Fetal Decapitation Research Articles

Risk factors and consequences of a rare obstetric complication: Intrapartum fetal decapitation

Intrapartum fetal decapitation is an extremely rare and devastating birth complication that involves the horizontal laceration and discontinuation of the neck and its contained soft structures. This article examines the limited literature on this topic, identifying risk factors and complications associated with fetal decapitation during childbirth. Risk factors such as macrosomia, high body mass index, cephalopelvic disproportion, high gestational age, prolonged second stage of labor, maternal diabetes, and breech position increase the likelihood of this traumatic event. Complications such as shoulder dystocia can progress to fetal decapitation, especially in cases involving vacuum-assisted deliveries. The article highlights the importance of appropriate management and ethical considerations in cases of fetal decapitation, emphasizing the need for transparency and communication with the parents. The involvement of medical staff’s competence and education is also addressed as a crucial factor in preventing such tragic outcomes. The article suggests that pre-birth checkups should assess the risk factors and guide obstetricians in determining the appropriate mode of delivery to minimize the chances of fetal decapitation. Effective risk management and improved staff qualifications are advocated to mitigate the occurrence of such rare but devastating events. Ultimately, this article underscores the importance of comprehensive evaluation, communication, and education to prevent fetal decapitation and ensure the well-being of both mothers and infants during childbirth.

Landslide Disaster Leading to an Unusual Case of Polytrauma with Uterine Rupture and Fetal Decapitation in Early Pregnancy

Landslide Disaster Leading to an Unusual Case of Polytrauma with Uterine Rupture and Fetal Decapitation in Early Pregnancy

Ultrasonographic Diagnosis of Intrauterine Fetal Decapitation Secondary to Amniotic Band Sequence: A Case Report

BackgroundAmniotic band sequence (ABS) is a rare disorder that can result in a wide spectrum of congenital craniofacial, limb, trunk, and viscera deformities. One of the more rare manifestations of ABS is intrauterine fetal decapitation. Case ReportThis case report presents the ultrasonographic diagnosis of first-trimester intrauterine fetal demise resulting from decapitation secondary to amniotic band sequence. Why Should an Emergency Physician Be Aware of This?This case report presents a rare and atypical presentation of intrauterine demise valuable for an emergency physician to recognize while performing or reviewing pelvic ultrasounds. It is important for the clinician to understand and counsel the patient that subsequent pregnancies will not be at increased risk due to a prior miscarriage from ABS, as opposed to other etiologies of first-trimester spontaneous abortion.

A Foreign Body in the Cervix after Spontaneous Abortion: A Rare Case of a Traumatic Fetal Decapitation

Although incomplete spontaneous abortions are common in early pregnancy, fetal decapitation does not specifically appear in the medical literature as a known complication of spontaneous abortion. We present a rare and unusual case of an incomplete spontaneous abortion occurring at home with the mother presenting to the emergency department (ED) with a decapitated fetus and a retained fetal head in the cervical os.

Fetal Decapitation Associated With Amniotic Bands

Amniotic band syndrome (ABS) occurs secondary to rupture of the amnion in early pregnancy. This may result in entrapment of fetal structures, which in turn can cause a wide range of congenital malformations, including constriction or amputation. Presented here is a case involving a live fetus at 13 weeks’ gestation with the rare finding of fetal decapitation caused by amniotic band syndrome.

GOT PURE BLOOD IN FETAL RATS?

Have you felt frustration when fetal blood is needed for your studies in rats, or have you been concerned about fetal rat “blood” collected from decapitation? The traditional approach has been to collect fetal blood from decapitation of fetuses. The new method of collecting fetal blood is from the fetal heart, and makes it possible to obtain pure fetal blood at near-term in rodents for fetal studies. This study also demonstrated a significant difference of fetal blood oxygen levels between the traditional and new methods of blood collection.

Hypothalamo-pituitary system controls the development of humoral immune response during prenatal ontogenesis in rats

We studied the influence of the neuroendocrine system on the development of humoral immune response to sheep erythrocytes in rat fetuses. The removal of brain in utero by decapitation of 18-day fetuses induced a fourfold increase in the number of antibody-forming cells in the liver, as compared to the unoperated fetuses. After the removal of the forebrain, including hypothalamus (encephalectomy), the number of antibody-forming cells was comparable to that in unoperated fetuses. The observed increase in the number of antibody-forming cells in the liver was not due to a disturbed migration of precursors of B-lymphocytes in the spleen, since their content in the spleen was also four times that in the encephalectomized and unoperated fetuses. The increased number of antibody-forming cells in decapitated fetuses could be due to an enhanced proliferative activity of the lymphocytes in the liver of these fetuses. It has been proposed that humoral immunity is controlled by the hypothalamo-pituitary-adrenal system already during prenatal development; the adrenocorticotropic hormone and glucocorticoids appear to be involved in this regulation.

