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Jayanthi 22 year Admitted on 29/4/10 in OG III taken over by Medicine III on 2/5/10 Para 1,39 weeks of Gestation

Wingdings 2:

Presenting Complaints h/o sudden onset abdominal pain and bleeding PV on 29/4/10 since 10 am Brought to hospital at 1.45 pm same day Had no perception of fetal movements since onset of symptoms O/E – BP-130/90 mm Hg , PR – 86/min Pallor +, Pedal edema + P/A – Foetal heart sounds not heard PV – bleeding present

Arial Black:

Emergency USG abd showed features suggestive of IUD Termination of pregnancy done on 29/4/10 9.50 pm by outlet forceps delivery Post-partum patient had episodes of seizures in early morning of 30/4/10- GTCS 2 episodes controlled with Inj.MgS04 Also developed hypertension , jaundice, fever , decreased urine output over course of two days from 29/4/10 to 1/5/10 Developed progressively increasing abdominal distension and b/l leg and hand swelling and breathlessness


Emg Ps showed Schistocytes,fragmented RBC’S,Low platelet count, and FDP was Positive. Patient was taken over by Medicine dept from OG in view of Severe sepsis,DIC and ARF and severe hepatic dysfunction in postpartum period. Shifted to MICU on 2/5/10


29/4 30/4 3/5 4/5 6/5 10/5 14/5 Hb 9.4 6.3 6.9 5.7 7.7 7.5 TC 11,000 44,100 39,700 35,200 24,500 21,900 12,300 DC N85L15 N76L22 N88L12 N86L14 N88L12 N79L19 M1 Platelets 60000 59000 83000 77000 99000 86000 2,44,000 Peripheral smear RBC WBC Platelets Hypo chromic, Mild aniso Poikilo cytosis Fragmented cells FDP +VE Leuco cytosis , Toxic change Reduced


LFT STP ALB AST ALT ALP TOTAL BILIRUBIN DIRECT BILIRUBIN 29/4 5.4 2.8 146 198 1103 10.3 3.3 2/5 4.6 2.3 36 85 474 4.1 1.3 3/5 3.8 2.0 154 53 329 3.4 1.2 4/5 4.2 2.0 212 84 366 11 6.4 5/5 4.4 2.3 163 87 346 13.8 6.5 6/5 3.9 2.3 92 42 309 9.7 3.2 7/5 4.1 2.3 123 95 513 9.5 2.5 11/5 5.9 2.4 52 37 314 7.6 2.5 14/5 5.7 2.8 10 27 204 6.4 2.4


S.Urea S.Creatinine B.Sugar Na K 29/4 52 1.4 135 136 4.0 1/5 88 3.1 111 120 4.6 2/5 110 2.5 62 116 4.8 3/5 ( Mrng) 127 2.9 66 120 5.1 3/5( evng )Pre Dialysis 167 3.4 60 126 5.7 3/5 Post Dialysis 87 1.5 61 132 4.1 4/5 107 2.3 60 131 4.36 5/5 132 1.8 318 130 3.2 6/5 Pre Dialysis 93 1.3 98 138 2.6 6/5 Post dialysis 60 1.0 60 141 3.4


S.Urea S.Creatinine B.Sugar Na K 7/5 78 1.1 63 147 4.3 10/5 37 1.2 74 139 3.6 11/5 27 68 144 3.8 12/5 33 63 144 2.9 13/5 40 1.3 72 138 4.3 14/5 26 73 137 5.0 15/5 16 84 135 5.4

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PT-INR HIV - Negative 29/4 - > 4 HBsAg - Negative 30/4 - 3.93 Anti – HCV - Negative 1/5 - 2.6 Blood C/S - Sterile 5/5 - 1.68 Urine C/S – Sterile 6/5 - 1.2 Wound C/S – Pseudomonas 11/5 – 1.4 aeruginosa resistant to all antibiotics Ascitic Fluid Total Protein:0.7gm/dl,albumin 0.3 gm/dl Cell count 6 Cells/µl

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ABG S.Uric acid 2/5 - 11.7 mg/dl 3/5 – 11.8 mg /dl Date PH PO2 PC02 Hco3 O2sat 2/5 7.36 82.5 24.7 18.1 96.1 3/5 7.43 153.3 30.2 22.8 99.1 5/5 7.42 121.5 33.6 23.1 98.4

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DIFFERENTIAL DIAGNOSIS Abruptio Placentae with DIC Sepsis DIC Eclampsia HELLP syndrome Acute fatty liver of pregnancy

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FINAL DIAGNOSIS Primi P1L0 Abruptio Placentae,Sepsis,DIC with Multiorgan Dysfunction.

