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082014100018
• DEEP VEINS THROMBOSIS
• PULMONARY EMBOLISM
DEEP VEINS THROMBOSIS
RISK FACTORS FOR THROMBOEMBOLISM IN
PREGNANCY
SPECIFIC TO PREGNANCY NON SPECIFIC TO
PREGNANCY CLINICAL FEATURES
1. Duplex ultrasonography/compression
ultrasonography
2. Magnetic resonance venography
3. Ascending contrast venography
4. D- dimer
MANAGEMENT
Bed rest
Therapeutic anticoagulation
Ambulate once symptom better
Elastic compression stockings
PULMONARY EMBOLISM
CLINICAL FEATURES
DIAGNOSIS
Unexplained tachycardia NON SPECIFIC TESTS
Dyspnea -chest x ray
Hypoxemia -ECG
Pleuritic pain -Arterial blood gases
Hemoptysis -ECHO
Sudden severe hypotension
SPECIFIC TESTS
-Ventilation-perfusion test
MANAGEMENT -CT pulmonary angiography
-Magnetic resonance pulmonary
Therapeutic angiography
anticoagulation -Pulmonary angiography
Venacaval filters
Thrombolytic therapy EVALUATION OF LOWER LIMBS FOR DVT
with t-PA -Duplex/compression ultrasonography
ANTICOAGULATION IN PREGNANCY
a) May be prophylactic , to prevent
thromboembolism in high risk women
b) Therapeutic for DVT and PE treatment
THERAPEUTIC USE OF LMW HEPARIN
INDICATIONS DRUG OF CHOICE
Established DVT or PE
Better bioavailability
Longer plasma half life
Predictable dose response
No lab More reduction in thrombus
monitoring size
Lower risk in major bleeding
Must be Lower recurrence
swithed to thromboembolism
Low risk of osteoporosis and
UFH at 36 wks
thrombocytopenia
Less frequent dosing
THERAPEUTIC USE UNFRACTIONED
HEPARIN
INDICATIONS
Immediate treatment of PE • Initially admisnisted
When delivery or/c section as IV
anticipated
After 36wks in all women with • Switch to SC
therapeutic LMW Heparin 12hourly after 7 to
10 days
UFH
70-100 units/kg IV Bolus
(5000-10000units)
15-20 units/kg Infusion
(1000units)/hour
Followed 7-10days later SC
By 10000 units 12 hourly
Acute Fatty Liver of Pregnancy
Intrahepatic Cholestasis
Viral Hepatitis
Gallstones
Constipation
Diarrhea
Hemorrhoids
GERD
Appendicitis
Acute Fatty Liver of Pregnancy
Rare complication of An excessive fetal fatty acid
pregnancy but can lead to accumulation released into
fulminant hepatic failure. maternal circulation
Often develops in second half
of pregnancy, closer to term.
May only be diagnosed after
delivery.
Increased load of long-chain fatty
Associated with autosomal acids in maternal liver tissue
recessive genetic error :
Maternal genetic mutation
Fetal LCHAD deficiency
(Long-chain 3-hydroxyacyl-
coenzyme A Impaired hepatic function
dehydrogenase)
SYMPTOMS RISK FACTORS
MANAGEMENT
1. Symptomatic treatment of the patient
Serum aminotransferase
Elevated > 1000-2000 U/L MANAGEMENT IN
ALT > AST PREGNANCY :
Serum total and direct bilirubin
Peak after elevation in ALT and AST Usually self limited.
Usually elevated > 10mg/dL Rest and balanced diet.
Serology : Avoid handling food for
Serum IgM for anti-hepatitis A virus (HAV) is the other family members.
gold standard for detection of acute illness Breastfeeding
Remains positive for 4-6 permissible with hygienic
months precautions.
Patients with fulminant
COURSE IN PREGNANCY : infectionequires :
• More severe with increasing gestational -Aggressive support
age. therapy
• Pregnancy complications :
-Transferred to a tertiary
• Preterm labor
• Placental abruption
care center
• PROM
• Perinatal transmission for the virus does
not occur!
POSTEXPOSURE PROPHYLAXIS
• Woman with close personal contact with someone
known to
• have acute hepatitis A infection should receive :
• Single 0.02 mL/kg IM dose of immunoglobin
• Should be given within 2 weeks exposure
• Provides protection for up to 3 months
• 80%-90% effective
Diagnosis of HBV is
made with detection of :
HBsAG
IgM antibodies to
HBcAG
Transmission to husband :
Her husband should be tested for HBsAG
If negative, he should receive the rapid immunization course with
hepatitis B vaccine (0,1, and 2 months)
Until vaccination completed, they should be advised to use
condom.
Effects on pregnancy :
Usually not severe.
Not associated with increased mortality or teratogenicity.
No indication for termination of pregnancy.
There is an increased risk of low birth weight and preterm birth.
MANAGEMENT :
MANAGEMENT :
Oral rehydration
Correction of potential electrolyte
abnormalities
Bananas and orange juice
Antidiarrheals
Loperamide is safe
Specific treatment for specific causes
HEMORRHOIDS
Varicosities in anal canal caused by pressure
from gravid uterus.
Common in 3rd trimester and immediately postpartum
(pushing
• effort during delivery).
Symptoms :
Pruritus, pain and bleeding, bulge at anal verge.
Management :
Relief of symptoms
Recurrent and severe hemorrhoids
Hemorrhoidectomy
GERD
Common, worsen from 1st to 3rd trimester
and disappear after delivery.
Tends to recur in subsequent pregnancy.
MANAGEMENT :
PATHOGENESIS :
• Lifestyle modifications
Intrinsic factors • Medications
Abnormal esophageal motility •Antacids
• Decreased LES pressure
Increased gastric pressure •Sucralfate
Mechanical factors •H2 blockers
Enlarged gravid uterus •PPI
• Increased intraabdominal
pressure
• Displacement of LES
APPENDICITIS
Commonest non-obstetric PHYSICAL SIGNS :
cause of acute abdomen in • Abdominal pain
•1st trimester : Right lower
• pregnancy. quadrant
Diagnosis may be delayed •2nd trimester : Umbilicus
because : •3rd trimester : Diffuse of right
upper
1. Many of the symptoms quadrant
considered to be due to • Nausea, vomiting and anorexia
pregnancy.
2. Displacement of colon by
enlarged uterus causing TREATMENT :
Appendicectomy
appendix changes
location.
REFERENCES
• Essentials of Obstetrics, Lakshmi Seshadri
& Gita Arjun