Complete uterine rupture with fetal decapitation by safety belt in 2 ND trimester pregnancy, after car accident

International Journal of Gynecology & ObstetricsVolume 70, Issue S1 p. A134-A134 Quality assurance Complete uterine rupture with fetal decapitation by safety belt in 2ND trimester pregnancy, after car accident L. Schmaltz, L. SchmaltzSearch for more papers by this authorJ. Duarte, J. DuarteSearch for more papers by this authorM. Vieira, M. VieiraSearch for more papers by this authorP. Rodrigues, P. RodriguesSearch for more papers by this authorO. Silva, O. SilvaSearch for more papers by this author L. Schmaltz, L. SchmaltzSearch for more papers by this authorJ. Duarte, J. DuarteSearch for more papers by this authorM. Vieira, M. VieiraSearch for more papers by this authorP. Rodrigues, P. RodriguesSearch for more papers by this authorO. Silva, O. SilvaSearch for more papers by this author First published: 10 December 2003 https://doi.org/10.1016/S0020-7292(00)83451-7AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume70, IssueS12000Pages A134-A134 RelatedInformation

Prolactin secretion and its dopamine inhibitory control in rat fetuses.

This study has determined in rats the ontogenetic schedule of the onset of pituitary prolactin (PRL) synthesis and release as well as of the establishment of the dopamine (DA) inhibitory control of PRL secretion. RIA recognized PRL traces in the pituitary at the 18th embryonic day (E18), although a clearly detectable amount of this hormone was first measured at E20, suggesting the onset of PRL synthesis. The PRL level in the pituitary increased significantly by E22, in females to a higher extent than in males. Decapitation of fetuses did not cause any change in the PRL plasma level in males showing no PRL release from the pituitary until term. Conversely, there was a slight but significant fall of plasma PRL in decapitated females, suggesting PRL release from the pituitary. An inhibition of DA receptors on lactotropes of fetuses resulted in an increased level of plasma PRL at E20, but not at E18, while the pituitary content of PRL remained unchanged. The same treatment at E22 caused a significant increase of the PRL concentration in plasma and a concomitant fall in the pituitary that could be prevented by preliminary encephalectomy. These data show that the tuberoinfundibular DA system begins to inhibit PRL release from lactotropes between E20 and E22, completely arresting PRL release from the pituitary in males but not in females.

Fetal decapitation: the application and safety of the stout embryotomy scissors.

Transverse lie with impacted shoulder and hand prolapse of the dead fetus was treated in 21 cases by decapitation of the fetus, performed with stout blunt-ended embryotomy scissors. Surgical complications were minimal and the procedure was simple, effective and safe.

Fetal control of calcium transport across the rat placenta.

Control of maternofetal calcium transfer across the in situ perfused rat placenta at day 21 of gestation (term 23 d) was investigated in both intact fetuses and those parathyroidectomized by decapitation on day 19. Decapitation resulted in significant fetal hypocalcemia. Injection of fetuses subcutaneously through the uterine wall with 0.43 micrograms bovine (b) PTH(1-84), 20 ng 1,25(OH)2D3 or 10 microL of the appropriate diluent resulted 2 h later in a raised fetal blood ionized Ca concentration only with bPTH(1-84) in both normal and decapitated fetuses. Fetal decapitation caused a significant (p less than 0.001) fall in the clearance of 45Ca across the placenta (Kmf45Ca), which was significantly (p less than 0.05) reversed after fetal bPTH(1-84) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) injection, but not back to normal levels. There was no effect of either hormone on Kmf45Ca in placentas from intact fetuses, or on Kmf51Cr-EDTA (used as an extracellular marker) in either group. When 4 ng/mL r[Nle8,21, Tyr34] PTH(1-34), 50 pg/mL 1,25(OH)2D3 or the appropriate diluent was perfused through placentas the only response observed was a significant (p less than 0.05) increase in Kmf45Ca with 1,25(OH)2D3 perfusion in placentas from decapitated fetuses, Kmf51Cr-EDTA being unchanged. Finally, perfusion with 10(-5) M forskolin (an activator of adenylate cyclase) stimulated Kmf45Ca in placentas from both normal and decapitated fetuses. Although there was also some effect on Kmf51Cr-EDTA in the latter, there was none in the placentas from normal fetuses, and here the effect on Kmf45Ca was dose dependent with an initial response at 10(-6) M.(ABSTRACT TRUNCATED AT 250 WORDS)

