Obstetric Case Reports 413 up 45 min later, with very strong contractions every 3 min. She emptied her bladder and called her midwife. At 21:50 her waters broke, something she had experienced on previous births, and half a cup of clear amniotic fluid came out at once. By 22:50, another half a cup of amniotic fluid had come out and she continued leaking in waves, but the contractions stopped. At 2 h after her waters broke, she went to the hospital where she was diagnosed for ruptured membranes and given steroids and antibiotics. She continued leaking for 36 h. At 36 h after ROM, the leaking completely stopped. She went home from hospital at 31 ⫹ 5 weeks. She delivered a healthy child at 41 weeks.
J Obstet Gynaecol Downloaded from informahealthcare.com by Nyu Medical Center on 06/09/15 For personal use only.
Case report 3 A 32-year-old woman, G6, with five previous term live births, experienced ROM at term, filling a cloth diaper with about 2 tablespoons of clear liquid every hour for 4.5 days, without any contractions. She experienced more leaking at night when lying down, particularly when moving from side to side. After this period, 1.5 days passed without any leaking fluid. On the 6th day after SROM, labour started. When the second stage of labour started and she gave the first push, the amniotic sac broke, releasing a cup of slightly green amniotic fluid (Figure 1).
Conclusion These case studies can either be explained by False ROM or holes in both layers of the sac, that repaired themselves after hours to days. False ROM seems the most likely scenario, since in all three cases, the hole was large enough to expel 30–350 cc of liquid in short time intervals; in two cases within a second. Closing such a hole while being pressured by the litre of amniotic fluid remaining inside the sac seems unlikely. The first two cases do not appear to be ‘high leaks’, since the water gushed out. Figure 1, taken of the placenta from the third case, documents a larger hole in the chorion and a smaller hole in the amnion. False ROM complicates the simplistic view that ROM is a vector for infection. The impact of False ROM on ascending infection remains to be elucidated. In-vitro studies have not been able to demonstrate the ability of Group B Strep. (GBS) to cross an intact amnion, even at concentrations of 1,000,000,000 CFU (Kjaergaard et al. 1999). GBS failed to invade amnion cells under a variety of assay conditions (Winram et al. 1998) and fetal membranes demonstrated an inhibitory effect on GBS (Kjaergaard et al. 2001). PCR assays of amniocentesis samples found traces of bacteria or mould RNA in 15% of 166 women all in preterm labour with supposedly intact membranes (DiGiulio et al. 2008). It would be interesting to know the amount of bacterial RNA present in cases without preterm labour. The reason we are still lacking a cohesive explanation for preterm labour (Wei et al. 2010) may be related to our lack of understanding of the physiology of the sac. Did the bacterial RNA in intact sacs slip in through holes in the sac that closed up? Is there a virulence factor which assists bacteria through the wall of the sac? If cytokine-stimulated collagenase production in the fetal membranes is responsible for the reduction of their tensile strength (Winkler and Rath 1996),
why does only the chorion rupture in about 10% of cases? How does maternal stress, drug addiction, smoking, obesity affect the ability to keep the chorion vs the amnion intact?
Questions for future research
• Can live bacteria enter a sealed amniotic sac? If so, how? • At term, what percentage of women have large amounts of fluid between the amnion and chorion? • Does the chorion produce amniotic fluid? • Is there such a thing as a high leak? • If there is such a thing as a high leak, does it involve both layers of membranes? • Can a high leak close up? If so, what is the mechanism? • When and why does the amnion produce prostaglandins, interleukin, cytokine? • How often does the chorion break before the amnion? • Why does the chorion sometimes break before the amnion? • How can we reliably test for True ROM vs rupture only of the amnion aside from when meconium or vernix is clearly seen? • Is there an increased risk of infection to the fetus or mother when only the chorion breaks or if there is a high leak? • What is the rate of successful induction vs caesarean surgery for women with False ROM vs True ROM? Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.
