Vascular problems in Gynecology and Obstetrics Dr. UMA GUPTA MD(OBG)FICMCH,Sr.Specialist,VPCIMS,LUCKNOW(UP)INDIA Dr.N.K.GUPTA, M.Ch,CTVS,Associate Prof,ERA’s LUCKNOW MEDICAL COLLEGE,LUCKNOW.INDIA
[email protected] [email protected]
08/01/09
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Vascular surgery evolution
The first elective operation for treatment of an aneurysm was reported by the most famous surgeon in Greek antiquity,ANTYLLUS, in the 2nd century.
AMBROSE PARE(1510-1590), mainly contributed – principles wound care-aneurysm operations.
After a century,RICHARD WISEMAN(16251686)”Father of English Surgery”described aneurysm in arm.
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contd
Sutures should be made with very fine needles while the wall is somewhat stretched.Stenosis or occlusion only occurs-faulty technique-which is still valid 100 years later. In 1910, he demonstrated that blood vessels could be kept in cold storage for long periods before transplanting them.
Carrel won the noble prize for this work in 1912 “in recognition of his work on vascular suture and 08/01/09 DrU.Gupta,Dr.N.K.Gupta
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Arterial Disorders
AntiPhospholipid Antibody Syndrome
Raynaud’s disease
Vasculitis
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Venous Disorders
Varicose Veins
Superficial Thrombophlebitis Deep Vein Thrombosis/ PE
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AntiPhospholipid Antibody Syndrome syn. Hughes Syndrome
Arterial and Venous thrombosis History
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First noted in pts positive for syphilis 1952- clotting disorder asso. with SLE 1957- linked to recurrent pregnancy loss 1963 & 1972 – term “Lupus anticoagulant” 1983 – Dr Graham Hughes – association between APL antibodies and arterial and venous thrombosis 1985 – ELISA test for detection of ACA DrU.Gupta,Dr.N.K.Gupta
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AntiPhospholipid Antibody Syndrome
Types:
PRIMARY
SECONDARY
Mechanism:
AUTOIMMUNE PHENOMENON ??? Tissue injury – Inflammation, Ischemia, trauma Classes Of Antibodies – a) Anticardiolipin Antibody (IgG,IgA,IgM) b) Lupus Anticoagulant c) Antibodies against specific molecules e.g.β-2-glycoprotein 08/01/09
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AntiPhospholipid Antibody Syndrome
Prevalence 2-4% 50% - Primary APLAS SLE – 30% will develop APLAS
ACA five times more common than Lupus Anticoagulant
Primary APLAS – 10% SLE, Mixed Conn. Tissue Ds 08/01/09
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AntiPhospholipid Antibody Syndrome
RISKS ASSOCIATED:
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MISCARRIAGES PRETERM LABOR PRE-ECLAMPSIA LOW BIRTH WEIGHT THROMBOCYTOPENIA (20-40%)
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AntiPhospholipid Antibody Syndrome
WHEN TO EVALUATE
08/01/09
Unexplained still birth/fetal death after 10 wks
Severe IUGR prior to term
Severe pre-eclampsia at <34 wks gestation
Unexplained arterial/venous thrombosis in any territory DrU.Gupta,Dr.N.K.Gupta
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AntiPhospholipid Antibody Syndrome
TREATMENT
Anticoagulation – Heparin → Oral
Long term → Life Long ( risks – 3% chance per year of major h’hage, 1/5th fatal)
Anti-platelet drugs – Aspirin LMWH Pregnancy – Heparin / LMWH
PROPHYLAXIS
08/01/09
(APLAS without thrombotic problems)
Aspirin Lifestyle Modification Control of Risk factors – HTN, Smoking, Cholesterol levels, Weight control DrU.Gupta,Dr.N.K.Gupta
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AntiPhospholipid Antibody Syndrome
Special Prenatal/Birth/Neonatal Considerations
Ideally, one should seek medical advice before becoming pregnant. Once pregnancy is achieved
to see Obstetrician - to decide on the need for treatment frequent office visits will be needed to:
Screen for preeclampsia, Fetal Monitoring Ultrasound examinations to check the growth of the baby.
For patients on heparin
extra blood tests may be needed to adjust the dose depending on the type of heparin being used, and the past history of the patient.