The Insulin-Like Growth Factor-Binding Proteins of Porcine Serum: Endocrine and Nutritional Regulation*

Several studies have shown that insulin-like growth factor-binding proteins (IGF-BPs) modify IGF activity. To investigate their role in regulating growth, the number and size of IGF-BPs in porcine serum and the role of nutritional and endocrine factors in controlling their relative abundance were determined. IGF-BPs were analyzed by ligand blotting; sera were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, then the separated proteins were transferred to nitrocellulose filters and probed with [125I]IGF-I or -II. The band intensities of various forms of IGF-BPs were quantified by scanning densitometry. Fetal and postnatal sera contained six IGF-BPs of 220,000, 43,000, 39,000, 34,000, 29,000, and 24,000 mol wt (Mr). The band intensity of all forms of IGF-BPs increased with advancing gestational age. Specifically, the intensities of the 43,000, 39,000, 34,000, 29,000, and 24,000 Mr IGF-BP bands were 2.8-, 2.7-, 4.3-, 4.4-, and 3.1-fold higher, respectively, in fetal plasma at 110 than at 45 days gestation. In fetal plasma the 34,000 and 29,000 Mr forms predominated, whereas postnatally, the 43,000 and 39,000 Mr IGF-BPs predominated. Fasting of newborn pigs for 24 h reduced the intensity of the 43,000, 39,000, 34,000, and 24,000 Mr forms to 11.5%, 7.2%, 69.8%, and 5.2% of control levels, respectively. However, the 29,000 Mr IGF-BP was 1.8-fold higher in fasted pig serum than in that of fed controls. The band intensities of the 34,000 and 29,000 Mr forms were increased in postnatal animals after hypophysectomy. In contrast, fetal decapitation resulted in a preferential decrease in only the 34,000 Mr form, which was reduced by 30% compared to that in age-matched controls. These studies indicate that porcine serum contains six IGF-BPs that can be detected by ligand blotting. The level of each of these proteins increases with advancing gestational age, although the increases are not uniform, suggesting that the proteins may be regulated differentially. In the postnatal animal both endocrine and nutritional factors modulate the levels of IGF-BPs by distinct controlling mechanisms.

Histochemical studies of muscle development in decapitated and hypophysectomized pig fetuses: blood vessel development.

In Exp. 1, fetuses were decapitated in utero on d 45 of gestation and examined at 110 d of gestation; in Exp. 2, fetuses were hypophysectomized (hypox) in utero with a cauterizing needle at d 70 of gestation and examined at 110 d of gestation. Semitendinosus muscles were sampled and transverse cryostat sections were cut from the medial portion of the muscle. Quantitative analysis of lectin-stained sections showed that capillary:fiber ratios (C/F) were lower (P less than .01) for sections from decapitated and hypox fetuses than for sections from control fetuses. The superficial and deep aspects of muscle sections from control fetuses had markedly different C/F ratios (deep region, 24.1 +/- 2; superficial region, 11.2 +/- .5). Fetal decapitation and hypophysectomy abolished differences in C/F ratios between deep and superficial regions of muscle sections (hypox fetuses; deep region, 6.9 +/- 1; superficial region, 6.4 +/- .6). Capillaries in sections from control fetuses were reactive for several enzymes, whereas capillaries in sections from experimental fetuses (decapitated and hypox) were not reactive for these enzymes. The number of small arterioles was reduced in sections from experimental fetuses (decapitated and hypox) compared with sections from control fetuses. These studies demonstrate that lowering the levels of pituitary hormones in the fetus retards the development of blood vessels in muscle tissue both quantitatively and qualitatively.

Differentiation of adipose tissue and muscle in hypophysectomized pig fetuses.

In the present study, fetuses were hypophysectomized (hypox) in utero on d 72 to 74 of gestation with an electrical cauterizing needle. One to six successfully hypox fetuses were removed on d 110 of gestation from each of five gilts. Subcutaneous adipose tissue samples and semitendinosus muscles were obtained from the hypox fetuses and an equal number of control fetuses. Body weights of control fetuses (n = 15; mean +/- SE, 1,195 +/- 33 g) were similar to weights of hypox fetuses (n = 15; 1,179 +/- 67 g). Fat cell size in the middle subcutaneous layer of adipose tissue was increased in hypox fetuses (P less than .01) compared with control fetuses. The number of obvious fat cell clusters (outer layer) in lipid stained sections was reduced (P less than .01) by 50% in hypox fetuses. Histochemical reactions for glucose-6-phosphate dehydrogenase, esterase and lipoprotein lipase (LPL) activities in middle layer cell clusters were considerably enhanced in sections from hypox fetuses compared with sections from controls. Quantitative analysis of percent light transmittance (Zeiss photometer) through LPL-stained cell clusters indicated an increase (P less than .001) in LPL staining in sections from hypox fetuses when compared with sections from control fetuses. Transverse muscle sections (cryostat) from hypox fetuses failed to show normal patterns (as seen in control muscles) of reactions for acid ATPase, malate dehydrogenase (NAD-dependent), NADH-TR and alpha-glycerol phosphate dehydrogenase (without NAD). The number of muscle fibers that were stained for these enzymes was greatly reduced in hypox fetuses compared with control fetuses. The number of lipid positive fibers was also reduced in hypox fetuses compared with control fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

