MRCOG FACTS

Doctor Patient Relationship

2011-11-10T15:40:00.000Z

Two simple models on doctor patient relationship.One is doctor as an expert adviser and the other is doctor in partnership.

Doctor as an expert adviser

Docotor defines the patient's needs
Doctor advises the patient what to do
Doctor solves problems for the patient
Doctor decide how much information to be given to the patient

Doctor in partnership

Doctor elicit the patient's problems & needs
Doctor explains the options to the patient
Doctor and the patient explore the solutions to gether
Doctor ask what information the patient wants

What is your style ?

Emanuel and Emanuel ( JAMA. 1992 Apr 22-29;267(16):2221-6.) elaborated four models of doctor patient relationships:

Paternalistic: physician makes decisions for the patient’s benefit independent of the patients values or desires
Informative: physician provides information, patient applies values and decides.
Interpretive: patient is uncertain about values, physician, as counselor, assists the patient in elucidating his or her values.
Deliberative: Patient is open to development, physician teaches desirable values

Interestingly another article,Physician-Patient Relations: No More Models, argues that one model doesn't fit all.Based on my experience,I agree with this article.What do you think?

Induction of labour

2011-10-31T10:04:00.001Z

Induction of labour

View more presentations from Ravimohan Ravimohan

Postpartum thyroiditis

2011-07-01T11:54:00.001+01:00

Definition:
(i)It is an autoimmune disorder

(ii)It is chracterised by lymphocyte infiltrate of thyroid gland

(iii)There is transient hyperthyroidism followed by hypothyroidism or one or other

(iv)It occurs in the first year of delivery.

The condition is more common on patients with family history of hypothyroidism, those with thyroid peroxidase antibodies and patients with type 1 DM.

3 phases of classical postpartum thyroiditis

(i)hyperthyroidism

(ii)hypothyroidism

(iii)recovery

1/3 of patients develop permanent hypothyroidism

Clinical features

presentation is usually between 3 to 4 months after delivery

(I)classical features of hyper or hypothyroidism is rarely observed
hyperthyroidism(palpitations,fatigue)
hypothyroidism(lethargy,depression)

(II)painless enlargement of the gland

(III)depression

Investigations

(I)thyroid function tests

(II)thyroid peroxidase antibodies.

(III) radioactive iodine uptake test may be necessary to differentiate from Graves' disease but this test can't be done in breast feeding mothers.

(*Thyroid receptor antibodies are present in Graves' disease)

Management

Most patients recover spontaneously.
Treatment should be determined by symptoms rather than biochemistry.

hyperthyroid phase needs treatment beta blockers but not with antithyroid drugs.

hypothyroidism needs with treatment thyroxine. Only 3-4 % of women remain permanently hypothyroid.

References

(i)Post-partum thyroiditis – a clinical updateElio Roti and Ettore degli Uberti.European Journal of Endocrinology (2002) 146 275–279
(ii)Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

(iii)Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

Uterine rupture

2011-03-06T21:08:00.000Z

2 types
(I) Uterine dehisence-separation of a preexisting scar without the disruption of parietal peritoneum.
(II)uterine rupture-full thickness disruption of uterine wall.

Risk factors

(I)previous caesarean section(Classical &Lower segment)
(II)Previous uterine surgery-myomectomy
(III)Grand multi parity
(IV)oxytocin
(V)prostaglandins

Clinical features

Uterine dehisence could be asymptomatic
(I)continuous lower abdominal pain
(II)fetal distress
(III)receding presenting part in labour
(IV)loss of uterine contractility during labour
(V) Haematuria/Bleeding per vaginum
(VI)Maternal tachycardia & hypo tension are late signs

Stair case sign-stepwise gradual decrease in contraction amplitude has been reported in uterine rupture.

Treatment

This is an Obstetrics emergency

resuscitation & surgery should go hand in hand.
call for Senior help(Obstetrician & Anaesthetist)
IV access
Arrange Cross matching of Blood(6-10 units)
Allocate one person to scribe the events
Keep the family informed during the procedure
Debrief at the end of procedure

If uterine rupture occurs prior to delivery emergency caesarean section should be done.
The following options can be selected according type of tear,state of the patient and ongoing blood loss.
(I)uterine repair
(II)Hysterectomy
(III)Internal artery ligation

Powerpoint on uterine rupture
References
(I)E Medicine
(II)Successful management of gravid uterine rupture.Taiwan J Obstet Gynecol. 2009 Sep;48(3):319-20.Authors: Fu PT Chen CH Wu GJ Yu MH.PMID: 19797032 [PubMed - indexed for MEDLINE]
(III)Spontaneous uterine rupture-Case report and review

Mnemonic for Chronic pelvic pain

2011-02-22T10:38:00.001Z

I found this very useful mnemonic in a book called Practical Gynecology -A Guide for the primary physician(Amazon Link)

OLD CAARTS

O-Onset When & How the pain started?
L-Location
D-Duration

C-Characteristic -colicky/stabbing/burning
A-Alleviating/Aggravating factors
A-Associated symptoms Gynacologic-Dyspareunia,dysmenorrhagia,vaginal discharge GI-constipation/diarrhoea/Rectal bleeding GU-frequency/dysuria/urgency/incontinence

R-radaition
T-Temporal what is the relationship to (i)time the day (ii)menstrual cycle
S-severity Sclae of 0-10

International criteria for painful bladder syndrome

(i) Urinary urgency,frequency,nocturia,and suprapubic or pelvic pain.
(ii)Final diagnosis for interstitial cystitis : with cystoscopic hydrodistension visualise
(i)Mucosal ulcers(Hunner's patch)
(ii)Glomerulations(small mucosal haemorrhages)
(iii) Urine cultures negative and no signs of malignancy

Rome III Criteria for Diagnosis of irritable Bowel syndrome

Recurrent abdominal pain for or discomfort for more than or equal to 3 days /month for the past 3 months associated with two or more of the following.

(i)Improvement with defecation and/or

(ii)Onset associated with a change in frequency of stool and /or

(iii) Onset associated with a change in form (appearnce) of stool

PDF source

Obgyn Twitter News paper

2011-01-29T22:47:00.000Z

Management of tubal ectopic pregnancy

2011-01-16T15:35:00.001Z

Check out this SlideShare Presentation:

Management of tubal ectopic pregnancy

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Peripartum cardiomyopathy

2011-01-03T13:11:00.000Z

Definition:

(1)development of heart failure in the last month of pregnancy within 5 months after delivery
(2)absence of a known cause
(3) without any heart disease prior to the last month of pregnancy
(4) documented systolic dysfunction

Risk factors
Advanced maternal age
Multiparity
PIH
Multiple pregnancy
Afro-Caribbean race

Symptoms

fatigue
Dyspnoea/paroxysmal nocturnal dysponea
palpitations
pulmonary oedema/peripheral oedema
features of peripheral/cerebral embolism

Signs

elevated JVP
Cardiomegaly
third heart sound

Mitral/Tricuspid regurgitation

crepitations
hepatomegaly
Ascites

Systemic embolism occurs in 25-40% of patients with cardiomyopathy.
Investigation-Diagnostic criteria

Left ventricular ejection fraction <45%>

Left ventricular end diastolic pressure (LVEDP) >2.7cm/m2

Fractional shortening <30%>Chest Xray-Cardiomegaly/Pleural effusion/patchy lower lung infiltrates vascular redistribution

ECG- may helpful in excluding other causes

Endomyocardial biopsy done some times.

Invasive haemodynamic monitoring is considered if there is not a good response to medical treatment.

