Obstetric Emergencies PDF

OBSTETRIC EMERGENCIES APH, POSTPARTUM COLLAPSE, ANTEPARTUM HAEMORRHAGE (APH) DR BAKARE.A ANTEPARTUM HAEMORRHAGE(APH) Bleeding from the genital tract / per vaginum after the 28th weeks of gestation and before delivery of the newborn. APH is an obstetric emergency...

OBSTETRIC EMERGENCIES APH, POSTPARTUM COLLAPSE, ANTEPARTUM HAEMORRHAGE (APH) DR BAKARE.A ANTEPARTUM HAEMORRHAGE(APH) Bleeding from the genital tract / per vaginum after the 28th weeks of gestation and before delivery of the newborn. APH is an obstetric emergency and it is associated with increased risk of maternal and perinatal morbidity and mortality. CAUSES OF APH Placenta praevia Placenta abruption Local causes (a) Cervical polyp (b) Cervical erosion (c) Carcinoma of the cervix (d) Cervicitis (e) Friable condyloma acuminata (f) Vaginitis (g) Trauma  The most common causes of APH are placenta praevia and placenta abruption.  These 2 conditions require prompt assessment to determine between conservative management and immediate delivery.  PLACENTA PRAEVIA Is defined as placenta that is wholly or partially located in the lower uterine segment. CLASSIFICATION It can be classified into 4 classes: Type i- The placenta encroaches on the lower uterine segment but does not reach the internal os. Type ii-The placenta reaches the internal os but does not cover it. Type 11 can be divided into (a) and (b); that is anterior and posterior respectively. Type iii- The placenta eccentrically reaches the internal os and crosses to the other side but cease to do so as the cervix dilate. Type iv – The placenta completely covers the internal os even when the cervix is dilated or undilated. PREDISPOSING FACTORS TO PLACENTA PRAEVIA Advanced maternal age Increased parity Previous uterine surgery including caesarean section Intrauterine synaechiae Multiple pregnancy Abnormality of endometrial vascularisation Prior trauma to the endometrium or myometrium including D&C Smoking  PRESENTATION  Placenta praevia is the leading cause of 3rd trimester bleeding per vaginum.  The bleeding per vaginum is painless and bright red.  Some women may have spotting during the 1st and 2nd trimesters of pregnancy.  As pregnancy advances, Braxton Hicks contractions may cause the lower segment to thin and even result in dilatation of the cervix.  DIAGNOSIS / CLINICAL FINDINGS  Placenta praevia may be asymptomatic but more often there is recurrent painless bleeding per vaginum.  Abdomen is usually soft with NO AREA OF TENDERNESS.  A high fetal head or presenting part of the fetus may be high.  The lie of the fetus may be abnormal.  The fetal heart tone is usually audible and regular.  Pelvic /vaginal examination is contraindicated in patients with APH since it might provoke further (serious) haemorrhage. However , a speculum examination can be done after excluding placenta praevia with ultrasound scan.  INVESTIGATIONS GENERAL  Pcv/ Hb  FBC  E, U and Creatinine  Urinalysis  Midstream urine for M/C/S SPECIFIC  Abdominopelvic ultrasound scan  Magnetic resonant imaging ( MRI) – Is the most precise method of diagnosing placenta praevia but it is an expensive method of tissue imaging.  TREATMENT EXPECTANT MANAGEMENT( MACAFEE REGIMEN) This is for foetuses remote from term. If the bleeding is slight and the gestation is less than 37weeks, ` conservative treatment is indicated till the end of 37weeks. The patient is hospitalised with bed rest and observed till delivery after 37 completed weeks of gestation Blood transfusion is commenced to replace any blood loss and raise the Hb concentration to at least 10g/dl or Pcv of 30%. At least 4 units of blood should be grouped and cross matched and saved for emergency situations.  In placenta praevia, maternal haemorrhage is most feared but fetal blood can also be lost during the process of placenta separation. If the patient is Rh negative, anti-D immune globulin should be administered. Fetal heart tones should be checked at least twice daily and fetal kick count instituted. The patient should keep a perineal pad and it should be inspected often to assess bleeding per vaginum. If the patient is in labour, vaginal delivery is allowed if the placenta is type I or II(a), vertex presentation and the pelvis is adequate  For TYPES I and II anterior placenta praevia, the treatment is artificial rupture of membranes followed by intravenous Oxytocin infusion to induce labour and effect delivery.  