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Edit Comment Close Premium member Presentation Transcript Chapter 28: High-Risk OB-GYN : Chapter 28: High-Risk OB-GYN Galveston College EMS Critical Care Paramedic 2009 Introduction (1 of 2) : Introduction (1 of 2) Pregnancy complications that mandate critical care transport can have multiple etiologies While some complications may be related to pre-existing medical conditions, others may be precipitated by the pregnancy, still others by the fetus Introduction (2 of 2) : Introduction (2 of 2) The critical care paramedic must be able to: Perform a proper physical assessment of both the mother and fetus Form a differential diagnosis and treatment plan Anticipate the risks and possible complications of any scenario so as to ensure the proper care and best possible outcome of both mother and fetus Anatomy and Physiology : Anatomy and Physiology Anatomy (1 of 4) : Anatomy (1 of 4) Courtesy Wendy Hiller Gee. Anatomy (2 of 4) : Anatomy (2 of 4) Courtesy Wendy Hiller Gee. Anatomy (3 of 4) : Anatomy (3 of 4) Anatomy (4 of 4) : Anatomy (4 of 4) General Information : General Information Female reproductive system consists of: Paired ovaries Paired fallopian tubes Uterus Vagina System functions to produce and secrete sex hormones; yield viable gametes; and support, protect, and deliver a developing fetus After birth, the female reproductive system nourishes the newborn infant Gestation : Gestation Time between fertilization of an oocyte until birth In human averages 266 days Gestation of fewer than 37 weeks is considered premature Gestation of greater than 42 weeks is considered postmature The gestational period is often broken into three trimesters, each 3 months long Fertilization and the First Trimester : Fertilization and the First Trimester Fertilization (1 of 2) : Fertilization (1 of 2) Usually occurs in distal one-third of the fallopian tube Fertilized egg termed a zygote Contains the normal human complement of 46 chromosomes Cell division in the zygote starts immediately Zygote travels down the fallopian tube to the uterus Fertilization (2 of 2) : Fertilization (2 of 2) From Nilsson, L. (1990) A child is born. New York: Dell Publishing. Development and Implantation : Development and Implantation Blastocyst formation Blastocyst adheres to uterine endometrium Differentiation Syncytial trophoblast Implantation Hyaluronidase Functional zone of endometrium Human chorionic gonadotropin (HCG) production Corpus luteum Progesterone Further prepares uterus for pregnancy Prevents start of new uterine cycle By Day 9 (1 of 2) : By Day 9 (1 of 2) Syncytial trophoblast has spread into the surrounding endometrium Surrounds and erodes endometrial capillaries Maternal blood leaking from the eroded capillaries flows through channels, called lacunae, in the syncytial trophoblast By Day 9 (2 of 2) : By Day 9 (2 of 2) Days 9–21 : Days 9–21 Chorionic villi form on the trophoblast and extend into the endometrium Embryonic blood vessels develop in the villi, and circulation in these vessels begins As large endometrial blood vessels become involved, more maternal blood flows through the lacunae First exchange between fetal and maternal blood occurs First steps in placenta creation By End of Week 4 : By End of Week 4 Embryo Is about 5 mm long Weighs about 0.02 g Has a heart beat Has begun to develop trachea, lungs, intestinal tract, liver, pancreas, eyes, and ears Week 5 : Week 5 Days 9–21 : Days 9–21 By the End of Week 8 : By the End of Week 8 Diaphragm, intestinal subdivisions, kidneys, axial and appendicular cartilage, and axial musculature have started to develop At this point, embryo is termed a fetus Week 20 : Week 20 By the End of the First Trimester (Week 28) (1 of 2) : By the End of the First Trimester (Week 28) (1 of 2) Gallbladder, gonads, brain, spinal cord, and appendicular musculature start to develop Fetus about 80 mm long and weighs about 25 g Placenta has fully developed and normally is in the fundal or body region of the uterus Typical human placenta is about 20 cm in diameter and 2.5 cm thick and weighs about 500 g By the End of the First Trimester (Week 28) (2 of 2) : By the End of the First Trimester (Week 28) (2 of 2) Primary functions Facilitate the exchange of nutrients and wastes between mother and fetus Developing fetus places significant demands on the mother Produce hormones needed to maintain pregnancy and fetal development Flow blood between the fetus and placenta via the umbilical cord Cord contains paired umbilical arteries and single umbilical vein Significant amount of maternal blood is redirected to the placenta The Second Trimester (1 of 2) : The Second Trimester (1 of 2) During the second and third trimesters, the placenta acts as an endocrine organ and takes over progesterone-releasing duties from the corpus luteum Placenta also produces the hormones HCG, estrogen, human placental lactogen, and relaxin During second trimester, organ system development nears completion The Second Trimester (2 of 2) : The Second Trimester (2 of 2) Fetus continues to mature rapidly Fetus is moving by the end of week 16 By the end of the second trimester, the developing fetus has taken on distinctive human