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Obstetric Emergencies Dr Mohamed Abdul Hakim Kotb,MBBCH,MSC,MD Anaesthesia & ICU.

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Presentation on theme: "Obstetric Emergencies Dr Mohamed Abdul Hakim Kotb,MBBCH,MSC,MD Anaesthesia & ICU."— Presentation transcript:

1 Obstetric Emergencies Dr Mohamed Abdul Hakim Kotb,MBBCH,MSC,MD Anaesthesia & ICU

2 Obstetric emergencies Massive obstetric haemorrhage Non-haemorrhagic shock: –Amniotic fluid embolism –Acute uterine inversion Shoulder dystocia Eclampsia Cord prolapse Cardiac Arrest AnaphylaxisTRAUMA

3 BASIC PRINCIPLES FOR OBSTETRIC EMERGENCIES. Physiological changes in pregnancy modify: Presentation of the problemPresentation of the problem Normal physiological variablesNormal physiological variables Response to treatmentResponse to treatment Both mother & fetus are affected by the pathology & subsequent treatment. Mothers welfare always takes precedence over fetal concerns --- Fetal survival is usually dependant on optimal maternal management.

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5 MASSIVE OBSTETRIC HAEMORRHAGE Major contributor to maternal mortality Definition –Blood loss requiring replacement of patients total blood volume –Transfusion requiring > 10 u of blood in 24 hs –50% replacement of blood vol. <3 hs period Difficult to estimate blood loss Problem of concealed bleeding –Uterus –Broad lig. –Peritoneal cavity

6 RECOGNISING SIGNIFICANT BLOOD LOSS 10 – 15% ml Normal BP No signs % ml BP ~ 100mmHg Dizziness, tachycardia 25-35% ml. BP ~ 70-80mmHg. Restlessness,pallor, oliguria.35-45% ml 50-70mmHg Collapse, air hunger, anuria

7 Factors contributing to maternal death from catastrophic PPH General Increased oxygen and cardiac output requirements of pregnancy may hamper adequate blood / volume replacement –Placental bed perfusion 600 mls/min Blood loss underestimated Delayed or inadequate management Inadequate resources / personnel Specific Failure to anticipate coagulopathy PET, abruption, sepsis, IUFD, AFE. Abnormal placentation Placenta praevia / accreta Jehovahs witness**

8 Mechanism of DIC 1) intravascular infusion of thromboplastic substances that initiate the extrinsic coagulation system –placental abruption, IUFD 2) conditions associated with endothelial cell damage, which activates both the extrinsic and intrinsic coagulation systems –eclampsia/ PET 3) indirect effects of other disease, such as G- sepsis, AFE etc

9 Preventative Management PPH Detect and treat antenatal anaemiaDetect and treat antenatal anaemia Active Management of Third StageActive Management of Third Stage Administration of a prophylactic oxytocin Administration of a prophylactic oxytocin Early cord clampingEarly cord clamping Controlled cord traction of the umbilical cord.Controlled cord traction of the umbilical cord. Advantage of active management = reduction in the incidence of PPH by 40% IV access plus collect blood for grouping and cross matching if assessed as at risk.

10 Available from Royal Womens Hospital, Carlton, Clinical Practice Guidelines: 3333

11 Management Principles Organisation restoration of blood volume correction of coagulopathy evaluating response to treatment monitoring PR, BP, CVP, ABG, UOP If resuscitation is adequate P & BP should return to normal treat the cause abruption placenta praevia uterine rupture placenta accreta

12 Available from Royal Womens Hospital, Carlton, Clinical Practice Guidelines: whcpg/womenshealth.cf m?doc_id=3333

13 NON-HAEMORRHAGIC OBSTETRIC SHOCK Uncommon but responsible for majority of maternal deaths in developed countries. -Amniotic fluid embolus -Acute uterine inversion

14 Amniotic Fluid Embolism – –Passage of amniotic fluid debris into maternal circulation – –Obstructs pulmonary circulation – –Cardio-respiratory arrest

15 AMNIOTIC FLUID EMBOLISM Clinical features –Multiparous women –Precipitous labour –Presence of intact membranes –Sudden dyspnea –Hypotension –Seizure activity not uncommon –If survive initial insult 70% suffer non-cardiogenic pulmonary oedema ARDS

16 AMNIOTIC FLUID EMBOLISM Diagnosis –Consider in all obstetric patients with sudden collapse. –Differential PTE Septic shock MI Aspiration pneumonia Allergy to drug

17 Management Secure airway treat cardiovascular collapse central venous line acute left ventricular failure: digoxin dopamine correct coagulopathy treat metabolic/electrolyte abnormalities

18 Acute Uterine Inversion Most commonly arises from mismanaged 3 rd stage

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20 Presentation Sudden collapse in 3 rd stage Degree of shock inconsistent with blood loss Shock is neurogenic in nature Traction on infundibular pelvic ligament May be no palpable fundus Mass in vagina/introitus

21 Management Avoid mismanagement of 3 rd stage of labour Once occurs –Anti-shock measures –If placenta still attached remove after uterus is replaced –Manual replacement of uterus –OSullivans hydrostatic pressure –Surgical correction