Newyork heart association classification can be used
I- asymptomatic
II-mild symptoms or symptoms only with extreme exertion
III-Symptoms on minimal exertion
IV- symptoms at rest Management

conventional treatment for heart failure is generally used.

Diuretics
vasodilators(hydralazine &/ nitrates)
cardio selective beta blockers(bisoprolol) or beta blockers with vasodilating action (carvedilol)

digoxin
ionotropes
ACEI-after delivery

salt restriction is recommended

Thromboprophylaxis

Elective delivery if antenatal.If cervix is favourable vaginal delivery is preferable,otherwise caesarean section may be chosen.Skilled epidural anaesthesia is useful for both routes of delivery.

Immunosuppressive therapy if myocarditis confirmed by endometrial biopsy.

Temporary support can be given by intraaortic balloon pumps & left ventricular assist devices.

Cardiac transplantation is indicated if intractable heart failure persists optimal medical therapy

Postpartum
Breast feeding isn't contraindicated.

Prognosis

Outcome of peripartum cardiomyopathy is variable.
Some patients recover rapidly but others may deteriorate to state requiring cardiac transplantation.
50% of patients make full recovery.
Echocardiography is repeated every six months to assess the recovery.
Prognosis depend on recovery of left ventricular size & function within 6 months.

Persistence of cardiac dysfunction beyond 6 months an indication of irreversible damage and such should be advised against pregnancy

Stress echocardiogram using dobutamine can be used to assess the contractile reserve.This would help in pre pregnancy counseling.Recurrence rate has been upto 50%

4.In future pregnancy women should have regular echocardiography

Sources

1.	Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

2	Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

3.E-medicine

4.	Peripartum Cardiomyopathy [Internet]. 2001 May 24 [cited 2009 Dec 12];Available from: http://content.nejm.org/cgi/content/extract/344/21/1629

free icons from

Sicke cell anaemia in pregnancy

2010-05-18T14:10:00.004+01:00

Genetics
Autosomal disorder
Single point mutation in β-Globin chain in haemoglobin.

Diagram explaining the inheritance

Types of sickling conditions

(i)Homozygous sickle-cell disease(HbSS)
(ii)Sickle cell/HbC(HbSC)
(iii)Sickle cell /Thalassaemia

Clinical features
Common features
(i)Anaemia due to chronic haemolysis- This is not so marked in HbSC
(ii)Vaso-occlusive crisis
(iii)Aplastic crisis

Other features
(i)leg ulcers
(ii)gall stones
(iii)acute chest syndrome-pleuritic chest pain,tachypnoea,fever

Sickling crisis in sickle cell trait patients is precipitated by severe anoxia,dehydration or acidosis.

Diagnosis

Diagnosis is made by haemoglobin electrophoresis.

Effect of pregnancy on disease

(i) sickle cell crisis is more common on pregnancy

Effect of disease on pregnancy
(i)fertility is generally unaffected.
(ii)Genetic transmission of the condition to the fetus
(iii)Perinatal & maternal mortality is increased
(iv) increased risk fetal complications : miscarriage,intrauterine growth restriction,preterm labour
(v) increased risk of maternal complications: thromboembolism,preeclampsia, abruption,infections(probably due to hyposplenism) like UTI,puerperal sepsis

Management

Prepregnancy
(i)Partner testing
(ii)Folic acid supplementation 5mg/day

Antenatal

(i)Multi disciplinary team involving haematologist,geneticist and obstetrician experienced in managing sickle cell disease.
(ii)Folic acid 5mg/day
(iii) Penicillin prophylaxis to prevent pneumococcal infection as a result of hyposplenism.
(iv)partner screening & genetic counselling -Fetal diagnosis by preimplantation genetics in IVF/CVS/Amniocentesis

(v)Regular checking of haemoglobin and mid stream urine

(vi)regular growth scan

(vii) Management of crisis
      (a)Rehydration
      (b)Pain relief-Morphine.NSAID can cause haemolysis.
      (c)early use of antibiotics if infection is likely
      (d)need to keep the patient warm ; well oxygenated.Pulse oxymetry & arterial blood gas may be necessary.
(viii)Blood transfusion may be necessary ex: to correct anaemia

(ix) Value of exchange transfusion is not well defined.Theoretically this increase the proportion of haemoglobin A and suppress the bone marrow from producing red cells with HbS. This may decrease the incidence of crisis but need to be balanced against the risks associated with transfusion.

(x) It is important to recognize & treat infection early.

(xi) The following treatments used to increase HbF need further evaluation in pregnancy
        (I) hydroxyurea
        (II)butyrate
(xii) Tourniquet should not be used.

Intrapartum care

(i)Avoid : dehydration/hypoxia/sepsis/acidosis
(ii)Epidural analgesia is recommended.
(iii) Sickle cell anaemia is not an indication for caesarean section
(iv)Give oxygen 4-6 l/min
(v)avoid blood loss as much as possible(Active management of third stage)

Postpartum

(i) Dehydration & infection should be avoided.

(ii) Risk assessment for thromboprophylaxis should be done.

(ii) Contraception should be discussed-Even though oral contraceptive pills have been implicated in increased risk of thrombo embolism , this is not based on any evidence.

RCOG guideline on management of sickle cell disease in pregnancy

Interventions for treating painful sickle cell crisis during pregnancy (Review)

Powerpoint on Sickle cell disease in pregnancy

Another presentation on sickle cell disease in pregnancy

Powerpoint on sickle cell disease

• Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.
• Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

Hepatitis C in Pregnancy

2010-05-17T15:54:00.006+01:00

Hepatitis C is a RNA virus.
It leads to chronic hepatitis in 70%,cirrhosis in 20-30% in about 10-30 years .
1-6% of cirrohotic patients develop hepatocellular carcinoma.

The commonest risk factor for hepatitis C infection in UK is past or present IV drug abuse.

Serological diagnosis
(I)Testing for Anti-HCV antibodies
(II)HCV RNA using PCR

Hepatitis C anti body indicates previous infection but positive PCR beyond six month indicates chronic infection.

Effect of disease in pregnancy
(i)Acute or chronic hepatitis C doesn't seem to adversely affect the pregnancy.
(ii) Vertical transmission is less frequent(3-5% of cases) than Hepatitis B virus.High viral load,Co-infection with HIV and active i.v. drug use are major risk factors for vertical transmission.
(iii) There is an increased risk of obstetric cholestasis.

Effect of pregnancy on liver disease
(i) pregnancy doesn't induce deterioration in liver disease.

Management.

Preconceptional care

(i) Vaccination against Hepatitis A & B should be offered.

(ii) Current IV drug users should be offered treatment programmes & needle exchange programmes.

Antenatal
(i) Routine screening isn't recommended.
    Selective screening is offered to high risk individuals:
       intravenous drug users
       patients who had multiple blood transfusion in the past
   women with HIV or HBV infection

(ii) Mutli disciplinary management with the involvement of hepatologist.

(iii)Perinatal transmission is uncommon, so there is no specific recommendations on delivery or breast feeding.

(iv) Patients should avoid alcohol in the interest of minimizing liver damage.

(v) Amniocentesis does not seem to significantly increase the risk of vertical transmission, but women should be counseled that very few studies have properly addressed this possibility.

Delivery
Universal precautions must be followed.
Caesarean section is not recommended.
There isn't enough evidence to make recommendation on artificial rupture of membranes,fetal scalp electrode and fetal blood sampling but these procedures are better avoided whenever possible.(SOGC guideline)
Pediatrician should be notified about the baby.

