It is relatively uncommon considering the high incidence of pulmonary embolism. Given the double pulmonary circulation (pulmonary circle and bronchial circle), the pulmonary infarction occurs only in 10% of cases of embolic occlusion of the pulmonary circle, while in the remaining 90% the bronchial circle compensates for the nutritional needs of the tissue.
It is characterized by the necrosis of a more or less extended tract of parenchyma as a consequence of an embolic (more rarely thrombotic) occlusion of a medium or small-caliber branch of the pulmonary artery (segmental, subsegmentary and lobular arteries) in a lung almost always altered due to hyperaemia. Th
e infarct usually takes on a hemorrhagic appearance and has its preferred location in the lower lobes, especially on the right (due to the greater amplitude of the main right branch of the pulmonary artery) and in the postero-inferior areas; the apices are almost always spared; in more than half of the cases the infarcts are multiple and often also in different stages of evolution due to recurrent phenomena of embolism.
Acute PI, a pulmonary manifestation of a circulatory problem, is a serious condition caused by obstruction of blood flow in one or more pulmonary arteries (PA). Almost all PIs are caused by a thrombus, but they also can result from fat globules, air, amniotic fluid, septic clots, or tumor fragments. The diagnosis of PE is correctly made in only 10% of patients over 70 years of age.
However, diagnosis is often missed in approximately 70% of cases and autopsy results show that up to 60% of deceased hospitalized patients have had a PE, a circumstance that has elicited to the condition the moniker the great masquerader.If left untreated, PI carries a 30% mortality rate.In patients with concurrent cardiac disease or cancer, that rate is about 20%, even with treatment of PI
In general we think about the following categories of patients:
-woman who gave birth
- elderly bedded with huge legs
- elderly with fractures of the femur and pelvis
- person with gynecological and / or andrological surgery
- septic patient
- patient with neoplastic cachexia
Based on experimental research, it is known that for the development of
pulmonary infarction, the following fundamental factors are necessary:
1. the anatomical, embolic or thrombotic occlusion of a medium or small-caliber
branch of the pulmonary artery, resulting in circulatory arrest and downstream
ischemia;
2. chronic pulmonary stasis which, as we have said, besides hindering the
creation of an effective collateral circulation mainly from the bronchial
arteries, favors the blood reflux from the pulmonary veins towards the ischemic
zone;
3. local vasomotor reflexes, with intense capillary vasodilation, which is
conditioned, through the permeability disorders, the red blood cells diapedesis.
Macroscopically, the recent pulmonary infarction presents itself as an area without air, dark red, compact and well delimited, conical or pyramidal with a base at the periphery and apex towards the hilum; in most cases the base corresponds to the pleural surface, which is often covered by a thin veil of fibrin (infarct pleurisy), very rare being the infarcts with a deep seat; at the apex of the triangle it is often possible to find the arterial vessel occluded by the embolus protruding from the small mouth of the dissected vessel.
The cutting surface, reddish, firm and dry, and the margins' relevance to the surrounding parenchyma are the characters that serve to differentiate the infarcts from the atelectasic areas, which may be reddish and cuneiform, but are soft, moist and reentrant on the external surface.
The size of the infarct
varies considerably from case to case, in relation to the caliber of the
occluded vessel and can range from those of a pea or a nut up to the involvement
of almost an entire lung lobe.
Histologically, in the recent infarct the alveoli, the alveolar ducts and the
small bronchi appear filled with densely packed red blood cells; the normal
pulmonary pattern is still recognizable but (contrary to what occurs in the
common haemorrhagic foci) the alveolar walls are necrotic, especially in the
central parts of the infarct. In the subsequent evolution, the red blood cells
go to the disfacmiento and the dissolved hemoglobin is partly transformed into
haemosiderin and hematoidin (the infarct therefore tends to discolor, assuming a
brownish-yellow color), while leucocytes and macrophages accumulate at the
periphery of the necrotic area :
Starting from the second week, a young granulation tissue, rich in blood vessels
and histiocytes, gradually invades the necrotic tissue and, little by little,
demolishes it and reassumes it; at the end, thanks to the fibroblasts and the
neoformation of collagen fibers, the whole outbreak is replaced by a connective
tissue in sclerotic evolution, so that a receding scar is covered by the
thickened pleura.
Contrary to what occurs in tuberculous scars, the infarct scar is often rich in newly formed elastic fibers. Also the embolus (or the thrombus) undergoes a process of organization with possible recanalization.
In the rare cases in which, especially because of the considerable size of the infarct, the organization process remains limited to the peripheral area of the infarct, the formation of a cyst is possible. The abscess or, more rarely, gangrenal transformation of the infarct occurs when the embolus that occludes the vessel is septic. Septic pulmonary infarcts are more often multiple and follow suppurative thrombophlebitis of the uterine veins (puerperal infection), of the venous sinuses of the dura mater (average otitis, panophthalmitis), of the veins of the neck (necrotic angina, tonsillar phlegmon) or of the limbs, especially lower.
Pulmonary infarction, arrows, CXR
show a wedge, and CT a triangular image
The patient with pulmonary infarction has dyspnea and tachypnea, thoracic stinging pain that is accentuated with the actions of the breath, due to pleural irritation; coughing with hemoptysis (from blood filling of the alveoli) and fever (from reabsorption of necrotic material).
SIGNS- INCIDENCE-
TACHYPNEA (respiratory rate >16/min)- 96%
CRACKLES ON CHEST AUSCULTATION- 58%
ACCENTUATED 2ND HEART SOUND- 53%
TACHYCARDIA-(heart rate >100/min) 44%
FEVER- 43%
DIAPHORESIS- 36%
S3 OR S4 GALLOP- 34%
THROMBOPLEBITIS SIGNS & SYMPTOMS- 32%
LOWER EXTREMITY EDEMA- 24%
CARDIAC MURMUR- 23%
CYANOSIS- 19%
In the ECG
a rotation of the frontal QRS axis to the right (resulting in a SI/QIII type),
a clockwise rotation of the horizontal axis, and often unspecific ST−T changes
are typical signs of pulmonary embolism. The chest radiograph may show
wedge-shaped or linear opacities of any size or shape, a pleural effusion, or an
elevated hemidiaphragm. Blood gases show a low PaO2 and a low PaCO2. D-dimers
are elevated in the plasma (>500 ng/L).
The diagnosis of pulmonary embolism is most often confirmed by a spiral CT, occasionally by lung scintigraphy, or pulmonary angiography.
Perfusional scintigraphy with macroaggregates of albumin, marked with Tc 99,
document non-perfused areas of the lung but also simple pulmonary infiltrates
can mislead.
-Angio TC (tac spiral of the thorax with mdc) allows to evaluate.