fig.2.5.)
Figure 2.5. Lympholeukosis.
-
chief diagnostic procedure is puncture of bone marrow, revealing its lymphoid
metaplasia (especially in aleukemic form when changes in peripheral blood are
lacking).
Lymphosarcoma (reticulosarcoma) is hyperplastic tumor arising from reticular
cells of lymph nodes and is characterized by aggressive infiltrative growth.
Diagnostic criteria of lymphosarcoma:
-
primary lymphosarcoma may develop in any age, including children;
-
condition of patient is quickly worsened: there is weakness, weight loss in
normal body temperature, cachexia ensues;
-
elements of lymphosarcoma grow across the lymph node capsule, enter the and
compress adjacent tissues and organs. Thus these patient will often have
dyspnea , dry cough, chest pain, cyanosis, facial and neck swelling;
-
peripheral lymph nodes are enlarged, dense, painless, cohere into large
conglomerates;
-
CBC finds include hyperchromic anemia, insignificant leucocytosis with
prevalence of band forms, lymphopenia, increased ESR;
-
negative tuberculin skin test is usually found in lymphosarcoma patient;
-
on X-ray there will be significant bilateral enlargement of all groups of
intrathoracic lymph nodes (adenopathy), which have tubercular appearance and
lack perifocal inflammation. Often pleuritis complicates lymphosarcoma
(Fig.2.6.);
Figure 2.6. Lymphosarcoma.
-
cytology of peripheral lymph nodes reveals up to 98% of lymphoid elements
with great nuclei;
-
fast tumor growth.
Sarcoidosis is systemic granulomatosis of unclear etiology and pathogenesis, leading to
formation of epithelioid non-caseation granulomas in different organs. These granulomas have
tendency for dissolution or hyalinization and for benign course.
Intrathoracic lymph nodes tuberculosis has to be differentiated from I stage of
sarcoidosis when intrathoracic lymph nodes are also affected. Typical sarcoidosis patient is
female of 20-45 years of age, but it also may develop in older children and teenagers.
Sarcoidosis may affect eyes, salivary and lachrymal glands, skin, heart, kidneys, liver, peripheral
lymph nodes.
Diagnostic criteria for sarcoidosis:
-
clinical course is often asymptomatic; intoxication is not characteristic.
Sarcoidosis is incidental find on X-ray.
-
gradual development of disease produces scarce symptoms. There is dyspnea ,
dry cough, chest pain, subfebrile body temperature. Sometimes one or two
symptoms are the only signs of sarcoidosis for many months or years, which
may be self-contained and then reappear again;
-
in acute onset there is Lefgren’ symptom, that is increase of body temperature to
38-39oC, nodular erythema, swelling and pain in joints, bilateral enlargement of
intrathoracic lymph nodes;
-
tuberculin tests are negative, and Qweim-Nikerson reaction is positive;
-
typical but not always present is Heerfordt symptom, which is association of
parotitis with uveitis and iridocyclitis;
-
wrist and foot bones may have cystic cavities;
-
leucopoenia, lymphopenia, eosinophilia, monocytosis, decreased albumins,
increased globulins (α2,γ) and calcium; albumin/globulin coefficient is <1;
-
X-ray picture in I stage of sarcoidosis is characterized by bilateral symmetric
enlargement of mainly bronchopulmonary lymph nodes and their separate
location. Because of that lung root shadow is enlarged and lengthened.
Enlargement is significant, contours are tubercular and nodes do not conjoin.
Pulmonary vascular tree around affected intrathoracic lymph nodes is not
changed; there is no compression of mediastinum (Fig.2.7.)
Figure 2.7. Sarcoidosis.
-
Diagnosis of sarcoidosis is based on finding of characteristic cellular elements
(epithelioid and giant cells, different from giant cells of Pirogov-Langhance) in
punctate of enlarged lymph nodes. Typical cells will have many nuclei and
round shape. Caseation and MBT is not found in sarcoidosis.
Cancer.
Intrathoracic lymph nodes tuberculosis has to be differentiated from central lung cancer.
Both diseases may have similar clinical and radiological symptoms (pathological shadows in the
root of the lung).
Diagnostic criteria for lung cancer:
-
typical patient with lung cancer will be male of 40 years and older;
-
broncho-pulmonary-pleural syndrome is characteristic for cancer rather then
intoxication syndrome;
-
progressing course;
-
sometimes there is enlargement of supraclavicular lymph nodes at the side of
metastasis;
-
CBC will show leucocytosis, increased ESR, anemia;
-
On X-ray cancer will have clear polycyclical contours, there will be
peribronchial infiltration (shadows of different length that do not become
thinner towards periphery);
-
Bronchoscopy will have the last word. Often bronchial narrowing will be seen.
Study questions.
1. What is intrathoracic lymph nodes tuberculosis?
2. What are X-ray forms of intrathoracic lymph nodes tuberculosis?
3. What are clinical symptoms of intrathoracic lymph nodes tuberculosis?
4. How intrathoracic lymph nodes tuberculosis is treated?
5. What are outcomes of intrathoracic lymph nodes tuberculosis?
6. What complications may intrathoracic lymph nodes tuberculosis have?
7. What are chief diagnostic criteria for intrathoracic lymph nodes tuberculosis?
8. What diseases should one differentiate intrathoracic lymph nodes tuberculosis from?
9. In suspicion of what diseases associated with enlargement of intrathoracic lymph
nodes in children and teenagers will you perform bronchoscopy?
10. What are diagnostic tests that should be done in child or teenager with infiltration of
pulmonary parenchyma and enlarged intrathoracic lymph nodes?
TUBERCULOSIS IN TEENAGER
Physiological peculiarities of teenage age. Teenage age is difficult period for
development of the child. Sexual maturation will influence defense and adaptation of the host.
Processes of excitation prevail over processes of inhibition. In early puberty chronic immune and
infectious and allergic
diseases will develop with marked exudative reactions, leading to
exacerbations of clinical symptoms. In second half of puberty inflammation will have productive
character and leads to chronic or latent course tending to relapse.
Tuberculosis in teenager. Teenagers are a “risk group” of phthisiology due to their
physiological peculiarities, their hormonal restructure and accelerated growth. Teenagers may
develop primary and secondary forms of tuberculosis.
Primary tuberculosis not only may manifest as typical primary forms (tuberculosis of
unknown primary site, intrathoracic lymph node tuberculosis, primary tubercular complex), but
also with focal or infiltrative pulmonary tuberculosis, which genetically related to infection of
intrathoracic lymph nodes and are really its complication. In teenager lymph nodes of the root
infected with tuberculosis, are not as much enlarged as they would be in children, so in most
cases only tomography will reveal them. But in accelerated growth pulmonary vessels at the root
will be wide, leading to possible hyper-diagnosing of intrathoracic lymph node tuberculosis.
