Is nuchal cord justified as a cause of obstetrician anxiety?

Purpose

Birth asphyxia leading to acidosis comprises 20–60 % of perinatal mortality. Nuchal cord (NC) is one of the possible causes of birth asphyxia. Majority of fetuses who are antenatally detected to have nuchal cord are able to achieve successful vaginal birth. The purpose of this study was to analyze the effect of nuchal cord on fetal acid base status and perinatal outcome in vaginal deliveries.

Study design

150 parturients were equally divided into three groups after vaginal delivery based on no NC, single and multiple loops. Umbilical cord arterial blood was analyzed for biochemical markers i.e. pH, PO₂, SPO₂, PCO₂, HCO₃ ^?, standard base excess and lactate for acidosis. Labor complications like abnormal FHR, meconium-stained liquor, prolonged second stage, instrumental vaginal delivery, third stage complications were compared. In neonates, birth weight, Apgar score ≤7 at 5 min, NICU admission and other morbidity and mortality during hospital stay were compared among groups using suitable statistical tests. Above parameters were also compared between tight and loose loops.

Result

Nuchal cord groups had significantly higher frequency of labor complications than no NC group, especially tight loops. Neonates with NC had significantly higher frequency of meconium-stained liquor, Apgar score ≤7 at 5 min, deranged biochemical markers, NICU transfer. However, none of the neonate had pH in acidosis range and majority were discharged in healthy condition.

Conclusion

Patients with NC are likely to have uneventful labor and delivery as cord compression is transient and most fetuses are able to compensate for reduce umbilical blood flow. Routine antenatal ultrasound scan is not advisable, as mode of delivery and labor management does not change with detection of NC antenatally. Therefore, vaginal delivery with routine labor protocol can be allowed in cases of nuchal cord.     

Unrecognized Acute Phosphate Nephropathy in a Kidney Donor with Consequent Poor Allograft Outcome

Acute phosphate nephropathy following a large phosphate load is a potentially irreversible cause of kidney failure. Here, we report on the unfavorable graft outcome in two recipients of deceased donor kidneys from a donor who had evolving acute phosphate nephropathy at the time of organ procurement. The donor, a 30-year-old with cerebral infarction, developed hypophosphatemia associated with diabetic ketoacidosis and was treated with intravenous phosphate resulting in a rise in serum phosphorus from 0.9 to 6.1 mg/dL. Renal biopsies performed on both recipients for suboptimal kidney function revealed acute tubular injury and diffuse calcium phosphate microcrystal deposits in the tubules, which were persistent in subsequent biopsies. A retrospective review of preimplantation biopsies performed on both kidneys revealed similar findings. Even though initial renal histology in both recipients was negative for BK virus, they eventually developed BK viremia with nephropathy but both had a substantive virologic response with therapy. The first patient returned to dialysis at 6 months, while the other has an estimated glomerular filtration rate of 12 mL/min, 17 months following his transplant. We conclude that unrecognized acute phosphate nephropathy in a deceased donor contributed substantially to poor graft outcome in the two recipients.     

Analysis of the osteoinductive capacity and angiogenicity of an in vitro generated extracellular matrix

In this study, the osteoinductive potential of an in vitro generated extracellular matrix (ECM) deposited by marrow stromal cells seeded onto titanium fiber mesh scaffolds and cultured in a flow perfusion bioreactor was investigated. Culture periods of 8, 12, and 16 days were selected to allow for different amounts of ECM deposition by the cells as well as ECM with varying degrees of maturity (Ti/ECM/d8, Ti/ECM/d12, and Ti/ECM/d16, respectively). These ECM-containing constructs were implanted intramuscularly in a rat animal model. After 56 days, histologic analysis of retrieved constructs revealed no bone formation in any of the implants. Surrounding many of the implants was a fibrous capsule, which was often interspersed with fat cells. Within the pore spaces, the predominant tissue response was the presence of blood vessels and young fibroblasts or fat cells. The number of blood vessels on a per area basis calculated from a histomorphometric analysis increased as a function of the amount of ECM within the implanted constructs, with a significant difference between Ti/ECM/d16 and plain Ti constructs. These results indicate that although an in vitro generated ECM alone may not induce bone formation at an ectopic site, its use may enhance the vascularization of implanted constructs.     

Incarcerated and Transmigrated Intrauterine Contraceptive Devices Managed at a Tertiary Care Teaching Hospital of East Delhi: A 5-Year Retrospective Analysis

The Journal of Obstetrics and Gynecology of India - Intrauterine contraceptive devices (IUCDs) are highly effective form of long-acting reversible contraception having least number of...     

Metachronous haemorrhagic epithelioid and spindle cell haemangioma of bone

We present the case of a 7-year-old boy with a haemorrhagic and spindle cell haemangiomas of the ring finger. The lesions appeared in a metachronous fashion initially in the distal phalanx and 16 months later in the proximal phalanx. Radiography revealed expansile lytic lesions of the phalanges. Haemorrhagic epithelioid and spindle cell haemangioma is a benign condition which, due to its unusual morphology, can be confused with more aggressive or malignant endothelial neoplasms. This condition with its possible multifocal presentation should be considered when diagnosing vascular lesions of bone in order that appropriate treatment can be implemented.     

Del Castello syndrome--an unusual presentation

Del Castello syndrome in a 28-year-old female, characterised by bilateral galactorrhoea, amenorrhoea and hyperinvoluted uterus, has been described. She had hyperprolactinaemia without any demonstrable pituitary tumour. She was successfully treated with two short courses of bromocriptine and was spontaneously cured after her second conception. The case is discussed with a brief review of the literature.     

Protein kinase C regulates [3H]D-aspartate release in auditory brain stem nuclei

We previously found that unilateral cochlear ablation altered transmitter release from glutamatergic synaptic endings in several brain stem auditory nuclei. To determine if this release activity could be regulated by protein kinase C (PKC), which has been associated with regulation of transmitter release, the electrically evoked release of [3H]d-aspartate ([3H]d-Asp) was quantified in vitro as an index of exocytosis from glutamatergic presynaptic endings in the major subdivisions of the cochlear nucleus (CN) and in the main nuclei of the superior olivary complex (SOC). Treating dissected tissues with a PKC activator, such as phorbol 12,13-diacetate (PDA) or phorbol 12,13-dibutyrate (PDBu) (3 microM), elevated the evoked release of [3H]d-Asp by 1.5- to 3.3-fold. The PKC inhibitor Ro31-8220 (50 nM) did not alter the evoked release but blocked the stimulatory effects of PDA and PDBu. These findings suggested that PKC could positively regulate transmitter release from glutamatergic presynaptic endings in brain stem auditory pathways. Seven days after unilateral cochlear ablation, when cochlear nerve endings had degenerated in the ipsilateral CN, PDBu elevated the evoked release bilaterally in each CN subdivision and SOC nucleus, implying that PKC could regulate glutamatergic release in the noncochlear pathways remaining in the ipsilateral CN and in the other pathways after unilateral hearing loss. After 145 postlesion days, Ro31-8220 blocked endogenous elevations in the evoked release in the ipsilateral SOC but did not alter the elevated or upregulated release in the other tissues. This suggested that the elevations of glutamatergic release activity in the ipsilateral SOC that appeared after unilateral cochlear ablation depended on endogenous activation of PKC.