Postnatal
(i) anti-HCV antibodies in the baby may be due to tranplacental maternal antibodies.Antibody testing should be delayed up to 18 months post delivery.
(ii)HCV RNA testing could be used.Undetectable levels(less than 100 copies/ml) at 3 months makes vertical transmission unlikely.
(iii) Mother should be referred to hepatologist for antiviral therapy (interferon and ribavirin). These drugs are contraindicated in pregnancy.
(iv) transmission by breast milk is uncommon.
(v)contraception must be discussed.

A past history of a child infected perinatally with HCV does not increase the risk of transmission in subsequent pregnancies.

The Reproductive Care of Women Living With Hepatitis C Infection-SOGC guideline

Sources
• Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.
• Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

	Hadzić N. Hepatitis C in pregnancy. Arch. Dis. Child. Fetal Neonatal Ed. 2001 May;84(3):F201-204.

Uterine inversion in pregnancy

2010-05-11T09:41:00.000+01:00

Clinical features

Severe lower abdominal pain in third stage

Haemorrhage

shock out of proportion to bleeding

Uterine fundus not palpable

Mass in the vagina

Management

two important aspects
(A) resuscitation
(B)repositioning of uterus

Help-Call for help(Obstetrician/Anaesthetist/Senior midwives)

Replacement of uterus should go hand in Hand with resuscitation measures

ABC-Airway,Breathing(Remember to give oxygen),Circulation

two wide bore (14/16 G) & Fluid replacement(crystalloid & colliods)

Bloods for FBC,coagulation studies and cross matching (4-6 units)

"Take bloods & label correctly"

The earlier the correction of inversion the more likely the success.

Analgesia should be given

The earlier the reposition of uterus the more likely the success.

Techniques for repositioning uterus

(I)Manual replacement(The Jhonsons Manoeuvre)-Using the fist to push the fundus through the cervix.

(II)Hydrostatic repositioning (O'Sullivan's technique)-
(a) patient is placed in the trendlenberg position
(b)one end of the long tube(2m) with a large nozzle is placed in the posterior fornix
(c) warm saline is infused
(d) leak is prevented by approximating the labia with the hand or a vacuum cup can also be used.

(III)Medical approach
(a)Magnesium sulphate 2-4 g infused over 5 minutes
(b)ritodrine 0.15 mg IV bouls
(c)terbutaline 0.25 mg slow IV bolus
(d) volatile agent as a part of general anaesthesia

(IV) Surgery

(a)Huntingdon's procedure-Allis forceps is used to grasp the dimple of the inverted uterus and then gentle traction is applied.Further application of forceps on the advancing fundus helps in the correction of uterine inversion.

(b)Haultin's technique-posterior aspect of cervical ring is incised to help the Huntingdon's procedure.

Oxytocics should be administered after the correction of uterine inversion.

Non Surgical approach is successful in the majority of the cases.

An excellent presentation on uterine inversion

MANAGEMENT OF UTERINE INVERSION

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Uterine inversion in pregnancy

2010-04-01T18:52:00.011+01:00

Clinical features

Severe lower abdominal pain in third stage

Haemorrhage

shock out of proportion to bleeding

Uterine fundus not palpable

Mass in the vagina

Management

two important aspects
(A) resuscitation
(B)repositioning of uterus

Help-Call for help(Obstetrician/Anaesthetist/Senior midwives)

Replacement of uterus should go hand in Hand with resuscitation measures

ABC-Airway,Breathing(Remember to give oxygen),Circulation

two wide bore (14/16 G) & Fluid replacement(crystalloid & colliods)

Bloods for FBC,coagulation studies and cross matching (4-6 units)

Analgesia should be given

The earlier the reposition of uterus the more likely the success.

Techniques for repositioning uterus

(I)Manual replacement(The Jhonsons Manoeuvre)-Using the fist to push the fundus through the cervix.

(II)Hydrostatic repositioning (O'Sullivan's technique)-
(a) patient is placed in the trendlenberg position
(b)one end of the long tube(2m) with a large nozzle is placed in the posterior fornix
(c) warm saline is infused
(d) leak is prevented by approximating the labia with the hand or a vacuum cup can also be used.

(III)Medical approach
(a)Magnesium sulphate 2-4 g infused over 5 minutes
(b)ritodrine 0.15 mg IV bouls
(c)terbutaline 0.25 mg slow IV bolus
(d) volatile agent as a part of general anaesthesia

(IV) Surgery

(a)Huntingdon's procedure-Allis forceps is used to grasp the dimple of the inverted uterus and then gentle traction is applied.Further application of forceps on the advancing fundus helps in the correction of uterine inversion.

(b)Haultin's technique-posterior aspect of cervical ring is incised to help the Huntingdon's procedure.

Oxytocics should be administered after the correction of uterine inversion.

Non Surgical approach is successful in the majority of the cases.

"Take bloods & label correctly"

Fluid replacement (colloids & crystalloids)

The earlier the correction of inversion the more likely the success.

An excellent presentation on uterine inversion

MANAGEMENT OF UTERINE INVERSION

See more presentations by ogundapo | Upload your own PowerPoint presentations

Carpal tunnnel syndrome in pregnancy

2010-03-29T21:01:00.007+01:00

Carpal Tunnel syndrome is due to the compression of median nerve at wrist leading to pain, sensory disturbance and sometimes motor weakness.
Clinical features
(i)Paraesthesiae & numbness in the thumb,index and half of middle finger
(ii) Tinel's sign

(iii) Phalen's sign

Causes
(i)Arthritis
(ii) hypothyroidism
(iii)pregnancy
(iv)diabetes
(v)acromegaly

There is an increased incidence of carpal tunnel syndrome in pregnancy and the possible reasons are

(I) water retention

(II) relaxin

(III)Musculoskeletal changes

Conservative treatments

physical therapy
wrist splints-Nocturnal splinting of the wrist in mid position is effective.
non-steroidal anti-inflammatory agents(may not be safe in pregnancy)
a low salt diet
hydrocortisone injections
surgery is indicated if there is progression to weakness of abductor pollicis brevis.

How to manage carpal tunnel syndrome in pregnancy?

Answer from TRIP data base

(i)Splints (ii)analgesia (iii)corticosteroid injections (iv) rarely surgery.

Sources

(I) The management of carpal tunnel syndrome
in pregnancy
F.Turgut1 MD, M. Çetins¸ahin1 MD, M.Turgut2 MD, O. Bölükbas¸i3 MD
1Department of Gynecology and Obstetrics, Aydin Maternity Hospital, and Departments of 2Neurosurgery and 3Neurology, Adnan Menderes University Hospital
(II)Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

HIV and pregnancy

2010-03-05T22:05:00.003Z

Check out this SlideShare Presentation:

HIV and pregnancy

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HIV in Pregnancy

2010-02-24T17:13:00.017Z

Clinical features of HIV

1-primary infection/seroconversion
Asymptomatic or
Accompanied by fever,fatigue,lymphadenopathy or rash

2-Latent phase

3.Symtomatic disease
Opportunistic infections-Ex.pneumocystis pneumonia
Secondary neoplasm-Ex.Kaposi’s sarcoma

Investigation

HIV antibody test-antibody to part of viral membrane/envelope
Another test is Polymerase chain reaction(PCR) for viral DNA/viral RNA
CD4 count reflect the current degree of immunosuppression
HIV-RNA level is the main predictor of disease progression.

HIV1 vs HIV 2
Less virulent clinical disease
Less likely to be vertically transmitted

Mother to child transmission
Non breast feeding women in Europe 15-20%
Breast feeding mothers in Africa 25-40%
Breast feeding is associated with 2 fold increase in transmission.

