OBSTETRIC EMERGENCIES

CONDITIONS

 


SHOCK VASA PREVIA CORD PRESENTATION AND CORD PROLAPSE AMNIOTIC FLUID EMBOLISM INVERSION OF UTERUS

1. SHOCK

Shock is defined as a state of circulatory inadequacy with poor tissue perfusion resulting in generalized cellular hypoxia leading to dysfunction of organs and cells

CLASSIFICATION
A.

HYPOVOLEMIC SHOCK:- The result of a reduction of intravascular volume Hemorrhagic shock: PPH, Post abortal hemorrhage, ectopic pregnancy, placenta previa, abruptio placenta, obstetric sx , rupture of uterus etc… Fluid loss shock: excessive diarrhoea, vomiting, rapid removal of amniotic fluid Supine hypotensive syndrome: compression of inferior venacava. Shock associated with DIC, intra uterine dead fetus syndrome, amniotic fluid embolism.

B. CARDIOGENIC SHOCK:-Impaired ability of the heart to pump blood  Failure of the left ventricular ejection in cardiac arrest and myocardial infarction  Failure of left ventricular filling associated with cardiac tamponade pulmonary embolism .

polynephritis and rarely postpartum endometritis. NEUROGENIC SHOCK: Chemical injury.Associated with aspiration of gastrointestinal contents during general anaesthesia . SEPTIC SHOCK Septic abortion.C. especially caesarean section  Drug induced associated with spinal anaesthesia D. chorioamnionitis. .

A. HYPOVOLEMIC SHOCK The body reacts to the loss of circulating fluid in stages as follows INITIA STAGE:Reduction in fluid or blood  decrease the venous return to the heart inadequate fill in ventricles reduction in stroke volume and cardiac output blood pressure decreases decreased supply of oxygen to tissue cell function will affect .

urinary output is reduced and exchange of gas in the lungs is impaired.COMPENSATORY STAGE:Drop in cardiac output 1. Pupils dilates. response from the sympathetic nervous system through the activation of receptors in the aorta and carotid arteries. . redistribution of blood to vital organs heart rate increases to improve cardiac output and BP Signs:. The sweat glands are stimulated and skin becomes moist and clammy.skin becoming pale and cool: peristalsis slows.

unless the fluid loss is replaced.2. Adrenaline and aldosterone from adrenal glands and anti diuretic hormone from posterior pituitary gland are secreted causing vasoconstriction an increased cardiac output and a decrease in urinary output Venous return to the heart will increase but. this will not be sustained .

low volume pulse. the respiratory rates becomes rapid. Peripheral circulation is poor. Colour of skin becomes ashen gray. Death ensures. Metabolic acidosis starts and for elimination of accumulated carbon dioxide.PROGRESSIVE STAGE This stage leads to multisystem failure. . Volume depletion caused further fall in blood pressure and cardiac output. With weak or absent pulses. oliguria and mental confusion occur. Compensatory mechanisms begin to fail. Multisystem failure and cell destruction are irreparable. with vital organs lacking adequate perfusion. The coronary arteries suffer lack of supply. LATE STAGE Hypotension continues and cannot be reversed by replacement of fluid because of stagnation of blood at the micro vascular level.

The priorities are to: Maintaining the airway Replace fluid (infusion and transfusion) Avoid warmth Control of hemorrhage.MANAGEMENT Urgent resuscitation is needed to prevent the mothers condition from deteriorating and causing irreversible damage. . 3. 1. 4. 2.