References Cohain JS. 2013. The less studied effects of amniotomy. Journal of Maternal-Fetal and Neonatal Medicine 26:1687–1690. Connon CJ, Nakamura T, Hopkinson A et al. 2007. The biomechanics of amnion rupture: An X-ray diffraction study. PLoS ONE 2:e1147. Cunningham FG. 2001. Williams obstetrics. 21st ed. New York: McGraw Hill. p 312. DiGiulio DB, Romero R, Amogan HP et al. 2008. Microbial prevalence, diversity and abundance in amniotic fluid during preterm labor: a molecular and culture-based investigation. PLoS ONE 3:e3056. Huebner M, Antolic A, Tunn R. 2010. The impact of pregnancy and vaginal delivery on urinary incontinence. International Journal of Gynecology and Obstetrics 110:249–251. Kjaergaard N, Hein M, Hyttel L et al. 2001. Antibacterial properties of human amnion and chorion in vitro. European Journal of Obstetrics, Gynecology, and Reproductive Biology 94:224–229. Kjaergaard N, Helmig RB, Schønheyder HC et al. 1999. Chorioamniotic membranes constitute a competent barrier to group b streptococcus in vitro. European Journal of Obstetrics, Gynecology, and Reproductive Biology 83:165–169. Wei SQ, Fraser W, Luo ZC. 2010. Inflammatory cytokines and spontaneous preterm birth in asymptomatic women: a systematic review. Obstetrics and Gynecology 116(2 Part 1):393–401. Winkler M, Rath W. 1996. The role of cytokines in the induction of labor, cervical ripening and rupture of the fetal membranes. Zeitschrift fur Geburtshilfe und Neonatologie 200(Suppl 1):1–12. Winram SB, Jonas M, Chi E, Rubens CE. 1998. Characterization of group B streptococcal invasion of human chorion and amnion epithelial cells in vitro. Infection and Immunity 66:4932–4941.
Superior mesenteric artery thrombosis: A rare and unknown complication after caesarean section L. Gaujal1, E. G. Simon1,2, I. Kellal1, A. Bleuzen3 & F. Perrotin1,2 Departments of 1Obstetrics, Gynaecology and Fetal Medicine, 2UMR INSERM U930 and 3Radiology, University Hospital Center of Tours François-Rabelais University de Tours, Tours, France DOI: 10.3109/01443615.2014.961908 Figure 1. Placenta showing larger hole in the chorion and fetal head sized hole in the amnion.
Correspondence: E. G. Simon, Department of Obstetrics, Gynaecology and Fetal Medicine, University Hospital Center of Tours, 2 Boulevard Tonnellé, Tours, 37000 France. E-mail: [email protected]
J Obstet Gynaecol Downloaded from informahealthcare.com by Nyu Medical Center on 06/09/15 For personal use only.
414
Obstetric Case Reports
Figure 1. Abdominal angioscan: superior mesenteric artery thrombosis, 14 days after caesarean section. (A) Thrombus in a sagittal plane (∗), (B) thrombus in an axial plane (arrow).
Case report
Discussion
We report the case of a superior mesenteric artery thrombosis in a 29-year-old woman, GI PI, 2 weeks after caesarean section. The woman had a body mass index of 18.5 and no medical history, apart from smoking 10 cigarettes/day, with complete smoking cessation in the 1st trimester of her pregnancy. Her uncle had a history of protein C deficiency. Her pregnancy was marked by excessive weight gain during the 3rd trimester and oedema of upper and lower limbs not related to gestational hypertension or pre-eclampsia. She entered spontaneous labour at 40 weeks’ gestation but needed a caesarean section for arrested cervical dilatation at 9 cm (total blood loss of 600 ml). The caesarean section was uneventful and she delivered a male baby weighing 3,660 g, with Apgar scores 10/10 at 10 min. Thromboprophylaxis with tinzaparin (3,500 IU/day) was started the day after delivery. The woman did not take contraception during the immediate postpartum. At 14 days after her caesarean section, the woman presented to the emergency department with acute and intense abdominal pain. The woman was afebrile and her abdomen was soft. Her blood pressure upon arrival was 120/90 mmHg, and an electrocardiogram showed a sinus tachycardia at 126/min. Blood test results showed: haemoglobin 11.6 g/dl; platelets 426 g/l; leucocytes 23 g/l; CRP 45 mg/l; and troponin 0.01 μg/l. An abdomino-pelvic ultrasound showed no anomaly. A CT of the abdomen and pelvis was carried out to search for an infection, but instead, led to the diagnosis of thrombosis of the superior mesenteric artery. The woman then underwent an emergency exploratory laparotomy and embolectomy. She was given anticoagulants, including heparin and aspirin and antibiotics. Aetiological assessment showed a severe protein C deficiency: the protein C level was only of 27%. No other risk factor for thrombosis was found. She was not a carrier of an autoimmune vasculitis disease. The woman was given protein C and supplements of vitamin K and 2 days later, a second-look laparotomy led to a 3 metre resection of the small intestine, cholecystectomy and terminal ileostomy. At 11 days after the surgery, she presented with severe sepsis with necrosis of the stoma. A CT of the abdomen and pelvis found an extension of thrombosis to the spleen, the liver and other areas of the digestive system (Figure 1). An emergency laparotomy was performed, which led to the resection of the totality of the small intestine, the right colon and the hemitransverse colon. The woman was then transferred to the hepato-digestive ICU. A cardiac ultrasound performed 1 month after thrombosis showed no valvulopathy, but did reveal a left intraventricular thrombus of 10 mm with a left ventricular ejection fraction of 40%. The woman went home 4 months after her caesarean section. She is currently waiting for a multivisceral transplant (small intestine, colon, pancreas and liver).