Primary tuberculosis in teenager may be complicated by bronchial tuberculosis, leading
to troublesome cough and atypical location of specific alterations in lungs or with atelectases
on X-ray. Sixteen percent of teenagers will be diagnosed with exudative pleuritis.
Tuberculosis in teenagers often begins and progresses with scarce clinical symptoms, but
it has marked tendency to progress, so the outcome will heavily depend on timely diagnosis.
Unfortunately almost 40% of tuberculosis is diagnosed in teenager upon seeking medical help.
Thus annual systematic tuberculin diagnostics and fluorography plays a major role in case finds.
In intoxication and bronchopulmonary syndromes fluorography is clinically indicated.
Bacterioscopy and bacteriology of sputum or bronchial wash are necessary in chronic
bronchopulmonary disease.
Treatment. Recovery is slow so long-term complex therapy with modern medication is
indicated. Basic chemotherapy course should last as long as 9-12 months, especially in
destructive forms of tuberculosis. Surgery is rarely indicated. Early diagnosis and treatment of
small forms of tuberculosis in teenager results into recovery without residual changes or into
insignificant post-tubercular alteration. But completed treatment of wide spread disease (2035%) leaves significant residual changes like pneumosclerosis, multiple dense foci in lungs, and
massive lymph node calcification. These may be a source for relapse of disease.
TUBERCULOSIS IN ADULT
Infection and disease of tuberculosis may happen after age of 18 years. At first disease is
asymptomatic, so it is diagnosed late. Individuals of this age group are rarely examined and
tuberculin tests are performed irregularly.
Location of pathological foci in adult is atypical for tuberculosis. Primary focus is located
in lower and medial lobes and in root area. Bronchial lymph nodes are not greatly enlarged (1-2
cm), and pathological changes in them happen earlier then in lung. These lymph nodes are
difficult to find on X-ray, but their shadows lead to widening of lung root. This sign is especially
important when periadenitis develops in addition to pathological changes in lymph nodes.
First sign of primary tuberculosis in adult is lymphadenitis, even if not greatly
pronounced one. Lungs are secondarily involved. Most often clinical forms of primary
tuberculosis include lymphohematogenic disseminated and focal tuberculosis.
Primary forms of tuberculosis in adults, even if timely diagnosed, lead to complications
like specific involvement of bronchus, bronchogenic seeding, fibrosis, atelectasis.
Except for local symptoms, these patients will have paraspecific signs like asthenia, joint
pain, encephalopathy, nodal erythema and glomerulonephritis. Primary forms of tuberculosis in
adults often exacerbate and relapse. Relapse results into infection of new pulmonary segments.
Tuberculin tests are weakly positive in one third of patients, and hyperergy is not
characteristic. Important diagnostic tool is virage of tuberculin reaction. Also important role
belongs to bronchoscopy with biopsy of a pathologically changed bronchial mucosa, as well as
bronchial wash. MBT are rarely found due to oligobacteriality (small number of bacilli in the
host).
Difference between primary and secondary tuberculosis is in typical age: for primary
tuberculosis it is below 25 years, rarely before 40 years. Differential diagnosis is helped by
dynamics of infection, enlargement of mediastinal and peripheral lymph nodes, often specific
infection of bronchus, oligobacteriality often with primary drug resistance of MBT, petrifaction
in lymph nodes, infection of pleura, and bilateral infiltrates.
Diagnostic criteria of primary tuberculosis in adults are as follows: marked intoxication,
often lymph node infection and polyserositis, paraspecific reactions (phlyctena, nodular
erythema, polyarthritis), hyperergic tuberculin tests.
SECONDARY TUBERCULOSIS
Disseminated pulmonary tuberculosis.
Disseminated pulmonary tuberculosis is characterized by multiple, usually bilateral
pulmonary foci of tubercular dissemination through lymphatic or blood flow with acute,
subacute or chronic course. Disseminated pulmonary tuberculosis is found in 20-25% of cases.
Pathogenesis. In disseminated pulmonary tuberculosis MBT enter lungs through
lymphatic or blood flow (or both). Hematogenous spread leads to symmetric dissemination in
both lungs, and in cortical area of lungs. Lymphatic spread results into retrograde infection of
pulmonary tissue from mediastinal lymph nodes, resulting usually in one-sided disseminated
pulmonary tuberculosis. Foci are located in root and apical areas where marked lymphangitis is
also found.
Conditions for development of disseminated pulmonary tuberculosis are:
-
mandatory tubercular bacteriemia (first described by Benda in 1884);
-
local hyper-sensitization to tubercular infection in organs with MBT;
-
marked decrease of resistance due to cold, hyper-insolation, metabolic and
nervous diseases, and non-specific diseases.
Portal of entry of MBT are as follows:
-
primary entrance of significant number of virulent MBT to blood flow;
-
through vascular wall due to its higher permeability, specific vascular
inflammation or opening of caseation focus into the vessel per se. Such
alterations take place in local primary tuberculosis, exacerbation of post-primary
foci in lungs or other organs (kidneys, bones, urinary system, etc).
-
MBT may enter blood flow from affected lymph nodes through thoracic or
jugular duct to upper vena cava and right heart (lymphohematogenous way).
Bacteriemia itself rarely results into hematogenous- disseminated tuberculosis because
MBT are killed by blood defense mechanisms.
Hematogenous-disseminated tuberculosis develops due to interaction of specific and nonspecific factors, leading to bacteriemia, increase of tissue reaction, decrease of defense
mechanisms in the host including the specific immunity.
There are acute, subacute and chronic disseminated pulmonary tuberculosis.
Acute hematogenous- disseminated tuberculosis is called miliary and is seen as separate
clinical form of tuberculosis.
Pathology. Alterations of vascular system precede formation of tubercular nodules.
These alterations include: fibrinoid vascular wall necrosis, formation of endotrombophlebitis and
hematomas. Tubercular foci form around these hematomas due to MBT entrance and seeding of
hematoma.
In hematogenous- disseminated tuberculosis exudative-necrotic phase results into
productive phase promoting interstitial sclerosis and resulting into fibrotic tissue and
emphysema. Fibrosis and emphysema form basis for bronchi deformation and formation of
bronchiectases. Besides specific infection leads to vascular narrowing and obliteration. Such
alterations lead to failure of blood flow in pulmonary circulation.
Subacute hematogenous- disseminated tuberculosis. Involvement of intralobular veins
and interlobular branches of pulmonary artery is characteristic for subacute hematogenousdisseminated tuberculosis; for this reason foci are large, soft and
converging. Foci have
tendency for sclerosis and thus become dense and turn to scars resulting into net fibrosis.
As subacute hematogenous- disseminated tuberculosis progresses, it involves also alveoli
and bronchi, resulting into pneumonic foci like infiltrates. In case of unfavorable outcome, these
infiltrates undergo destruction and replaced by caverns. These caverns are different from caverns
in other forms of tuberculosis, because they do not have fibrotic walls, thus they are thin-walled,
or they are said to be “stamped”. Caverns may appear in one or both lungs on symmetric areas.
