OBSTETRIC EMERGENCIES OBSTETRIC EMERGENCIES Dr. Malak Al Hakeem.

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Presentation transcript:

OBSTETRIC EMERGENCIES OBSTETRIC EMERGENCIES Dr. Malak Al Hakeem

MAJOR HAEMORRHAGE Definition Blood loss >25% of circulating volume. >1500 mL blood loss heavy continuing blood loss (it would be irresponsible to wait until 1500 mL of blood have been passed before implementing prompt management).

Common causes of major obstetric haemorrhage A) Antepartum Placenta praevia Abruptio placenta Uterine rupture Difficult haemostasis at Caesarean section

B) Postpartum Uterine atony Lower genital tract trauma (perineal, vaginal and cervical lacerations; uterine rupture) Retained products of conception Uterine inversion Amniotic fluid embolism.

MANAGEMENT The aims are: 1- to stop blood loss 2- to resuscitate the patient and restore/maintain oxygen carrying volume to tissues. Summon all extra staff especially a senior anesthetist. Inform blood bank. Take 20 mL of blood for cross match (at least six units), FBC, clot­ting studies, renal and liver function tests.

Administer oxygen by face mask. Insert two 14 G iv lines. Insert a Foley catheter. Give a plasma expander (crystalloid or colloid). Beware, of, fluid overloading especially those with severe pre-eclampsia.

Give blood as soon as possible. Wait for cross-matched blood if the blood pressure improves with fluids and remains stable. Otherwise give ABO compatible blood or even O Rhesus -ve blood if the loss is more than 40%. Use a compression cuff if the volume expansion is needed rapidly.

Consider central venous pressure (CVP)/Arterial lines. Recheck, clotting parameters and blood biochemistry at regular intervals. Give FFP, platelets and cryoprecipitate as appropriate (via consultation with consultant haematologist who should be involved). Consider transfer to intensive treatment unit.

Severe Preeclampsia BP > I60/110 with protienuria > 3gms. Persistent symptoms of epigastric pain, headache, nausea, vomiting and visual disturbance.

Hyperreflexia, papilloedema, epigastric tenderness, cyanosis, and pulmonary Oedema worsening biochemistry (uric acid,, Urea, and liver enzymes.) abnormal coagulation profile(platelets, fibrinogen, fibrinogen degradation products (FDP))PT and APPT. decreasing urinary output

The major risks from uncontrolled severe hypertension are cerebrovascular accidents and placental abruption. Pre-eclampsia carries additional risks of eclampsia, pulmonary Oedema (often iatrogenic due to fluid overload) and DIC..

Management Of Sever PET If the patient has severe hypertension, symptoms or signs suggestive of severe disease or rapidly deteriorating blood test results, involve senior staff, obtain intravenous access and then; 1) Transfer to delivery suite

2) Stabilize the blood pressure Aim to bring the blood pressure to ( )/(90-100). This should be gradual. Patients with pre-eclampsia have a lower circulating blood volume and may tolerate a drop in BP poorly. Excess reduction of BP decreases placental perfusion.

HYPOTENSIVE DRUGS Hydralazin IV 10 mgs. State, followed by infusion ( 5-40mg/hour). Labetelol 20 mgs. State, followed by infusion ( mg/hour).

3) Fluid management Aim to restrict fluid intake to 100 mL/h (remember to calculate the fluids used in antihypertensive and synto. infusions). Urine volume of <30 mL/h can be tolerated for a few hours as the risks of acute tubular necrosis are outweighed by those of pulmonary and cerebral oedema.

Central venous pressure measurements (or even pulmonary capillary wedge pressure) may be necessary to accurately monitor fluid status. Diuretics should not be used to increase urine output unless there is good evidence of fluid overload. Extra colloid can be used if the central venous pressure is low but 'blind' fluid challenges are to be avoided.,

4)Seizure prophylaxis Eclamptic fits can be prevented by using intravenous magnesium sulphate infusion. Give 4-6 gms. of mg. Sulphate IV state followed by 1-3 gms hourly.

5) Delivery Delivery of the placenta is the only way of actually treating the underlying patho - physiological processes of pre-eclampsia. The options are induction and Caesarean section according to cervical status.

An epidural may be helpful in reducing blood pressure by producing vasodilatation and reducing afferent pain stimulation. It is safer than a spinal or general anaesthetic if Caesarean section is required. A coagulopathy is a contraindication to regional anaesthesia and platelet counts of <100 may limit the options for analgesia Don't use methergin or syntometrine in third stage due to its hypertensive action.