Mesenteric infarction is a serious condition, the prognosis depending on the underlying aetiology. There are four distinct forms: arterial occlusion by embolism or by thrombosis, venous thrombosis and non-occlusive mesenteric ischaemia. The mortality rates of these different forms are, respectively, 54%, 77%, 32% and 72% (Brandt and Boley 2000). Prompt diagnosis is a crucial factor for the prognosis of women who present with the typical clinical and biological features of mesenteric ischaemia (Sise 2014). However, diagnosis of this condition may sometimes be challenging. A normal abdomino-pelvic ultrasound scan in a case of acute postpartum abdominal pain should be followed by a CT of the abdomen and pelvis. An angioscan is the gold standard to diagnose this pathology (Cudnik et al. 2013; Sise 2014). Acute mesenteric ischaemia due to arterial occlusion (Brandt and Boley 2000; Sise 2014) may sometimes be caused by arterial embolism from cardiac disease (arrhythmia, valvular disease, myocardial infarction, thrombus or myxoma). It may also occur in the context of an atheromatous disease, vasculitis or thrombosis. The cause of the acute mesenteric ischaemia reported in this case is highly unusual. One case report in the literature documented a similar event that occurred on the 8th day postpartum after a vaginal delivery (Ducarme et al. 2008). The cause of this event remained unknown. Another paper reported an acute mesenteric ischaemia as an immediate complication of caesarean section, but the aetiology remained unclear (Singhal et al. 2005). In our case, we highlight protein C deficiency as a substantial contributing factor. In the literature, several cases of protein C deficiency associated with venous thrombosis have been described while, to our knowledge, none associating protein C deficiency with arterial has been reported. Histological analysis of the thrombus showed elements included in the fibrin, similar to those observed in venous thrombosis associated with protein C deficiency. However, there were no platelets and there was no sign of inflammation and no pathogenic agents, which are often observed in arterial thrombosis. The protein C deficiency may be responsible for the worsening of the thrombosis, despite appropriate surgical and medical intervention. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Brandt LJ, Boley SJ. 2000. AGA technical review on intestinal ischemia. American Gastrointestinal Association. Gastroenterology 118:954–968.
Obstetric Case Reports 415 Cudnik MT, Darbha S, Jones J et al. 2013. The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis. Academic Emergency Medicine 20:1087–1100. Ducarme G, Lidove O, Leduey A et al. 2008. Postpartum thrombosis of the superior mesenteric artery after vaginal delivery. Obstetrics and Gynecology 111:535–537. Singhal SR, Sharma D, Singhal SK. 2005. Acute mesenteric ischemia: an unknown cause of immediate postcesarean mortality. Acta Obstetricia et Gynecologica Scandinavica 84:299–300. Sise MJ. 2014. Acute mesenteric ischemia. Surgical Clinics of North America 94:165–181.
J Obstet Gynaecol Downloaded from informahealthcare.com by Nyu Medical Center on 06/09/15 For personal use only.