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AntiPhospholipid Antibody Syndrome
PREGNANCY:
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Pre Pregnancy Counselling Heparin (s/c)± Low Dose Aspirin LMWH Aspirin ± Prednisone X X X X Low Dose Aspirin Intravenous Immune Globulin (IVIG) Immunosupression Steroids Catastrophic Plasmapheresis DrU.Gupta,Dr.N.K.Gupta
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Raynaud’s disease 1862 – Maurice Raynaud Prevalence – 3-5% Episodic events – vasoconstriction (digital arteries, precapillary arterioles & cutaneous AV shunts) vs Acrocyanosis Exaggeration of the physiologic response to cold temperature or stress. Manifestation of generalised vasospastic disorder.e.g.pts who have Prinzemetal’s angina, migraines, or scleroderma.
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Raynaud’s disease
H/o sensitivity to cold/ episodic pallor or cyanosis Triphasic reaction (white>blue>red) Involves- fingers, toes, tip of the nose, ear lobes. PRIMARY*
SECONDARY
SYMMETRIC
ASYMMETRIC
ABSENCE OF
PAINFUL ISCHAEMIC SKIN LESIONS
-TISSUE NECROSIS
-GANGRENE
C/f s.o. CONN. TISSUE DISORDERS (arthritis,myalgia,
-SECONDARY CAUSE
abnormal lung fn,fever etc)
-ULCERATION
H/o drug use/toxic agent NORMAL NAIL FOLD CAPILLARIES MICROVASCULAR DS NORMAL ESR 08/01/09 NEGATIVE
ESR ↑
ANA TEST DrU.Gupta,Dr.N.K.GuptaANA ±
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*Adapted from LeRoy and Medsger
Raynaud’s disease
Complete evaluation – to R/o underlying cause
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H/o or current drug use H/o repetitive trauma e.g.vibratory tools Positional changes triggering the event. e.g.Tho Outl Obst. Carpel tunnel syndrome Neurapathic conditions Malignancy Hypothyroidism Dysproteinemias Vasculitis Emboli Vascular Occlusive disease
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Raynaud’s disease
Treatment
NonPharmacological
Calcium channel Blockers Other Agents
Sympatholytic drugs ARBs Fluoxetine I.V. Prostaglandins
Awaited
Avoidance of cold temp / prolong vibrations Reduce emotional stress Avoid Smoking
Cilostazole Sildenafil Bosentan (endothelin receptor inhibitor)
Sympathectomy
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Proximal ??? Localised Digital DrU.Gupta,Dr.N.K.Gupta √√
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Vasculitis
AutoImmune Disease
Inflammation of the blood vessels
Symptoms – depend on which blood vessels are inflamed
08/01/09
Fatigue Sleep disturbances Memory Loss Emotional Liability Depression Low Thyroid Function G I disturbances Headaches/Chemical Sensitivity Fungal Infections Low Blood Sugar Pain – Tingling/Ringing ears/Cold Toes/Cold Fingers Overdoing Fluttering Heart/Tachycardia/Panic Attacks/Mitral valve Prolapse DrU.Gupta,Dr.N.K.Gupta
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Vasculitis
IMMUNE SYSTEM MALFUNCTION
CONSUMPTION OF ASPARTATE (IN DIET DRINKS/ARTIFICIAL SWEETNERS etc.) CHLORINATED AND FLORIDATED WATER ???