characteristics Eyebrows and eyelashes are well formed, all eye components are developed Hands and startle reflex are evidents Footprints and fingerprints are forming Alveoli are developing The Third Trimester (1 of 2) : The Third Trimester (1 of 2) Early in the third trimester, most organ systems have matured and become fully functional Baby born at 36 weeks has good chance of survival and is considered full term from weeks 37 through 40 The Third Trimester (2 of 2) : The Third Trimester (2 of 2) Third trimester characterized by rapid growth of fetus Has grown to about 345 mm long and weighs about 3.2 kg at full gestation Exhibits other developmental markers Rapid deposition of body fat Rhythmic breathing movements Lungs are not fully mature, however Fully developed though soft and pliable bones Stores of iron, calcium, and phosphorus Changes in Maternal Physiology : Changes in Maternal Physiology Systems affected in pregnancy include: Cardiovascular Respiratory Reproductive Gastrointestinal Urinary Cardiovascular System Changes (1 of 3) : Cardiovascular System Changes (1 of 3) Increased blood volume and red blood cell production By end of gestation, maternal blood volume has increased by 45 to 50 percent Results in: Increased resting heart rate Increased cardiac output Possible flow murmurs on auscultation Slight decreases in peripheral vascular resistance Causes slight decrease in blood pressure during first and second trimesters Cardiovascular System Changes (2 of 3) : Cardiovascular System Changes (2 of 3) System returns to prepregnancy levels during third trimester Peripheral edema Secondary to intravascular fluid shifts into the intracellular space in dependent areas Supine hypotensive syndrome Not true physiologic change Transient decrease in venous return to the heart and subsequent hypotension can occur when the gravid uterus compresses the inferior vena cava Occurs most often when the pregnant female is supine Cardiovascular System Changes (3 of 3) : Cardiovascular System Changes (3 of 3) Hypercoagulable state Secondary to: Increase of clotting factors Decrease in fibrinolytic activity Increase in platelet activation Venous stasis Respiratory System Changes (1 of 3) : Respiratory System Changes (1 of 3) O2 demand increases 10 to 20 percent increase in O2 consumption Progesterone secretion weakens costal cartilage Greater movement of the rib cage 35 to 40 percent increase in tidal volume Respiratory System Changes (2 of 3) : Respiratory System Changes (2 of 3) Respiratory rate increases mildly This, with the increase in tidal volume, increases minute volume Mild, compensated respiratory alkalosis occurs Creates a greater CO2 gradient and greater diffusion of CO2 between mother and fetus Reproductive System Changes (3 of 3) : Reproductive System Changes (3 of 3) Uterus enlarges Achieves 30 cm length, 1,000 g weight, 5 liter volume Receives about 15 percent of maternal blood volume by gestation’s end Gastrointestinal System Changes (1 of 2) : Gastrointestinal System Changes (1 of 2) Abdomincal organs are compressed and displaced Peristalsis slows, delaying gastric emptying Bloating, nausea, and constipation are common Maternal nutritional requirements increase 10 to 30 percent Gastrointestinal System Changes (2 of 2) : Gastrointestinal System Changes (2 of 2) Glomerular filtration rate (GFR) increases by about 50 percent As result, glucose may be insufficiently reabsorbed and is subsequently excreted in the urine Urine production increases Glucosuria manifests General OB/GYN Assessment : General OB/GYN Assessment History Medical history should include: Entire medical history Obstetric history Medical history concerns Pregnancy Can exacerbate or complicate history Diabetes Seizure disorders Heart disease Hypertension Neuromuscular disorders Medications and allergies to medications Should be identified and recorded Obstetric History Concerns (1 of 5) : Obstetric History Concerns (1 of 5) Gravida/para (G/P) status Number of living children? Complications with previous pregnancies or deliveries? History of preterm delivery? Gestational age? Outcome? History of lective or spontaneous abortion? D&C performed? Obstetric History Concerns (2 of 5) : Obstetric History Concerns (2 of 5) Have all previous births been vaginal or was cesarean section performed? Has patient delivered vaginally after a cesarean section? When was, and what was length of, last labor? With regard to current pregnancy, what is estimated date of confinement (EDC)? Has patient received adequate, limited (three or fewer visits), or no prenatal care? Obstetric History Concerns (3 of 5) : Obstetric History Concerns (3 of 5) Any problem with pregnancy identified? If so, what? Diagnostic tests like ultrasound done? If so, what were results? Is patient taking any medications for obstetric or nonobstetric reasons? If so, which medication(s), what dose(s), and compliant schedule(s)? Obstetric History Concerns (4 of 5) : Obstetric History Concerns (4 of 5) Drug or alcohol abuse suspected? If so, which substance(s), frequency of use, date of last use? Patient smoking? Pregnancy weight gain normal, or patient malnourished or obese? Is patient having contractions? If so, when did they begin, and what