Lacking fibrotic wall they are elastic, thus they may undergo collapse and even scarring.
Especially high percentage of caverns heal after antimycobacterial therapy.
Clinical symptoms. Subacute hematogenous- disseminated tuberculosis develops slowly
and has different beginning and course. Sometimes it has acute onset and course: fever as high as
38-390C, sweating, weakness, loss of appetite and weight.
Oftener beginning of disease is gradual. Complaints increase in the course of weeks and
even months. In some patients this form of tuberculosis takes course of influenza, focal
pneumonia or chronic bronchitis.
There are also extrapulmonary symptoms of subacute hematogenous- disseminated
tuberculosis like infection of larynx and vocal cords. Disease may manifest with pain on swallow
and hoarse voice. Tuberculosis may affect kidneys, bones, joints, and pleura (exudative
pleuritis). Patients will have pronounced bronchial-pulmonary-pleural syndrome: productive
cough, sometimes hemoptysis, dyspnea .
Blunted sound over apical area and tympanic sound over lower lung area due to
emphysema is found on percussion. On auscultation there is weakened breathing in lower lung
and puerile breathing in the apical lung with scattered dry rales. As disease progresses infiltrates
and caverns ensue then wet rales can be auscultated.
Diagnosis.
X-ray symptoms of subacute hematogenous- disseminated tuberculosis are:
-
symmetric foci with similar shape and density in upper lung (small and medium)
5-6 mm to 10 mm in size with irregular and unclear contours (‘snow flake’
symptom);
-
infiltration foci;
-
multiple or single ‘stamped’ caverns (‘spectacles’ symptom);
-
pleura is often involved;
-
net fibrosis;
CBC will find elevated leucocyte count (12-14x109/L) and band forms, monocytes, ESR.
Lymphocyte count is decreased. Tuberculin reaction may be positive of negative.
Figure 2.8. Subacute lymphogenous - disseminated tuberculosis.
In lymphogenous - disseminated tuberculosis (Fig.2.8) foci primarily localize unilaterally
at the root of lung; lymphatic vessels are involved.
Outcome.
Outcome is said to be favorable when there is complete dissolution of foci and healing of
caverns.
Outcome is relatively favorable when foci dissolve in part and calcify, there is net
fibrosis, emphysema, chronic disseminated tuberculosis ensues.
Unfavorable outcome is when fibrotic-cavernal pulmonary tuberculosis or caseation
pneumonia ensues.
Chronic disseminated tuberculosis develops as result of acute or subacute disseminated
pulmonary tuberculosis. Foci of different intensity and size among fibrotic pulmonary tissue are
characteristic (Fig.2.9)
Figure 2.9. Chronic disseminated tuberculosis
If foci localize at the apical lung, this form is said to be local; but if all segments of lungs are
involved, this form of tuberculosis is said to be generalized.
Clinical symptoms. Chronic disseminated tuberculosis has wave-like course: symptoms
decrease in remission and increase in exacerbation. This form of tuberculosis is associated with
almost no intoxication. Often patients feel quite well. Detailed history finds generalized
weakness, dyspnea on physical exertion. MBT seeding starts with destruction of pulmonary
tissue and cavern formation. Progress leads to destruction in lungs and intoxication, hemoptysis
may follow. In the same time develops cor pulmonale: dyspnea , diffuse cyanosis.
Fibrosis in patients with chronic disseminated tuberculosis leads to apical bronchiectases;
thus blunted sound on percussion. Lower lungs develop emphysema thus tympanic sound on
percussion. There are dry, rarely wet rales in paravertebral area on auscultation.
Diagnostics.
X-ray symptoms of chronic disseminated tuberculosis are
-
asymmetric polymorphous foci of different sizes and density (‘star sky’
symptom). Most dense foci are found in apical lung;
-
‘stamped’ caverns;
-
fibrosis in lungs (‘weeping willow’ or ‘falling rain’ symptom);
-
bronchiectases, emphysema, emphysematous bullas.
CBC finds will include leucocytosis with prevalence of band forms, monocytosis, increased
ESR. In stable course CBC may be unchanged.
Treatment.
Patients with subacute disseminated tuberculosis are treated as patients of 1 and 2
category, and patients with chronic disseminated tuberculosis are treated according to 2 or 3
category.
Outcome.
Favorable: consolidation and petrifaction of foci.
Relatively favorable: fibrosis, emphysema, and bronchiectases.
Unfavorable: proceeding to fibrotic-cavernal pulmonary tuberculosis or caseation
pneumonia.
Differential diagnostics of disseminated tuberculosis is done with bilateral focal
pneumonia, bronchiolitis, metastatic tumor in lungs, pneumoconiosis (silicosis, silicotuberculosis), sarcoidosis, chronic pulmonary failure, rheumatic diseases, cystic fibrosis.
Pneumonia: bilateral focal pneumonia has X-ray symptom of pulmonary dissemination.
It is caused by Staphylococci, Streptococci, Pneumococci, viruses, Pneumocysts, Legionellae.
Culture and antibiotic sensitivity testing should be performed in pneumonia.
Diagnostic criteria of non-specific pneumonia:
-
significant intoxication, grave general state of patient;
-
broncho-pulmonary syndrome if more pronounced then in tuberculosis: cough is
dry, then wet, there is dyspnea ;
-
multiple dry and wet rales are auscultated over pneumonic area;
-
no cavity of destruction; metastatic foci are absent;
-
no MBT on bacterioscopy;
-
high leucocytosis on CBC (over 15x109/L) with prevalent band forms and
increased ESR;
-
unilateral foci of moderate intensity and unclear contours found in lower lung
and root of the lung on X-ray; apical lung is usually not involved (Fig.2.10) In
case of abscess there is cavity with horizontal air-fluid level, oftener in medial
or lower lung;
-
non-specific inflammation resolves in 2-3 weeks of non-specific wide-spectrum
antibiotics.
Bronchiolitis – is widespread infections of small bronchi and bronchioles,
leading to marked obstruction and thus respiratory failure. Most often seen in spring and winter
with influenza or other acute respiratory infection.
Diagnostic criteria of bronchiolitis:
-
acute respiratory infection or influenza usually precedes bronchiolitis;
-
fever subsides in bronchiolitis to normal in 4-5 days;
-
multiple dry and wet rales of different caliber;
-
small foci and infiltrates (converged foci) in root and lower lung areas on X-ray;
-
physical and X-ray symptoms quickly subside.
Metastases of cancer into lungs.
Malignant tumors of breast, thyroid, bones, reproductive organs, adrenal glands, and
lungs may metastasize into lungs resulting into X-ray syndrome of pulmonary dissemination.
History of surgery or suspicion for tumor in other organs suggest correct diagnosis.
