DOCSLIB.ORG

F F Placental Infarction in Teenage Pregnancy F 16 22 2 2550 77

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
F F Placental Infarction in Teenage Pregnancy F 16 22 2 2550 77 Placental infarction in teenage pregnancy ..* ,-. " % & 4 '+! #> #!7)+=&7+# (') *+ 16 ./ 0 *1 +6 2+' 5 ') ')+ * 20 '.# % Abstract .&% #7+1+ 8 %7+#. 9&0 * .:( &#'#$ + *+# A- 16 year-old primigravida woman had ') 28 '.# 9&+ * 36 '.# ' the first visit antenatal care at the health station '=" #$% & !& #> near home, when the gestational age was 20 +6 week 71+7+#++!+ +#&%$ *+'? # by certained date, bood serology all negative. There 9+9# 1.3 ? 9> was a problem of the fundal height less than the #= 9+7)+"#@ &9+& gestational age at 32 week of pregnancy but early 1#'# ) 1 >+ '9>'= detection and further investigation was not done. " * & # %A %8'# At 36 weeks of pregnancy, she came to +# 7)+.B > A1= the Taphanhin Crown Prince Hospital with the chief 9+ ' 250 ' >8C complain of abnormal vaginal bleeding and labor pain &#7+9# 1 ? 35 ? ) 1 and the ultrasound findings were abnormal placenta >+%D $) C (9 APGAR score (thickness 1.5 cm. and focal hypoechogenicity = 0, 3, 4 ) ' 1,260 ' Maturity Score 34 especially at the placental margin and the maternal '.# %@' %("!>= *&#' floor ) and oligohydramnios. while she was being &* &9#++?%=&#' admitted to the labor room, the fetal distress was '=+! =%&! >! D#>2 ' detected so the cesarean section was done. The * 7 ! " #$% & !& %' '# % ./1 22 @'1 2 ' 2550 77 intraoperative findings were wide placental infarction 9>1 7+".+= 7+=>8 (more than 1/3 of the placenta), 250 grams by weight, * &7)+ D#>>+& 25 9+ (') * umbilical cord diameter is 1 cm., with average length #1D* &?>+=#o (3) +D$ of 35 cm., severe oligohydramnios and the female 2> 7)+ A1=9+7)+ newborn (APGAR score = 0, 3, 4 ) 1,260 grams by %&8+7+#1%&D.) ?A1 = >#* & weight, breech presentation and Maturity score was %("!>= * 7+= *D#>(4,5) 34 weeks. The diagnosis was severe IUGR and severe birth asphyxia. After birth the newborn was intubated and resuscitated, and then transferred to the Phichit 8>.p (D * + 16 ./ Hospital, 4 day later she was dead due to severe %'qCA./1 3 +! '%>'1 D. * sepsis. + *+' >+ %' '# % 3 ,-2 .&% #7+ ')#> '1 28 .B 1&D " 9+ 2 2549 (% D#>+&1 +) # #& ' "#%&!71++& +# '1 5 2550 .sq #& &#7+9+'#9+# >1 '( > 0 * ')9&+ * 20 +6 2 .& 7+ .B1.1+ & '.# 121+'# + *+' >+ ++?%%# ') >1> %' '# % '#% 5 ') 87+#. n+"1% .B& ') * 2 % ) '+') * 58 "' 156 D#>% 71 21') 7 8 '.# (1) "# ? #'! 23.7 "'+ 71+9>D1+%&2+ 9+ @##&' %'((! .&D D9 D#> "#%& $.B>+7)+71++#>=9+8' 9 7+) =.: & 8 % '#+ #& 9>%& >7)+# (2) &q'?. %'A0 * 9>9+7)+= *&&%&.B$# .:( &+#1 +& * D.%D1 1. ) '9A) 17 "'*= 4 9+') * 71++ *9A)'%#9> #7+9&+ * 20 +6 - 35 +3 '.# &#.B 7+ .%'9A) #'&+% 78 " % %A % 50 g 1 hr 9&+ * 28 +3 - HEENT : not pale conjunctivae, no '.# D#> 130 mg% icteric sclera , no thyroid enlargement 2. 9##$ + *') - Heart and Lung : . 28 '.# = >.& '#)# DD#> +'>? # - Abdomen : FH 2 > (29 cm.) , 4 7+7 > 1 FHR positive, irregular uterine contraction Interval 4 6 , Duration 30 , severity 1 2 + - .sq" .&% ' .sq > & D!'# >+ .sq 1 #71 7+=!> # - Speculum exam : bloody discharge - '+C''&# 2 cc at post fornix, no active bleeding , - Extremities : no deformities, no edema - #+ 40 ./ .B 5 ./ 5 56- 7, '1 + D#># 1 10 ?