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Towards the end of pregnancy <5% of women have a
platelet count <150 × 109/l. This gestational thrombocytopaenia
carries no significance, but requires exclusion of
other disorders (Table 29.4). If the platelet count is <100× 109/l, further investigations are
required (Table 29.5).

Immune thrombocytopaenic purpura

ITP results in thrombocytopaenia from autoantibodymediated
destruction of platelets. Such antibodies occur
idiopathically and also in association with other disorders
(Table 29.6). ITP mostcommonly presents as asymptomatic
maternal thrombocytopaenia, but transplacental
passage of antibodies can result in fetal thrombocytopaenia
in 9–15% and intracerebral haemorrhage in 1.5% of
babies with affected mothers. The diagnosis of ITP in
pregnancy is by exclusion of other disorders [33].

Spontaneous bleeding is unlikely with platelets >20 × 109/l and monitoring of the patient and
platelet count

Haematological problems in pregnancy 275

Table 29.4 Thrombocytopaenia in pregnancy
Spurious (i.e. clumping or poor sampling)
Immune thrombocytopaenic purpura (ITP)
Heparin-induced thrombocytopaenia (HIT)
Post-transfusion purpura (PTP)
Acute fatty Liver of pregnancy
Pre-eclampsia (PET)/ HELLP syndrome
Thrombotic thrombocytopaenic purpura (TTP)/ Haemolytic
uraemic syndrome (HUS)
Disseminated intravascular coagulation (DIC)
Drug induced thrombocytopenia
Systemic lupus erythematosis (SLE)/antiphospholipid
Congenital thrombocythemias/thrombocytopaenia
Type IIb vonWillebrands disease
Marrow dysfunction/haematinic deficiency
Table 29.5 Investigation of thrombocytopaenia
Blood film to exclude platelet clumps, MAHAor other
haematological disorders
Coagulation screen (to include fibrinogen and D-dimer levels)
Renal and liver function tests
Antiphospholipid antibodies
Anti-DNA antibodies to exclude SLE (antinuclear antibody is
sufficient as a screening test)
Table 29.6 Causes of ITP
Helicobacter pylori
Lymphoma/chronic lymphocytic leukaemia

are often all that is required, with the aim often attaining
an adequate platelet count for delivery.Aspontaneous
vaginal delivery or Caesarean Section can take place when
platelets are >50×109/l. If the woman wishes or requires
epidural or spinal anaesthesia then a platelet count of
>80 × 109/l is recommended [33].
When required, treatment with either oral corticosteroids
or IVIgG produces 50–70% response rates. The

Like HUS. as the nadir in platelets is most often 24–48 h after delivery.7). but is more commonly due to an acquired autoantibody.ADAMTS-13. although there is a congenital form that may recur.IVIgG response usually lasts 2–3 weeks and repeated dosing may be required. ticlopidine. TTP is more often associated with neurological abnormalities and nonrenal organ ischaemia. cyclosporine. Secondary treatments include high-dose methylprednisolone or azathioprine. there is a significant crossover and it is often difficult to distinguish between the two [34–36]. Thrombotic thrombocytopaenic purpura/haemolytic uraemic syndrome Thrombotic thrombocytopaenic purpura (TTP) and Haemolytic Uraemic Syndrome (HUS) are characterized by thrombocytopaenia. low platelets (HELLP) syndrome. There is no evidence. Thus. clopidogrel. coli-0157 HUS Pregnancy Infection (cytotoxin producing E. ITP: THE MANAGEMENT OF DELIVERY The baby’s plateletcountcannotbe reliably predicted from any maternal features. The resultant excess of circulating ultra-large multimers leads to platelet aggregation and consumption. A cord blood platelet countshould be determined in all babies and close monitoring is required over the next 2–5 days. elevated liver. on release from the endothelium.g. 276 Chapter 29 this can be due to a congenital deficiency of ADAMTS13. Furthermore. it may also occur secondary to other influences (Table 29. enzymes. cleaved by the metalloprotease. procedures in labour and atdelivery thatpose an additional bleeding risk should be avoided (fetal scalp electrode. HUScan also be associated with haemolysis. ventouse and rotational forceps). while patients with HUS have predominantly renal manifestations and usually occurs post-partum. but Table 29. coli or Shigella) Drugs (e. In TTP. However. microangiopathic haemolytic anaemia (MAHA) and multiorgan failure. quinine. fetal sampling is hazardous or prone to spuriously low results. is bestcarried outbet ween 13 and 20 weeks’ gestation.g. tacrolimus) Combined contraceptive pill Bone marrow transplant SLE Malignancy HIV E. Other treatments (vinca alkaloids and cyclophosphamide) are notsuit able in pregnancy and splenectomy is also best avoided. fetal blood sampling. TTP occurs most often as an idiopathic single episode. Von Willebrand factor is. that Caesarean section is safer for the thrombocytopaenic fetus than an uncomplicated vaginal delivery. chemotherapy) if essential.7 Causes of TTP/HUS TTP Congenital Pregnancy Drugs (e. however. resulting in the correct balance of vWF multimers. . TTP/HUS is characterized by a failure of this cleavage. or a combination of these therapies with IVIgG.

may be sufficientin congenital disease.leading to microvascular thrombosis. However. ADAMTS-13 is normal and. which should be instituted within 24 h of presentation and although the optimal regime and fluid replacementis notcert ain. FFP alone may be beneficial and. but as the disease progresses there may be coagulation activation and DIC. both are often considered as a single syndrome when considering therapy. or does not respond. although cryosupernatant may be preferred. TTP. indeed. haemolysis. the physiological coagulation changes in pregnancy may predispose to the condition. or frequency of exchanges. usually presents before 24 weeks of pregnancy. Dewhurst's Textbook of Obstetrics and Gynaecology 7th Ediotion halaman 289 . particularly recurrent TTP. haemolysis. platelet transfusions should be avoided in TTP. a reduction in ADAMTS-13 is not specific to TTP/HUS. higher volume. the exact mechanism is not fully understood. it is unlikely that a clear distinction between the two syndromes will be possible in the majority of pregnancyrelated cases. thrombocytopaenia. particularly as there may be benefit in plasma exchange (PEX) in non-toxin-related HUS [37]. However. When exchange is notimmediat ely available. As a consequence. However. fresh frozen plasma (FFP – virally inactivated if possible) is the common standard. DIAGNOSIS HUS typically presents post-partum with thrombocytopaenia. and renal failure. indeed. The mainstay of treatment is PEX. CNS signs and renal dysfunction. all five are only present in around 50% of cases. While TTP is a classic pentad of fever. TREATMENT With the exception of endotoxin-related HUS (where supportive care is the main requirement) and congenital TTP. If the patient deteriorates. in HUS. Consequently. and in many cases of TTP. or differentr eplacementfluid is recommended. Routine blood clotting tests are often normal in the early stages of TTP/HUS. Intravenous methylprednisolone and aspirin (when platelets >50 × 109/l) are often added to PEX therapy.