Prevention
Maternal child transmission is prevented by

Antenatal HIV screening
Antiretroviral therapy
Elective Caesarean section
Avoiding breast feeding

Reduced from 25-30% to less than 2 %

Effect of pregnancy on HIV
CD4 counts fall during pregnancy but return to pre pregnancy levels post partum.
No increased risk of accelerated immunosuppression.

Effect of HIV in pregnancy

Fertility-reduced (may be due to other STD)
Increased spontaneus abortion
Preterm birth-may be due to HIV/may be due to confounding variable
Small for gestational age-statistically significant but modest effect on fetal growth

Antenatal management

Screening for HIV should be offered early in pregnancy because appropriate antenatal interventions can reduce maternal-to-child transmission of HIV infection.
positive HIV antibody test result should be given to the woman in person by an appropriately trained health professional.

multidisciplinary team

HIV positive patients should be managed by a multidisciplinary team.

HIV physician
an Obstetrician
a Midwife
a Paediatrician
a Psychiatric team
support groups

Confidentiality
Confidentiality is important.
Information may be disclosed to a known sexual contact of the woman ,where she can’t be persuaded to do so.Link

Booking visit
Additional tests requested are

Lymphocyte subsets
Quantitaive RNA PCR measurement of viral load
Hepatitis B & C
Cervical & vaginal swaps to check for STDs,Bacterial vaginosis & Group B streptococcus.
CD4 count should be tested every trimester or more frequently if maternal viral load is high.

Antiretroviral therapy
2 reasons

1. prevention of mother-to-child transmission (therapy usually discontinued at, or soon after, delivery)
2.secondly for treatment of the mother to prevent maternal disease progression (therapy continued indefinitely after delivery)

anti-retroviral therapy is recommended for all HIV positive women during pregnancy and at delivery to prevent MTCT.

The optimal regimen is determined by an HIV physician on a case-by-case basis.

The decision to start,modify or stop anti-retroviral therapy

– should be undertaken by an HIV physician
– in close liaison with other health professionals

obstetrician
paediatrician.

Antiretroviral therapy

Women who are not on HIV treatment for their own health need anti-retroviral therapy to prevent mother-to-child transmission.

Anti-retroviral therapy is usually started between 28 and 32 weeks of gestation and should be continued intrapartum.

A maternal sample for plasma viral load is taken at delivery.

Maternal anti-retroviral therapy is usually stopped soon after delivery but the precise time of discontinuation should be discussed with the HIV physician.

Zidovudine is usually administered orally to the neonate for four to six weeks.

Antiretroviral therapy

Timing
– Antenatal(consider possibility of preterm Ex.Twins)
– Intrapartum
– Neonatal period(4-6 weeks)
Choice of antiretroviral therapy & Timing is decided by HIV physician.

Plasma viral load & CD4 counts regularly monitored.

Timing of prophylaxis

When to start prophylaxis in women who doesn’t require treatment for their disease?

ACTG076(AIDS clinical trial group ) recruited from 14-36 weeks & median gestation was 26 weeks.

If shorter exposure
• Less chance of possible long term complications
• Less chance of selecting zidovudine resistant species
– BUT risk of inadequate therapy incase of preterm labour

• Antiretroviral therapy......

Patients on antiretroviral therapy should be monitored for toxicity
• full blood count
• urea and electrolytes
• liver function tests
• Lactate
• blood glucose
• Patients should also have detail ultrasound scan to detect foetal anomalies.

Drug toxicity
• Presentation with symptoms or signs of pre-eclampsia/ Cholestasis or other signs of liver dysfunction during pregnancy may indicate drug toxicity and early liaison with HIV physicians should be sought.
• Lactic acidosis
– is a recognised complication of certain HAART regimens.
• presenting symptoms
• often nonspecific
• include
– gastrointestinal disturbance
– fatigue
– fever
– breathlessness.

Types of HIV drugs
• Reverse transcriptase inhibitors
– Nucleoside reverse transcriptase inhibitors
– Non nucleoside reverse transcriptase inhibitors
• Protease inhibitors
• Entry inhibitors
• Integrase inhibitors
• Maturation and assembly inhibitors
• Other viral proteins
– More information at aidsmap

• Drug safety in pregnancy
• Category B (animal studies fail to show risk to fetus) ddI ,saquinavir,ritonavir,nelfinavir
• Category C(animal studies have either not been done or have shown abnormalities Indinavir,nevirapine
• Efavirenz has shown teratogenic potential
• Mitochonrial toxicity is another concern-Review

Prophylaxis of Pneumocystis carinii

• PCP prophylaxis is usually administered when the CD4 T-lymphocyte count is below 200 106/l.
• The first line treatment is cotrimoxazole(a folate antagonist).
• Folic acid 5 mg should also be given
• Nebulised pentamidine is another alternative.

Screening for genital infections

All pregnant women who are HIV positive should be screened genital infections.

When to do ?
This should be done as early as possible in pregnancy
• repeated at around 28 weeks.
• Any infection detected should be treated according to UK national guidelines.

Antenatal care
• Screening for Down syndrome and fetal anomalies should be offered.
• A detailed ultrasound scan for fetal anomalies is important after first-trimester exposure to HAART and folate antagonists used for prophylaxis against PCP.
• invasive prenatal diagnosis
• The risk of mother-to-child transmission with chorionic villus sampling or second-trimester amniocentesis are hasn’t been estabilished.
• If invasive prenatal diagnosis is contemplated, the advice of the fetal medicine specialist and HIV physician should be seeked and prophylaxis with HAART considered.

Prevention of MTCT
• 2 choices of antiretroviral therapy
– Single agent-Zidovudine
– START(short term antiretroviral therapy)- HAART for short duration in pregnancy and continued intrapartum

Zidovudine Vs START

Disadvantage of Zidovudine -

may allow the emergence of resistant virus

START

advantgage-

maternal plasma viraemia is more likely to be suppressed to undetectable levels

Disadvantage-

exposure of the mother and fetus to larger numbers of potentially toxic drugs

Advanced HIV
• likely to have symptomatic HIV infection and
– a falling or low CD4 T-lymphocyte count (less than 350 106/l)
– and/or a high viral load (greater than 10 000–20 000 copies/ml).
• advanced HIV
• These women should be treated with a HAART regimen.
• The start of treatment should be deferred until after the first trimester, if possible, and should be continued after delivery.
• advanced HIV
• Women who conceive while taking HAART should continue their HAART regimen if it is effectively suppressing plasma viraemia.
• For women whose regimen is not suppressing viraemia, a change in therapy after the first trimester may be indicated.

Mode of delivery
• Elective Caesarean section is beneficial
– HIV positive women who are not taking HAART during pregnancy
– for women with a detectable plasma viral load
• Value of elective caesarean section is uncertain
– in women taking HAART who have an undetectable plasma viral load at the time of delivery.

LSCS in HIV women

• A zidovudine infusion
– should be started four hours before beginning the caesarean section
– Should continue until the umbilical cord has been clamped.
• A maternal sample for plasma viral load should be taken at delivery.
• The cord should be clamped as early as possible after delivery and the baby should be bathed immediately after the birth.

LSCS in HIV women....
• a technique of ‘bloodless’ caesarean section may further reduce the risk of mother-tochild transmission.
– opening the uterus with a staple gun,which simultaneously cuts and giveshaemostasis.
• Casarean section
• This should be sheduled at 38 weeks to reduce the risk of spontaneus labour or membrane rupture.
• Contamination of the baby with maternal blood should be avoided
– Secure the bleeding points
– Allowing the membrane to be present along uterine incision prior to the rapid delivery of baby
• Cord clamped as soon as possible

Casarean section
• Drainage should be used sparingly and they should be used to closed suction system
• Universal precautions :gloves, aprons & face protection should be employed.