Assess central venous pressure and fluid balance for adequacy for circulating volume Watch for occurrence of any further bleeding Detailed observation charts are to be maintained and the mother may be transferred to a critical care unit . Assess skin colour and temperature hourly.Clinical observations for the mother in shock       Assess the level of consciousness. Signs of restlessness and confusion are to be noted Monitor blood pressure every 30 minutes or continuously.

obstetric trauma or in the presence of retained placental tissue.SEPTIC SHOCK Infection commonly from gram negative organisms (E.coli. prolonged rupture of membranes. The body’s primary response to infection is alteration in the peripheral circulation. Cells damaged by the infecting organisms release histamine and enzymes that contribute to vasodilation and increased permeability of the capillaries. . or Pseudomonas) female genital tract Endotoxins present in their cells trigger body’s immune response The placental site is the main point of entry for an infection associated with pregnancy and childbirth. Proteus. This may occur following septic abortion.

which either could be due to the events of childbearing or because of disseminated intravascular coagulation As vasodilatation continues. Temperature rise varies between 1010 to 1050F Tachycardia. tachypnoea and rigors occur. there is marked flushing of the face and the skin feels warm.Clinical signs      In the initial phase. Hemorrhage may be present. hypotension leads to kidney damage with reduced glomerular filtration acute tubular necrosis and oliguria .

    If the shock conditions does not improve. . cardiac or respiratory distress and coma will occur Disseminated intravascular coagulation is also a feature Multisystem organ failure will result as an effect of the continued hypotension and myocardial depression. and death result. She remains cold and clammy with ashen-gray cyanotic appearance Anuria. brain and respiratory system follows. Failure of the liver. the patient passes clinically to the stage of irreversible shock.

Management of septic shock Management is based on preventing further deterioration by restoring circulatory volume and eradication of the infection. Antibiotics: Broad spectrum antibiotics are given to start after confirming the sensitivity. specifics antibiotics are given intravenously  . A full infection screening should be carried out including a high vaginal swab. Retained products of conceptions if detected on ultrasound should be removed. midstream urine and blood cultures.

      Intravenous fluids and electrolytes: Septic shock associated hemorrhagic hypotension is treated with liberal infusion and blood transfusion. dopamine and dobutamine are administered to increase the cardiac contractility. In unresponsive septic shock following septic abortion or puerperal sepsis. noradrenaline. heparin may be given. Oliguria with high specific gravity is an indication for liberal fluid administration Correction of acidosis: Bicarbonate is administered to correct metabolic acidosis. Maintenance of blood pressure: Inotropic agents such as adrenaline. Corticosteroids are given to exert an antiendotoxin effect As a prophylactic measure for DIC. hysterectomy may be done to eliminate the source of infection. .

VASA PREVIA This term is used when a foetal blood vessel lies over the os in front of the presenting part. This usually occurs when foetal vessels from a velamentous insertion of the cord cross the area for the internal os to the placenta and also succenturiatelobe. Vas previa occurs in less than 0.2% of pregnancies.3. .

Diagnosis     Bimanual examination A speculum examination may be done to visualise the blood vessel. Fresh vaginal bleeding. may be due to ruptured vasa previa. . which commences at the time of rupture of membranes. It may be also visualised on ultrasound.

If the mother in 2nd stage delivery should be expected and a vaginal birth may be achieved.Management       Immediate consultation with physician Monitor fetal heart rate If fetus is alive emergency LSCS. Paediatrician should be present May require blood transfusion for the baby .

CORD PRESENTATION AND CORD PROLAPSE There are three clinical types of abnormal descent of the umbilical cord by the side of the presenting part.  Occult prolapse: The cord is placed by the side of the presenting part and is not felt by the fingers on internal examination  Cord presentation: The cord is slipped down below the presenting part and is felt lying in the intact bag of membranes  Cord prolapse: the cord is lying inside the vagina or outside the vulva following rupture of membranes .

These are same for both presentation and prolapse of cord Malpresentations Prematurity Multiple pregnancy Polyhydramnions High head High parity .        Incidence: the incidence of cord prolapse is about 1 in 300 Predisposing factors.

Diagnosis     Occult prolapse: this is difficult to diagnose. A loop of cord may be visible at the vulva: . The possibility should be suspected if there is (1)persistence of variable deceleration of fetal heart rate pattern detected on continuous fetal monitoring in an otherwise normal delivery or (2) persistent fetal soufflé with irregular heart sounds. Cord presentation: Bimanual examination Cord prolapse The cord is felt below or beside the presenting part on vaginal examination.