For TYPES II posterior, III and IV, the treatment is caesarean section.  DOUBLE SET- UP EXAMINATION  This was done/ performed to rule out placenta implantation in the lower uterine segment.  It was done in centres with no ultrasound facility.  Double set-up is performed at 37 weeks gestational age where there is suspicion of placenta praevia.  It is done in the theatre in the presence of two obstetricians.  One obstetrician performs the digital examination and the other is scrubbed and gowned in preparation for the C/S if excessive vaginal bleeding occur.  ABRUPTIO PLACENTAE Is the premature separation of a normally situated placenta before the delivery of the fetus. AETIOLOGY The cause is unknown but there are some associated factors which include: 1)Maternal hypertension 2)Severe preeclampsia / eclampsia 3)Direct trauma to the abdomen 4)High parity 5)Advanced maternal age 6)Low socio economic status 7)Rapid decompression of the uterus following rupture of fetal membrane.( as could occur in polyhydramnios and multiple pregnancy. 8)Uterine fibroids 9)Smoking 10)Use of cocaine 11)Folic acid deficiency CLASSIFICATION 1)Revealed 2)Concealed 3)Mixed 1. REVEALED- Bleeding is revealed through the vagina. 2. CONCEALED- There is no obvious bleeding through the vagina, when there is bleeding into the myometrium and it causes a woody hard tender uterus otherwise known as COUVELAIRE UTERUS. If the above process continues, there will be release of tissue thromboplastin into maternal circulation and microvasculature. DIC sets in; which might trigger the coagulation cascade system with depletion of fibrinogen, platelets and other clotting factors. CLINICAL FEATURES 1.Vaginal bleeding (80% of patients) 2.Abdominal discomfort / pain ( which increases in severity) 3.There may be uterine contractions 4.Backache 5.Absence of fetal movements. CLINICAL SIGNS 1.Signs of shock  Pallor  Cold clammy extremities  Rapid pulse 2.Abdominal examination  Tense, tender woody hard uterus.  Fetal parts are difficult to palpate and fetal heart beat maybe be absent. The uterus may be noted to relax in between contractions, if the patient is in labour.  Increased abdominal girth may be observed if the abruption is continuing.  Vaginal examination is performed after excluding placenta praevia.This will show evidence of bleeding in the revealed or mixed type of abruption placenta.  The cervix may also be dilated, if the patient is in labour.  MANAGEMENT The initial assessment of placental abruption should be swift and decisive since the prognosis for the fetus and the mother is worsened by delay. An intravenous line is set up and the infusion of crystalloid solution begun. Blood should be taken for Hb estimation, coagulation studies profile (platelet count, fibrin degradation products, PT/PTTK) FBC Group & crossmatching of at least 2 units of blood. A crude bedside clotting time should be done. If the clot does not form within 10 to 12 minutes or forms and lyses within 30minutes  A coagulation defect should be suspected and FFP should be started before the coagulation results are retrieved.  Blood loss should be corrected as soon as possible.  E, U, Creatinine  Urinalysis  Mid stream urine for M/C/S  Abdominopelvic USS- This helps to locate the placenta, exclude placenta praevia and confirm fetal viability.  Negative ultrasonographic findings does not exclude abruption placenta.  Intravenous O2 should be given if necessary and an indwelling self- retaining catheter passed to monitor the urinary output, which should be at least 30mls/hour.  If the pregnancy is at term and both the mother and fetus are stable, cautious induction of labour with vaginal delivery may be attempted.  Amniotomy might hasten the onset of labour and the uterine contractions as well as reduce uterine bleeding.  