++ ' CBC : Hb 12.3 mg/dl, Hct 39%, wbc ' > 10 ./ 20,000 neutrophil 89%, lymphocyte 7% normal rbc - + 18 ./ %'qCA./1 3 morphology, platelet smear 253,000, M.C.v. 81, +! 9'2'%> .sq" .&% ' 1 2 M.C.H 26, M.C.H.C 32 3 + ' D1 + UA : sp.gr. 1010, albumin negative, 8>.p ''1" sugar negative, ketone negative, rbc 30 50, epith #$% & !& '1 13 2550 cell 10 9&+ * 36 '.# #> 71+. #>+o ') Coaglulogram : PT ., PTT . &7+#.$>+++%!+ +# LFT : SGOT 32, SGPT 14 3 !'1 "+" .sq#%$ 7+ FBS : 80 mg% BUN : 6 mg% +' Triglyceride : 170 Creatinin : 0.9 mg% 5 Cholesterol : 207 - vital sign : BP 120/80 mmHg, PR ANA : negative y 88/min, RR 18/min, BT 37.1 C CXR : . - General appearance : a young EKG : . pregnant, good intelligent, BW 76 kg. ./1 22 @'1 2 ' 2550 79 * 1 1 NST * & Late decelelation, baseline 150 bpm, moderate variability &+++&> ( 71+ C) * 1 2 +'? # : Single viable fetus, * 1 3 +'? ## 1.3 transverse lie, FHR positive, FM positive, AFI = 4 ? + posterior lower, ' fetal parameter HC : ratio 1 9>#"#@ &9+& 1# '# 80 " % .28 8>.p D#>' %@' 1. Primigravida teenage prenancy 2. IUGR with non reassuring FHR 3. R/O Abruptio placenta 9& 8') * * & progression of labor & FHR # (#'.) %*= .#.# 1 cm. effacement 75%, MI, station -2 * 1 4 Severe variation / late decelelation, FHR : baseline 120-140 bpm, moderate variability : no accelelation 9 - Set OR for : emergency cesarean section due to fetal distress. - Post operative diagnosis : Severe IGUR with fetal distress. - Operation : Low transverse cesarean section with Breech extraction. - Finding : Non gravid uterus, normal both adnexa, oligohydramnios. D $) +# >+ #$"#D>+> 9#>8C 10 ? ..B # 7)+?#&9$.B > A1=9+ "#@ &#>#&+#9+, ) ' 250 ', no retroplacenta blood clot, >8C&#7+ 1 ? (A : v = 2 :1) ./1 22 @'1 2 ' 2550 81 * 1 5 #* 7)+.B > A1=9+7)+ #>?>##>#, * 9 #* ## * 1 6 #* '#9 * 1 7 #* ' +# 2 ' C (9 , APGAR 1 = 10 cc vein push, Dopamine 30 mg in 5% d/w 50 cc 0, 5 = 3, 10 = 4 ( HR = 2, = 2 ) drip 1 cc/hr, Ampicillin 50 mg vein add Gentamycin ) ' 1,260 ' .. D =% ' 9 4 mg intravenous ' '+" % ' ) ' =%>>+ 80 ')/ D#> '18+* +# 4 ' & ! >! .B 15 &=+! =% ! 71+%#!7)+*=&7+# + 3, A 7 ?, ON UvC line, DTX stat 27 mg% = > adrenaline (1 : 10,000) 0.2 cc % 7 dose, 0.9% NSS 10 cc/hr, 10% glucose 82 " % 5: 9>9+7)+#.B >& 9# ') *= ' % '# 9+ NST Late Decelelation ?A1#2A* & + +'" (WHO) 7+ ') *9&+ ++?% +1 D2A 20 ./ "#=.&C1 ' ' % 8#' 9>>%&+q= ') *= '.&>+& 15 - 20 9+ 8>.p )D#> #* & uteroplacenta insufficiency +#&2A>+& 85 9++'') *= = ># fetal decompensate .B IUGR %&'1 ''1 " (6) "#>+& 33 9+ '1') * #* &9#++?%= = >7+#)D =!> # !#1 1=# # ..: &##* & oligohydramnios * &?>++ (7) +#) ' ?A1= >1# Perinatal morbid & mortality +#>+= '#%89+ +#+ D#>9A) # 7+ '* & SGA "# ) ' * & uteroplacenta insufficiency.9+ +#>+ 19A).& 1.2 & SGA 8>.p )D#>7 =# ! #' 1%("!>= * 19A).& " " &7)+71+1 ' * &?# * & 1.3 (8,9,10,11) 8"#9++#' #!7)+= * & "*! ?A1D * & ) ' +#>+'D!'#% #' 9>> vasoactive agents (cocaine , nicotine) 8>.p 1.B ( '') *1 %&.B %+C'+'#&1 .:( %("!> ')+ * 28 1 .& 10 / ' ?A1D#>' '1% '.# DD#>'7 >&' 9&18>.p 8>+71%&* &11%&#* &?>+o '1" '1"# 1 5 / ' (') * + * 36 '.# +'? # 1 1 %& +#) '>+ ( + * 28 +2 '.# ') *1D 1 .& 458 ' (12) & ( EFW 1,200 gram ?A1 < 10 percentile ') *1 # 1& ') * %& +# Body weight ) '@1 1'D #.& 120 ' AFI = 4 ')o1 %&.B! 1) 1 %&' ) '>+ 1#% ( # 7+ 36 '.