The puerpera fully understood and signed a written informed consent to publish the case report. A 26-year-old puerpera with 39 weeks of menolipsis was hospitalized on November 14, 2018, and lack amniotic fluid of unknown reasons. The examinations of color Doppler ultrasound indicated that all tests were normal except the presence of only 64 mm amniotic fluid index, which might have been ceased by the malfunction or dysfunction of the placenta.
Labor And Delivery Presentation
On November 15, an intravenous drip of oxytocin was administered to the puerpera for odinapoeia until 5:15 pm. At 8:50 pm, she had a fever up to 39°C associated with chills and shivering. Blood tests showed the increases in the leukocyte count, neutrophil ratio, and C-reactive protein level. The fetal membrane was ruptured, the amniotic fluid was degree 1 turbid, fetal tachycardia occurred and irregular contractions of uterine were observed, implying intrauterine infection. At 9:50 pm, a cesarean section was performed to terminate the pregnancy, and the amniotic fluid of the puerpera was determined to be 3 degrees turbid. The puerpera gave birth to a baby boy at 10:11 pm.
Postpartum
The patient began severe vomiting at 10:55 pm, November 15. Her blood pressure dropped down to 82/45 mmHg, her heart rate raised up 131/min, and many places of capillary hemorrhage were observed in the omentum majus. Her nasal cavity spontaneously began to bleed, lasting for 7 minutes. And unexpectedly the patient’s blood did not manifest coagulation, resulting in the suspicion of disseminated intravascular coagulation (DIC). During hemorrhage of the greater omentum suture, the patient had obvious infiltration of the abdominal wall muscles and subcutaneous fat, and her DIC score reached 10 points (primary disease, 2 points; PLT 50×109/L, 1 point; PT 21.1 s, 2 points; FDP significantly increased, 4 points; Fib < 1 g/L, 1 point). Based on the dominant DIC International Standard of Thrombus and Hemostasis Committee (ISTH Standard) assessment, revealing that she was in a state of severe hypo-coagulation or coagulopathy.
Teg Diagnosis And Intervention
A critical condition of PPH patient with DIC needed to be urgently treated. Therefore, TEG was employed to measure the coagulation state after sampling. Surprisingly, the TEG assay showed that the patient’s R value was extended and the line was sustained over 30 min. At 11:18 pm, based on the laboratory results, the patient was given 10 U of cryoprecipitate and 4 U of RBC, and adjunctive use of anti-fibrinolytic and anti-infective drugs, unfortunately, the patient continued to bleeding (Table 1).
Table 1
History of medical examinations from the puerpera during the critical period.
Date | | 2018-11-15 | 2018-11-16 |
Acquisition time | | 7:00 pm | 9:10 pm | 11:18 pm | 11:40 pm | 0:54 am | 1:17 am | 1:27 am | 2:43 am | 4:41 am |
Routine blood | WBC (×109/L) | 7.8 | 14.7 | 11.0 | | 10.2 | | 9.4 | 19.6 | 20.7 |
HGB (g/L) | 125 | 146 | 92 | | 77 | | 90 | 95 | 92 |
PLT (×109/L) | 183 | 113 | 77 | | 50 | | 37 | 74 | 71 |
Coagulation function | APTT (s) | | 41.0 | 106.1 | | 71 | | 48.5 | 40.1 | 44.3 |
PT (s) | | 13.4 | 21.1 | | 19.8 | | 15.4 | 14.8 | 13.3 |
FiB (g/L) | | 2.4 | 0.5 | | 0.8 | | 2.6 | 3.0 | 2.9 |
TT(s) | | 21.3 | 28.7 | | 25.2 | | 15.9 | 15.2 | 18.8 |
| DIC score | | 4 | 11 | | 10 | | 6 | 5 | |
| FDP (µg/mL) | | 33.4 | 116.2 | | 98.6 | | 36 | 32 | |
| ATⅢ % | | | 22.6 | | 39.2 | | | | 58.2 |
TEG | | CK | CK | CK | CKH | Protamine intervention | CK | CKH | Protamine intervention | CK | CK | CK |
R (min) | 7.8 | 15.1 | 70.2 | 8.5 | 12.5 | 48.2 | 8.0 | 8.6 | 9.0 | 10.3 | 11.8 |
Angle | 35.7 | 20.3 | | 22.9 | 20.3 | | 23.6 | 21.6 | 57.1 | 52.6 | 38.8 |
MA (mm) | 48.7 | 30.1 | | 34.7 | 30.1 | | 34.0 | 30.0 | 53.0 | 54.4 | 62.4 |
Inflammatory biomarkers | PCT (µg/L) | | 26.1 | | | | | | | 150.0 |
CRP (mg/L) | | 0.08 | | | | | | | 58.36 |