6) Continuous observation and monitoring Vigilance must be maintained throughout for complications and deterioration in maternal or fetal condition. BP and urine output hourly.

Oxygen saturation by pulse oximetry. Central venous pressure if oliguric. Serial measurements of platelet count, clotting times, renal and liver functions and serum magnesium levels if having magnesium sulphate.

7) After delivery Continue intensive treatment for at least 24 hours after clinical, biochemical and haematological indices have stabilised. Antihypertensive medications may be necessary for a number of days postpartum. Advise at least a 5-day hospital stay after the delivery.

8)Follow-up This should be at 6 weeks to test urine and BP. If the BP remains raised or protienuria persists, investigate for renal or connective diseases.

ECLAMPSIA Occurrence of convulsions in association with signs and symptoms of preeclampsia. An incidence of 4.9: maternities in the UK (1:2000).

About 40% occur before labour, 20% during labour and 40% after delivery (up to 7 days). Eclampsia is more likely to occur in teenagers (x3) and in multiple pregnancy (x6). The differential diagnosis includes cerebral bleed, local anaesthetic toxicity, and epilepsy.

TREATMENT Summon help. Obtain iv access and if still fitting give diazepam bouls 10 mg iv. Check airway for obstruction and give oxygen. Stabilize blood pressure (as for pre- eclampsia). Transfer to delivery suite and inform senior obstetric and anaesthetist consultants

Commence magnesium sulphate with a bolus dose of 4 -6 g ( mLs of 20% solution) given over 20 minutes. Maintenance dose is 1 -3 g/h (5 g in 500 mL normal saline and run at lOOmL/h). Magnesium sulphate causes central and therefore respiratory depression.

Respiratory rate, oxygen saturations and patellar reflexes should be recorded regularly before giving it to detect toxicity. This is more likely if renal function is poor. One gram of calcium gluconate iv over 2—3 minutes is used to reverse toxic effects of mg. Sulphate.

THROMBOEMBOLISM Incidence An incidence of 1 per 1000 on going pregnancies and 2 per 1000 recently delivered pregnancies. Venous thromboembolism (VTE) is the commonest cause of direct maternal death.

Risk factors for thromboembolism immobility surgery (relative risk of VTE is increased 10 times after LSCS) thrombophilias (lupus anticoagulant; antithrombin III, protein S and C deficiencies and activated protein C resistance) multiparity obesity age over 35 previous history of TE family history of TE infection pre-eclampsia.

DIAGNOSIS Most cases present in the third trimester and up to 6 weeks after delivery with leg pain, swelling and erythema or dyspnoea, chest pain and sometimes haemoptysis. Diagnosis on clinical features alone is unreliable

For suspected deep vein thrombosis arrange Doppler flow ultra­sound. This has a high sensitivity (94%) for iliac/femoral vein thrombosis although it may not be able to distinguish external compression from occlusion and will not exclude calf vein thrombosis

limited venography is the investigation of choice for suspected below knee thrombosis. The radiation dose to the fetus is small and is justifiable in view of maternal risk

If a pulmonary embolus is suspected check arterial blood gases and a chest X- ray (with shielding of the abdomen there is no risk to the fetus and it excludes other causes of chest pain). A perfusion lung scan should be carried out and once again the radiation risk should be considered less than the risk of missing the diagnosis.

Treatment Treatment with iv heparin should commence as soon as the clinical diagnosis of a DVT or PE is made or strongly suspected.

Start an intravenous infusion of IU heparin/h after a loading dose IU. Check the activated partial thromboplastin time (APTT) 6 hours later and adjust to maintain a level of

After resolution of clinical symptoms convert to subcutaneous heparin( during pregnancy) iu bd subcutaneously or low molecular weight heparin units per day monitored by factor Xa heparin assay (appropriate range = ).

Check maternal platelet count at regular intervals, especially around a week to ten days after commencing treatment. Heparin can cause an immune-mediated thrombocytopenia with paradoxical thrombotic episodes

For delivery reduce the heparin to IU bd and normalize the APTT. Have FFP available for bleeding. Resume iv heparin IU/24 h after delivery and then convert to warfarin for 6-12 weeks. Warfarin is safe to use whilst breastfeeding.