# ?A1' * &) 1 ') *1D 1 .& 39 ' #'') >+$' 'q' 9#9+ ) '1 +#% (1 1%&% (1D 1.& 153 ' (13) ./1 22 @'1 2 ' 2550 83 = 1.&+ 3,000 !# 9#9+%& 19A)+ *& nicotine .B1+'1#&8&+ 2 .D#> =.s' 7)+ 71+%.B1&D#>=D9' = > '# 9+ 71+%&# & 8D#> (14) &#' nicotine 19A)=&7+# #$ "#'1 D.% 9+ %& 9+#%&&>= ># 19A)9+ ''.# + * &>+1%& 4 - 5 catecholamine .B8= > #'" #9A) (16) ? "#'1 D.> ' 23 '.# D #71+9+71+% 19A)9+ >+ 1.5 ? &D 5 % collgen = chorionic villi & ' 9+ ?"#* &%& = >7+#9+9# subtrophoblastic basement membrane # + &++?% ')9'2 9++ # #9A)71+% 1% +D#++D?#&9+D#>>+ (22,23) 9+ syncytial buds & 9 apoptosis 9A)=9+8>1 1 &71++ 4 #9+ = >#.1+ & ++?%%# (15) 8 = >#* & !"# ) '#>+& IUGR (17) $% &'()' $ +++D?#%& = >#* &7+# ** +,) %, '- ./& % 71+%D.%''$#7+## (18) = > $*+(0 ++?%#&71+" $&>= >#* & * (& 0/ / +#7+# #' %A = >#* & hypoxia =7)+ ('1 + " & 9+8>1 1 D.#9+ placental 7)+71+1 ' * &?# * &#!7)+= * & hormone &#%$ *+ #D#>(19) "*! 7+D#>' #!# ! (') *1 1 %& = ># cocaine, nicotine #'') %@' & * &?>++ ! &1 +' + '* &7)+ ')7 >D#>')+ # 7)+ &#$) '' >+ (20) & = *#%&! = ># perinatal outcome 1# * &?>++ ! . #" early neurodevelopmental impairment, behavioral problem, > > (21) 84 " % 4 7. Julie AQ. Sharon FE. The impact of continuing, illegal drug use on teenage pregnancy 1. Kazzi GM, Evans MI, Sokol RJ, outcomes a prospective cohort study. Br J Sabbagha RE. Placental maturation and thickness. In : obstetric Gynecol 2002 ; 109 : 1148 - 53. Sabbagha RE, editor. Diagnostic ultrasound applied 8. Agustin CD, Juse MB, Cristing L. to Obstetrics and Gynecology . 3rd ed. Philadelphia : Maternal-perinatal morbidity and mortality associated JB Lippincott Company ; 1994 : 289 98. with adolescent pregnancy in Catin America: cross 2. Muller LMM . Ultrasound assessment of sectional study American Journal obstetric the placenta , and clinical assessment of the placenta Coynecol 2005 ; 192 : 342-9. growth. In : Redmann CWG, Sargent IL and Starkey 9. Chineta RE, Michael Kl, William LG. PM, editors. The human placenta. Oxford : Blackwell Risk of adverse pregnancy outcomes in young Scientific Publications ; 1993 : 155-89. adolescent parturients in an inner-city hospital. 3. Spirt BA, Gordon LP. The placenta and American journal obstetric Gynecol 2002 ; 186 : cervix. In : McGahan JP, Porto M , editors. Diagnostic 918-20. obstetrical ultrasound . Philadelphia : JB Lippincott 10. Moini A, Riazi K, Mehrparvar AH. Company ; 1944 : 84 88. Pregnancy and labor complications in teenagers in 4. Smith SC, Baker PN, Symonds ME. Tehran. Inter J Gynecol Obstet 2002 ; 78 : 245-7. Placental apoptosis in nomal human pregnancy. Am J 11. Hugh SM, Karen BL, kathryn LR. Obstetrics Gynecology 1997 ; 177 : 57-65 Adolescence and very low birth weight infants a 5. Barclay D, Evans K , Fox R . Ultrasound disproportionate association. Obstetric Gynecol 1996 ; diagnosed placental infarction in a women with 87 : 83-6. recurrent fetal growth restriction, Journal obstetrics 12. Roquer JM, Figueras J, Botet F, and Gynecology
Load more

Recommended publications
  • Clinical Correlates of Histopathological Entities of the Placenta