If there is IUFD, the mother should be stabilised before vaginal delivery.  If there is fetal distress and cervix is not fully dilated or there is severe maternal bleeding, caesarean section must be performed.  If the fetus is preterm, the mother is haemodynamically stable, blood loss is minimal and there is no evidence of fetal distress, careful expectant management with corticosteroids to accelerate fetal lung maturity can be initiated. The fetus should be continuously monitored till it is safe to be delivered.  COMPLICATIONS OF ABRUPTION PLACENTA MATERNAL Haemorrhage which could be life threatening and lead to hypovolemic shock. Increased risk of PPH.Atonic uterus is managed by oxytocin infusion containing 20 -40 IU of oxytocin in 500mls of N/S to run for at least 4 hours. Clotting disorder – Clotting time should be done 4 hourly for early detection. DIC results from release of thromboplastin from the placental site and fibrinogen is converted to fibrin by activation of the extrinsic clotting cascade system. Increased caesarean delivery.  Ischaemic necrosis of distal organs especially the kidneys, resulting in acute tubular necrosis or bilateral cortical necrosis.  Renal failure is usually the result of prolonged hypovolemic shock, hypertension and DIC.  Oliguria.  Uraemia.  Maternal death.  FETAL COMPLICATIONS Hypoxia Anaemia IUGR for conservative management. IUFD  LOCAL CAUSES OF ANTEPARTUM HAEMORRHAGE  Cervical erosion  Cervical polyp  Cervical carcinoma  Varicosities of the vulva or introitus  Vaginitis  Trauma  MANAGEMENT CERVICAL EROSION- Bleeding from cervical erosion is usually slight and will stop without any treatment. Cauterisation in pregnancy should be avoided. CERVICAL POLYP- Should be left alone unless there is active bleeding when gentle avulsion can be performed. Bleeding from the base after removal of the polyp will usually stop after some hours once pressure is applied. CERVICAL CARCINOMA- It is usually friable and readily bleeds to touch. VARICOSE VEIN- May rupture and cause bleeding. Apply pressure which may stop the bleeding. Occasionally the ruptured vein may be ligated. TRAUMA- If the trauma is from postcoital laceration, the laceration site should be repaired. VAGINITIS- Most infections causing bleeding clear readily when treated with appropriate agents.  VASA PRAEVIA This is bleeding from the fetal vessels. It often results from velamentous insertion of the umbilical cord. The cord inserts at a distance from the placenta and it is not protected by whartoms jelly. The umbilical cord vessels traverse between the chorion and amnion without protection ( below the fetal presenting part) and might cross the os. Spontaneous or artificial rupture of membranes or dilatation of the os might lead to rupture of these fetal vessels.  Bleeding from the fetal vessels is usually associated with abnormal fetal heart pattern and delivery should be rapid by emergency caesarean section.  The total blood volume of a term fetus is approximately 375ml and shock will occur in the fetus when the blood loss is approximately 72mls  A high index of suspicion is required to diagnose and rapidly manage ruptured vasa praevia.  The incidence is approximately 1 per 5000 singleton deliveries.  The fetal mortality rate is as high as 75 to 100%  APT TEST Is used in the diagnosis of vasa praevia by mixing suspected bloody vaginal fluid with water and after centrifuging, the supernatant is mixed with 1%NaoH. The pink colour after another centrifuge indicates the presence of fetal blood. The physiology behind this test is that fetal oxyhaemoglobin is more RESISTANT TO ALKALINE than adult oxyhaemoglobin is converted to alkaline globin haematin (denatured). SUDDEN POSTPARTUM COLLAPSE  OUTLINE INTRODUCTION AETIOLOGY / CAUSES SIGNS AND SYMPTOMS DIAGNOSIS MANAGEMENT CONCLUSION  Signifies an abrupt acute event after delivery involving the brain, heart and / or lungs and may ultimately result in death. - Nutritional intake is restricted during labour and consequently leads to development of dehydration, ketoses and mild pyrexia. - Changes in circulating volume, shivering and the emotional climax of delivery all contribute