Labour in HIV woman
• Women who opt for a planned vaginal delivery should have their membranes left intact for as long as possible.
• Use of fetal scalp electrodes and fetal blood sampling should be avoided.
• Women should continue their HAART regimen throughout labour .
• If an intravenous infusion of zidovudine is required it should be commenced at the onset of labour and continued until the umbilical cord has been clamped.
• A maternal sample for plasma viral load should be taken at delivery.
• The cord should be clamped as early as possible after delivery and the baby should be bathed immediately after the birth.
• HIV infection per se is not an indication for continuous electronic fetal monitoring
• Vaginal delivery
• Forceps preferred to Vacuum
• Remove maternal blood stain with alcohol wipe prior to Vitamin K injection
• Universal precautions :gloves, aprons & face protection should be employed.

Women scheduled for Emergency caesarean section presents in early labour
– Studies have shown no benefit with non elective caesarean
– In case of
• Early stages of labour
• Patient presenting immediately after SROM
• Probability of prolonged labour
– LSCS still may be protective
• If quick delivery is likely one could wait for vaginal delivery.

SROM in HIV
• SROM-spontaneus rupture of Membranes
– ruptured membranes for more than four hours were associated with double the risk of HIV transmission.
– These studies also demonstrated a 2% incremental increase in transmission risk for every hour of rupturedmembranes up to 24 hours.
– The relevance of these studies for women taking HAART who have undetectable viral loads is uncertain.

PPROM in HIV
• PPROM-preterm prelabour rupture of membranes
– If there is preterm rupture of membranes, with or without labour, the risk of HIV transmission should be set against the risk of preterm delivery.
– Preterm infants are more likely to be infected with HIV.
– There is no known contraindication to the use of short-term steroids to promote fetal lung maturation.

Postpartum
• In UK women with HIV advised not to breast feed
• Neonate infections.
– PCR is done as maternal antibodies cross the placenta
– Typically, tests are carried out at birth, then at three weeks, six weeks and six months.
– definitive test is the HIV antibody test: a negative result at 18 months of age confirms that the child is uninfected.

Management of the neonate

• All infants born to women who are HIV positive should be treated with anti-retroviral therapy from birth.
• Usually treatment is discontinued after four to six weeks

IVF pregnancy in HIV patients
• This is ethically acceptable
– Life expectancy of couple is improved HAART
– Vertical transmission can be reduced to less than 2%

• Pre pregnancy counselling should be done.
• IVF pregnancy in HIV patients.

If Male HIV Negative-

artificial insemination at the time of ovulation, and quills, syringes and Gallipots may be provided.

If Female HIV negative-

‘Sperm washing’-spermatozoa are separated from surrounding HIV-infected seminal plasma by a sperm swim-up technique

Needle stick injury
• In case of needle stick injury post exposure prophylaxis has to be started with in 1-2 hours

More information
HIV Association

Sources
• Greentop guideline
• Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.
• Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

Eczema in pregnancy

2010-02-06T21:46:00.019Z

This is the commonest dermatosis associated with pregnancy. Eczema is a multifactorial disease controlled by genetic predisposition & environmental factors.

Effect of pregnancy on Eczema
25% of pregnant women with eczema improve but more than 50% deteriorate.
Deterioration occur at anytime but more common in second trimester.

Effect of Eczema on pregnancy

Generally eczema doesn't affect fertility or the pregnancy.Genetic & environmental factors determine the development of eczema in a child.It is important to recognize & treat eczema herpeticum as this could lead to serious maternal mortality & morbidity.Aciclovir should be commenced on clinical suspicion and the diagnosis can be confirmed by viral swab.

Preconceptional counselling

(i)Optimize the control of eczema by avoiding the irritants & allergens,using emollients & topical steroids.

(ii)Patients who had systemic treatment should ensure adequate drug free interval
Example conception should be avoided for three months after methotrexate (males & females)

During pregnancy:

The streroids should be used in minimum strengths & quantities.

Sedative antihistamine would help with sleep.

Secondary infections often require systemic antibiotics therapy.

The following are safe treatments options :
emollients,topical steroids (mild, moderate, or potent),Ultraviolet B

These options are relatively contraindicated:very potent topical steroids,oral steroids,Ciclosporin,azathioprine,topical calcineurin inhibitors
The following options are contraindicated:methotrexate,psoralens plus ultraviolet A (PUVA)

ciclosporin crosses the placenta but data from transplant patients indicate it is relatively safe.These patients need regular assessment of full blood count,renal function & blood pressure.

Azathioprine crosses the placenta but the fetal liver lacks the enzyme to convert it into active metabolite.Patients on azathioprine has to have regular full blood count & liver function tests.

More information on topical calcineurin inhibitors

Example :tacrolimus and pimecrolimus

Systemic therapy is teratogenic but absorption from topical treatment is very small.The patient should be counseled about the risk.

Eczema of nipple

Emollients & low to moderate potency steroids are first line treatment.These are applied after breast feeding and should be washed away just before the next feed.
Ultraviolet B is safe but methotrexate & ciclosporin should be avoided.

What are emollients? more information on emollients?

Cochrane review on topical steroids in pregnancy

An excellent article on common skin disorders in pregnancy

Another article

A link on skin diseases in pregnancy

How to treat skin problems in pregnancy?

References
(1)Treatment of Recurrent Eczema Herpeticum in Pregnancy With Acyclovir Richard A. Lattacorresponding author1 and David A. Baker2 .Infect Dis Obstet Gynecol. 1996; 4(4): 239–242. doi: 10.1155/S1064744996000452.

2.Eczema Herpeticum in Pregnancy and Neonatal Herpes Infection,DiCarlo, Angela; Amon, Erol MD; Gardner, Morey MD; Barr, Susan MD; Ott, Kelly MD, Obstetrics & Gynecology: August 2008 - Volume 112 - Issue 2, Part 2 - pp 455-457, doi: 10.1097/AOG.0b013e318169ce19, Case Reports.

							3.Weatherhead S, Robson SC, Reynolds NJ. Eczema in pregnancy. BMJ. 2007 7;335(7611):152-154-An excellent review on this topic.
							4.Oxford text book of medicine,third edition,Voulme 2 pp1805.

ARDS in pregnancy

2010-01-12T20:18:00.012Z

What is ARDS?

It is form of acute respiratory failure
characterized by (i) alveolar hypoxemia (ii) increased capillary permeability
resulting from diffuse & ongoing pulmonary inflammation.

Current definition
(i)acute onset
(ii) a PaO2/FIO2 ratio, or hypoxia score,of <=200, regardless of positive end expiratory pressure (iii) bilateral infiltrates on chest radio graph (iv) a pulmonary artery occlusion pressure of <=18 mm Hg or the absence of clinical evidence of left atrial hypertension. 4phases
(i)exudative phase-increased capillary permeability resulting in alveoli filled with fluid.(0-4days)
(ii)proliferative phase(4-8days)
(iii)fibrotic phase(>8 days)
(iv)recovery

2 type of causes

(i) Direct-(pulmonary causes)direct lung injury Example: Aspiration
(ii)Indirect(extrapulmonary causes) Ex:Acute pancreatitis in pregnancy

3 categories in pregnancy
(A)Pathogeneses Minimally Affected by Pregnancy (i)Sepsis with prolonged hypotension
(B)Pathogeneses Affected by pregnancy (i)aspiration (ii)acute pyelonephritis
(C)Pathogeneses unique to pregnancy (i)preeclampsia

Differential diagnosis
(i)Cardiogenic pulmonary odema
(ii)volume overload

Management
Multidisciplinary management involving Obstetrician, Intensivists, Anaesthetists and Neonatologist.