    Clinical Clinical correlates of histopathological entities of the placenta Admire Matsika PLACENTAL EXAMINATION has a critical research on the understanding of the role in understanding adverse fetal clinical implications of placental lesions in and maternal outcomes in pregnancy. obstetric and neonatal care. Background General and allied health practitioners However, progress in correlating placental This review provides medical caring for pregnant women and neonates pathology with clinical phenotypes has practitioners with an update on new often encounter placental histopathological been hampered by methodological issues terminology and status quo of research on reports with esoteric diagnostic entities of in many studies published.1 Additionally, placental entities of clinical significance contentious clinical significance such as there appears to be a knowledge disparity that may recur in subsequent pregnancy chronic villitis, massive perivillous fibrin between perinatal pathologists reporting and for which alteration of obstetric care deposition, chronic histiocytic intervillositis, microscopic changes seen in the organ and may improve outcomes. With the advent materno-fetal vascular malperfusion and delayed villous maturation. These lesions understanding of the clinical significance of the electronic My Health Record may recur in subsequent pregnancies. of placental histopathological diagnoses by system implemented Australia-wide, obstetric care providers.2 When reported patients will have direct access to their Objective and interpreted
    [Show full text]
  • Associations Between Phenotypes of Preeclampsia and Thrombophilia
    European Journal of Obstetrics & Gynecology and Reproductive Biology 194 (2015) 199–205 Contents lists available at ScienceDirect European Journal of Obstetrics & Gynecology and Reproductive Biology jou rnal homepage: www.elsevier.com/locate/ejogrb Associations between phenotypes of preeclampsia and thrombophilia a, a a b Durk Berks *, Johannes J. Duvekot , Hillal Basalan , Moniek P.M. De MAAT , a a Eric A.P. Steegers , Willy Visser a Department of Obstetrics and Gynecology, Division of Obstetrics and Prenatal Medicine, Erasmus MC, University Medical Center Rotterdam, The Netherlands b Department of Hematology, Erasmus MC, University Medical Center Rotterdam, The Netherlands A R T I C L E I N F O A B S T R A C T Article history: Objectives: Preeclampsia complicates 2–8% of all pregnancies. Studies on the association of preeclampsia Received 29 July 2015 with thrombophilia are conflicting. Clinical heterogeneity of the disease may be one of the explanations. Received in revised form 4 September 2015 The present study addresses the question whether different phenotypes of preeclampsia are Accepted 17 September 2015 associated with thrombophilia factors. Study design We planned a retrospective cohort study. From 1985 until 2010 women with Keywords: preeclampsia were offered postpartum screening for the following thrombophilia factors: anti- Fetal growth restriction phospholipid antibodies, APC-resistance, protein C deficiency and protein S deficiency, hyperhomo- HELLP syndrome cysteineamia, factor V Leiden and Prothrombin gene mutation. Hospital records were used to obtain Pre-eclampsia information on phenotypes of the preeclampsia and placental histology. Retrospective study Thrombophilia Results: We identified 844 women with singleton pregnancies who were screened for thrombophilia factors.