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CLINICAL COURSE AND TREATMENT 22 year Primi,admitted in 39 th week of gestation, with abd pain and bleeding PV,detected to have IUD,termination of Pregnancy done->developed postpartum seizures,sepsis,DIC,ARF and severe hepatic dysfunction She required intubation in MICU and was on ventilator support from 3/5/10 to 5/5/10(GCS-3/15) Intermittent Hemodialysis done twice (on 3/5/10 and6/5/10) for ARF Pt given 6 unit Packed RBC transfusion,6 units Platelet transfusion and 10 units of FFP transfusion. Also given Inj.Vit.k for correction of coagulopathy

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Sepsis treated with antibiotics Meropenem and flagyl.She had also received Magnex for 1 st 3 days Prior to shifting to ICU. Inj.Lasix given later for fluid overload after 2 dialysis sessions->Significant Weight decline and decrease in abdominal and limb swelling Weight- 56 kg on 5/5/10 decreased to 43 kg on 17/5/10 Abdominal girth 91 cm on 1/5/10 decreased to 71 cm on 17/5/10

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Causes and trimester of liver disease in pregnancy

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Algorithm of abnormal liver tests

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Physiological Changes during Pregnancy

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Abruptio Placentae( placental abruption,Accidental haemorrhage,Ablatio placentae) Definition Premature separation of the normally implanted placenta from the uterine wall.


Etiology Mechanism : hemorrhage into the decidua basalis, leading to premature placental separation and further bleeding. Associated factors: Maternal hypertension Sudden decompression of the uterus Trauma Maternal cocaine use


Diagnosis Classic clinical presentation: vaginal bleeding Tender uterus Uterine contractions Fetal distress


Coagulation abnormalities Hypofibrinogenemia Increaseing levels of fibrin degradation products decreasing platelet count Increasing prothrombin time and partial thromboplastin time Decreasing other serum clotting factors

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Ultrasonography: relatively large retroplacental clots may be detected Placental examination The extent of placental abruption of the maternal surface of the placenta on which a clot is detect at the time of delivery

Causes and trimester of liver disease in pregnancy:

Management Maintain hemodynamic stabilization ( Transfusion therapy ) Crystalloid transfusion Whole blood therapy Component therapy Correct coagulation status

Algorithm of abnormal liver tests:

Delivery When the fetus is mature,vaginal delivery is preferable unless there is evidence of fetal distress or hemodynamic instability. When the fetus is not mature and placental abruption is limited,observation with close monitoring of both fetal and maternal status.

Physiological Changes during Pregnancy:

Disseminated Intravascular Coagulation DIC is a clinicopathologic syndrome characterized by widespread intravascular fibrin formation in response to excessive blood protease activity that overcomes the natural anticoagulant mechanisms

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Common Clinical Causes of Disseminated Intravascular Coagulation Sepsis   Bacterial    Staphylococci, streptococci, pneumococci, meningococci, gram-negative bacilli    Viral   Mycotic    Parasitic    Rickettsial Trauma and tissue injury   Brain injury (gunshot),   Extensive burns  , Fat embolism  , Rhabdomyolysis


Vascular disorders   Giant hemangiomas (Kasabach-Merrit syndrome)    Large vessel aneurysms (e.g., aorta) Obstetric complications   Abruptio placentae   Amniotic fluid embolism    Dead fetus syndrome   Septic abortion Cancer   Adenocarcinoma (prostate, pancreas, etc)    Hematologic malignancies (acute promyelocytic leukemia


Immunologic disorders   Acute hemolytic transfusion reaction   Organ or tissue transplant rejection   Graft-versus-host disease Liver disease   Fulminant hepatic failure    Cirrhosis    Fatty liver of pregnancy Envenomation   Snake    Insects

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Drugs   Fibrinolytic agents    Aprotinin    Warfarin (especially in neonates with protein C deficiency)    Prothrombin complex concentrates    Recreational drugs (amphetamines) Miscellaneous   Shock    Respiratory distress syndrome   Massive transfusion

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The Mechanism of Disseminated Intravascular Coagulation

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A normal blood smear Black arrow = PLT Blue arrow =lymphocyte. Red cells uniform size & shape. Central pallor of red cell equals about 1/3 of diameter.