Severe visual loss following obstetric forceps delivery-related ocular trauma in a neonate K. Shah, R. Roy, S. Guha, M. Bhargava, S. V. Shah, A. Lobo, D. Das & A. K. Majumder Aditya Birla Sankara Nethralaya, Kolkata, West Bengal, India DOI: 10.3109/01443615.2014.969205 Correspondence: Dr. Rupak Roy, Aditya Birla Sankara Nethralaya, 147, E. M Bypass, Mukundapur, Kolkata 700099, West Bengal, India. E-mail: rayrupak@ gmail.com
Report of a case Parents of a 20-hour-old male baby brought him to the hospital with white reflex and bleeding in the right eye following obstetrics forceps delivery. The circumstances and indications of forceps application could not be ascertained from baby’s medical records. His systemic examination was within normal limits. On examination vision could not be assessed in the right eye, and left eye was apparently normal. There was linear full-thickness corneal tear extending from superior to central portion of cornea (6 mm) with severe corneal oedema (Figure 1a). Patient underwent primary corneal suturing under general anaesthesia on the same day (Figure 1b). Post-operatively media was hazy due to corneal oedema. Ultrasonography of the eye was performed the following day, which revealed total retinal detachment. The baby underwent combined penetrating keratoplasty, lensectomy, pars plana vitrectomy with endolaser and silicone oil tamponade for retinal reattachment. Intraoperatively there was vitreous haemorrhage and multiple blotchy pre-retinal haemorrhages with a giant retinal tear (GRT) of 3 clock hours causing total retinal detachment (Figure 1c). Post-operatively corneal graft was clear and retina was attached (Figure 1d). At 1-month follow up, the baby developed inferior retinal re-detachment. The baby underwent membranectomy, endolaser and repeat silicone oil injection. Unfortunately at follow-up the eye became phthisical. Stock shell was placed in the socket to prevent contracture of the orbit.
Introduction Ophthalmic injuries have been reported secondary to instrumental vaginal deliveries (Jain et al. 1980). A variety of complications have been described involving anterior and posterior segment of the eye due to obstetric trauma. We report a case of grievous ocular injury in a neonate following forceps delivery, its management and outcome.
Discussion A wide spectrum of ocular injuries has been reported due to birth trauma more so following forceps delivery. Various anterior segment complications secondary to obstetric forceps injury include absence of globe (Wiegand 1990), facial palsy, lid lacerations, subconjunctival haemorrhage, corneal abrasion, corneal abscess,
Figure 1. (a) Pre-operative photograph showing full-thickness corneal tear (6 mm) with surrounding oedema and blood-stained cornea (arrow). (b) Post-operative photograph showing sutured corneal wound with air bubble in anterior chamber (arrow). (c) Intra-operative photograph showing multiple blotchy pre-retinal haemorrhage (long arrow) and GRT (arrow head) during vitreous surgery. (d) Post-operative photograph following corneal transplant with clear corneal graft.
J Obstet Gynaecol Downloaded from informahealthcare.com by Nyu Medical Center on 06/09/15 For personal use only.
Case report 3 A 32-year-old woman, G6, with five previous term live births, experienced ROM at term, filling a cloth diaper with about 2 tablespoons of clear liquid every hour for 4.5 days, without any contractions. She experienced more leaking at night when lying down, particularly when moving from side to side. After this period, 1.5 days passed without any leaking fluid. On the 6th day after SROM, labour started. When the second stage of labour started and she gave the first push, the amniotic sac broke, releasing a cup of slightly green amniotic fluid (Figure 1).
Conclusion These case studies can either be explained by False ROM or holes in both layers of the sac, that repaired themselves after hours to days. False ROM seems the most likely scenario, since in all three cases, the hole was large enough to expel 30–350 cc of liquid in short time intervals; in two cases within a second. Closing such a hole while being pressured by the litre of amniotic fluid remaining inside the sac seems unlikely. The first two cases do not appear to be ‘high leaks’, since the water gushed out. Figure 1, taken of the placenta from the third case, documents a larger hole in the chorion and a smaller hole in the amnion. False ROM complicates the simplistic view that ROM is a vector for infection. The impact of False ROM on ascending infection remains to be elucidated. In-vitro studies have not been able to demonstrate the ability of Group B Strep. (GBS) to cross an intact amnion, even at concentrations of 1,000,000,000 CFU (Kjaergaard et al. 1999). GBS failed to invade amnion cells under a variety of assay conditions (Winram et al. 1998) and fetal membranes demonstrated an inhibitory effect on GBS (Kjaergaard et al. 2001). PCR assays of amniocentesis samples found traces of bacteria or mould RNA in 15% of 166 women all in preterm labour with supposedly intact membranes (DiGiulio et al. 2008). It would be interesting to know the amount of bacterial RNA present in cases without preterm labour. The reason we are still lacking a cohesive explanation for preterm labour (Wei et al. 2010) may be related to our lack of understanding of the physiology of the sac. Did the bacterial RNA in intact sacs slip in through holes in the sac that closed up? Is there a virulence factor which assists bacteria through the wall of the sac? If cytokine-stimulated collagenase production in the fetal membranes is responsible for the reduction of their tensile strength (Winkler and Rath 1996),
why does only the chorion rupture in about 10% of cases? How does maternal stress, drug addiction, smoking, obesity affect the ability to keep the chorion vs the amnion intact?