Diagnostic criteria of cancer metastases:
-
history of surgery or other treatment of tumor;
-
finding of tumor from other organ;
-
scarce symptoms at the beginning (dry cough, weakness, low appetite,
sometimes fever);
-
worsening of general state of patient: progressing dyspnea , chest pain, dry
cough;
-
chief complaints are cough and dyspnea , which is not relieved;
-
X-ray finds include multiple bilateral foci of different size, usually of similar
shape. Foci have clear contours and are localized primarily in lower lungs,
closer to the roots (Fig.2.11);
-
pulmonary vascular tree is not seen on the background of foci;
-
CBC is similar in tuberculosis and metastases, but anemia and marked increase
of ESR is more characteristic for metastases;
-
Mantoux skin test in usually negative in metastatic disease.
Pneumoconiosis is diagnosed when patient had history of work in high dust-polluted
areas (mine, quarry).
Silicosis is occupational disease due to pulmonary damage with dust and minute particles
of mineral rock. Among pneumoconioses, tuberculosis is most often associated with silicosis.
Diagnostic criteria of silicosis:
-
occupational history;
-
gradual development without intoxication symptoms, characteristic for
tuberculosis, but with symptoms of bronchitis and emphysema. Clinical
symptoms include productive cough, chest pain, increasing dyspnea ;
-
weakened breathing sound on auscultation of lungs due to emphysema, dry rales
due to bronchitis;
-
X-ray symptoms include pneumosclerosis, emphysema of mainly basal areas of
lungs; bilateral symmetric foci (silicone nodules) 3-5 mm in size with clear
contours and prevalent in lower lung. Sometimes lymph nodes at the root of
lungs are calcified on periphery (‘egg shell’ appearance);
-
lung roots are widened and dense;
-
in II-III stage multiple disseminated foci may appear; sometimes foci converge
into large conglomerates ; emphysema, dense interlobar and costal pleura;
-
absent MBT on bacterioscopy;
-
absent positive result of antimycobacterial therapy.
Presence of MBT in sputum is sign of mixed disease called silicotuberculosis.
Diagnostic criteria of silicosis and silicotuberculosis are found in table 2.1.
Table 2.1. Diagnostic criteria of silicosis and silicotuberculosis
Silicosis
Silicotuberculosis
Complaints
Cough, dyspnea, chest pain
Additionally: symptoms of intoxication
Physical exam
Signs of bronchitis, emphysema (dry rales,
tympanic sound over lower lungs)
Additionally: local wet rales, when infiltrates
present there is blunted sound on percussion
over apical lungs
Laboratory testing
Normal CBC; MBT-
Possible leucocytosis, prevalent band forms,
lymphopenia, increased ESR, MBT+
Radiography
Deformation of pulmonary vascular tree,
nodular shadows in medial and lateral areas,
‘cut down’ lung roots
Additionally: new polymorphous foci, infiltrates
or cavities, especially in upper areas of lungs
Sarcoidosis on its II stage, like disseminated tuberculosis, often has asymptomatic
beginning, or with scarce symptoms like dry cough, insignificant dyspnea and chest pain.
Diagnostic criteria of II stage sarcoidosis:
-
Lefgren symptom (fever of 38-390C, joint pain, skin itching);
-
scarce auscultation data even with significant spread of disease;
-
possible damage to eyes, salivary glands, skin, heart and other organs,
enlargement of separate groups of peripheral lymph nodes;
-
foci have similar shape, their number is decreased peripherally from the roots;
-
pulmonary form of sarcoidosis without enlargement of intrathoracic lymph
nodes will have focal shadows and interstitial densities in midportions of lungs.
When intrathoracic lymph nodes are enlarged, there is homogeneous shadow,
clearly separate from surrounding tissues; cavities of destruction are absent.
-
Tuberculin tests are negative or weakly positive;
-
CBC finds include leucopoenia, lymphopenia, insignificant increase of ESR;
-
In sarcoidosis often there is hypercalciemia, high angiotesin-converting enzyme.
Qwaim test is used when corresponding antigen is present.
-
Bronchoscopy finds include tender vascular net on bronchial mucosa,
sarcoidosis plaques and atrophic bronchitis.
-
Antimycobacterial therapy is not effective, corticosteroids will have positive
effect.
Congested lungs.
Congested lungs develop as result of left ventricle failure due to decompensated mitral
valve defects, hypertension, heart ischemia, cardiosclerosis etc. Congested pulmonary circulation
may also cause bilateral focal shadows, like those found in disseminated tuberculosis.
Gradual and chronic congested lungs are difficult to diagnose especially when
concomitant tubercular changes are present in lungs.
Figure 2.12. Mitral valve defect. Congested lungs. Transsudate in pleural cavity.
Diagnostic criteria of congested lungs:
-
history of rheumatic fever and other heart diseases;
-
there is no intoxication in congested lungs;
-
progressing dyspnea , cough (dry, sometimes wet) with normal body
temperature;
-
change in heart shape and size, cardiac arrhythmia, heart murmur, pathological
ECG, sometimes swelling and enlargement of liver;
-
X-ray finds foci primarily on lower and root areas of lungs; roots are widened
(congested). Possible collection of transudate in pleural cavity, resembling
disseminated pulmonary tuberculosis complicated with pleuritis (Fig.2.12);
-
Administration of diuretics and cardiac glycosides leads to clinical and
radiological improvement.
One has to consider that a patient with congestive heart failure may also contract pulmonary
tuberculosis, so detailed examination with multiple MBT search is necessary in each case.
Rheumatic diseases.
Several connective tissue and vascular disorders are collected under this term: rheumatic
fever, rheumatoid arthritis, systemic lupus erythematosus, polyarteritis nodosa, scleroderma, and
dermatomyositis). Clinical symptoms in these diseases (fever, weight loss, chest pain, productive
cough, sometimes hemoptysis, dyspnea , cyanosis, rales) and radiological symptoms (focal
alterations, cavities, pleuritis) are similar to ones in tuberculosis. Sometimes there is bilateral
dissemination and pleural transudate, which is feature of disseminated pulmonary tuberculosis
(Fig. 2.13)
Figure 2.13. Damage to lungs in rheumatoid arthritis.
Diagnostic criteria for rheumatic diseases:
-
rheumatic disease usually features vasculitis (resulting in hemoptysis and
dyspnea ) and perivascular sclerosis manifested on X-ray as increased
pulmonary vascular tree and focal shadows, resembling disseminated pulmonary
tuberculosis;
-
rheumatic disease features multiple organ damage: skin, joints, kidneys, lungs,
lymph nodes, pleura, heart etc;
-
each rheumatic disease has characteristic features;
-
blood biochemistry finds high fibrinogen, α and γ globulins, significant increase
in ESR.
