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LETTER TO EDITOR
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 146-148

Successful recovery from disseminated intravascular coagulation in a patient with abruptio placentae who presented for emergency lower-segment cesarean section


Department of Anaesthesiology, B. J. Medical College, Ahmedabad, Gujarat, India

Date of Submission09-Aug-2014
Date of Acceptance12-Nov-2014
Date of Web Publication17-Mar-2016

Correspondence Address:
B Patel Kiran
50, Raichandnagar Society, Near Visat Petrol Pump, Sabarmati, Ahmedabad 382424, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.178897

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  Abstract 

Healthy pregnancy is accompanied by changes in the hemostatic system that convert it into a hypercoagulable state vulnerable to a spectrum of disorders ranging from venous thromboembolism to disseminated intravascular coagulation (DIC). DIC is always a secondary phenomenon triggered by specific disorders such as abruption placentae and amniotic fluid embolism due to intravascular release of thromboplastin or endothelial damage resulting from pre-eclampsia and sepsis. Delivery of the fetus and placenta in the early stage of accelerated disease progression is the definitive therapy. Uncompensated DIC, associated with pre-eclampsia, is monitored with serial hematological investigation of platelet count, fibrin degradation products, and serum fibrinogen level. Removal of triggering mechanisms with supportive measures associated with or without mechanical ventilator support is key to successful management. Outcome depends on our ability to deal with the triggers primarily and not only on correcting coagulation and providing mechanical ventilatory therapy.

Keywords: abruption placentae, noninvasive mechanical ventilation, pre-eclampsia, termination of pregnancy, uncompensated disseminated intravascular coagulation


How to cite this article:
Kiran B P, Bidyut B, Ananyaruchi S S. Successful recovery from disseminated intravascular coagulation in a patient with abruptio placentae who presented for emergency lower-segment cesarean section. Ain-Shams J Anaesthesiol 2016;9:146-8

How to cite this URL:
Kiran B P, Bidyut B, Ananyaruchi S S. Successful recovery from disseminated intravascular coagulation in a patient with abruptio placentae who presented for emergency lower-segment cesarean section. Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2019 Sep 18];9:146-8. Available from: http://www.asja.eg.net/text.asp?2016/9/1/146/178897


  Introduction Top


Disseminated intravascular coagulation (DIC) is a severe complication secondary to abruptio placentae associated with pre-eclampsia resulting in increased risk of adverse outcome for both the mother and the fetus. Pre-eclampsia is one of the predisposing factors for abruption of the placenta [1] . Abruption may be missed because clinical signs are hidden by onset of labor associated with a hyperkinetic and hypertonic uterus in a young healthy parturient [2],[3] . Before delivery, aggressive obstetrical management is directed toward stabilization of the affected organ systems and, if possible, termination of pregnancy, and delivery of the fetus and placenta in the early phase of accelerated disease progression is the definitive therapy.

Case history

A 22-year-old primigravida with pregnancy-induced hypertension and severe anemia with 28 weeks' amenorrhea was referred to the Civil Hospital, Ahmedabad, on 6 November 2013 at 5 a.m. with severe abdominal pain and bleeding per vagina, which was diagnosed as a case of pregnancy-induced hypertension with abruptio placentae. Intrauterine fetal death was confirmed on the ultrasound. Initially, the patient was given a tablet of 25 mg misoprostol vaginally and an attempt was made to artificially rupture the membrane for vaginal delivery; however, the attempt failed and her vitals became unstable. On physical examination her blood pressure was found to be 150/90 and heart rate was 100 beats/min; laboratory investigations revealed hemoglobin 6.03 g/dl, white blood cell 18 200/mm 3 , blood urea 50.3 mg/dl, serum creatinine 1.8 mg/dl, platelet count 78 000/mm 3 , fibrin degradation product more than 5 mcg/ml, D-dimer assay more than 9000 mcg/ml, and serum fibrinogen 94 mg/dl, which suggested DIC. On catheterization, blood-stained urine was observed; therefore, prompt decision was taken to terminate the pregnancy by lower-segment cesarean section on an emergency basis. A well informed ASA grade III E consent was taken on account of patient's clinical condition.