3 aspects of management
(i)initial stabilization
(ii)confirming the diagnosis & identifying the aeitiology
(iii)assessing fetal well being & making the delivery plan

Treatment principles
(A) treat primary problem
(B)physiological support(lungs & other organs)
(C) avoid complications

Different methods of ventilatory support
(i)Noninvasive Positive-Pressure Ventilation-There is limitation in pregnancy due to raised risk of air way compromise & aspiration.
(ii)Lung-Protective Conventional Ventilation-(endotracheal intubation)

Advanced options :
(a)airway pressure-release ventilation (APRV)
(b)high-frequency oscillatory ventilation(HFOV)
(c)lung recruitment maneuvers(LRMs)
(d) prone positioning
(e) inhaled nitric oxide

Timing & mode of delivery
The available evidence is limited,so timing & mode of delivery should be as per standard obstetric practice.

PowerPoint presentations on ARDS (I) (II)
Excellent PowerPoint on Critical care in pregnancy

References
(1)Acute respiratory distress syndrome in pregnancy;Daniel E. Cole, MD; Tara L. Taylor, MD; Deirdre M. McCullough, MD; Catherine T. Shoff, DO;Stephen Derdak, DO (Crit Care Med 2005; 33[Suppl.]:S269 –S278)

(2)Acute Respiratory Distress Syndrome inPregnancy and the Puerperium: Causes,Courses, and Outcomes
VAL CATANZARITE, MD, PhD, DAVID WILLMS, MD, DAVIES WONG, MD,
CHARLES LANDERS, MD, LARRY COUSINS, MD, AND DAVID SCHRIMMER, MD.
Obstetrics & Gynecology:May 2001 - Volume 97 - Issue 5 - p 760-764

Conn's Syndrome in pregnancy

2010-01-11T18:37:00.015Z

In pregnancy there is physiological up regulation of renin-angiotension-aldosterone system.

A powerpoint explaining Conn's syndrome

Image explaining Renin-Angiotensin-Aldosterone cascade

Aeitiology
(I)Adrenal adenoma(60-80%)
(II)Adrenal hyperplasia(20-40%)
(III)Adrenal carcinoma rare

Clinical features
(I) Hypertension
(II)Muscle weakness

Investigation
(I)hypokalaemia
(II)radioactive selenium cholesterol test should be delayed until after delivery.
(III)suppressed renin activity
(IV) increased plasma aldosterone
(V)MRI of abdomen

Treatment
Multidisciplinary care involving Obstetrician,Endocrinologist and Physicians.
Hypertension should be controlled by anti hypertensives (labetolol,methyldopa,nifidipine)

Hypokalaemia managed by
(A) Potassium supplementation
(B)Potassium sparing diuretics Amelioride is preferred over spironolactone because of anti androgenic property of the latter that could lead to feminizing a male fetus.

Surgery is effective in adrenal adenoma or carcinoma but the value is limited in adrenal hyperplasia.Surgery could be postponed until after delivery.If surgery is indicated for

Labour
(i) Fluid & electrolyte balance should be maintained.

References
(I) Pituitary and adrenal disorders complicating pregnancy:Chandraharan, Edwin; Arulkumaran, Sabaratnam

Current Opinion in Obstetrics and Gynecology:April 2003 - Volume 15 - Issue 2 - pp 101-107

(2)Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

(3)Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

(4)Laparoscopic treatment of primary hyperaldosteronism in a pregnant patient
(5)Primary aldosteronism in pregnancy.Matsumoto J, Miyake H, Isozaki T, Koshino T, Araki T.J Nippon Med Sch. 2000 Aug;67(4):275-9

Cushing's Syndrome in Pregnancy

2010-01-03T18:04:00.035Z

Physiology of adrenal gland

Image of adrenal gland

Excellent Powerpoint on Cushing's syndrome

Aeitiology

(i)adrenal adenoma-disproportionately more common in pregnancy(40-50% Vs 17-19%)

(ii)Cushing's Disease-Pituitary ACTH increased-(What is the difference between Cushing's disease and Cushing's syndrome?)

(iii)ectopic ACTH

Clinical features

(I) Weight gain
(II) Hypertension
(III)Glucose intolerance
(IV)Purple striae

The above features aren't uncommon in pregnancy.

(V)Proximal myopathy

Changes in normal pregnancy

raised (i)total cortisol (ii)free cortisol levels (iii) urinary cortisol (iv) cortisol binding globulin

Corticotropin releasing hormone is secreted by placenta.

How does Cushing's Syndrome affects pregnancy?

(I) In untreated Cushing's syndrome hypothalamic pituitary axis is suppressed,so the patients tend to infertile.

(II) most common complications are hypertension & diabetes

(III) less frequent complications are osteoporosis,delayed wound healing and psychiatric complications

(IV) fetal complications -miscarriage,prematurity,intrauterine growth restriction & still births.

Maternal cortisol can cross the placenta.

(i)Increased rate of miscarriage
(ii)Premature delivery
(iii)Still birth

Investigations

Tests used for diagnosis

Pregnancy specific ranges should be examined

(i) 24 hour urinary free cortisol-Higher cutoff need to be used in pregnancy.

(ii)midnight serum cortisol -Physiological nocturnal drop is the serum cortisol level is also observed Cushing's syndrome.Higher cut off values should be used.

(iii)dexamethasone suppression test-

2 types of test

(A)overnight dexamethasone suppression test-1mg dexamethasone given at 23.00 hrs and serum cortisol is measured at 9am

(B)48 hour dexamethasone suppression test 0.5 mg given

6 hourly(9.00,15.00,21.00,3.00 hrs).Serum cortisol measured 9.00 at

the start & end of test.

The suppression effect on cortisol by dexamethasone is diminished in normal pregnancy.

So the usefulness of dexamethasone suppression is limited in pregnancy.

Once the Cushing's syndrome is confirmed, further tests done find the aeitiology.

If ACTH level is low adrenal imaging with MRI is useful.However adrenal' incidentaloma'(non secreting adrenal tumors can be found in 2-1% of abdominal CT's.It is important to correlate the CT findings to clinical & biochemical findings.

If ACTH level is elevated,high dose dexamethasone suppression test helps in differentiating between pituitary source vs ectopic ACTH.MRI of head or MRI of chest & abdomen can be arranged accordingly.

High dose of dexamethasone suppress cortisol in Cushing's disease but the suppression fails in adrenal adenoma & ectopic ACTH secretion.

ACTH measurement-ACTH level reduced in adrenal adenoma.

CRH (corticotropin releasing hormone) stimulation test-Pituitary tumors would show rise in cortisol but adrenal adenoma & Ectopic ACTH wouldn't.

Treatment

Multidisciplinary approach involving Obstetrician,Endocrinologist,Anaesthetist and Surgeon is important.

It's important to control the blood pressure and diabetes mellitus.

Definitive treatment options depend on aeitiology.
(I) Adrenal adenoma-Adrenalectomy
(II)Cushing's disease-Transsphenoidal treatment,Medical treatment or adrenalectomy.

adrenalectomy in Pitutary adenoma could lead to Nelson syndrome

(III)Ectopic ACTH-resection of the source.

medical treatment can be used but generally surgery is the preferred.