    [Show full text]
  • Superb Microvascular Imaging of Retained Placenta with Placenta
    PICTURE OF THE MONTH Superb Microvascular Imaging of Retained Placenta with Placenta Accreta Spectrum Toshiyuki Hata1, Uiko Hanaoka2, Ayumi Mori3, Kenta Yamamoto4, Chiaki Tenkumo5, Nobuhiro Mori6, Kenji Kanenishi7, Hirokazu Tanaka8 ABSTRACT We present our first experience of using superb microvascular imaging (SMI) with an 18-MHz linear probe to diagnose placenta accreta spectrum (PAS) in the retained placenta after vaginal delivery. In the first case, irregular minimal invasion of the retained placenta into the anterior myometrium and a thin uterine wall were clearly noted. In the second case, SMI clearly demonstrated the loss of myometrium anterior to fundal lesions and abnormally dilated, torturous, stem villous vessels invading until the uterine serosa. SMI with the use of an 18-MHz linear probe may be a novel diagnostic tool for the diagnosis of PAS in the retained placenta after delivery. Keywords: 18-MHz linear probe, High-resolution ultrasound, Placenta accreta spectrum, Retained placenta, Superb microvascular imaging. Donald School Journal of Ultrasound in Obstetrics and Gynecology (2019): 10.5005/jp-journals-10009-1600 INTRODUCTION 1–8 Department of Perinatology and Gynecology, Kagawa University A placenta accreta spectrum (PAS) is one of the most serious and Graduate School of Medicine, Miki, Kagawa, Japan potentially life-threatening conditions for both a pregnant woman 1 Corresponding Author: Toshiyuki Hata, Department of Perinatology and fetus. The precise prenatal diagnosis of PAS improves the and Gynecology, Kagawa University Graduate School of Medicine, prognosis of the patient and reduces maternal morbidity.2 The Miki, Kagawa, Japan, Phone: +81-87-891-2174, e-mail: toshi28@med. European Working Group on PAS has proposed standardized kagawa-u.ac.jp 3 ultrasound descriptors of this spectrum.
    [Show full text]
  • Pathological Examination of the Placenta: Raison D'être, Clinical
    Review Article Singapore Med J 2009; 50(12) : 1123 Pathological examination of the placenta: Raison d’être, clinical relevance and medicolegal utility Chang K T E ABSTRACT pregnancy outcome; Formal pathological examination of the (3) Improved management of subsequent pregnancies placenta provides valuable information to by the identification of conditions known to have the obstetrician, neonatologist, paediatrician recurrence risks or which may be either treatable or and family. This article aims to provide the preventable; clinician with an overview of the significance of (4) Identification of a pathological condition requiring placental examination in relation to common or timely clinical intervention; important pathological processes, and the utility (5) Understanding of antenatal and intrapartum events of information obtained therein in explaining that contribute to long-term neurodevelopmental adverse outcomes, management of subsequent sequelae, with early identification of such changes pregnancies, and assessment of newborn risk for making possible early interventions and improvement the development of short- or long-term sequelae. in long-term outcome; General guidelines for placental examination, and (6) Assessment of factors contributing to poor outcome logistical and practical issues are also discussed. as a factual basis for resolving medicolegal issues. Finally, the role of the placenta in the defence of The multidisciplinary team approach is well obstetricians and other healthcare workers in established in oncology.(4) A similar model for perinatal cases of poor neonatal outcome is described. medicine is appropriate,(5) and may involve obstetricians, neonatologists, ultrasonographers, obstetrical Keywords: medicolegal, placenta, placental anaesthetists, clinical geneticists, paediatric surgeons and pathological examination, poor neonatal paediatric pathologists. This may serve both as a working outcome conference to review and discuss current case issues, and Singapore Med J 2009; 50(12): 1123-1133 as a teaching conference.
    [Show full text]
  • Placental Abruption: Clinical Features and Diagnosis
    Official reprint from UpToDate® www.uptodate.com ©2017 UpToDate® Placental abruption: Clinical features and diagnosis Authors: Cande V Ananth, PhD, MPH, Wendy L Kinzler, MD Section Editor: Charles J Lockwood, MD, MHCM Deputy Editor: Vanessa A Barss, MD, FACOG All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: May 2017. | This topic last updated: Feb 23, 2017. INTRODUCTION — Placental abruption (also referred to as abruptio placentae) is bleeding at the decidual-placental interface that causes partial or complete placental detachment prior to delivery of the fetus. The diagnosis is typically reserved for pregnancies over 20 weeks of gestation. The major clinical findings are vaginal bleeding and abdominal pain, often accompanied by hypertonic uterine contractions, uterine tenderness, and a nonreassuring fetal heart rate (FHR) pattern. Abruption is a significant cause of maternal and perinatal morbidity, and perinatal mortality. The perinatal mortality rate is approximately 20-fold higher in comparison to pregnancies without abruption (12 percent versus 0.6 percent, respectively) [1]. The majority of perinatal deaths (up to 77 percent) occur in utero; deaths in the postnatal period are primarily related to preterm delivery [1-4]. However, perinatal mortality associated with abruption appears to be decreasing [1]. INCIDENCE — Placental abruption complicates approximately 1 percent of pregnancies [5,6], with two-thirds classified as severe due to accompanying maternal, fetal, and neonatal morbidity [7]. The incidence appears to be increasing in the United States, Canada, and several Nordic countries [5], possibly due to increases in the prevalence of risk factors for the disorder and/or to changes in case ascertainment [8,9].
