This document presents the case of a 29-year-old pregnant female who presented with epigastric pain, vomiting, diarrhea and later coughing up blood and nosebleeds. Investigations showed leukocytosis, low blood pH, high blood sugar, and sepsis. She had a spontaneous abortion due to sepsis and developed disseminated intravascular coagulation (DIC) and bilateral pulmonary embolism. Her condition improved with treatment but she was found to have a protein C deficiency, which can cause hypercoagulability and venous thromboembolism. The document provides details on her hospital course and explains DIC, its causes, diagnosis, and inherited and acquired hypercoagulable states.

1. CASE PRESENTATION

2.  29 year old female pregnant G2p1+0 9wks
gestation presented complaining of
epigastric pain, vomiting & diarrhea on day of
admission. Later on the day started c/o
productive cough with streaks of blood &
epistaxis. She was also c/o mild exertional
dyspnea 2wks before admission.pt not known
to be D.M nor HTN & no h/o any chronic
illness before

3.  Investigations:
 Leukocytosis: wbc-14.9
 ABG: ph-7.02 / Hco3-8 /Pco2-27
 Blood sugar-526
 She had being admitted to MICU and
managed as a case of Sepsis & Lactic
acidosis.

4. Investigations on day of admission:
 ABG: PH:7.02→→7.3
HCO3 :8→→12
Pco2 :27→→24
 CBC: WBC:14.9
RBC:4.4
Hb:12.2
Plt:47→18→13
 U/E/C:Na: 137→142
K:2.5→4.8
Cr:1.4→1.2
BUN:9→11
 Glucose:526→398→225→69

5.  LFT: ALT:455
ALP:98
AST:678
GGT:97
 Coagulation profile: PT: 38.9
APTT:71.6
INR:3.45
 Bl.groupe: O +ve
 ß-HCG titre :5865

6.  On the 2nd day she had intrauterine gestational sac




with no fetal heart. She had more bleeding &had
complete spontaneous abortion due to sepsis. Then
was transferred to MICU because of multiple bruises
all over the body;
Investigations of 2nd day:
CBC: WBC: 14
Hb:11.3→ 9
Plt:9→10→31→26
Coag. Pro.: PT:71→48.2→52.5
APTT:99→58.7→56.5
INR:6→4.3→4.73
D-dimer:6496.9

7.  LFT:ALT:458





AST:712
ALP:110
GGT:99
Amy:168
Lipase:227
LDH:1730
ABG:PH:7.24→7.53
HCO3:9→7→18
Pco2:22
ECG: inverted T wave LIII & deep s in LI.
total CK:1533
MMB:2.7
Trop.I:3.2
 She developed DIC.

8.  On 3rd day U/S abd: liver not congested ,not
enlarged, no splenomegaly, pancrease and both
kidneys are normal ,only minimal ascites in
douglas pouch.
 CT angiography of pulmonary vessels →→
massive bilateral pulmonary empolism with mild
pleural effusion

9.  S/R: unremarkable.
 Obestatric & Gynae H/O:
 P1+1 she’s being married for 4 years, her 1st
pregnancy developed bleeding at three months
gestation, recieved tablets then it resolved, and had
normal vaginal delivary with no complications and
breast fed her baby for 10 months. Then she had
two years of secondary infertility , sought medical
advice gave her clomid for induction of her 2nd
pregnancy which was aborted in this admission .
 PMH/PSH: NAD
 Family H: NAD
 Allergy: not known.

10.  On physical ex.:
 Pt was concioeus, oriented, not jaundice,not pale
,no LAP, no LLO ,b.p=80/50 ,pulse=72, afebrile.
 CVS: s1+s2+0
 Respiratory: good air entry bilateral with no added
sounds but decrease tactile vocal resonanse in
middle zone bilat but mainly in left side.
 Abdomen: distended, multiple bruises in the flank
areas, soft not tender , no organomegaly and –ve
shifting dullness.
 CNS: normal

11. 