Medical treatment options

(I)cyproheptadine

(II)ketoconozole-This crosses the placenta,so there is a theoretical risk of inhibition of fetal adrenal cortex. Ketaconozole is also teratogenic in animal studies.

(III)metyrapone-can cause severe hypertension.

Medical treatment isn't currently recommended due to potential adverse side effects on fetus.

Post natal

(I) lactation is discouraged because

(a)there is possibility permanent galactorrhoea.

(b)drugs may be secreted into breast milk(ex.cyproheptadine)

(II) Neonate should be reviewed for potential intrauterine suppression of hypothalmic pituitary adrenal axis suppression.

References
(i) Cushing's syndrome in pregnancy: an overview.Vilar L, Freitas Mda C, Lima LH, Lyra R, Kater CE.
Arq Bras Endocrinol Metabol. 2007 Nov;51(8):1293-302.

(ii)Cushing syndrome in pregnancy .Deborah J. Cook, MD, FRCPC,Robert H. Riddell, MD, FRCPath,John D. Booth, MD, FRCPC. CMAJ, VOL. 141, NOVEMBER 15, 1989,pp1059-1061

(3)Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

(4)Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

(5)Pituitary and adrenal disorders complicating pregnancy:Chandraharan, Edwin; Arulkumaran, Sabaratnam

Current Opinion in Obstetrics and Gynecology:April 2003 - Volume 15 - Issue 2 - pp 101-107

Congenital adrenal hyperplasia in Pregnancy

2009-12-24T14:45:00.019Z

Information on Congenital adrenal hyperplasia for Public

Congenital adrenal hyperplasia occurs as a result of gene mutation.

This results in defective glucocorticoid & mineralocorticoid synthesis.

Excellent Power point explaining congenital adrenal hyperplasia is here

Diagram explaining adrenal hormone synthesis

Mode of inheritance is autosomal recessive.

Clinical features

3 catergories of diseasse - depending on the type of mutation

(I)Salt Wasting(SW)

(II) Simple Virilising(SV)

(III) Non-Classic(NC)

The condition is usually diagnosed in infancy

(A) Female infant-ambigious genetalia

(B)Acute illness due to hyponatraemia (salt losing crisis due to mineralocorticoid defeciency)

90% due to 21 hydroxylase enzyme deficiency.These patients have both glucocorticoid & mineralocorticoid defeciency.

5-8% due to 11 hydroxylase deficiency.These patients have excess deoxycortisol, that shows mineralocorticoid activity,leading to hypertension.

How the disease affect pregnancy?
(A)Reduction in fertility , especially in patients with salt wasting type disease.

Reasons: (i) inadequate control of hyperandrogenism
(ii)Inadequate introitus due to poor surgical repair

(B) Disease inheritance by fetus

(C) Risk of Miscarriage,pre-eclampsia & IUGR increased

(D) Masculinization can lead to android type pelvis that may lead to failure to progress in labour.

Management

Antenatal

2 Types of Clical problems

(I) Pregnant women with Congenital adrenal hyperplasia

(II)Women who is carrier for Congenital adrenal hyperplasia with previously affected child( or with a heterozygous partner)

Genetic counselling

(I) This is a autosomal recessive disorder.

(II)Prenatal diagnosis is possible with a battery of gene probes through chorionic villus sampling at 10 weeks

(III) In the past diagnosis made by estimation of 17 hydroxy progestrone & androgen levels in amniotic fluid.

(IV)Zygosity of partner for Congenital adrenal hyperplasia gene can be done.In case gene deletion ,30% of heterozygous , diagnosis can be made accurately.The other 70 % has gene mutation which can be mimicked by pseudo genes of normal individuals. So negative gene testing in the partner reduces the probability of heterozygosity from 1:50 to 1:70.

Differentiation of female genitalia occurs between 9-10 weeks,so even a diagnosis at 10weeks would be late in preventing masculinization of a female fetus with congenital adrenal hyperplasia.

Dexamethasone,the steroid which is capable of crossing the placenta, can be used to suppress the fetal adrenal gland to avoid masculinization. The therapy should be started at least by the fifth week.It may even be started preconceptually. This treatment regime isn't always successful in preventing masculinisation.

Maternal compliance is shown by reduced urinary cortisol or oestriol level.

If the chorionic villus sampling shows a female fetus with congenital adrenal hyperplasia(CAH), the treatment should be continued till delivery.In case of female fetus with congenital adrenal hyperplasia ,termination is also an option.

In a pregnancy with CAH in a male fetus or unaffected fetus the treatment should be discontinued.

Fetal sex determination by ultra sound scan is helpful as maternal androgen excess has minimal effects on male fetus.

Pregnant women with congenital adrenal hyperplasia
On the other hand some steroids can cause masculinization but patients need steroid to suppress their disease activity.However the placental aromatase activity is sufficient to prevent masculinization of fetus.

Hydrocortisone, cortisone acetate, prednisone, methylprednisolone are inactivated in the placenta but dexamethasone crosses the placenta and causes neonatal adrenal suppression.

Regular assessment of clinical status,serum electrolytes and serum androgen levels to adjust the glucocorticoid and mineralocorticoid therapy.

Generally the patients with 21-hydroxylase deficiency doesn't require alteration in dosage during pregancy.

Serum testosterone & free testosterone levels should me measured every 6 weeks in first trimester & every 8 weeks thereafter.Aim is to maintain free testosterone levels at high to normal levels for pregnancy.

Labour & delivery

Elective caesarean is indicated in patients who had genital reconstructive surgery.

Caesaren section rate among these patients is increased and this could be attributed to android type pelvis resulting from masculinization.

Stress dose glucocorticoid therapy ( Hydrocortisone 100 mg IM ) is indicated for patients undergoing labour.

Newborn should be examined for ambiguous genitalia.Female pseudohermaphroditism is either due to maternal hyperandrogenism or fetal 21 hydroxylase deficiency(if father is a carrier).

Affected fetuses would require steroid treatment but even the unaffted fetus would require short term steroid support when its adrenal activity is suppressed in utero as the result of treatment of mother.

Source

1.Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

2.Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

3.1.E.Medicine

4.K. Hagenfeldt , P.O. Janson , G. Holmdahl , H. Falhammar , H. Filipsson , L. Frisén , M. Thorén , and A. Nordenskjöld
Fertility and pregnancy outcome in women with congenital adrenal hyperplasia due to 21-hydroxylase deficiency Hum. Reprod. Advance Access published on July 1, 2008, DOI 10.1093/humrep/den118.Hum. Reprod. 23: 1607-1613.

Artificial heart valve in pregnancy

2009-12-01T21:04:00.016Z

Preconceptual evaluation

(A)cardiac function should be assessed-Clinical/Echo/Exercise testing
moderately or severely symptomatic (class III and IV) should be advised against pregnancy

(B)Fetal risks-abortion/prematurity/intrauterine growth restriction/congenital abnormalities-due to warfarin/inheritance in patient's with congenital heart disease

Inheritance of congenital heart disease

(C)Anticoagulation should be discussed-if anticoagulation is altered there is an increased risk thromboembolism. If thromboembolism occurs during pregnancy the risk to the fetus increased again.

(D) management planned by multi disciplinary team(Obstetrician/cardiologist/Cardiothoracic surgeon)

2 major types of valves

1.mechanical- Suggested INR is 3-4.Failure to anti coagulate could result in valve thrombosis and stroke.Subcutaneous heparin anti coagulation may inadequate in patients with artificial valves.
three categories : caged-ball tilting-disc bi leaflet valves

2.bio prosthetic or homo graft-
three categories hetero grafts homo grafts auto grafts.