General anesthesia was planned, and the patient was attached to all available monitors. She was premedicated intravenously with 0.2 mg glycopyrollate, 8.0 mg ondansetron, and l50 µg fentanyl. After 3 min of preoxygenation, anesthesia was induced with 350 mg thiopentone and 70 mg succinylcholine intravenously and the patient was intubated with an endotracheal cuffed tube No.7.0 mm internal diameter and maintained on sevoflurane, 50% nitrous oxide in oxygen. Mechanical ventilation was instituted after atracurium. Two units of packed cells (packed cell volume), 4 U of fresh frozen plasma, and 4 U of platelet concentrate were transfused intraoperatively. An intrauterine dead baby weighing 1.4 kg was delivered and 20 U of oxytocin infusion was started intravenously. Surgery was completed uneventfully, and after extubation the patient was shifted to the postoperative recovery ward for observation as her urine output was diminished.

After 4 h the patient became tachypnic and complained of cough and difficulty in breathing. She was conscious, with blood pressure 160/110 mmHg and pulse rate 160/min. Bilateral creps were seen on auscultation. Blood samples were sent for laboratory analysis. Renal function (blood urea, 56.8; serum creatinine, 1.75) were elevated and arterial blood gas showed metabolic acidosis with compensatory respiratory alkalosis, which was thought to be due to acute renal shutdown. We decided to shift her to the ICU and she was connected to a noninvasive ventilator (biphasic positive airway pressure) with continuous monitoring. Central venous pressure was taken, which was found to be mildly elevated. Frusemide at 40 mg was given intravenously. Antibiotics and supportive therapies were started. Six units of packed cell volume, 5 U of fresh frozen plasma, 3 U of whole blood, and 1 U of platelet concentrate were given the next day after her urine had cleared and was adequate. When arterial blood gas and chest radiography were normal, and she was weaned off the ventilator on the second day in the ICU. Her coagulation profiles gradually returned to normal and she was shifted to the ward after 4 days, from where she was discharged home.


  Discussion Top


Obstetric hemorrhage remains a serious complication, contributing to maternal morbidity and mortality. Placental abruption is defined as separation of the placenta from the decidua basalis after 20 weeks of gestation, before delivery of the fetus. Bleeding occurs from exposed decidual vessels and may be extensive. Fetal distress occurs because of loss of area for fetomaternal gas exchange. Abruption is an important cause of intrauterine growth retardation, premature labor, and fetal death [1],[2] . According to the Page classification of abruptio placentae, our patient was in stage III, which is indicative of a severe form with coagulation defects and fetal death in utero. According to the Sher classification, our patient was in stage IIIB, which is indicative of a severe form of abruptio placentae with intrauterine fetal death and coagulopathy [1] . Obstetric hemorrhage is the second leading cause of all pregnancy-related deaths. The classical hemorrhagic picture includes thrombocytopenia, depletion of fibrinogen, and prolonged plasma thromboplastin times. Acute renal failure may accompany DIC, reflecting fibrin deposition in the renal arteries and fetal distress reflecting loss of functional placenta and decreased uteroplacental perfusion, as seen in our case [3] .

DIC is an acquired consumption coagulopathy occurring secondarily in the course of severe forms of disease. It is a thrombohemorrhagic disorder with simultaneous activation of the coagulation and fibrinolytic paths and is considered a hematological emergency indicating a clotting catastrophe requiring critical care [4],[5],[6] . The placenta plays a major role in the activation of the coagulation system as a large placental site behaves as an open wound. Pregnancy has been described as a hypercoagulable stage, as there is significant rise in levels of serum fibrinogen, factor VII, factor VIII, factor IX, and factor X [7] . Factors V and II remain almost the same, whereas factors XI and XIII are decreased to almost 70% of the nonpregnant level [8] . In our case, because of coagulopathy, it was unwise to consider regional anesthesia and because of the possible risk for intraoperative hypotension and bleeding we instituted general anesthesia.