POOR CELLULAR COMMUNICATION
HEAVY MOL WT CARBOHYDRATES (LONG CHAINED)
OVER ACTIVATED, OUT OF BALANCE IMMUNE SYSTEM
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PROVIDE INGREDIENTS FOR CELL MARKERS HIGHLY ANTI-INFLAMMATORY CODING CAPACITY BETTER THAN AMINO ACIDS *
Stress Infections – Bacterial , Fungal (Candida), Viral (e.g.Herpes) Toxins – produced by infecting organism, from environment Liver dysfunction Steroids Enzyme deficiency – Digestive/Metabolic Hypercoagulation/ HypoOxygenation Glutathione Deficiency DrU.Gupta,Dr.N.K.Gupta
*Acta Anatomica
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Vasculitis
Management
Weighing the available options Steroids Chemotherapeutic Agents
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Antioxidants/ Digestive Enzymes Treat underlying disorder Lifestyle modification
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Venous Disorders
Varicose Veins
Superficial Thrombophlebitis Deep Vein Thrombosis/ PE
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Varicose Veins
08/01/09
Pregnancy
Increased blood volume
Pressure on veins
Relaxation effect of hormones
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Varicose Veins
Management
Non Operative
Self resolving (within six weeks)
After 6 weeks
if problematic/ unacceptable
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Graduated Compression Stockings Surgery DrU.Gupta,Dr.N.K.Gupta
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Varicose Veins
Before Treatment 08/01/09
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After Treatment 26
Varicose Veins
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Superficial Thrombophlebitis Benign /Self limiting Disease Can progress to DVT(11%) Associated with Abnormalities in blood coagulation
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Superficial Thrombophlebitis
Traumatic Varicose Veins Oral contraceptives Pregnancy Infection (e.g. Staph., Pseud., Kleb., Anaerobes) Migratory (e.g. Cancer, Vasculitis, Buerger’s) Mondor’s Disease Unusual forms
palmar digital veins
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Superficial Thrombophlebitis
Diagnosis
Painful cord like structure Redness along the vein Tenderness Fever
Investigations
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Duplex scan
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Superficial Thrombophlebitis
Management
08/01/09
Underlying disorder Remove offending agents (e.g.IV cannula) Antibiotics NSAIDs Anticoagulation Excision of the suppurating vein Application of massive warm wet compresses Elevation of the extremity Immobilization DrU.Gupta,Dr.N.K.Gupta
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
LEADING CAUSE OF DEATH
1-3 /1000 PREGNANCIES
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Pathophysiology
5 times higher in pregnancy ↑ venous stasis of pregnancy Physiological changes asso. with pregnancy
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Pathophysiology
Independent risk factors Prolong Bed rest Multiparity (>3) Advanced Maternal Age (>35yrs) Overweight Personal or family history of VTE Pre-eclampsia
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Pathophysiology
Alteration in Coagulation/Fibrinolytic System Factor II, VII, X ↑ (middle of Pregnancy) Fibrin Protein S Protein C Fibrinolytic System inhibited (mostly 3rd trimester)
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Diagnosis
Calf veins or Ilio-femoral segment Predilection for Left side
S/s
Swelling Tenderness Skin Discolouration Warm to touch Unusual firmness /hardness in the leg Calf discomfort on dorsiflexion Prominent tender cord like subcut. vein DrU.Gupta,Dr.N.K.Gupta
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Diagnostic tests
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Venography
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Diagnostic tests
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Duplex Ultrasonography
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Diagnostic tests
Spiral CT Venography
No filling of calf veins 08/01/09
Opacification of collaterals
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Diagnostic tests
08/01/09
Nuclear Imaging IPG MRI D-dimer
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Radiation Exposure
Procedure CXR Limited Venography Perfusion Lung Scan Ventilation Lung Scan CT Chest Pulm Angio (femoral) Pulm Angio (brachial) 08/01/09
Fetal radiation dose (mrads) <1 <50 6-12 1-19 30 221-374 <50 DrU.Gupta,Dr.N.K.Gupta
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VENOUS THROMBOEMBOLISM DURING PREGNANCY Blood Tests
08/01/09
Factor V Leiden Protein C Protein S ACA and LA antibodies Activated Protein C resistance (APC-R) AntiThrombin III Homocystein Prothrombin gene mutation DrU.Gupta,Dr.N.K.Gupta
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Pulmonary Embolism
Major nonobstetric cause of maternal mortality Cause of Death
08/01/09
2 / 100,000 maternities
Maximum – Peripartum More after operative intervention Subtle presentation