    [Show full text]
  • Placental Findings in Preterm and Term Preeclampsia
    Published online: 2021-08-30 THIEME 560 Review Article | Artigo de Revisão Placental Findings in Preterm and Term Preeclampsia: An Integrative Review of the Literature Achadosplacentáriosnapré-eclâmpsiapré-termoea termo: Uma revisão integrativa da literatura Luciana Pietro1,2 José Paulo de Siqueira Guida2 Guilherme de Moraes Nobrega2 Arthur Antolini-Tavares3 Maria Laura Costa2 1 Institute of Health Sciences, Universidade Paulista, Campinas, SP, Address for correspondence Maria Laura Costa, Department of Brazil Obstetrics and Gynecology The University of Campinas, 101 2 Department of Obstetrics and Gynecology, Universidade Estadual de Alexander Fleming St, Campinas, SP, Brazil Campinas, Campinas, SP, Brazil (e-mail: [email protected]). 3 Department of Pathology, Universidade Estadual de Campinas, Campinas, SP, Brazil Rev Bras Ginecol Obstet 2021;43(7):560–569. Abstract Introduction Preeclampsia (PE) is a pregnancy complication associated with in- creased maternal and perinatal morbidity and mortality. The disease presents with recent onset hypertension (after 20 weeks of gestation) and proteinuria, and can progress to multiple organ dysfunction, with worse outcomes among early onset preeclampsia (EOP) cases (< 34 weeks). The placenta is considered the root cause of PE; it represents the interface between the mother and the fetus, and acts as a macro- membrane between the two circulations, due to its villous and vascular structures. Therefore, in pathological conditions, macroscopic and microscopic evaluation can provide clinically useful information that can confirm diagnosis and enlighten about outcomes and future therapeutic benefit. Objective To perform an integrative review of the literature on pathological placental findings associated to preeclampsia (comparing EOP and late onset preeclampsia [LOP]) and its impacts on clinical manifestations.
    [Show full text]
  • HELLP Syndrome, Multiple Liver Infarctions, and Intrauterine Fetal Death in a Patient with Systemic Lupus Erythematosus and Antiphospholipid Syndrome
    □ CASE REPORT □ HELLP Syndrome, Multiple Liver Infarctions, and Intrauterine Fetal Death in a Patient with Systemic Lupus Erythematosus and Antiphospholipid Syndrome Yoko Wada 1, Yuichi Sakamaki 1, Daisuke Kobayashi 1, Junya Ajiro 1,2, Hiroshi Moro 3, Shuichi Murakami 1, Izumi Ooki 4, Akira Kikuchi 4, Koichi Takakuwa 4, Kenichi Tanaka 4, Takehiro Sato 5, Masaaki Nakano 6 and Ichiei Narita 1 Abstract We report a case of HELLP syndrome, multiple liver infarctions, and intrauterine fetal death in a woman in the 17th week of pregnancy with SLE and APS who had been in remission on a regimen of low-dose prednisolone and aspirin. An increase in the dosage of corticosteroid together with intravenous heparin infu- sion led to improvement of the clinical symptoms, laboratory parameters, and multifocal low-density liver le- sions detected by computed tomography. Early onset and signs of severe organ involvement are the character- istic features of HELLP syndrome associated with APS, and patients that are at risk should be followed up carefully. Key words: HELLP syndrome, systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), mul- tiple liver infarction, catastrophic antiphospholipid syndrome (CAPS) (Inter Med 48: 1555-1558, 2009) (DOI: 10.2169/internalmedicine.48.2284) function, impaired placental vascular perfusion, and Introduction ischemia-producing oxidative stress, which stimulate the re- lease of factors that injure the vascular endothelium via acti- The syndrome of hemolysis, elevated liver enzyme levels vation of platelets, vasoconstrictors, and loss of normal vas- and low platelet count (HELLP) is a multisystemic throm- cular relaxation in pregnancy (3, 4). botic microangiopathy that complicates pregnancy.