22 Shoulder Dystocia

23 Erbs palsy

24 It all comes, said Pooh crossly, of not having front doors big enough

25 It all comes, said Rabbit sternly, of eating too much

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27 Risk Factors Macrosomia (>4kg) –maternal diabetes –post dates –maternal obesity –high maternal wgt gain in pregnancy –advanced maternal age –previous large infant –previous shoulder dystocia Intrapartum –protracted late active phase –prolonged 2nd stage –delay in head descent in 2nd stage –mid-pelvic operative delivery The combination of macrosomia and delay in 2nd stage predicts 35% of shoulder dystocia

28 Eclampsia 1/1500

29 Complications Cerebrovascular injury pulmonary oedema coagulopathy maternal/fetal death HELLP syndrome

30 Presentation Hypertension, hyperreflexia, clonus, headache, visual changes, seizure 20% have diastolic BP<90, normal reflexes, and urinary protein <2+ 70% of deaths due to intracerebral haemorrhage

31 Management Goals: Goals: – Stabilization of the mother/seizure control MgSO4 therapy: 4-6 g over 20 min followed by MgSO4 therapy: 4-6 g over 20 min followed by infusion of 1-3 g/hr, OR Thiopental or diazepam followed by MgSO4 Thiopental or diazepam followed by MgSO4infusion – Airway management – Avoiding aspiration

32 Prolapsed Cord 1/500 deliveries Most occur during ARM

33 Presentation Cord visible outside the introitus CTG abnormalities appear –variable decelerations –fetal bradycardia Note: fetal or maternal injury due to hasty intervention

34 Management Keep cord warm - replacing in vagina may help Keep pressure off cord by gloved hand in vagina lifting fetal part off the cord Positioning,Maternal O 2, IV access If fetus is alive, operative delivery - CS if not able to deliver vaginally If fetus is dead, vaginal delivery if presentation allows

35 Anaphylaxis vasodilatation, smooth muscle contraction, glandular secretion, increased capillary permeability Management: –oxygen –colloid –bronchodilator –adrenaline (despite Ux stimulatory effect) –anti-histamine (if angioneurotic oedema) –steroid (for refractory bronchospasm)

36 Maternal cardiac emergency Acute: –AMI –Tocolytic therapy –Aortic dissecting aneurysm –Peripartum cardiomyopathy: 1 in 50000, 50% progress to end-stage heart failure (heart Tx), 50% recurrence. Suspect if acute SOB, chest pain, abN ECG, signs LVF/RVF –Traumatic myocardial contusion: ie: MCA

37 Drug Overdose Illicit drugs: heroin, cocaine and amphetamines (these 2 can cause hypertension, ^ C.O., decrease Uterine blood flow, APH, cerebral haemorrhage, convulsions, arrhythmias). Drug overdose Drug error Anaphylaxis Hypermagnesaemia: –wide QRS on ECG, 5-6mmol/l lose tendon reflex –resp. paralysis, SA and AV node block –cardiac arrest. Treatment: CaGluconate 10% 10ml slow IV

38 CARDIO-PULMONARY ARREST Cardiac arrest rare in pregnancy (1 in deliveries) Usually associated with particular obstetric complications like amniotic fluid embolism, drug toxicity from Magnesium sulphate & local anesthetics.

39 Technique for external cardiac massage: External cardiac massage in non-obstetric patient provides 30% cardiac output. External cardiac massage in non-obstetric patient provides 30% cardiac output. After 20 weeks reduced further due to veno-caval compression. After 20 weeks reduced further due to veno-caval compression. Relief of aorto-caval compression part of BLS: Relief of aorto-caval compression part of BLS: left lateral tilt --- decreased efficacy of compressions left lateral tilt --- decreased efficacy of compressions wedge 27 0 angle allows 80% of maximal force to be dissipated wedge 27 0 angle allows 80% of maximal force to be dissipated rescuers thigh as wedge. rescuers thigh as wedge. Sodium bicarbonate controversial as it leads to fetal acidosis but pH has to be kept above 7.30 to prevent uterine vasoconstriction. International Liaison Committee on Resuscitation (ILCOR) if there is no response to ALS, peri-mortem caesarean delivery should be made within 5 minutes of arrest if there is no response to ALS, peri-mortem caesarean delivery should be made within 5 minutes of arrest

40 TRAUMA Occurs in 6-7% of all pregnancies. Hospital admissions only % of all pregnancies. 1% of all trauma cases are pregnant. Maternal deaths associated most commonly with head injuries & severe hemorrhage. Fetal deaths associated with placental abruption & maternal death. Fetal deaths associated with placental abruption & maternal death.

41 Management Initial resuscitation should follow normal plan of ABC. Hypotension may not be present until 35% or more blood volume is lost. Aorto-caval compression release Rule out pelvic fractures, uterine injury & retro-peritoneal hemorrhage Fetal monitoring with cardio-tocographic monitor Rh immunoglobulin – within 72 hours. Radiation hazards: 1 st trimester >5 rads Chest x-ray < 5 rads Chest x-ray < 5 rads Pelvic film <1 rads Pelvic film <1 rads Abdomino-pelvic CT scan 5-10 rads Abdomino-pelvic CT scan 5-10 rads

42 BURNS Increased levels of prostaglandins predispose to pre-term labour. Replacement of fluids vis-à-vis increased volumes in pregnancy. Inhalational injury- hypoxia & carbon monoxide poisoning Infections- prophylactic antibiotics controversial Topical Povodine iodine- affects fetal thyroid functions

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