Atonicity of the uterus is the commonest cause of primary PPH, while retained bits of placenta and membranes usually cause secondary PPH. We present a case of primary PPH during caesarean section due to massive fibrinoid debris over placental site.
A 23 years primigravida with an irregular antenatal check up from a private clinic was admitted in our hospital at 37 weeks 5 days with pre eclampsia and labor pain on 5.03.08. Her antenatal record showed she had mild PIII since 32 weeks of gestation. On examination; she had pallor, pulse rate 84/min BP 150/100 mmHg. The baby was term size. While monitoring her labor she had spontaneous rupture of membranes and the liquor was meconium stained together with a fetal heart rate irregularity. An emergency caesarean section was performed for fetal distress under spinal anesthesia and a male baby weighing 2.3 kg was delivered. Placenta was delivered by controlled cord traction. As the placenta was expelled there was profuse uterine bleeding from the placental bed. We saw a copious amount of thick edematous leaf like fleshy masses were hanging from the placental bed, the largest one being 6.5 9 3.0 9 0.6 cm3. The uterus remained flabby, but the masses were too adherent to be removed easily and hence, were removed with sponge forceps. Simultaneously 40 IU oxytocin and prostaglandin F2a (250 mcg) was given and the PPH was controlled. On histopathological examination the fleshy masses were reported to be fibrinoid necrosis with a marked decidual reaction (Fig. 1).
Fibrinoid deposition occurs within the decidua basalis and usually is confined to placental floor [1]. The fibrin, however, can extend into the intervillous space to envelop the villi, which then atrophy and may cause maternal floor infarction [1]. Adams et al. [2] described that maternal floor infarction is an uncommon phenomenon occurring in 0.006% delivery cases causing adverse neonatal neurodevelopmental outcome. Fibrinoid degeneration is usually associated with preeclampsia and an unfavourable fetal outcome due to a chronic placental insufficiency and oligohydramnios as was evident in this case. But what was unique in this case was that the extent of the degeneration was so huge that it behaved like retained placental masses causing severe PPH which is a very rare clinical experience. We present this case because of its rarity and to consider this factor during management of PPH.