    [Show full text]
  • Overview of Neo-Vascular Lesions After Delivery Or Miscarriage
    Journal of Clinical Medicine Review Overview of Neo-Vascular Lesions after Delivery or Miscarriage Yuji Shiina Department of Obstetrics and Gynecology, Yamagata Prefectural Shinjo Hospital, Shinjo, 12-55 Wakabacho, Yamagata 996-0025, Japan; [email protected]; Tel.: +81-233-22-5525; Fax: +81-233-29-2693 Abstract: The concept of intrauterine neo-vascular lesions after pregnancy, initially called placental polyps, has changed gradually. Now, based on diagnostic imaging, such lesions are defined as retained products of conception (RPOC) with vascularization. The lesions appear after delivery or miscarriage, and they are accompanied by frequent abundant vascularization in the myometrium attached to the remnant. Many of these vascular lesions have been reported to resolve spontaneously within a few months. Acquired arteriovenous malformations (AVMs) must be considered in the differential diagnosis of RPOC with vascularization. AVMs are errors of morphogenesis. The lesions start to be constructed at the time of placenta formation. These lesions do not show spontaneous regression. Although these two lesions are recognized as neo-vascular lesions, neo-vascular lesions on imaging may represent conditions other than these two lesions (e.g., peritrophoblastic flow, uterine artery pseudoaneurysm, and villous-derived malignancies). Detecting vasculature at the placenta–myometrium interface and classifying vascular diseases according to hemodynamics in the remnant would facilitate the development of specific treatments. Keywords: placental polyps; retained products of conception; arteriovenous malformations; neo- vascular lesion Citation: Shiina, Y. Overview of Neo-Vascular Lesions after Delivery or Miscarriage. J. Clin. Med. 2021, 10, 1084. https://doi.org/10.3390/ 1. Introduction jcm10051084 The sudden onset of critical vaginal bleeding 12 years after pregnancy was reported in 1884 in Philadelphia [1].
    [Show full text]
  • Placental Morphology in Hypertensive Disorders and Its Correlation to Neonatal Outcome
    Tangirala S, kumari D. Placental morphology in hypertensive disorders and its correlation to neonatal outcome. IAIM, 2015; 2(11): 35-38. Original Research Article Placental morphology in hypertensive disorders and its correlation to neonatal outcome Sudha Tangirala1*, Durga kumari1 1Assistant Professor, Department of Obstetrics and Gynaecology, King George Hospital, Visakhapatnam, Andhra Pradesh, India *Corresponding author email: [email protected] International Archives of Integrated Medicine, Vol. 2, Issue 11, November, 2015. Copy right © 2015, IAIM, All Rights Reserved. Available online at http://iaimjournal.com/ ISSN: 2394-0026 (P) ISSN: 2394-0034 (O) Received on: 25-10-2015 Accepted on: 02-11-2015 Source of support: Nil Conflict of interest: None declared. How to cite this article: Tangirala S, kumari D. Placental morphology in hypertensive disorders and its correlation to neonatal outcome. IAIM, 2015; 2(11): 35-38. Abstract Background: Placenta is a fetomaternal organ which is vital for maintaining normal pregnancy and promoting growth of the foetus. Pregnancy complications like Preeclampsia are reflected in the placenta both morphologically and microscopically as blood supply to the placenta is impaired in preeclampsia due to failure of trophoblastic invasion. Aim: To correlate morphological changes of placenta with the severity of hypertension in the mother and to assess the neonatal outcome. Materials and methods: It was a comparative study conducted on 200 women out of which 100 were having hypertensive disorders and remaining 100 were taken as control group. Placenta was collected from these women and studied for morphological changes and correlated with severity of hypertension. Neonatal outcome in the form of birth weight, Apgar score, need for neonatal resuscitation and admission to NICU were noted.