to the picture. - If a pathological event supervenes the situation becomes dramatic with shock and its attendant symptoms. - Poor monitoring of patients results in the early warning signs for disaster /postpartum collapse not being detected. CAUSES (A)OBSTETRIC CAUSES Eclampsia Obstetric Haemorrhage Pulmonary Thromboembolism Amniotic Fluid embolism Uterine inversion (B) NON OBSTETRIC CAUSES Anaesthetic toxicity Aspiration pneumonitis Cardiac arrhythmia Myocardial infarction ( rare in a healthy women) Cerebrovascular Accident Peritoneal haemorrhage due to a ruptured aneurysm such as splenic artery aneurysm, hepatic artery aneurysm, or the aorta itself, ruptured liver or spleen. C. OTHERS INTRACRANIAL HAEMORRHAGE Spontaneous Subarachnoid haemorrhage Pre-eclampsia – associated intracerebral haemorrhage (ii)ENDOCRINE * Hypoglycaemia (iii)Miscellaneous Septic shock Anaphylactic shock Adverse drug reaction. SYMPTOMS General feeling of unease Vomiting Dizziness Fainting attack Chest pain Difficulty in breathing.  SIGNS Pallor Cyanosis Tachycardia Hypotension Poor peripheral Perfusion Alteration in level of consciousness  MANAGEMENT GENERAL History taking, physical examination investigation and treatment of the cause. While taking the history, resuscitation of the patient is commenced and ABC (Airways, Breathing, Circulation) drill is followed with a large-bore Cannula inserted to immediately infuse 1 litre of Normal saline - The airways are cleared and suctioned of there are secretions - Bedside clotting Time - As the general physical examination is continued to know the came of the collapse, other investigation that could be done include: - Arterial blood gases - CXR - ECG - Ventilation / Perfusion Scan - CT Scan of the Brain - Pulmonary angiography - A urethral Catheter should be passed to monitor urine output on an hourly basis. - A abdominopelvic ultrasound will show free fluid in the peritoneal cavity (intraperitoneal bleeding) or if there is retained product of conception.  SPECIFIC Depends on the cause of the postpartum collapse history, physical examination and investigation. PPH – Most common cause of obstetric haemorrhage and postpartum collapse Uterine atomy-rub up uterine contraction and set up on I.V. line. Give I.V Ergometrine (0.5mg), if she is not hypertensive, or I.V 10 i.U. of Oxytocin slowly.  If the uterus is not well contracted, peform bimanual compression of the uterus and inject prostaglandin /or Ergometrine into myometrium or intramuscularly. If all conservative measures fail to control bleeding, perform emergency laparotomy. At laparotomy, check for uterine rupture and repair or perform hysterectomy (subtotal or total) if there is an extensive rupture. Uterine artery ligation could be done.  If the uterus contracts and relaxes and there is no rupture internal iliac artery ligation or hysterectomy. B-LYNCH (BRACE) SUTURE-Is a compression suturing technique with sutures passed around the uterus both anteriorly and posteriorly after exteriorising the uterus. Intervention radiography - Selective transarterial embolization (gel foam) - Selective arterial infusion of Vasopressin.  The radiographic approach to obstetric haemorrhage has some advantages over the surgical approach. - Anaesthetic and surgical risks are reduced - Specific vessels can be identified and selectively occluded. - Hysterectomy can be avoided. In the absence of coagulopathy, the success rate of arterial embolization is >90%. GENITAL TRACT LACERATION EUA and suture the laceration PELVIC Vulvar Haematoma HAEMATOMAS Vaginal Haematoma Retroperitoneal Haematoma. Linear incision of the mass and evacuate the blood and clots UTERINE INVERSION Fundus of uterus turning “inside out” Is a life-threatening event. 1 in 2,000 deliveries. Treatment involves annual vaginal replacement of the uterine fundus Uterine-relaxing agents may be used if need be. Once uterus is replaced, oxytocin infusion should be administered to produce uterine contraction. Occasionally, if it is impossible to reposition the inverted uterus vaginally, perform a laparotomy. AMNIOTIC FLUID EMBOLISM (AFE) Is a rare but frequently fatal obstetric emergency 1 in 80,000 births. The definitive diagnosis of AFE require the demonstration of FETAL SQUAMES and LANUGO in the maternal circulation (pulmonary vascular space).  