Invasive pulmonary aspergillosis in a premature neonate

Invasive pulmonary aspergillosis in a premature neonate

IAP 2014 ABSTRACTS S33 Pediatric and Perinatal Pathology: SY21-1 corticoids and antibiotics in neonatal intensive care units. Aspergillus species a...

34KB Sizes 2 Downloads 171 Views

IAP 2014 ABSTRACTS

S33

Pediatric and Perinatal Pathology: SY21-1

corticoids and antibiotics in neonatal intensive care units. Aspergillus species are ubiquitous, being present in the soil and dust. The usual port of entry is the respiratory tract. However, most neonatal invasive aspergillosis described are complication of cutaneous aspergillosis, where the port of entry are venous arm boards, tape used to secure catheters, etc. Most infections reported are due to Aspergillus fumigatus followed by A. flavus and occasional cases of A. niger. The current case is a premature monochorionic monoamniotic twin born at 25 þ 4 weeks gestation. The placenta showed chorioamnionitis without fetal response to the infection. He developed a large subcapsular hepatic hematoma and died with multiorgan failure at 27 þ 3 weeks gestation. There were no cutaneous lesions. At autopsy there was invasive pulmonary aspergillosis and disseminated intravascular coagulopathy. The organism responsible was Aspergillus flavus.

LATE-ONSET AND REVERSED CHRONIC TWIN-TOTWIN TRANSFUSION SYNDROME

Pediatric and Perinatal Pathology: SY21-2

pregnant again. The ALKP was monitored and rose to 1497 U/L. Fetal monitoring was increased. The baby was delivered at 38 weeks with evidence of IUGR (2400 g) with a placental disc weight of 356 g. Assessment of both placentas revealed moderatemassive chronic intervillositis associated with a mild chronic basal villitis and moderate chronic decidualitis. Placental tissue cultures grew no organisms. The features were those of chronic intervillositis of unknown etiology (CIUE). CIUE is a rare entity with an increased risk of poor pregnancy outcome including IUGR and stillbirth and a high recurrence rate. It is thought to be consequence of an abnormal maternal immune response to the fetal allograft. Serum ALKP can be a useful antenatal marker of CIUE to aid management.

Phillip M. Cox West Midlands Perinatal Pathology, Birmingham Womens NHSFT, Birmingham, UK Chronic twin-to-twin transfusion syndrome (cTTTS) complicates 4–35% of monochorionic diamniotic (MCDA) twin pregnancies and untreated carries a mortality of some 80%, with significant neurological disability in 30–35% of survivors. MCDA twin pregnancies are usually closely monitored for cTTTS, which is identified by discordant growth of the twins with polyhydramnios and a distended bladder in the larger one (the recipient) and oligohydramnios and an absent (i.e., collapsed, empty) bladder in the smaller (the donor). Onset is usually in the late second trimester and later onset is usually associated with mild disease. Occasionally, whilst a pregnancy with cTTTS is being monitored, prior to, or following intervention, the cTTTS is seen to reverse, with the donor appearing to become the recipient and vice versa. Alternatively a previously stable MCDA pregnancy suddenly develops rapidly progressive, severe cTTTS in the third trimester. Understandably, the fetal medicine team and the family want an explanation for these occurrences. I shall present 3 different causes of late-onset or apparent reversal of cTTTS. 1) Spontaneous occlusion of protective anastomoses. 2) Fetal abnormality. 3) Post-laser ablation of anastomoses. Careful examination of the placenta and of the twin fetuses by the pathologist may provide an explanation in these unusual cases.

Pediatric and Perinatal Pathology: SY21-2 INVASIVE PULMONARY ASPERGILLOSIS IN A PREMATURE NEONATE Irene Scheimberg The Royal London Hospital The incidence of opportunistic invasive infections has risen dramatically in the last years and morbidity and mortality remains high. Invasive aspergillosis has been described in immunocompromised patients (bone marrow transplant, haematological malignancies, solid transplant organ recipients). Neonates and in particular those born prematurely, are at especial risk of infection due to the immaturity of their immune system and the use of

COMPLICATIONS OF TREATMENT IN THE NEONATAL PERIOD Helen Wainwright1,2 1NHLS D7 Laboratory, Groote Schuur Hospital, Cape Town, South Africa, and 2Department of Anatomical Pathology, UCT Faculty of Health Sciences, Cape Town, South Africa The lifesaving therapies and procedures used in the care of neonates may result in untoward effects and complications. Retinitis of prematurity (ROP) may present as a spectrum of disease ranging from spontaneously resolving vasculopathy to retinal detachment and blindness. Total parenteral nutrition (TPN) is found in 40–60% of infants requiring prolonged intravenous feeding for intestinal failure. Host factors combined with deleterious components of TPN play a role. There is cholestasis, steatosis, portal inflammation and oedema, ductopenia and fibrosis. Sudden unexpected death (SUD) is the typical presentation of cardiac tamponade due to TPN solution entering the pericardial sac. Arterial cannulation for frequent blood pressure monitoring and blood sampling may be complicated by vasospasm, thrombosis, haematoma, infection, breakage, migration, displacement, peripheral nerve damage, ischaemia and tissue necrosis. The immature central nervous system is particularly susceptible to cerebrovascular damage. Periventricular leukomalacia (PML) with destruction of white matter and severe germinal matrix haemorrhage with intraventricular rupture and infarction may occur. Bronchopulmonary dysplasia (BPD) in the post-surfactant era is confined to very low birth weight infants. There is disturbed alveogenesis with large and simplified airspaces, interstitial fibrosis, and disruption of microvascular development.

Pediatric and Perinatal Pathology: SY21-2 CONGENITAL HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS PRESENTING AS NEONATAL LIVER FAILURE Nicole Graf1 and Nick Evans2 1Histopathology Department, The Childrens Hospital at Westmead, Sydney, and 2Neonatal Intensive Care Unit, Royal Prince Alfred Hospital, Sydney, NSW, Australia

Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.