Questions for future research
• Can live bacteria enter a sealed amniotic sac? If so, how? • At term, what percentage of women have large amounts of fluid between the amnion and chorion? • Does the chorion produce amniotic fluid? • Is there such a thing as a high leak? • If there is such a thing as a high leak, does it involve both layers of membranes? • Can a high leak close up? If so, what is the mechanism? • When and why does the amnion produce prostaglandins, interleukin, cytokine? • How often does the chorion break before the amnion? • Why does the chorion sometimes break before the amnion? • How can we reliably test for True ROM vs rupture only of the amnion aside from when meconium or vernix is clearly seen? • Is there an increased risk of infection to the fetus or mother when only the chorion breaks or if there is a high leak? • What is the rate of successful induction vs caesarean surgery for women with False ROM vs True ROM? Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.
References Cohain JS. 2013. The less studied effects of amniotomy. Journal of Maternal-Fetal and Neonatal Medicine 26:1687–1690. Connon CJ, Nakamura T, Hopkinson A et al. 2007. The biomechanics of amnion rupture: An X-ray diffraction study. PLoS ONE 2:e1147. Cunningham FG. 2001. Williams obstetrics. 21st ed. New York: McGraw Hill. p 312. DiGiulio DB, Romero R, Amogan HP et al. 2008. Microbial prevalence, diversity and abundance in amniotic fluid during preterm labor: a molecular and culture-based investigation. PLoS ONE 3:e3056. Huebner M, Antolic A, Tunn R. 2010. The impact of pregnancy and vaginal delivery on urinary incontinence. International Journal of Gynecology and Obstetrics 110:249–251. Kjaergaard N, Hein M, Hyttel L et al. 2001. Antibacterial properties of human amnion and chorion in vitro. European Journal of Obstetrics, Gynecology, and Reproductive Biology 94:224–229. Kjaergaard N, Helmig RB, Schønheyder HC et al. 1999. Chorioamniotic membranes constitute a competent barrier to group b streptococcus in vitro. European Journal of Obstetrics, Gynecology, and Reproductive Biology 83:165–169. Wei SQ, Fraser W, Luo ZC. 2010. Inflammatory cytokines and spontaneous preterm birth in asymptomatic women: a systematic review. Obstetrics and Gynecology 116(2 Part 1):393–401. Winkler M, Rath W. 1996. The role of cytokines in the induction of labor, cervical ripening and rupture of the fetal membranes. Zeitschrift fur Geburtshilfe und Neonatologie 200(Suppl 1):1–12. Winram SB, Jonas M, Chi E, Rubens CE. 1998. Characterization of group B streptococcal invasion of human chorion and amnion epithelial cells in vitro. Infection and Immunity 66:4932–4941.
Superior mesenteric artery thrombosis: A rare and unknown complication after caesarean section L. Gaujal1, E. G. Simon1,2, I. Kellal1, A. Bleuzen3 & F. Perrotin1,2 Departments of 1Obstetrics, Gynaecology and Fetal Medicine, 2UMR INSERM U930 and 3Radiology, University Hospital Center of Tours François-Rabelais University de Tours, Tours, France DOI: 10.3109/01443615.2014.961908 Figure 1. Placenta showing larger hole in the chorion and fetal head sized hole in the amnion.
Correspondence: E. G. Simon, Department of Obstetrics, Gynaecology and Fetal Medicine, University Hospital Center of Tours, 2 Boulevard Tonnellé, Tours, 37000 France. E-mail: [email protected]
J Obstet Gynaecol Downloaded from informahealthcare.com by Nyu Medical Center on 06/09/15 For personal use only.
414
Obstetric Case Reports
Figure 1. Abdominal angioscan: superior mesenteric artery thrombosis, 14 days after caesarean section. (A) Thrombus in a sagittal plane (∗), (B) thrombus in an axial plane (arrow).