The ultrastructure of normal fetal and neonatal pig testis germ cells and the influence of fetal decapitation on the germ cell development.

The development of germ cells in the male pig was investigated ultrastructurally in normal and decapitated fetuses. The age ranged respectively from 30 days p.c. till one month after birth and from 52 days p.c. until birth. The ultrastructural organization of the germ cells changes dramatically between 30 days p.c. and 52 days p.c. which coincides with the formation of 'true' sex cords. From 52 days p.c. onwards the morphology is rather stable: cells show a 'hydrated' appearance and typical cell bridges. There is no obvious difference in the ultrastructure of germ cells in decapitated animals, their normal littermates and control animals. Therefore germ cell development in the pig is likely to be insensitive to gonadotropins during the fetal period. The development of pig germ cells follows closely the pattern described for several species. Quantitatively there is an increase in the ratio of germ cell/Sertoli cell per cross sectional diameter in the decapitated animals.

Pre-adipocyte proliferation and differentiation in response to hormone supplementation of decapitated fetal pig sera.

Growth hormone and thyroid hormones have been implicated as important serum factors for adipocyte development in cell culture. Fetal decapitation removes these factors from serum of the growing fetal pig and results in development of fewer adipocytes than in intact fetuses. These experiments examined the effects of growth hormone or thyroxine supplementation to decapitated fetal pig sera upon pre-adipocyte proliferation and differentiation. Hormones were supplemented to concentrations present in sera from intact pig littermates (reference). Sera +/- hormones were analyzed for their effects upon pre-adipocyte proliferation as determined by [3H]-thymidine incorporation; enzyme expression as determined by sn-glycerol-3-phosphate dehydrogenase activity; and induction of complete differentiation into lipid filled adipocytes as based upon a pre-adipocyte proliferation and enzyme expression than reference sera. Growth hormone had no effect in decap sera upon these parameters. Decap sera permitted detection of 54% more lipid-accumulating, newly formed adipocytes on percol gradients than reference sera, but growth hormone reduced detection to 29% of reference sera. Thyroxine specifically stimulated pre-adipocyte proliferation more than decap sera, but not to the level of reference sera. Complete differentiation, a formation of lipid-accumulating adipocytes was promoted also by thyroxine in comparison to basal decap sera. The results of these experiments indicate thyroid hormones are an important component of fetal sera for regulation of adipocyte development, whereas growth hormone may only affect cellular metabolism and not promote pre-adipocyte growth and development.

Regulation of rabbit fetal glycogen: effect of in utero fetal decapitation on the metabolism of glycogen in fetal heart, lung, and liver.

To understand the control mechanisms involved in the regulation of fetal glycogen, we have studied the effect of in utero fetal decapitations on glycogen metabolism in rabbit fetal heart, lung, and liver. In utero fetal decapitations were performed between days 18 and 21 of gestation. Two to four fetuses on one side of the horn were decapitated. Fetuses were delivered between days 23 and 26 or between days 28 and 30 of gestation. Fetal heart, lungs, and liver were analyzed for DNA, protein, glycogen, glycogen synthase (I and D forms), glycogen phosphorylase (a and b forms), phosphofructokinase, pyruvate kinase, and lactic dehydrogenase. In fetal heart and lung, no difference was observed in any of the above measurements in the intact and decapitated fetuses. In contrast, fetal liver does not appear to develop the glycogen system as indicated by the very low levels of glycogen (0.02 mg/mg DNA) in decapitated fetuses as compared with intact fetuses (0.4 mg/mg DNA). Similarly the levels of glycogen synthase and phosphorylase were two to three times lower in livers from decapitated fetuses as compared with the livers from intact fetuses. The three enzymes phosphofructokinase, pyruvate kinase, and lactic dehydrogenase were not affected by fetal decapitation in all three tissues. These results indicate that the fetal hypothalamic-pituitary-adrenal (thyroid) axis is not required at least after day 18 of gestation for the normal accumulation and subsequent utilization of glycogen in fetal heart and lungs, while it is an absolute requirement for the development of the fetal liver glycogen system.(ABSTRACT TRUNCATED AT 250 WORDS)

Enzyme histochemical studies in an ontogeny study of muscle development in Ossabaw and decapitated fetuses: cellular reactions.