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Pulmonary Embolism
Diagnostic tests
Pulmonary Angiography
Spiral CT Scan
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Pulmonary Embolism Diagnostic tests Nuclear Imaging
08/01/09
(Ventilation-Perfusion Scan)
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VENOUS THROMBOEMBOLISM DURING PREGNANCY Management
Medical/Pharmacological
Surgical
IVC Filter placement
Others
08/01/09
Venous Thrombectomy Thrombolysis
Endovascular
Anticoagulation Anti-platelet agents
Hydration Early Mobilization Graduated Compression Stockings Pneumatic compression devices DrU.Gupta,Dr.N.K.Gupta
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Medical/Pharmacological
Unfractionated Heparin/LMWH
Oral Anticoagulation
Antiplatelet agents
New Molecules
Direct Thrombin Inhibitors
08/01/09
Lepirudin, Desirudin, Argatroban, Ximelagatran DrU.Gupta,Dr.N.K.Gupta
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Surgical
Venous Thrombectomy –
08/01/09
Ilio-femoral DVT
Pulmonary Embolectomy
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Surgical
08/01/09
Thrombolysis
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Endovascular
08/01/09
IVC Filter placement
Temporary
Permanent
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Others
Hydration Early
Mobilization Graduated Compression Stockings Pneumatic compression devices
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
PROPHYLAXIS
Risk Assessment
Present status
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
PROPHYLAXIS
Past h/o DVT in pregnancy, no other thrombotic risk factors
Antenatal thrombo-prophylaxis
S/c Heparin+/- GCS
S/c Heparin/LMWH → Warfarin (INR 2-2.5) GCS 6-12 wks (if anticoagulation contraindicated)
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BMJ 1992 53
VENOUS THROMBOEMBOLISM DURING PREGNANCY
PROPHYLAXIS
Known inherited/acquired thrombophilia
Postpartum +/- Antepartum thromboprophylaxis Individual consideration
No past h/o DVT/Thrombophilia, but with other risk factors in combination
Postpartum thromboprophylaxis
08/01/09
S/c Heparin
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BMJ 1992 54
VENOUS THROMBOEMBOLISM DURING PREGNANCY
PROPHYLAXIS IN CAESERIAN SECTION
Low Risk
Moderate Risk
Elective C-section – uncomplicated pregnancy No risk factors Age, Weight, Parity, Varicose Veins, Immobility, Sepsis, Pre-eclampsia, Emergency C-section, Major Current Illness
High Risk
08/01/09
3 or more mod risk factors, Extended major pelvic/abd surgery e.g.Caeserian hysterectomy Personal/family H/o DVT/PE/thrombophilia, Paraparesis DrU.Gupta,Dr.N.K.Gupta 55 Pt with APLAS
VENOUS THROMBOEMBOLISM DURING PREGNANCY
PROPHYLAXIS IN CAESERIAN SECTION
Low Risk Early Mobilization Hydration
Moderate Risk
One of variety of prophylactic measures
Subcutaneous Heparin Mechanical devices
High Risk
Heparin Prophylaxis +/- Leg Stockings
Report08/01/09 of the RCOG Working Party on prophylaxis (andDrU.Gupta,Dr.N.K.Gupta management) against Thromboembolism in Gynaecology and Obstetrics. 56 London: Royal College of Obstetricians and Gynaecologists, 1995
VENOUS THROMBOEMBOLISM DURING PREGNANCY
Key Points
Even 1st trimester carries risk of thrombosis (2/3rd antepartum deaths) Additional risk factors/ family history / known thrombophilia may indicate thromboprophylaxis Close attention should be paid to any pregnant woman c/o leg/chest symptoms for e/o DVT/PE All women undergoing C-section should be assessed for prophylaxis against VTE Midwives, GPs & other medical staff should take particular attention of women with chest or leg symptoms after vaginal delivery Women with risk factors for DVT should be carefully screened and considered for thromboprophylaxis
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VENOUS THROMBOEMBOLISM DURING PREGNANCY
Prevention:
Weight control Avoid prolong immobility Leg elevation Avoid OCPs containing high dose of Estrogens Adequate hydration Avoid Smoking/Alcohol intake
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VENOUS THROMBOEMBOLISM DURING PREGNANCY Take Home Message
08/01/09
VTE is an uncommon but very serious complication of pregnancy Pregnant women are at increased risk for VTE, and may present in subtle ways Suspected VTE in pregnancy should be investigated thoroughly Risk of VTE can be reduced in appropriate patients with judicious use of anticoagulants DrU.Gupta,Dr.N.K.Gupta
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Vascular Control in Gynaecological Surgery
MODALITIES AVAILABLE
Open Vascular
Endovascular
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Vascular Control in Gynaecological Surgery
OPEN VASCULAR
08/01/09
Uterine artery Ligation Ovarian Artery ligation Internal Iliac Artery Ligation Common Iliac artery control Control over Aorta
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Vascular Control in Gynaecological Surgery
ENDOVASCULAR
Balloon Occlusion Stent Graft Embolisation –
08/01/09
Coil Foam particles etc.
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08/01/09
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