Case report
Discussion
We report the case of a superior mesenteric artery thrombosis in a 29-year-old woman, GI PI, 2 weeks after caesarean section. The woman had a body mass index of 18.5 and no medical history, apart from smoking 10 cigarettes/day, with complete smoking cessation in the 1st trimester of her pregnancy. Her uncle had a history of protein C deficiency. Her pregnancy was marked by excessive weight gain during the 3rd trimester and oedema of upper and lower limbs not related to gestational hypertension or pre-eclampsia. She entered spontaneous labour at 40 weeks’ gestation but needed a caesarean section for arrested cervical dilatation at 9 cm (total blood loss of 600 ml). The caesarean section was uneventful and she delivered a male baby weighing 3,660 g, with Apgar scores 10/10 at 10 min. Thromboprophylaxis with tinzaparin (3,500 IU/day) was started the day after delivery. The woman did not take contraception during the immediate postpartum. At 14 days after her caesarean section, the woman presented to the emergency department with acute and intense abdominal pain. The woman was afebrile and her abdomen was soft. Her blood pressure upon arrival was 120/90 mmHg, and an electrocardiogram showed a sinus tachycardia at 126/min. Blood test results showed: haemoglobin 11.6 g/dl; platelets 426 g/l; leucocytes 23 g/l; CRP 45 mg/l; and troponin 0.01 μg/l. An abdomino-pelvic ultrasound showed no anomaly. A CT of the abdomen and pelvis was carried out to search for an infection, but instead, led to the diagnosis of thrombosis of the superior mesenteric artery. The woman then underwent an emergency exploratory laparotomy and embolectomy. She was given anticoagulants, including heparin and aspirin and antibiotics. Aetiological assessment showed a severe protein C deficiency: the protein C level was only of 27%. No other risk factor for thrombosis was found. She was not a carrier of an autoimmune vasculitis disease. The woman was given protein C and supplements of vitamin K and 2 days later, a second-look laparotomy led to a 3 metre resection of the small intestine, cholecystectomy and terminal ileostomy. At 11 days after the surgery, she presented with severe sepsis with necrosis of the stoma. A CT of the abdomen and pelvis found an extension of thrombosis to the spleen, the liver and other areas of the digestive system (Figure 1). An emergency laparotomy was performed, which led to the resection of the totality of the small intestine, the right colon and the hemitransverse colon. The woman was then transferred to the hepato-digestive ICU. A cardiac ultrasound performed 1 month after thrombosis showed no valvulopathy, but did reveal a left intraventricular thrombus of 10 mm with a left ventricular ejection fraction of 40%. The woman went home 4 months after her caesarean section. She is currently waiting for a multivisceral transplant (small intestine, colon, pancreas and liver).
Mesenteric infarction is a serious condition, the prognosis depending on the underlying aetiology. There are four distinct forms: arterial occlusion by embolism or by thrombosis, venous thrombosis and non-occlusive mesenteric ischaemia. The mortality rates of these different forms are, respectively, 54%, 77%, 32% and 72% (Brandt and Boley 2000). Prompt diagnosis is a crucial factor for the prognosis of women who present with the typical clinical and biological features of mesenteric ischaemia (Sise 2014). However, diagnosis of this condition may sometimes be challenging. A normal abdomino-pelvic ultrasound scan in a case of acute postpartum abdominal pain should be followed by a CT of the abdomen and pelvis. An angioscan is the gold standard to diagnose this pathology (Cudnik et al. 2013; Sise 2014). Acute mesenteric ischaemia due to arterial occlusion (Brandt and Boley 2000; Sise 2014) may sometimes be caused by arterial embolism from cardiac disease (arrhythmia, valvular disease, myocardial infarction, thrombus or myxoma). It may also occur in the context of an atheromatous disease, vasculitis or thrombosis. The cause of the acute mesenteric ischaemia reported in this case is highly unusual. One case report in the literature documented a similar event that occurred on the 8th day postpartum after a vaginal delivery (Ducarme et al. 2008). The cause of this event remained unknown. Another paper reported an acute mesenteric ischaemia as an immediate complication of caesarean section, but the aetiology remained unclear (Singhal et al. 2005). In our case, we highlight protein C deficiency as a substantial contributing factor. In the literature, several cases of protein C deficiency associated with venous thrombosis have been described while, to our knowledge, none associating protein C deficiency with arterial has been reported. Histological analysis of the thrombus showed elements included in the fibrin, similar to those observed in venous thrombosis associated with protein C deficiency. However, there were no platelets and there was no sign of inflammation and no pathogenic agents, which are often observed in arterial thrombosis. The protein C deficiency may be responsible for the worsening of the thrombosis, despite appropriate surgical and medical intervention. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References Brandt LJ, Boley SJ. 2000. AGA technical review on intestinal ischemia. American Gastrointestinal Association. Gastroenterology 118:954–968.