    [Show full text]
  • 19 Diseases of the Placenta Deborah J
    19 Diseases of the Placenta Deborah J. Gersell . Frederick T. Kraus Normal Anatomy and Development .............. 1000 Insertion . 1054 Umbilical Vessels . 1056 Abnormal Placentation and Villous Development . 1003 Anomalous Shapes . 1003 Clinical Syndromes and Their Pathologic Extrachorial Placenta . 1004 Correlates in the Placenta ......................... 1059 Placenta Accreta, Increta, and Percreta . 1005 Preeclampsia . 1059 Mesenchymal Dysplasia . 1007 Essential Hypertension . 1060 Diabetes Mellitus . 1060 Multiple Pregnancy ................................ 1007 Preterm Birth, Preterm Labor, and Preterm Twin Gestation . 1007 Rupture of Membranes . 1060 Complications of Multiple Pregnancy . 1013 Post-Term Pregnancy . 1060 Higher Multiple Births . 1021 Fetal Growth Restriction, Intrauterine Growth Restriction (IUGR) . 1060 Placental Inflammation and Intrauterine Neonatal Encephalopathy (NE), Cerebral Infection ........................................... 1022 Palsy (CP), and ‘‘Birth Asphyxia’’ . 1061 Ascending Infection and Acute Fetal and Placental Hydrops . 1061 Chorioamnionitis . 1022 Nucleated Red Blood Cells in the Fetal Subacute Chorioamnionitis . 1027 Circulation . 1062 Villitis and Hematogenous Infection . 1027 Thrombophilias . 1063 Other Patterns of Placental Inflammation . 1032 Acute Fatty Liver of Pregnancy and HELLP Syndrome . 1063 Circulatory Disorders .............................. 1033 Sickle-Cell Trait/Disease and Other Maternal Circulation . 1034 Hemoglobinopathies . 1063 Fetal Circulation . 1042 Storage Disorders . 1064
    [Show full text]
  • Anatomical and Histopathologic Analysis of Placenta in Dilation and Evacuation Specimens
    Forensic Medicine and Anatomy Research, 2014, 2, 17-27 Published Online April 2014 in SciRes. http://www.scirp.org/journal/fmar http://dx.doi.org/10.4236/fmar.2014.22005 Anatomical and Histopathologic Analysis of Placenta in Dilation and Evacuation Specimens Taha M. M. Hassan1, Ahmad M. S. Hegazy2*, Mohammed M. Mosaed3 1Pathology Department, Bani-Sowif University, Bani-Sowif City, Egypt 2Anatomy Department, Benaha Faculty of Medicine, Benha University, Banha City, Egypt 3Anatomy Department, Al-Azhar Faculty of Medicine, Al-Azhar University, Assuit City, Egypt Email: *[email protected] Received 18 December 2013; revised 7 January 2014; accepted 20 January 2014 Copyright © 2014 by authors and Scientific Research Publishing Inc. This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/ Abstract Background: Anatomical and histopathologic examination of placenta in cases of abortion is cru- cial as to clarify the underlying causes of many adverse pregnancy outcomes. Dilation and evacua- tion (D&E) is the most common mode of uterine evacuation that commonly examined in pathology sections. The aim of this study is to discuss the various placental pathologies, and to demonstrate the importance of careful pathologic examination of D&E material, also to review the anatomy of placenta and to compare our findings with other publications worldwide. Material and Methods: A retrospective descriptive study for 200 placental tissues was collected in 18 months period and revised for normal anatomy and various placental pathologies. These placentas were obtained by dilation and evacuation (D&E) technique. All cases were undergone for histopathological sections that were stained by Hematoxylin and Eosin (H&E).
    [Show full text]
  • Hematologic Effects of Placental Pathology on Very Low Birthweight Infants Born to Mothers with Preeclampsia
    Journal of Perinatology (2009) 29,8–12 r 2009 Nature Publishing Group All rights reserved. 0743-8346/09 $32 www.nature.com/jp ORIGINAL ARTICLE Hematologic effects of placental pathology on very low birthweight infants born to mothers with preeclampsia KJ Zook1,2, AB Mackley1, J Kern1 and DA Paul1,2 1Department of Pediatrics, Section of Neonatology, Christiana Care Health System, Newark, DE, USA and 2Department of Pediatrics, Thomas Jefferson University, Philadelphia, PA, USA Introduction Objective: To investigate the effect of placental pathology on neonatal Preeclampsia is a common disorder of pregnancy affecting nearly 5 neutrophils, platelets, hematocrit and nucleated red blood cells in very low to 8% of pregnant women annually in the United States. The NIH birthweight (VLBW) infants born to mothers with preeclampsia. reported in 2000 that preeclampsia had risen by one-third over the Study Design: Retrospective cohort study of infants with birthweight previous decade.1 Preeclampsia is known to be a common cause of < 1500 g born to mothers with preeclampsia from july, 2002 to july, 2006 neonatal neutropenia and thrombocytopenia. It has previously at a single level III neonatal intensive care unit. Placental pathology been postulated that both neonatal neutropenia and was reviewed for the presence of placental infarction and vasculopathy. thrombocytopenia result from decreased production of WBCs and Hematologic parameters from day of life 0, 1 and 2 were obtained. platelets (Plt) from placental insufficiency.2–9 Statistical analysis included repeated-measures analysis of variance Preeclampsia is also known to have associated placental and multivariable analysis using logistic regression. pathology.10 Different placental histopathologies are associated with Result: The study sample included 203 infants with estimated specific clinical features of preterm preeclampsia.
    [Show full text]