The danger is more in vertex presentation. which involves the risk of anaesthesia. especially when the prolapse through the anterior segment of the pelvis or when the cervix is partially dilated.  . blood loss and infection.  Fetal The fetus is at risk of anoxia due to acute placental insufficiency from the moment cord is prolapsed.Risk to mothers Maternal The maternal risks are incidental due to emergency operative delivery.

she is kept in exaggerated Sim’s position to minimise compression .Management of cord presentation The aim is to preserve the membranes and to expedite delivery  The midwife should discontinue vaginal examination in order to reduce the risk of rupturing the membranes  Medical help should be summoned immediately  Fetal heart should be auscultated as frequently as possible or obtained through continuous electronic monitoring.  Caesarean section is the most likely method of delivery  During the time of preparing the woman for operative delivery.

    Immediate action Calls for urgent assistance. The fingers should be placed inside the vagina until definitive treatment is instituted . the aim of immediate management to minimize pressure on the cord until such time when the woman is prepared for assisted delivery of risk transferred to an equipped hospital. The mother and her family must be given explanation about the findings and the emergency measures that will be needed. Stop oxytocin infusion If the baby is alive. For this. the gloved fingers are to be introduced into the vagina to lift the presenting part of the cord.Management of cord prolapse 1.

High trendlenberg position or knee chest position. it should be replaced in to the vaginal to minimize vasospasm due to irritation and to maintain the temperature. which has been traditionally mentioned. If much of the cord are outside the vulva. it should be covered with sterile wet gauze.   Postural treatment is given until the delivery of the baby. The woman is placed in exaggerated elevated Sim’s position with pillow under the hip. either vaginally or by caesarean section. to prevent spasm of the umbilical vessels . The foot end of the bed may be elevated. is very tiring and distressing to the woman If the cord lies outside the vagina.

labour is allowed to proceed. This is possible only with vertex presentation and carries high fetal risks.  If the head is engaged. awaiting spontaneous termination. With breech engaged. . is manually pushed above the presenting part under general anaesthesia. reposition of the cord wrapped in a large piece of sterile roller gauze.2. Definitive management  Caesarean section is the ideal management  If immediate caesarean section is not possible or the baby is too premature. if necessary. delivery is completed by forceps. This is followed by stimulation of uterine contraction with oxytocin drip. a breech extraction is done  If fetus is confirmed dead. ventouse traction may be applied to deliver the baby. When the cervix is about three fourths dilated.

and cardiovascular collapse. with hemorrhage and coagulation disorder followed y pulmonary edema.AMNIOTIC FLUID EMBOLISM This condition occurs when amniotic fluid enters the maternal circulation through a tear in the membranes or placenta.  The body responds in two phases – this initial phase is one of vasospasm causing hypoxia. . hypotension.  Mortality and morbidity are very high  .This second phase is the development of left ventricular failure.

Predisposing factors       Transfer of amniotic fluid from the uterus to the maternal circulation Amniotic fluid under pressure may enter maternal circulation in the first phase of hypoxia during hypertonic uterine activity Procedures such as insertion of an intrauterine catheter and artificial rupture of membranes In cases o placental abruption It can occur during a ceasaren section or termination of pregnancy. Trauma may occur during intrauterine manipulation such as internal podalic version .

Clinical features       Sudden onset of maternal respiratory distress: the woman becomes severely dyspnic and cyanosed There is maternal hypotension and uterine hypertonia Fetal distress in response to hypoxia caused by hypertonia Fetal distress in response to hypoxia caused by hypertonia Cardiopulmonary arrest follows quickly in minutes Many others present with convulsions immediately preceding the collapse .