During pregnancy, acute kidney injury (AKI) is associated with increased mortality and morbidity. An understanding of the renal physiologic changes that occur during pregnancy is essential for proper evaluation, diagnosis, and management of AKI. As in the general population, AKI can occur from prerenal, intrinsic, and postrenal causes. Major causes of prerenal azotemia include hyperemesis gravidarum and uterine hemorrhage in the setting of placental abruption. Intrinsic etiologies include infections from acute pyelonephritis and septic abortion, bilateral cortical necrosis, and acute tubular necrosis. Particular attention should be paid to specific conditions that lead to AKI during the second and third trimesters, such as pre-eclampsia, HELLP syndrome, and acute fatty liver in pregnancy [9] . The cellular profile exhibits extensive arterial, arteriolar, and glomerular fibrinoid thrombi [10] . Treatment of prerenal acute renal failure in pregnancy involves correcting the underlying cause, replacing lost volume or blood substitutes, and treating sepsis. In our case, we also corrected lost volume and blood substitutes to avoid renal shutdown.


  Conclusion Top


Lower-segment cesarean section may entail reduced risk of perinatal mortality in case of placental abruption with a live baby, but vaginal delivery is recommended if the baby is dead. General anesthesia is required because of the high probability for maternal hypovolemia due to hemorrhage, coagulopathy, and potential for further intraoperative bleeding. Abruptio placentae with DIC requires a multidisciplinary approach for diagnosis and management. Early decision to remove triggers and perioperative management including mechanical ventilatory support with strict monitoring, laboratory parameter checks, and transfusion of blood substitutes will result in successful outcome.


  Acknowledgements Top


Conflicts of interest

Non declared.

 
  References Top

1.
Ducloy AS, Lee J. Obstetric anaesthesia-placental abruption. Updat Anaesth 2002; 14:46-47.  Back to cited text no. 1
    
2.
Chamberlain G, Steer P. ABC of labour care: obstetric emergencies. BMJ 1999; 318:1342-1345.  Back to cited text no. 2
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3.
Hines R, Marschall K Chapter-23: obstetric haemorrhages. In: Hines R, Marschall K, eds. Stoelting's anaesthesia and co-existing diseases. 5th ed.. Philadelphia: Churchill Livingstone 2008; 1-5.  Back to cited text no. 3
    
4.
DeLoughery TG. Critical care clotting catastrophies. Crit Care Clin 2005; 21:531-562.  Back to cited text no. 4
    
5.
Asthana B, Sharma P, Ranjan R, Jain P, Aravindan A, Chandra Mishra P, Saxena R Patterns of acquired bleeding disorders in a tertiary care hospital. Clin Appl Thromb Hemost 2009; 15:448-453.  Back to cited text no. 5
    
6.
Levi M. Disseminated intravascular coagulation (DIC) in pregnancy and peri-partum period. Thromb Res 2009; 123:63-64.  Back to cited text no. 6
    
7.
Elby CS. A review of a hypercoagulable state. Hematology-Oncol Clin North Am 1993; 7:1121-1142.  Back to cited text no. 7
    
8.
Hobisch-Hegan P, Mortl M, Schobersberger W. Haematostatic disorders in pregnancy and peripartum period. Acta Anesthesiol Scand 1997; 111:216-217.  Back to cited text no. 8
    
9.
Nwoko R, Plecas D, Garovic VD. Acute kidney injury in the pregnant patient. Clin Nephrol 2012; 78:478-486.  Back to cited text no. 9
    
10.
Prakash J, Tripathi K, Pandey LK, Gadela SR, Usha. Renal cortical necrosis in pregnancy-related acute renal failure. J Indian Med Assoc 1996; 94:227-229.  Back to cited text no. 10
    




 

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