-
often there is short term and self-contained asthmatic component to rheumatic
disease;
-
on X-ray there is bilateral symmetric damage, but tubercular damage is localized
in upper and middle portions of lung and rheumatoid damage localizes in lower
and root areas;
-
pleuritis is found in both diseases, but unilateral pleuritis is rather sign of
tuberculosis while bilateral self-contained pleuritis is feature of rheumatoid
disease;
-
cavity formation in tuberculosis is associated with MBT seeding, while
rheumatoid disease may lead to thin walled cavities patients are MBT negative;
-
corticosteroid therapy results into prompt improvement of rheumatoid disease
damage to the lungs.
Differential diagnostic tests should include bronchoscopy, skin and muscle biopsy. One
should also consider easier contraction of tuberculosis by patient on long-term corticosteroid
therapy. Thus this group of patients requires detailed physical, radiological, tuberculin and
multiple cultures for MBT.
Cystic fibrosis (mucoviscidosis) is congenital disorder characterized by viscid mucus
obstructing exocrine glands (pancreas, gastrointestinal tract, respiratory tract, sweat, lachrymal,
and salivary glands).
Diagnostic criteria of cystic fibrosis:
-
history of relapsing and difficult to treat bronchitis and pneumonias (often
bilateral) leading to long-term polysegmental atelectases;
-
most characteristic feature of disease is troublesome cough with viscid and hard
to cough up sputum; such cough may sometimes result in vomiting;
-
most patients (80%) will have gastrointestinal symptoms: diarrhea and
constipation, fat malabsorbtion, right upper quadrant pain due to cholecystitis;
-
chronic nasal discharge is also characteristic feature of cystic fibrosis;
-
there are wet and dry rales on auscultation due to mucus obstruction and
pulmonary infection. Upper lungs may have weakened breathing due to
emphysema;
-
X-ray symptoms are diffuse, right upper lobe is affected most often. Pulmonary
vascular tree is increased and deformed with coarse net-like structures.
Sometimes lobular, subsegmental and segmental atelectases are present. Upper
segments may be hyperlucid due to emphysema. Often there is pneumonic
infiltration;
-
bronchography finds include typical picture of :’cut off’ bronchi, fragmented
contrasting, irregular contours. More then one third of patients will be diagnosed
with bronchiectases of lower segments;
-
sweat test is highly informative for diagnosis and differential diagnosis of cystic
fibrosis. Sweat chloride concentration over 60 mmol/L and sweat sodium
concentration over 70 mmol/L are considered an absolute indication of cystic
fibrosis in children.
Study questions.
1. What is disseminated tuberculosis?
2. What are portals of entry of MBT into blood flow?
3. What are forms of disseminated tuberculosis?
4. What symptoms are characteristic of subacute disseminated pulmonary tuberculosis
and what are signs of it on physical examination?
5. What complaints suggest tuberculosis of larynx in subacute disseminated pulmonary
tuberculosis?
6. What are X-ray features of subacute and chronic disseminated pulmonary
tuberculosis?
7. Why cavern in subacute disseminated pulmonary tuberculosis is called ‘stamped’
cavern?
8. What are outcomes of subacute disseminated pulmonary tuberculosis?
9. What are diagnostic criteria for disseminated pulmonary tuberculosis?
10. What are diseases to be considered for differential diagnosis in disseminated
pulmonary tuberculosis?
Focal pulmonary tuberculosis.
Focal pulmonary tuberculosis characterizes by presence of different foci up to 10 mm in
diameter in 1-2 segments of one or both lungs. It usually has scarce symptoms.
Among individuals with primary tuberculosis 15-20% have focal forms of tuberculosis.
Its basic features are local infection in apex or upper lobe of lung. There is soft-focal and
fibrous-focal pulmonary tuberculosis. According to contemporary classification of tuberculosis,
soft-focal tuberculosis is focal tuberculosis in phase of infiltration, young form of disease which
needs to be treated.
Fibrous-focal is focal tuberculosis in the phase of consolidation and calcification. This
form of tuberculosis develops as a result of incomplete dissolution and consolidation of soft
focal, infiltrative, acute disseminated pulmonary tuberculosis.
All foci classified by three groups: small (up to 3 mm), medium (4-6mm) and large (7-10
mm).
Pathogenesis. Very rarely focal tuberculosis can be primary. Usually this type of disease
is secondary due to: a. exogenous superinfection, b. endogenous reactivation of old calcified
tubercular foci, scars or induration fields after tuberculosis in the past.
Reactivation of post-tubercular alterations takes place due to reversion and multiplication
of L-forms. Reversion of L-forms may be due to acute and chronic diseases (acute and chronic
respiratory infections, diabetes mellitus, gastric and duodenal ulcer, pneumoconioses, drug
addiction, alcoholism, AIDS, mental disorders), and exogenous superinfection.
Pathology. Exogenous superinfection alters apical lobular bronchi causing caseation panbronchitis. Further exudative and productive inflammation spreads to alveoli. These foci were
first described by O.I. Abricosov in 1904.
Under endogenous reactivation leucocytes enter focus and melt caseation necrosis.
Fibrotic capsule infiltrates by lymphocytes and becomes soft; perifocal infiltration develops nonspecific inflammation. Further damage is done to bronchi due to lymphatic spread of MBT
spread of caseation masses onto peribronchial tissue resulting into pan-bronchitis. Treatment
leads to complete dissolution of foci or scar formation. Fibrotic capsule surrounds some foci
resulting into fibrotic-focal tuberculosis.
Clinical symptoms. Most patients with focal tuberculosis do not notice any symptoms of
disease. Along with that focal tuberculosis may produce symptoms of intoxication and damage
to respiratory system. Intoxication manifests with long-term subfebrile body temperature, loss of
appetite and working capacity, sweating, and weakness. Other complaints include cough with
scarce sputum production. Intoxication is characteristic for focal tuberculosis in phase of
infiltration (Fig.2.14, 2.15); in respiratory tuberculosis intoxication is characteristic for focal
tuberculosis in phase of consolidation. Infiltration phase of focal tuberculosis does not alter
percussion findings. One can auscultated rales when tissue destruction is present.
Focal tuberculosis in phase of consolidation and calcification often leads to
bronchiectases and so productive cough, sometimes hemoptysis. Apical lungs undergo fibrosis,
so supra-clavicle and infra-clavicle fossae can be clearly seen. There is blunted sound on
percussion, and auscultation may reveal weakened or puerile breath sounds and wet rales due to
marked fibrosis and bronchiectases.
Treatment. Patients with focal tuberculosis in phases of infiltration and scarring during
exacerbations should receive treatment according to 1, 3 or 2 category.
Figure 2.14. Focal tuberculosis
Figure 2.15. Focal tuberculosis. Tomogram.
Outcomes. Favorable: complete dissolution of pathological foci (usually foci under 5
mm).
Relatively favorable: petrifaction, segmental pneumosclerosis.