The amniotic fluid induces acute vaso- constriction of the small pulmonary vessels and not total mechanical occlusion of the pulmonary vessels. 50% of patient with AFE die within 1 hour of onset of illness; mainly due to circulatory failure. 25% of deaths may be attributed to coagulopathy. The remainder are related to pulmonary complications.  The classic clinical presentation of AFE are as follows: (a)Respiratory distress (b)Cyanosis (c)Cardiovascular collapse (d)Haemorrhage (e)Coma.  Treatment of AFE is mainly SUPPORTIVE - Endotracheal intubation and antificial ventilation. - Cardiopulmonary resuscitation - 02 is given intranasally 6-7 litres / min - Circulatory support by intravenous line (Normal saline) with wide-bore cannula. - Treat heart failure with inotropic agent such as I.V. Dopamine / Dobutamine - I.V. Steroids may be useful - Correct coagulopathy with FRESH WHOLE BLOOD FRESH FROZEN PLASMA or CRYOPRECIPITATE as soon as they are available. - Haematology should be invited.  ANAESTHETIC TOXICITY To avoid this the anaesthetist should take a thorough history and exam the patient. Anaesthetist should be alert when administering the anaesthetic agents. ASPIRATION PNEUMONITIS It is a serious and fatal complication of general anaesthesia. It could prevented by: - Placing the patient on NPO at least 8-12hours prior to an elective operation. - In Emergency cases, an N-G tube may be passed to aspirate gastric contents - About 30 minutes before the operation, 30mls of a clear, non-particulate antacid, such as 0.3M sodium citrate is administered to decrease gastric acidity.  In elective Caesarean Sections, 150mg of Raniditine is given the night before operation and repeated 2 hours before the operation to reduce the volume of gastric acid and increase the pH of gastric contents.  PULMONARY THROMBOEMBOLISM The incidence in pregnancy is 1 per 2,500 pregnancies. 75% occur in the immediate postpartum period. It is one of the 3 leading causes of maternal deaths in industrialized nations Pregnancy predispose gravid patients to an increased risk of thromboembolism Puerperal infection increase the risk of venous thromboembolism  The major source of pulmonary emboli are DEEP VEINS THROMBOSES in the veins of the calf and iliofemoral system. Septic pulmonary emboli are most likely to arise from the veins of the pelvis. CLINICAL MANIFESTATIONS - Anxiety - Retrosternal pain - Tachycardia - Dyspnea - Apnea - Cyanosis - Loss of consciousness - Shock. PHYSICAL FINDINGS - Haemoptysis - Pleural friction rub - Fixed splitting of the second heart sound - S gallop 3  DIAGNOSIS Ventilation – Perfusion (V-P) Scan is the most accurate non-invasive means of diagnosis. A normal V-P scan reliably excludes the diagnosis of pulmonary embolism. If the V-P scan is equivocal, pulmonary angiography should be performed.  MANAGEMENT OF PULMONARY EMBOLISM (MEDICAL THERAPY) Maintain a patent airway. Maintenance of ventilation and Oxygenation Hypotension should be corrected by administration of isotonic crystalloids. Anticoagulation is indicated once the diagnosis of pulmonary embolism is confirmed. Administration of an initial intravenous bolus of 5000 to 10,000 units of heparin followed by a continuous infusion. I.V heparin should be continued for a minimum of 7-10 days.  SURGICAL THERAPY PULMONARY EMBOLECTOMY - Patients with massive embolus in the proximal portion of the main pulmonary arteries.  MYOCARDIAL INFARCTION (M.I) Is an unusual complication of pregnancy In 10,000 to 1 in 42,000 pregnancies. The majority of cases occur in the 3rd trimester and the immediate puerperium. The maternal mortality is approximately 35-45%.  