| TM (TU/mL) | | 11.8 | 14.9 | | 23.6 | | | | |
| tPAI-C (ng/mL) | | 14.7 | 27.5 | | 32.3 | | | | |
| Drug intervention | | | Tranexamic acid injection 2 g | Protamine injection 40 mg | Protamine injection 40 mg | Fibrinogen freeze-dried powder 4 g | | | Tranexamic acid injection 2 g |
| Transfusion of blood products | | RBC4U | Cryo 20 U | FFP 600 mL | RBC 6 U | Cryo 15 U | PLT 20 U | | Cryo 10 U |
Normal reference values of the coagulation index: APTT: 26.0–37.0ན, TT: 12.0–17.0ན, PT: 9.0–13.0ན, Fib: 2.0–4.0 g/L, FDP: 0–5 µg/mL. Normal thromboelastic reference values are plotted as R: 5–10 min, MA: 50–70 mm, Angle: 53°-72°. CRP 0–10 mg/L; WBC (4–10) ×109/L; HGB 120–160 g/L; PCT 0-0.1 µg/L; ATⅢ 81.5-121.3%; TM 3.8–13.3 TU/mL; tPAI-C < 10.5 ng/mL. |
Combined with the prolong and expansion of activated partial thromboplastin time (APTT) extension, thrombin time (TT), and R value, the hmTEG was also performed to measure the patient’s sample again. The results showed that the coagulation state had significantly improved after the neutralization of heparinase, and the TEG results (R 8.5 min, angle 22.9º, MA 34.7 mm) were also verified. These results indicated that the patient had severe heparinization (Fig. 1), which could be due to the self-production of heparin substance which was not derived from any heparin-related medication definitely. Definitely, no heparin administration upon closure was performed and this state was reconfirmed by the surgical team. Immediately, the patient's coagulation function was significantly improved (R 12.5 min, angle 20.3°, MA 30.1 mm) after 40 mg of protamine intervention, indicating that the heparin was offset (Table 1 and Fig. 1).
However, the coagulation results still revealed a lack of fibrinogen and platelets. Platelets were not available, and 10 U of cryoprecipitate and 4 U of RBCs slightly promoted the coagulation. At 00:54 am on November 16, the patient’s condition became worsen again, as evidenced by 200 mL of blood exuding from the wound without clotting. Unexpectedly, the results showed that the R value was extended, the line was sustained to 30 min, and the antagonism of heparinase had improved (R 8 min, angle 23.6°, MA 34 mm). These results showed the abnormality of the coagulation again, and endogenous heparinization counteraction was deteriorated. After urgent injection with 40 mg protamine again, the patient’s coagulation function was significantly improved (R 8.6 min, angle 21.6°, MA 30 mm). After 24 U of cryoprecipitate, 2 doses of curative platelets and 4 g of fibrin preparation were transfused. The patient’s coagulation function gradually returned to normal at 02:43 am. The patient was sent to the ICU for further medicare and treatment at 03:50 am on November 16.
Laboratory Tests
In the meantime, we also examined two indicators: thrombo-regulatory protein (TM 3.8–13.3 TU/mL) and tissue plasminogen activator inhibitor 1 complex (tPAI-C < 10.5 ng/mL) of vascular endothelial cell injury. At 09:10 pm on November 15, 2018, TM was 11.8 TU/mL and tPAI-C was 14.7 ng/mL, respectively; and subsequently TM was 14.9 TU/mL and tPAI-C was 27.5 ng/mL at 11:18 pm. TM was 23.6 TU/mL and tPAI-C was 32.3 ng/mL at 00:54 am, November 16, 2018. ATIII (81.5–121.3%) level was 22.56% at 11:18 pm, November 15, 2018. At 01:27 am on November 16, ATIII level was 39.21%, but the level was elevated to 58.23% at 04:41 am on November 16 (Table 1).
During the treatments, the patient presented the symptoms of double lung respiratory sounds and wet rales. Bedside chest X-ray revealed double lung patch shadows and pleural effusion, and the hemogram of the patient exhibited persistent symptoms of infection. Blood was cultured on November 15, and the results showed that the patient had an Escherichia infection. After anti-infection treatment, the patient became gradually stable and was discharged from the hospital on November 28, 2018.