Unfavorable: progress to focal tuberculosis, phase of destruction, followed by fibroticcavernal tuberculosis.
Differential diagnosis. Tuberculosis in infiltration phase should be differentiated from
bronchopneumonia, peripheral lung cancer, and metastatic lung cancer.
Bronchopneumonia is non-specific inflammation within segment, lobule or acinus.
Diagnostic criteria for bronchopneumonia:
-
often follows acute respiratory infection, overcooling;
-
has acute onset with marked clinical symptoms (fever, weakness, loss of
appetite, productive cough, chest pain, dyspnea at rest);
-
puerile breathing with wet and dry rales on lung auscultation;
-
CBC finds marked leucocytosis, prevalence of band forms, increased ESR;
-
On X-ray there are bilateral focal shadows 1-1.5 cm in size having week density
and unclear contours often in lower lungs (sometimes in upper lung but not in
the apex)
-
Pulmonary vascular tree is increased along pulmonary fields; lung roots are
widened;
-
Wide-spectrum antibiotics gives positive result in 7-10 days (dissolution of
foci).
When diagnosis is difficult, a trial treatment is given with antibiotics not used to treat
tuberculosis. Dissolution of foci in 2-3 weeks confirms diagnosis of bronchopneumonia.
Small peripheral lung cancer characterizes with hidden course, that is absence of
clinical symptoms at the beginning (just like tuberculosis). On X-ray cancer shadow is small, has
irregular polygonal shape with unclear contours, resembling tubercular focus. Pulmonary tissue
is not altered around such tumor. Tumor develops typical radiological symptoms only when
grown to 2 cm in size.
Diagnostic criteria for Small peripheral lung cancer:
-
typical patient is heavy smoking male over 40 years old;
-
asymptomatic beginning; clinical symptoms appear at the final stages of cancer,
with prevalent broncho-pulmonary-pleural symptoms (chest pain, cough,
hemoptysis, unexplained dyspnea );
-
X-ray finds one focus with unclear shadows on an unchanged background; most
often in III, IV and V segments and lower lobe.
-
in most cases small peripheral cancer has irregular round shape with unclear
tubercular shadows, sometimes radiating into pulmonary tissue. These give an
appearance of ‘malignant crown’ (‘corona maligna’); peripheral cancer shadow
has ulcer of Rigler;
-
Shadow has medium intensity, non-homogenous, (as if consisting of several
small converging foci); there are no calcification;
-
Mantoux skin test with 2 TU PPD-L may be negative, unlike in focal
tuberculosis;
-
CBC finds anemia and increased ESR;
-
Treatment with antitubercular medications does not stop progress of malignant
disease.
Diagnosis is verified by bronchoscopy catheterization with biopsy for cytology and
bacteriology tests.
Metastatic cancer features several similar coin shaped foci with clear contours in
different areas of lung.
Study questions.
1. What is focal infiltrative tuberculosis?
2. What is pathogenesis of focal pulmonary tuberculosis?
3. What are clinical and radiological types of focal tuberculosis?
4. What are radiological symptoms of focal tuberculosis in phase of infiltration?
5. What are clinical symptoms of focal tuberculosis in phase of infiltration?
6. What forms of tuberculosis precede fibrotic-focal tuberculosis?
7. In what segments focal tuberculosis localize typically?
8. What diseases should focal tuberculosis be differentiated with?
9. What are diagnostic criteria for focal pulmonary tuberculosis?
10. What are possible outcomes of treatment of focal pulmonary tuberculosis?
Infiltration pulmonary tuberculosis
Infiltration pulmonary tuberculosis is specific exudative progressing pneumonic process
larger then 10 mm. Among primary tuberculosis cases 60% will have infiltration pulmonary
tuberculosis.
Pathogenesis. Infiltrate is tubercular focus with perifocal inflammation around new or
old foci. New foci develop due to a. exogenous superinfection, and b. endogenous reactivation.
Pathology. Characteristic feature of infiltration pulmonary tuberculosis is prevalence of
perifocal exudative inflammation. Each infiltrate will have foci of caseation. Due to exogenous
superinfection with MBT, new foci develop in bronchioles and then to alveoli forming
pneumonic foci. Exacerbation of old foci left after treatment of other forms of tuberculosis
features endogenous reactivation. Exudative perifocal inflammation starts around these foci; its
contents melts. Further inflammation spreads to lymphatics and bronchial wall and enters its
opening, from where it spreads to alveoli with exudative inflammation foci.
Infiltrate develops due to hyper-sensitized lung tissue first appearing in primary infection
of the host with MBT. Second exposure to MBT produces hyper-reaction in this sensitized
tissue. According to A. Rich (1944) hyper-sensitization zones are acquired feature of pulmonary
tissue. Hyperergic reaction develops in great number and fast multiplication of pathogen in
pulmonary tissue.
Concomitant diseases, overheating, psychological traumas, pregnancy, childbirth,
abortion and other factors decreasing resistance of the host promote infiltrate formation.
There are following forms of infiltrate according to clinical and radiological symptoms
(Fig.2.16-2.20):
Lobular – heterogeneous shadow consisting of large and small foci, converged into one
or few conglomerates with destruction in its center;
Round (Fig.2.17) (Assmann-Redecker’s) round homogeneous shadow of low intensity
and clear contours; possible destruction of pulmonary tissue;
Cloud-like (Fig.2.18) (Rubinstine’s) is tender, weakly intensive homogeneous shadow
with unclear contours. Often there is prompt destruction of pulmonary tissue and cavity
formation;
Lobitis (Fig 2.19) is infiltrate spread over the lobe of lung. Shadow often is
heterogeneous with single or multiple cavities of destruction (very large size cavities may form).
Most often right upper lobe is involved.
Peri-cisuritis (Fig 2.20) is large infiltrative shadow with clear contour on one side and
unclear on the other. Such shadow is explained by involvement of interlobar pleura, sometimes
with collection of exudate. Pulmonary tissue destruction may be present as in other forms.
Tubercular infiltrate most often is located in upper lung segments, but 3% patient will
have it in lower lobe.
Fig 2.16. Types of infiltrates.
a-lobular; b-round; c-lobitis; d-cloud-like; e- peri-cisuritis; e – lobar caseation
pneumonia.
Fig.2.17. Round infiltrate with cavity of destruction in its center.
Clinical symptoms. Infiltration tuberculosis does not have typical clinical picture.
Beginning may be acute, gradual or asymptomatic. Most often it starts as other diseases like
influenza, pneumonia, acute respiratory viral infection, pulmonary cancer. Often patient
complains on weakness, prompt fatigue, loss of appetite. Cough may first be scarce and does not
trouble a patient, it is productive with small amount of sputum which coughs up easily.
Infiltration tuberculosis is one of ‘fresh’ types of disease, so physical examination may
not reveal significant signs of disease. Percussion data depend on size of infiltrate. If infiltrate is
larger then 4 cm in diameter, there is blunted sound on percussion and bronchial breathing with
small focus of wet rales on auscultation. When destruction is present then MBT are found in
sputum.