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Microangiopathic smear Small black arrows = “helmet cells,” Large black arrows = other fragmented red cells, Blue arrows =microspherocytes. Low platelets: red arrow points to a large platelet resulting from destruction.

Disseminated Intravascular Coagulation:


Common Clinical Causes of Disseminated Intravascular Coagulation:

Characteristics of common liver diseases in pregnancy Pre-eclampsia and eclampsia Trimester-2nd or 3rd Incidence-5% to 10% Signs and symptoms Nausea; vomiting epigastric pain edema ,hypertension; mental status changes,jaundice (late presentation )

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Laboratory findings ALT <500 U/L ,proteinuria ,DIC (7%) Complications Maternal: Hypertensive crisis; renal impairment; hepatic rupture/infarct; neurological (seizures, cerebrovascular disease) Fetal: Abruptio placentae; prematurity;IUGR leading to increased perinatal morbidity and mortality

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HELLP syndrome Trimester-3 rd Incidence -0.10% (4% to 12%of women with pre-eclampsia Signs and symptoms Symptoms of pre-eclampsia (hypertension, headache blurred vision); epigastric or right upper quadrant pain; nausea; vomiting hematuria; jaundice (late presentation)

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Laboratory findings Hemolysis, ALT <500 U/L,platelets <100×109/L ,elevated LDH, DIC (20%–40%) Complications Maternal: Seizures; acute renal failure , hepatic rupture, hematoma or infarct, increased mortality (1% to 3%) Fetal: Abruptio placentae, increased mortality (35%)

The Mechanism of Disseminated Intravascular Coagulation:

Acute fatty liver of pregnancy Trimester-3 rd (can occur during 2nd) Incidence - 0.01% Signs and symptoms Malaise; upper abdominal pain; nausea; vomiting, jaundice (very common) encephalopathy(late presentation) Laboratory findings ALT <500 U/L; hyperbilirubinemia; hypoglycemia; elevated ammonia; leukocytosis ,DIC (>75%) thrombocytopenia, prolonged PT,hypofibrinogenemia

A normal blood smear:

Complications Maternal: Acute renal failure; encephalopathy; ascites; sepsis; wound seroma; pancreatitis, increased mortality Fetal: Increased mortality (13% to 18%) from asphyxia; prematurity; IUGR; LCHAD deficiency and its complications

Microangiopathic smear:

Intrahepatic cholestasis of pregnancy Trimester-2nd or 3 rd Incidence - 0.1% to 0.2% Signs and symptoms Intense pruritus; jaundice (20% to 60%, 1 to 4 weeks after pruritus); steatorrhea Laboratory findings ALT <500 U/L; markedly elevated ALP and GGT increased bile acids bilirubin (<103 μ mol/L)


Complications Maternal: Predisposed to cholestasis on subsequent pregnancies Fetal: Still birth; prematurity; fetal mortality (3.5%)

Characteristics of common liver diseases in pregnancy:

Drug-induced hepatitis Trimester-Any Incidence - Unknown Signs and symptoms Usually none; nausea vomiting; pruritis; jaundice (in cholestatic hepatitis) Laboratory findings Variable Complications Unknown

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Viral hepatitis Trimester-Any Incidence - Same as general population Signs and symptoms Nausea; vomiting fever Laboratory findings ALT greatly elevated (>500 U/L); elevated bilirubin; positive serology tests Complications Maternal: Increased mortality with hepatitis E

HELLP syndrome:

The Mechanism of Disseminated Intravascular Coagulation

Acute fatty liver of pregnancy:

The central mechanism of DIC is the uncontrolled generation of thrombin by exposure of the blood to pathologic levels of tissue factor Suppression of physiologic anticoagulant mechanisms and abnormal fibrinolysis further accelerate the process. systemic fibrin deposition in small and mid-sized vessels. The duration and intensity of the fibrin deposition can compromise the blood supply of many organs, especially the lung, kidney, liver, and brain, with consequent organ failure.

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The sustained activation of coagulation results in consumption of clotting factors and platelets Leads to systemic bleeding Aggravated by secondary hyperfibrinolysis. Fibrinolytic system is suppressed at the time of maximal activation of coagulation. In APL, a severe hyperfibrinolytic state often occurs in addition to the coagulation activation. Release of proinflammatory cytokines interleukin 6 and tumor necrosis factor play central roles in mediating the coagulation defects in DIC and symptoms associated with systemic inflammatory response syndrome

Intrahepatic cholestasis of pregnancy:

The form of DIC depends on the rapidity and force of the initiating event, leading to the two primary forms of DIC: Acute decompensated DIC Chronic compensated DIC. If activation occurs slowly, the coagulants that are produced dominate, and thrombosis is the primary complication. In this case, the liver is able to compensate for the factors that are consumed. This is the chronic form.