PREDISPOSING FACTORS OF M.I.. - Pre-existing atherosclerotic heart disease. - Hypertension - Hyperlipidaemia - Age >35years - Cigarette smoking - Insulin-dependent diabetes - Obesity - Sedentary life style. CLINICAL PRESENTATION OF M.I. - Severe crushing substernal pain - Nausea, vomiting - Dyspnea - The pain may radiate into the neck and down along the left arm. - Shock - Loss of consciousness - Pulmonary edema - Arrhythmias. Diagnosis of M.I. - ECG and Cardiac Enzymes are the most commonly used test to establish the diagnosis. - ECG findings include ST – segment elevation - Cardiac isoenzyme profile initially demonstrate an elevation in creatine phosphokinase. Concentrations increase within 4-6 hours after the infarction, reach a max. at 24hrs and return to normal within 3 days. - The aminoacid transferase enzymes (SGPT and SGOT) begin to increase 6-8 hours after the acute event, peak at 24-48 hours, and return to baseline within 4 days. - Lactic acid dehydrogenase (LDH) does not increase until approximately 12 hours after the infarction. The concentration reaches a maximum in 3-6 days and then decreases to normal within 14 days.  COMPLICATIONS OF M.I. Cardiac arrhythmia such as ventricular tachycardia, ventricular fibrillation, complete heart block and asystole. Left ventricular dysfunction lead to congestive heart failure. Cardiogenic shock Death  MANAGEMENT OF M.I. 1st objective is identification of women who are at risk for M.I. Efforts should be made during labour to ensure that these patients are well oxygenated and relatively free of pain. Wide variations in blood pressure, heart rate and cardiac output are most effectively prevented by utilization of regional anaesthesia. If acute infarction develop in the immediate puerperium, emergency management is directed towards securing the patients airway and providing effective ventilation. - Closed cardiac massage may be necessary initially to support the circulation. - Dopamine and dobutamine are the preferred vasopressor agents to sustain the perfusion pressure. - Life threatening arrhythmias (e.g. ventricular tachycardia and fibrillation) must be treated immediately by countershock. - Complete heart block should be treated initially with atropine until a cardiologist is available to insert a transvenous pacemaker - Once the patient is stabilised, she should be transferred to a coronary care unit for definitive management by medical specialists. - The cardiologist must be involved in cases of sudden postpartum collapse due to cardiac arrhythmias, myocardial infarction and CVA.  PERITONEAL HAEMORRHAGE - Due to ruptured aneurysm – Hepatic artery, splenic artery. An emergency laparatomy has to be performed with the General surgeon in attendance for further and expert management. INTRACRANIAL HAEMORRHAGE After this has been confirmed by the CT-Scan, the Neurosurgeon must be involved in the management. HYPOGLYCAEMIA * 50mls of 25% glucose is given intravenously.  SEPTIC SHOCK - Central venous pressure monitoring - Intravenous fluids to maintain blood pressure and adequate kidney perfusion. - Intranasal 02 / 02 by face mask - Vasopressor agent - Digitalis - Corticosteroids - Broad Spectrum Antibiotics.  ANAPHYLACTIC SHOCK - 0.5ml of Adrenalin 1:1000 - Antihistamine - Hydrocortisone - Intravenous fluids. CONCLUSION - Sudden postpartum Collapse (SPC) is a rare and terrifying obstetric complication that is caused by a limited number of disorders as discussed above. - The usual clinical manifestations are apnea, cyanosis, shock and generalized tonic-clonic seizures. - The immediate objective in the management of SPC is to provide ventilation and oxygenation and to initiate fluid resuscitation. CONCLUSION (CONTINUED) - Selected laboratory studies should be performed to determine the cause of SPC such as arterial blood gas analysis, ECG, evaluation of haemodynamic monitoring and examination of blood aspirated from the central circulation. - SPC can be minimised by examining patients more thoroughly, by improving clinical documentation and close monitoring of patients in hospital, especially in the postpartum period. CONCLUSION (CONTINUED) - Inviting specialist in other specialities in the management of SPC is important as at when due. - Obtaining autopsies would also help in making accurate diagnosis. - Having done the above, maternal mortality will be reduced to the barest minimum in our environment. THANK YOU FOR LISTENING