Emergency management    The mother may be in a state of collapse and resuscitation must be started at once. Specific management of the condition is life support and high levels of oxygen are required. Mothers who survive may suffer neurological impairment. .

Complications Disseminated intravascular coagulation (DIC)  Acute renal failure occurs due to heavy bleeding and the prolonged hypovolemic hypotension Effect on the fetus Perinatal mortality and morbidity are high where amniotic fluid embolism occurs before the birth of the baby.  .

000 deliveries . The incidence is about 1 in 20.INVERSION OF UTERUS   It is an extremely rare but a life threatening complication in third stage in which the uterus is turned inside out partially or completely.

Varieties First degree – there is dimpling of the fundus which still remains above the level of internal os.the fundus passes through the cervix but lies inside the vagina  Third degree (complete) – the endometrium with or without the attached placenta is visible outside the vulva.  Second degree. It may occur before or after separation of placenta  . The cervix and part of the vagina may also be involved in the process.

short umbilical cord. It is more common in women with collagen disease. sneezing or bearing down effort. morbid adherent placenta.Etiology     Spontaneous (40%): this is brought about by localised atony on the placental site over the fundus associated with sharp intra abdominal pressure as coughing. Fundal attachment of the placenta. prolonged labour. Pulling the cord – when the uterus is atonic specially when combined with fundal pressure fundal pressure – while the uterus is relaxed – faulty technique or manual removal common risk factors are uterine over enlargement. and manual removal of placenta. short cord and placenta accrete are often associated. uterine malformations. Iatrogenic(60%) : This is due to the mismanagement of third stage of labour. fetal macrosomia. .

it may lead to – infection.Dangers Shock  Haemorrhage  Pulmonary embolism  If left uncared for. uterine sloughing and chronic one Diagnosis Symptoms : acute lower abdominal pain with bearing down sensation Signs :  Abdominal examination – cupping or dimpling of the fundal surface. bimanual examination not only helps to confirm the diagnosis but also the degree  Songraphy can confirm the diagnosis when clinical examination is not clear  .

Prevention   Do not employ the method to expel the placenta out when the uterus is relaxed. Avoid pulling the cord .

urgent manual replacement even without anaesthesia. .Management   Call for help Before shock develops.

the hand should remain inside the uterus until the uterus becomes contracted by parenteral oxytocin The placement is to removed manually only after the uterus which facilitates replacement –a) to reduce the bulk which facilitates replacement or b) if partially separated to minimise the blood loss Usual treatment of shock including blood transfusion should be arranged simultaneously .      Principal steps To replace that part first which is not inverted . To apply counter support by the other hand placed on the abdomen After replacement.

.

.After the shock develops Principal steps are  The treatment of shock should be instituted with an urgent normal saline drip and blood transfusion  To push the uterus inside the vaginal if possible and pack the vagina with antiseptic roller gauze  Foot end of bed is raised  Replacement f of the uterus either manually or hydrostatic method (o Sullivan)under general anaesthesia is to be done along with resuscitative measures. Hydrostatic method is quite effective and less shock producing.

Additional fluids may be required.  Insert the hand into the vagina with the open end of the tubing near the posterior fornix.HYDROSTATIC REDUCTION (O’SULLIVAN’S TECHNIQUE)  Hydrostatic reduction is a method of reinverting the uterus by infusing warm saline into the vagina.  Infuse warmed fluid under gravity. Several litres of fluid may be required. round ligaments and the ovaries.  Obtain a seal at the vaginal entrance by enclosing the labia around the wrist/hand to prevent fluid leakage.  . Method one  Attach a 2 x 1 litre bags of warmed saline to a Cystoscopy giving set.  The women may be placed in the Tredelenburg position to assist gravity and reduce traction on the infundibulo-pelvic ligaments.

reposition may be done by abdominal operation (Haultain’s operation) .Sub acute stage  To improve the general condition by blood transfusion  Antibiotics are given to control sepsis  Reposition of the uterus either manually or by hydrostatic method may be tried  If fails.