Treatment. Patients with infiltration tuberculosis are treated according to 1,3, or 2
category.
Figure 2.18. Cloud-like infiltrate.
Figure 2.19. Lobitis.
Figure 2.20. Peri-cisuritis.
Outcome. Favorable: complete dissolution, seen with infiltrates of smaller sizes.
Relatively favorable: a. scar formation, not seen on X-ray; b. fibrotic-focal tuberculosis
formation, when perifocal inflammation dissolves completely, caseation focus partially dissolves
and partially calcifies; c- tuberculoma formation, when different in size caseation foci develop.
Unfavorable: transformation into fibrotic-cavernal tuberculosis, when caseation masses
liquefy, separate and are coughed up.
Infiltration tuberculosis is different from caseation pneumonia due to its prevalent
perifocal alteration over caseation and lack of propensity to prompt progress.
Differential diagnosis of infiltration tuberculosis is done most often with pleuropneumonia, pulmonary infiltration eosinophilia, lung infarction, lung cancer (central and
peripheral), actinomycosis, candidosis.
Pleuro-pneumonia is inflammation of segment, lobe or several lobes of lung and pleura.
Diagnostic criteria for pleuro-pneumonia:
-
acute onset after over-cooling or bronchitis, tracheitis, pharyngitis, sinusitis;
-
marked symptoms of intoxication (hectic fever 40-410C, headache, weakness)
and broncho-pulmonary-pleural syndrome (chest pain, productive cough with
reddish sputum, dyspnea );
-
many scattered wet and dry rales on auscultation and signs of pneumonia on
percussion;
-
marked leucocytosis (20x109/L), band forms increase over 15%, marked
increase of ESR;
-
on X-ray there is intensive homogeneous infiltration of a segment (lobe or
lobes) often located in the medial and lower lobes, rarely in the upper lobe; three
is convexity of affected lobe and pleuritis (Fig.2.21)
-
prompt clinical and radiological improvement after administration of antibiotic.
Effective antibiotics are β-lactamase resistant penicillines, macrolides,
fluoroquinolones, II and III generation cephalosporins.
Atypical viral pneumonia. Atypical viral pneumonia characterizes with scarce
symptoms and sometimes has gradual beginning. CBC finds normal leucocyte count, moderate
increase of band forms, monocytosis, increased ESR up to 20 mm/h. Pneumonia may last as long
as 2 months.
Diagnostic criteria of atypical viral pneumonia:
-
patient complains on marked chest pain, dyspnea and headache. In infiltration
tuberculosis these symptoms are absent or moderate;
-
X-ray picture is different due to marked net-like picture due to peribronchial and
perivascular infiltration spreading from widened and inflamed lung root;
Pulmonary infiltration eosinophilia ( pulmonary eosinophilia,
pneumonia,
eosinophilous
Loeffler syndrome) is caused by allergens like parasite (ascariasis,
opisthorchiasis, trichinellosis etc), medication (antibiotics, aspirin, furadonin), chemical
substances, plants and food allergens. Clinical picture is first described by Loeffler.
Diagnostic criteria for pulmonary infiltration eosinophilia:
-
history of allergies, contact with allergens, worm infestation;
-
scarce symptoms at the beginning, sometimes acute onset;
-
clinical picture is characterized by moderate symptoms of intoxication;
-
productive cough with yellowish sputum due to crystals of Sharko-Leyden
formed from died eosinophils;
-
high count of eosinophils in sputum (10-70%);
-
On x-ray there is one or several homogeneous low intensity shadows of different
shapes and sizes, and vague contours (‘cotton swab’ shadow) (Fig.2.22). These
shadows promptly appear and disappear.
-
Anti-allergic medications will quickly improve clinical and X-ray picture.
Sometimes condition is self-contained and does not require medical treatment.
-
Positive skin reaction to respective allergen.
Fig. 2.22 Pulmonary infiltration eosinophilia
Pulmonary infarction is necrosis of lung area due to failure of pulmonary artery
circulation following its thrombembolia. Recovery of infarction leads to complete dissolution of
thrombus or formation of linear scar.
Diagnostic criteria for pulmonary infarction:
-
history of lower limb and pelvic venous thrombophlebitis, septic endocarditis,
rheumatic carditis, congenital heart defects, myocardial infarction, bone
fracture, childbirth, surgical operation;
-
sudden beginning usually coincides with moment of impaction of thrombus or
embolus into branch of pulmonary artery;
-
typical clinical triad is cough, acute chest pain (due to reactive pleuritis at the
infarction basis), hemoptysis. There is dyspnea , tachicardia, fever up to 37.2390C;
-
blunted sound on percussion, bronchial breathing, crepitating rales, pleural
friction rub, accented and bitonal II heart murmur over pulmonary artery on
auscultation;
-
on X-ray there is homogeneous or heterogeneous triangle shaped shadow with
apex faced to lung root (Fig.2.23).Shadow may also have round, oval or
irregular shape, and well rounded or unclear contours. Often there is elevation of
unilateral diaphragmatic cupola;
-
ECG shows right heart overload;
-
hypercoagulation and depressed fibrinolysis in blood chemistry testing.
Lung cancer is malignant tumor arising from bronchial epithelium or from mucosal
glands of bronchial wall (bronchogenic cancer, bronchial carcinoma), rarely from alveolar and
terminal bronchioles epithelium (alveolar cell cancer, pulmonary adenomatosis).
There is central and peripheral type of cancer depending on location.
Central cancer is found in 65% of lung cancer cases. It affects main, lobar and openings
of segmental bronchi leading to their obstruction. Central cancer may exhibit endobronchial and
peribronchial growth.
Peripheral cancer affects distal segmental bronchi. Small peripheral pulmonary cancer
develops in small and smallest size bronchi. There is round, pneumonia-like type and apical
cancer. Peripheral pulmonary cancer may be asymptomatic and be an incidental finding on Xray.
Clinical symptoms of pulmonary cancer resemble those of infiltration tuberculosis: lung
cancer, especially at the beginning may have asymptomatic course or manifest with non-specific
symptoms. Clinical symptoms are rather seen in central lung cancer then in peripheral one.
Tumor may localize in upper lobe, it may have small size and unclear contours.
Moderate leucocytosis can be found in both diseases. Of importance is multiple cytological
sputum examination for MBT.
Diagnostic criteria of lung cancer:
-
typical patient is male over 40 years old;
-
history of repeated or difficult to treat pneumonia, chronic bronchitis, long
history of smoking;
-
bronchial-pulmonary-pleural symptoms like cough (bouts of dry or low
productive cough) which can be troublesome; hemoptysis (‘raspberry jelly’
sputum), chest pain unrelated to breathing phase, dyspnea (in small changes on
X-ray). Gradually these symptoms become pronounced.