Investigations from 3rd day to date of discharge:
Bone marrow: reactive B.M with periphral thrombocytopenia.
CT abdomen on 8th day showed signs of Budd Chiari syndrome.
CBC: WBC: 12.6→8→5
Hb:8.4→10.6
plt:26→19→13→31→108→→→292
Coag. Pro.: PT:28.2→→→→16.5
APTT:105→→→→34.8
INR:2.46→→→→1.4
ESR:3
Fib:0.8
U/E/C: normal
Glucose: 118→→→→98

12. 




Protien C: 26.5↓↓
Protien S: 91.8↔
Factor v leiden:0.89↔
Tip of central line c/s: Gm –ve rods
LFT: ALT:942→342→→→98
AST:562→372→→→71
ALP: 104→99
GGT:103→77
LDH:1730→→→310
Alb:3.5
lipase:609
 CT abdomen on 20th day showed normal liver with
signs of Budd chiari.

13. Disseminated intravascular
coagulation
 One of acquired bleeding disorders.
 Initiated by a variety of different mechanisms:
a. Endothelial damage due to many causes e.g.
Endotoximia due to Gm –ve bacteria causes
septicemia, results in tissue factor expression which
leads to activation of the coagulation cascade
through the extrinsic pathway.
b. Intravascular coag. Takes place with consumption of
plts, factor v, factor vlll and fibrinogen.
c. This results in a potential heamorrhagic state, due
to depletion of heamostatic components, which
may be exacerbated by activation of the fibrinolytic
system secondary to the deposition of fibrin.

14. Definitive diagnosis of DIC depends on the finding of:
 Thrombocytopenia
 Prolonged PT ,APTT
 Decrease fibrinogen concentration
↑↑↑D- dimer.
Causes of DIC:
 Infections:
E. Coli ,neisseria meningitids ,streptococcus pneumonie, malaria.
 Obstetrics:
Placental abruption, pre-eclam psia , retained dead fetus, amniotic
fluid embolism.
 Cancer:
Lung , pancreas and prostate.
N.B: DIC from malignancy may have normal or even elevated
platelet count.

15.  Causes of hypercoagulable state:
Acquired:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Heparin- induced thrombocytpenia.
Nephrotic syndrome.
Antiphospholipid antibody syndrome.
Microangiopathic hemolytic anemia ( TTP, DIC ,HUS)
Myeloproliferative disorder
Old age
Immobility
Surgery
Pregnancy
Hormone therapy
Malignancy
1.
2.
3.
Defciencies of protien C , S, and antithrombin lll
Prothrombin gene mutation
Activated protien C resistance( factor v leiden gene
polymorphism)
Hyperhomocysteonemia.
Inherited:
4.

16. There may also be heritable hypercoagulable states
precipitated by persistent elevation of coagulation
factors vlll , lx, xl.
Screening should be performed for a young patients
with +ve family history or H/O recurrent thrombus
e.g:
 Protien C, S ,antithrombin lll levels may be reduced
during an active thrombosis, which can create false
+ve test result.
 Warfarrin will reduce the activity of the vit.kdependent modulators of clotting factors, protien
C, S.
 Heparin and warfarrin may affect results for lupus
anticoagulant, and this diagnosis is best established
after anticoagulants is discontinued.

17.  Defciencies protien C ,protien S, Antithrombin lll :
These three protiens are synthesized in the liver and have
modulatory function in hemostasis of the coagulation
cascade.
Protien S is a cofactor of activated protien C that serves to
inactivate factors va &vllla.
Antithrombin lll inhibits factors ll ,xa, xla, xlla ,lxa
Heparin complexes with anti lll greatly potentiating the
serine protease inhibitory activity of anti lll.
These enzymes can be quantitatively or qualitatively
abnormal in hypercoagulable individuals.
Severe defciencies of these enzymes may result in VTEat
young age.
They are uncommonly detected in the general
population, but they are responsible for 5%- 15% of
idiopathic VTE.

18. THANK YOU