Fetuses were decapitated in one uterine horn in each of 14 sows at 45 d of gestation. Control (C) and decapitated (D) fetuses were removed by Caesarean section from three sows at 65 d of gestation (total of 10 D and 10 C fetuses), two sows at 85 d (six D and six C fetuses) and nine sows at 110 d (nine C and nine D fetuses) of gestation (Exp. 1). In Exp. 2, four to six fetuses were removed from each of two Ossabaw (O) gilts and three crossbred (C, Landrace X Yorkshire) gilts at 70 d of gestation, from three C and O gilts at 90 d of gestation and from three C and two O gilts at 110 d of gestation. In Exp. 1, one semitendinosis muscle was removed for histochemistry, whereas the contralateral muscle was removed and weighed. A medial portion of biceps femoris muscle was removed and used for histochemistry in Exp. 2. In both experiments, transverse sections (cryostat) of muscle were stained for lipid, glycogen (PAS) and the following enzymes: acid ATPase, NADH-TR, NADPH-TR, malate dehydrogenase (NAD- and NADP-dependent reactions; MDH), succinate dehydrogenase (SDH), alpha-glycerol phosphate dehydrogenase (with and without NAD; alpha-GPDH), isocitrate dehydrogenase (NAD dependent; ICDH), esterase, lipoprotein lipase and lipase. In Exp. 1, body and muscle weights of the two groups were not significantly different (P greater than .05) at 65 d of gestation, whereas D fetuses were smaller and had lighter weight muscles (P less than .05) at 85 d of gestation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of fetal decapitation upon porcine placental metabolism. Evidence for a fetal influence in placental metabolism.

This experiment was performed to determine if the fetus can influence its placental metabolism. Fetal pigs were decapitated at 45 days of gestation and their placentas compared at 110 days to within litter controls. No histological or histochemical differences were observed. Glycogen levels were elevated in the fetal placenta of decapitated pigs by 107%. Fatty acid synthesis was increased in the fetal placenta of decapitated animals (12.9 +/- 1.5 vs. 3.4 +/- 0.7 nmol acetate units/100 mg/2 h). Fetal decapitation increased fetal placental fatty acid esterification by 43% and oxidation by 125%. The altered lipid metabolism of the fetal placenta was reflected in enzymes associated with substrate utilization (pyruvate kinase and lactate dehydrogenase). Maternal placenta lipogenesis was also altered by fetal manipulation. Leucine conversion to its alpha ketoacid was increased in the fetal placenta of the decapitated pigs (14.8 +/- 1.7 vs. 8.6 +/- 1.4 nmol/100 mg/2 h) indicating amino acid metabolism was affected by this treatment. The ability of an altered fetal endocrinology and metabolism to affect the placental metabolism supports the concept of a fetal influence on placental metabolism.

Histochemical and cellular aspects of adipose tissue development in decapitated pig fetuses: an ontogeny study.

Adipose tissue from fetuses decapitated at 45 d of gestation was removed and structurally and histochemically analyzed at 65, 85 and 110 d of gestation. Subcutaneous adipose tissue from decapitated and control fetuses at 65 d of gestation was histologically and histochemically similar. A reduced number of fat cell clusters in the outer layer of subcutaneous tissue and a poorly developed dermis was evident in decapitated fetuses at 85 d of gestation. Fat cell size was similar for control and decapitated fetuses at 65 d of gestation, whereas cells in 85 d-old decapitated fetuses were larger than cells in control fetuses. Adipocytes from control and 85 d-old decapitated fetuses were histochemically similar except for an elevated number of esterase positive cells in decapitated fetuses. At 110 d of gestation, adipocytes from decapitated fetuses had higher activities of the following enzymes than did control adipocytes: malate dehydrogenase (NADP dependent) glucose 6-phosphate dehydrogenase NADP dependent), isocitrate dehydrogenase (NADP dependent), alpha-glycerol phosphate dehydrogenase (NADP dependent), NADPH-tetrazoleum reductase and esterase. Levels of succinate dehydrogenase, glutamate dehydrogenase and NADH-tetrazoleum reductase were similar in cells from controls and decapitated fetuses. These data indicate that fetal decapitation probably exerts a positive influence on enzymes involved in lipid synthesis. However, fetal decapitation also exerts a negative influence on fat cell hyperplasia.