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Clinical manifestations of DIC Bleeding ranging from oozing from venipuncture sites, petechiae, and ecchymoses to severe hemorrhage from the gastrointestinal tract or lung or into the central nervous system. In chronic DIC the bleeding symptoms are discreet and restricted to skin or mucosal surfaces. The hypercoagulability of DIC manifests as the occlusion of vessels in the microcirculation and resulting organ failure.

Drug-induced hepatitis:

Thrombosis of large vessels and cerebral embolism can also occur. Hemodynamic complications and shock are common among patients with acute DIC. The mortality ranges from 30 to >80% depending on the underlying disease, the severity of the DIC, and the age of the patient

Viral hepatitis:

Laboratory abnormalities in DIC Prolongation of PT and/or aPTT; Platelet counts 100,000/mm 3 , or a rapid decline in platelet numbers Presence of schistocytes (fragmented red cells) in the blood smear Elevated levels of FDP. The most sensitive test for DIC is the FDP level. DIC is an unlikely diagnosis in the presence of normal levels of FDP.

The Mechanism of Disseminated Intravascular Coagulation:

The D-dimer test is more specific for detection of fibrin (but not fibrinogen) degradation products and indicates that the cross-linked fibrin has been digested by plasmin. Fibrinogen has a prolonged half-life, plasma levels diminish acutely only in severe cases of DIC. High-grade DIC is also associated with levels of antithrombin III or plasminogen activity <60% of normal

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Treatment The morbidity and mortality associated with DIC are primarily related to the underlying disease The control or elimination of the underlying cause should therefore be the primary concern. Patients with severe DIC require control of hemodynamic parameters, respiratory support, and sometimes invasive surgical procedures. Attempts to treat DIC without accompanying treatment of the causative disease are likely to fail

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Management of Hemorrhagic Symptoms The control of bleeding in DIC patients with marked thrombocytopenia (platelet counts <10,000–20,000/mm 3 ) and low levels of coagulation factors will require replacement therapy. The PT (>1.5 x normal) provides a good indicator of the severity of the clotting factor consumption. Replacement with FFP is indicated (1 unit of FFP increases most coagulation factors by 3% in an adult without DIC).

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Low levels of fibrinogen (<100 mg/dL) or brisk hyperfibrinolysis will require infusion of cryoprecipitate (plasma fraction enriched for fibrinogen, FVIII, and vWF). The replacement of 10 U of cryoprecipitate for every 2–3 U of FFP is sufficient to correct the hemostasis. The transfusion scheme must be adjusted according to the patient's clinical and laboratory evolution. Platelet concentrates at a dose of 1–2 U/10 kg body weight are sufficient for most DIC patients with severe thrombocytopenia.

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Clotting factor concentrates are not recommended for control of bleeding in DIC Only limited efficacy afforded by replacement of single factors (factor VIII or IX concentrates) High risk of products containing traces of activated blood proteases (PCCs)-> further aggravates the disease.

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Replacement of Coagulation or Fibrinolysis Inhibitors Drugs to control coagulation heparin, antithrombin III (ATIII) concentrates, or antifibrinolytic drugs have been tried in DIC. Low doses of continuous infusion heparin (5–10 U/kg per h) in patients with low-grade DIC associated with solid tumor or APL or in a setting with recognized thrombosis. Heparin for the treatment of purpura fulminans, during the surgical resection of giant hemangiomas, and during removal of a dead fetus. In acute DIC, the use of heparin is likely to aggravate bleeding. Use of heparin in severe DIC patients is of no proven survival benefit.

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The use of antifibrinolytic drugs, EACA, or tranexamic acid to prevent fibrin degradation by plasmin may reduce bleeding episodes in patients with DIC Drugs can increase the risk of thrombosis, and concomitant use of heparin is indicated. Patients with APL or those with chronic DIC associated with giant hemangiomas may benefit from this therapy.

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The use of protein C concentrates to treat purpura fulminans associated with acquired protein C deficiency or meningococcemia has been proved effective. The results from the replacement of ATIII in early phase studies are promising but require further study

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