-
enlargement of peripheral lymph nodes especially in supra-clavicle area is
feature of tumor metastasis;
-
cancer has scarce auscultative symptoms unless complications develop; dry rales
and blunted sound on percussion over small area features malignant tumor;
-
CBC finds increased ESR which grows as disease progresses, moderate
leucocytosis, anemia;
Diagnostic criteria of central lung cancer:
-
malignant tumor usually compresses adjacent organs;
-
first complaint of patient may be troublesome cough, chest pain and
troublesome dyspnea when main bronchus is affected;
-
X-ray symptoms include: a- endogenous cancer growth leads to hypoventilation
or atelectasis of segment, lobe or lung. When tumor does not obstruct bronchus
completely there is bronchial filling defect on bronchography; when obstruction
is complete there is ‘bronchial stump’ (‘bronchial amputation’) on
bronchography. Only lobar or lung atelectasis result in significant clinical
symptoms. On X-ray atelectasis, as opposed to tubercular infiltrate, has
homogeneous, clear shadow and often concave contours. Tomography
(computed tomography) is necessary to find cancer node; b – peribronchial
growth leads to coarse structures spreading in a fan-like fashion peripherally
from the root. On this background bronchial openings can be seen with their
thickened walls (‘broom’s symptom’). Tomography features longer bronchus
whose apical branch is visible for 2-3 cm instead of normal 0.5-1 cm.
Diagnostic criteria for pneumonia-like peripheral cancer, which features on X-ray as
syndrome of pulmonary infiltration eosinophilia:
-
chest pain of different character and intensity (dull or acute, local or spread,
periodical or constant, unrelated to breathing or that which is made worse on
inhalation);
-
dyspnea is rare. Its first appearance and growth is due to metastatic tumor in
mediastinal lymph nodes or miliary dissemination in lungs;
-
productive cough and hemoptysis appear when tumor affects large bore
bronchus;
-
X-ray symptoms:
o Preferred site in 3 (anterior) segment and lower lobe of right lung;
o Contour of shadow of peripheral cancer is tubercular due to irregular growth
of different parts of tumor;
o Unclear contour is due to tumor’s spread along bronchi, lymphatic and blood
vessels giving it appearance of tender ‘radiant crown’ (‘malignant crown’)
(Fig.2.24)
o Presence of Rigler’s cut;
o Heterogeneous structure of shadow as if it consists of several small round
shadows closely adjacent to each other (symptom of ‘multinodularity’);
Figure 2.24. Peripheral cancer in S2 in right lung. ‘Radiant crown’ spread of
tumor from its outer contour peripherally.
-
CBC has increased ESR, moderate leucocytosis, anemia; sputum has malignant
cells;
-
Bronchoscopy finds tumor primarily localized in anterior segment of upper lobe
of right lung; 3-4 cm nodes have round shape, 1-1.5 cm nodes have polygonal
shape with different sizes of their sides’
-
Progressing course.
Apical pulmonary cancer (Pancoast tumor) is characterized by symptoms of
compression of sympathetic trunk:
-
forearm muscle atrophy;
-
plexitis: pain in shoulder joint, shoulder, and fingers;
-
Horner triad: ptosis, myosis, and enophthalmos;
-
Apical cancer has relatively homogeneous structure and convex lower contour
(Fig.2.25). It can be complicated by destruction of I-II ribs and transversal
processes of thoracic vertebrae.
Figure 2.25. Cancer of upper lobe of right lung. Metastatic foci in left lung.
Actinomycosis is chronic granulomatouse pulmonary damage. It belongs to
pseudomycoses. Disease is caused by Actinomycetes, which take intermediate place between
bacteria and fungi and exist in human host as saprophyte. When resistance is low (long-term
chronic diseases, administration of cytostatics and corticosteroids) endogenous infection
activates and spreads from other organs to lungs, although exogenous infection through air is
also possible.
Diagnostic criteria of actinomycosis:
-
broncho-pulmonary form (characteristic central location of focus in lungs)
develops gradually with scarce clinical signs. Patient complains on cough, dull
chest pain, irregular fever, sweating. Further sputum becomes clear and
suppurative with traces of blood. Sputum contains dense seeds, or druses of
actinomycetes;
-
pleuro-pulmonary form (characteristic subpleural
location involving pleura)
features intense chest pain made worse by cough, inhalation and brisk
movements of a patient. Cough is dry and severe. Infection spreads gradually to
soft tissues and adjacent bones. Chest wall develops woody-dense infiltrates,
sometimes followed by fistula formation. This also resembles tuberculosis for
which infection of lungs, pleura and bones is characteristic;
-
lung abscesses are formed in both variants of disease as they progress;
-
actinomycosis leads to prompt fibrotic transformation;
-
there are wet and dry rales on lung auscultation;
-
CBC finds marked leucocytosis and increased ESR.
-
X-ray finds dense infiltrate of segment or lobe. Lower lung are affected most
often, but upper lung location is also possible. Bronchogenic dissemination foci
are absent. Pleura is thickened;
-
Diagnosis is verified by finding of actinomycetes druses in sputum, fistula
discharge and histology of bioptates;
-
Penicillines, aminoglycosides, and sulfonamide antibiotics lead to prompt relief
of symptoms.
Candidiasis of lung is acute or chronic disease due to Candida fungi. Most often culprit
is Candida albicans, which is saprophyte for human as they it is cultured in 30-80% of cases of
healthy individuals. Lower resistance of the host due to chronic disease or massive dose of
antibiotics may lead to activation and multiplication of fungi.
Diagnostic criteria for candidiasis:
-
acute or chronic development due to chronic disease or use of antibiotics;
-
often is associated with candidosis of pharyngitis, glossitis, and laryngitis;
-
cough productive with scarce clear sputum, fever of 37-390C, hemoptysis;
-
dry and wet rales over medium and lower parts of lungs, but sometimes rales are
absent;
-
unclear contour infiltrate in medium and lower parts of lungs on X-ray;
-
Candida found in sample of sputum taken during bronchoscopy;
-
Positive agglutination test with Candida on dilution to 1:200 and higher;
-
Prompt positive dynamics with antimycotic therapy.
Study questions:
1. What is infiltration tuberculosis?
2. What is pathogenesis of pulmonary infiltration tuberculosis?
3. What forms of infiltrate do you know?
4. What form of infiltration tuberculosis is called lobitis?
5. How do you describe peri-cisuritis? Why one border of peri-cisuritis has clear
contour?
6. What are ‘masks’ of pulmonary infiltration tuberculosis?
7. What data may be found in physical examination of patient with pulmonary
infiltration tuberculosis?
8. What are outcomes of pulmonary infiltration tuberculosis?
9. What diseases should pulmonary infiltration tuberculosis be differentiated from?
10. What are diagnostic criteria of pulmonary infiltration tuberculosis?