Obstetric Case Reports 415 Cudnik MT, Darbha S, Jones J et al. 2013. The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis. Academic Emergency Medicine 20:1087–1100. Ducarme G, Lidove O, Leduey A et al. 2008. Postpartum thrombosis of the superior mesenteric artery after vaginal delivery. Obstetrics and Gynecology 111:535–537. Singhal SR, Sharma D, Singhal SK. 2005. Acute mesenteric ischemia: an unknown cause of immediate postcesarean mortality. Acta Obstetricia et Gynecologica Scandinavica 84:299–300. Sise MJ. 2014. Acute mesenteric ischemia. Surgical Clinics of North America 94:165–181.
J Obstet Gynaecol Downloaded from informahealthcare.com by Nyu Medical Center on 06/09/15 For personal use only.
Severe visual loss following obstetric forceps delivery-related ocular trauma in a neonate K. Shah, R. Roy, S. Guha, M. Bhargava, S. V. Shah, A. Lobo, D. Das & A. K. Majumder Aditya Birla Sankara Nethralaya, Kolkata, West Bengal, India DOI: 10.3109/01443615.2014.969205 Correspondence: Dr. Rupak Roy, Aditya Birla Sankara Nethralaya, 147, E. M Bypass, Mukundapur, Kolkata 700099, West Bengal, India. E-mail: rayrupak@ gmail.com
Report of a case Parents of a 20-hour-old male baby brought him to the hospital with white reflex and bleeding in the right eye following obstetrics forceps delivery. The circumstances and indications of forceps application could not be ascertained from baby’s medical records. His systemic examination was within normal limits. On examination vision could not be assessed in the right eye, and left eye was apparently normal. There was linear full-thickness corneal tear extending from superior to central portion of cornea (6 mm) with severe corneal oedema (Figure 1a). Patient underwent primary corneal suturing under general anaesthesia on the same day (Figure 1b). Post-operatively media was hazy due to corneal oedema. Ultrasonography of the eye was performed the following day, which revealed total retinal detachment. The baby underwent combined penetrating keratoplasty, lensectomy, pars plana vitrectomy with endolaser and silicone oil tamponade for retinal reattachment. Intraoperatively there was vitreous haemorrhage and multiple blotchy pre-retinal haemorrhages with a giant retinal tear (GRT) of 3 clock hours causing total retinal detachment (Figure 1c). Post-operatively corneal graft was clear and retina was attached (Figure 1d). At 1-month follow up, the baby developed inferior retinal re-detachment. The baby underwent membranectomy, endolaser and repeat silicone oil injection. Unfortunately at follow-up the eye became phthisical. Stock shell was placed in the socket to prevent contracture of the orbit.
Introduction Ophthalmic injuries have been reported secondary to instrumental vaginal deliveries (Jain et al. 1980). A variety of complications have been described involving anterior and posterior segment of the eye due to obstetric trauma. We report a case of grievous ocular injury in a neonate following forceps delivery, its management and outcome.
Discussion A wide spectrum of ocular injuries has been reported due to birth trauma more so following forceps delivery. Various anterior segment complications secondary to obstetric forceps injury include absence of globe (Wiegand 1990), facial palsy, lid lacerations, subconjunctival haemorrhage, corneal abrasion, corneal abscess,
Figure 1. (a) Pre-operative photograph showing full-thickness corneal tear (6 mm) with surrounding oedema and blood-stained cornea (arrow). (b) Post-operative photograph showing sutured corneal wound with air bubble in anterior chamber (arrow). (c) Intra-operative photograph showing multiple blotchy pre-retinal haemorrhage (long arrow) and GRT (arrow head) during vitreous surgery. (d) Post-operative photograph following corneal transplant with clear corneal graft.