They don't require anti coagulation but shorter lives than mechanical valve.Patients may need anti coagulation if they develop Atrial fibrillation.

Opinion varies as to whether pregnancy accelerate homo graft valve deterioration.

Fetal risks of Warfarin
1.Miscarriage
2.Teratogenesis
Chodrodysplasia punctata
Optic atropy
Microcephaly

Factors determining the choice of anticoagulation
1.Site of valve replacement(mitral more thrombogenic aortic)

2.Type of valve ( ball & cage more thrombogenic than bi leaflet valves)

3.Past history of thromboembolic events

4.No of mechanical valves

5.patient choice

Anticoagulation regimens-3 broad possibilities

1.Warfarin throughout the pregnancy
2.Heparin & warfarin alternatively Heparin between 6-12 weeks & after 36 weeks
3.Heparin throughout the pregnancy

Aspirin is a useful adjunct when heparin is used.

If LMWH is used anti Xa levels should be monitored 4-6 hrs post injection.LMWH doesn't cross placenta

Advantages of LMWH

1.fewer bleeding complications
2.lower frequency of thrombocytopenia
3.lower incidence of osteoporosis
4.longer half life
5.more predictable dose response

The following is the commonly used regime

Conception is difficult to time & risk of congenital malformation is likely to be minimal in the first 4 weeks, so patient could conceive on warfarin.

Then patients are given intravenous heparin aiming to double APTT during 6-12 weeks.

Patient can be converted to warfarin from 12 weeks.

At 37 weeks patient us converted to continuous intravenous heparin.

If patients goes into labour while on warfarin vitamin K & FFP should be given & heparin should be commenced.
Heparin & LMWH can be reversed with protamine sulphate.

Postpartum patient continues on heparin for 3-7 days.Patient can breast feed while in heparin or warfarin.

Patients on dindevan shouldn't breast feed.

Antibiotic prophylaxis is indicated in patient with artificial valve.
Current recommendations amoxicillin 2g i.v & gentamicin 1.5 mg/kg i.v

Heart failure in pregnancy

medicine that can be used:digoxin, diuretics, nitrates, hydralazine, and
beta blockers.

medicine that should be avoided:angiotensin-converting enzyme
inhibitors and angiotensin receptor antagonist amiodarone sodium nirtotroprusside

Valve thrombosis in pregnancy

Thrombolysis is the first line approach
Surgery is reserved for patients in thrombolysis is contraindicated.

Patient information leaflet :Breast feeding while on anticoagulation

References

1.	Nelson-Piercy C. Handbook of obstetric medicine. Taylor & Francis; 2002.

Swiet MD. Medical disorders in obstetric practice. Wiley-Blackwell; 2002.

3.	Elkayam U, Bitar F. Valvular Heart Disease and Pregnancy: Part II: Prosthetic Valves. J Am Coll Cardiol. 2005 Aug 2;46(3):403-410.

4.The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy

Evidence-Based Guidelines

Mnemonic for Obstetric Haemorrhage

2009-11-26T22:43:00.003Z

Management of Atonic Obstetric Haemorrhage-"HAEMOSTASIS"

General medical management

H-call for help

A-assess (vital signs/blood loss) & resuscitate

E-Establish aeitiology(4T-Tone/Tissue/ Trauma/Thrombin)

E-Ecbolics(syntometrine/ergometrine/bolus syntocinon)

E-Ensure availability of blood products

M-Massage the uterus

O-Oxytocin infusion,prostaglandins(intravenous,rectal,intramuscular,intramyometrial)

Specific surgical management

S-shift to operating theatre(bimanual compression anti-shock garment,especially if tranfer is required

T-Tissue & trauma to be exculded & balloon tamponade or uterine packing

A-apply compression sutures

S-sytematic pelvic devascularisation(uterine,ovarian,quadruple,internal iliac)

I-interventional radiology,uterine artery embolisation

S-Subtotal/Total hysterectomy

Source:

Mukherjee S, Arulkumaran S. Post-partum haemorrhage. Obstetrics, Gynaecology & Reproductive Medicine. 2009 5;19(5):121-126.

More Mnemoinics

Cystic fibrosis in Pregnancy

2009-11-17T22:03:00.012Z

This is a multisystem disorder with impaired cellular secretion.
Commonest autosomal recessive disorder in U.K.
In Carrier rate 1:25 in Caucasians.In USA 1:30 American is a symptomless carrier.

Most common single mutation in Nonhispanic Caucasians is deltaF508.This occurs in approximately 65-70% of cases.DNA probes exist to detect 95% of mutations.If the couple already had a affected child,the defective gene could be identified and then prenatal diagnosis can be done to exclude cystic fibrosis.

Clinical features
1.recurrent lung infection/bronchiectasis/respiratory failure

2.pancreatic deficiency-malnutrition & diabetes.

Effect of Cystic fibrosis in Pregnancy
Fertility
Female: Fertility is reduced due to 1.thick cervical mucous 2.low lean body mass 3. voluntary infertility due to fear of producing affected children.

Male:
Most are infertile due to atresia of the vas & epididymis.

Pre pregnancy counselling

Factors to consider

1.cor pulmonlae

2.uncontrollable recurrent respiratory tract infection.

3.vital capacity - Patients with vital capacity less than 50% recommended termination.Many cystic fibrosis patients and patients with kyphosis with such vital capacity have normal pregnancy.

4.Right ventricular cavity size at end diastole is a good prognosticator of clinical outcome.

5.Patients may have diabetes and/or liver disease.Screening for diabetes need to be done.

6.Presence of Burkholderia cepacia is also an important risk factor.

Women's life span is reduced,so implications for parenting should be discussed.

Contraindication to pregnancy

1.Pulmonary hypertension
2.Cor pulmonale
3.FEV1 <30-40 class="ii gt">

Genetics
If father is a carrier-50% of babies wold be born with cystic fibrosis,other 50% would be carriers.

If father's carrier status unknown, the risk of CF baby is 2-2.5% as the carrier status is UK general population is 1:25.

Antenatal
1.risk of spontaneous abortion not increased.
2.complication in pregnancy

(A)prematurity
(B)IUGR-due to chronic hypoxia

Principles of antenatal management

1.antenatal screening- Power point on Cystic Fibrosis screening
2.support maternal nutrition

3.regular physio therapy
4.prevention & early treatment of infections.
5.avoid prolonged hypoxia
6.regular growth monitoring-Growth restriction can be managed by bed rest, nutritional supplements & oxygen.

Antibiotic treatment

Generally risk of infection is greater than the side effects of antibiotics.
Penicillin,cephalosporins and erythromycin are safe in pregnancy.
Tetracycline should be avoided.
Monitoring of drug levels should be done when intravenous aminoglycosides are used.
Data on new drugs like imipenam is limited.

The patient is managed by joined care between cystic fibrosis center & specialized obstetric center.

Screen for diabetes mellitus around 20 weeks

Presence of resting hypoxia(oxygen saturation 80-90%) is an indication for admission for bed rest & oxygen therapy.

Intrapartum

1.care with fluid & electrolyte as patients may easily become hyponatraemic & fluid overload should be avoided in corpulmonle.

2. epidural or caudal anaesthesia is preferred as there is risk post anaesthetic atelectasis.

3.risk of pneumothorax- be wary of chest pain

4.instrumental delivery could be used avoid prolonged second stage.

Postpartum
Breast feeding isn't contraindicated.Sodium & protein content of breast milk is normal.

Most medications used in the management of cystic fibrosis are safe in pregnancy.

Effect of pregnancy on disease

Pregnancy didn't affect the rate of annual decline in FEV1.

Sources