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    10 views3 pages

    Embrio de Bazo

    Uploaded by

    Alejandra Saravia

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    © All Rights Reserved
    Download as PDF or read online from Scribd
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    of 3
    T. Yee Khong This chapter focuses on the morphological aspects. of the spleen and thymus, Maternal and neonatal hematological problems that can contribute to. adverse pregnancy or neonatal outcome are dis- cussed in Chapter 8. Spleen Normal Development The spleen is derived from mesenchymal cells found between the layers of the midline dorsal mesentery (mesogastrium) between the aorta and. stomach, developing in the 5th week. Rotation of the stomach and growth of the mesentery results in the left-sided location of the spleen. The left surface of the dorsal mesentery fuses with the peritoneum overlyingtheleftkidney. These events. eave a lienorenal ligament between the kidney and the spleen and a gastrosplenic ligament between the spleen and the stomach. It is lobu- lated in the fetus, but the lobules are lost by term, being represented throughout life by notches or clefts on the superior border. Hemopoiesis begins. in the organ at about 12 weeks and lymphoid fol- licles appear at 22 to 24 weeks (Figs. 25.1 and 25.2), Splenic weight increases 10-fold in the second half of pregnancy. Gestation related. normal weights are tabulated (Table 25.1). Developmental Anomalies ‘The term polyasplenia has been coined to en- compass the spectrum of disorders of asplenia and polysplenia (Opitz 1985). There is commonal- ity of malformations in other organ systems, and bboth asplenia and polysplenia have been described in the same family. Asplenia is usually accompanied by major abnormalities of the cardiothoracic and abdomi- nal organs, including right atrial isomerism, trilo- bbation of both lungs, and bilateral epartezial Ibronchi (Ivemark’s syndrome) (Ivemark 1955) (Table 25.2). Anomalous pulmonary venous drainage, persistent left superior vena cava, and atrioventricular abnormalities may also bbe present. The cardiovascular anomalies in this syndrome are complex and highly variable (see ‘Chapter 21). This syndrome is overrepresented among hydropic fetuses with cardiovascular anomalies (see Chapter 14), and malrotation of ‘the intestines or malpositioning of the viscera is also seen. Isolated congenital aspleniais rare, with ‘only about 65 reported cases (Halberisma et al. 2005) and can even be familial (Gilbert et al. 2002). ‘An uncommon association of asplenia is horse- ‘shoe adrenal gland but itis seen in over 50% of ‘horseshoe adrenal gland (Strouse et al. 2002). Fused adrenal gland and anal atresia or stenosis, are exclusive to asplenia of the heterotaxy syn- ‘dromes (Ticho etal. 2000), Other midline defects in heterotaxy syndromes include cleft palate and absent corpus callosum (Noack etal. 2002). In addition to multiple spleens in the dorsal mesogastrium, polysplenia is associated with ‘other abnormalities—left atrial isomerism, bilat- ‘eral hyparterial bronchi, and bilobed iungs—and ‘complex and unpredictable visceral arrangements FFeause 25.1. Spleen at 18 weeks with red pulp and averle sdevid of perarerar empha, in the abdomen are found. Cardiovascular anom- alies are frequent but not as severe as those accompanying asplenia. The splenic mass is ‘usually divided into fairly equally sized masses ‘that together equal the mass of a normal spleen. ‘Accessory spleens (splenunculi) are seen in 10% of postmortems, most commonly adjacent to ‘he tail of the pancreas or the hilum of the defini- ‘tive spleen. One or more splenic masses are seen around a normally sized spleen; accessory spleens differ from polysplenia by the absence of te vis-

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