are their frequency and duration? Patient with urge to defecate? Obstetric History Concerns (5 of 5) : Obstetric History Concerns (5 of 5) Has patient’s amniotic sac ruptured? If so, at what time, and was it a trickle or gush? Was meconium in the fluid, or did fluid smell foul? Has patient bled vaginally? If so, accompanied by pain? If pain, is it associated with contractions or constant? Has patient or transporting facility used sanitary napkins or other absorbent devices to soak up blood? If so, how much? Physical Exam (1 of 8) : Physical Exam (1 of 8) Abdominal exam for pregnant patients is basically same as that for nonpregnant patients Displacement and compression of abdominal organs by the gravid uterus makes identifying abdominal landmarks challenging Physical Exam (2 of 8) : Physical Exam (2 of 8) Palpate for pain, tenderness, guarding, masses, and uterine contractions During uterine contractions, palpate the fundus for contraction strength, frequency, and duration Use tocodynamometer Records strength, duration, and time between contractions Records and prints continuously while the patient is hooked to the monitor Physical Exam (3 of 8) : Physical Exam (3 of 8) Measure fundal height (FH) of uterus, in centimeters, from the symphysis pubis to the most superior portion of the fundus Each centimeter of FH corresponds roughly to gestational age in weeks Fetus position can be determined by palpating the uterus for the head and buttocks Fetal spine can often be palpated, as well Physical Exam (4 of 8) : Physical Exam (4 of 8) Fundal height (FH) Physical Exam (5 of 8) : Physical Exam (5 of 8) Examine external genitalia for discharge, blood, mucus, a prolapsed cord, or crowning Evaluate for crowning during a contraction Do not conduct internal vaginal exam Not normally in scope of practice of the critical care paramedic May be justified in doing physician examination of the patient’s cervix before transport Physical Exam (6 of 8) : Physical Exam (6 of 8) External genitalia Physical Exam (7 of 8) : Physical Exam (7 of 8) Assess vital signs every 15 minutes or as often as the situation warrants Pulse Blood pressure Respiratory rate Temperature SpO2 Physical Exam (8 of 8) : Physical Exam (8 of 8) Assess and monitor fetal heart tones (FHT) throughout transport Conduct electronic fetal monitoring Evaluate and monitor uterine contractions and fetal heart rate electronically Intrapartum Fetal Heart Rate Monitoring (1 of 2) : Intrapartum Fetal Heart Rate Monitoring (1 of 2) Intrapartum FHR monitoring was introduced as way to prevent intrapartum fetal compromise, death, and asphyxia-induced brain damage A change in FHR is earliest indication of insult to fetal circulation and developing hypoxia secondary to umbilical cord insult or uteroplacental insufficiency Asphyxia is said to have occurred when hypoxia with a resulting metabolic acidosis presents Intrapartum Fetal Heart Rate Monitoring (2 of 2) : Intrapartum Fetal Heart Rate Monitoring (2 of 2) FHR monitoring has very good rate of detecting fetuses at risk of developing asphyxia (about 90 percent) False negatives are rare In most cases, normal FHR tracings are adequate to conclude clinically that fetal perfusion status is normal FHR monitoring specificity is poor False-positive rates between 50 and 75 percent Most newborns with abnormal FHR records do not present with hypoxia and metabolic acidosis at birth Indications for FHR Monitoring : Indications for FHR Monitoring Antepartum risk factors Multiple gestation, preeclampsia, chronic hypertension, and maternal diabetes Intrapartum risk factors Cases of active or suspected abruptio placentae, placenta previa, meconium staining, prematurity, and the documentation of abnormal FHR patterns FHR monitoring is also suggested in cases of active labor with the use of analgesia, anesthesia, or oxytocin Effective OB/GYN Assessment : Effective OB/GYN Assessment Familiarize with FHR monitoring terminology Know normal FHR parameters Be able to recognize normal and abnormal FHR tracings Baseline FHR : Baseline FHR Defined as average FHR during 10-minute period rounded to the nearest 5 beats/minute For baseline FHR, must be at least 2 minutes of 10 with no: Eisodic changes Periods of significant FHR variability Segments with differences greater than 25 beats/minute Normal baseline FHR is 110–160 bpm Bradycardia (1 of 2) : Bradycardia (1 of 2) Exists when FHR is less than 110 bpm for more than 10 minutes Not uncommon for a term or postmature fetus to have baselines between 100 and 110 bpm Bradycardia occurs secondary to increased fetal parasympathetic tone and causes decreased cardiac output, hypoxia, and, eventually, metabolic acidosis Bradycardia (2 of 2) : Bradycardia (2 of 2) Can occur secondary to: Umbilical cord compression or occlusion Maternal hypotension Uterine hyperstimulation resulting in increased intrauterine pressure during contractions As with the use of oxytocin Chronic hypoxia Fetal bradycardia is late, ominous sign May be inadvertent measure of maternal pulse Tachycardia (1 of 2) : Tachycardia (1 of 2) Defined as FHR greater than 160 bpm for more than 10 minutes Early, immediate compensatory reaction is to increase cardiac output in instances of hypoxia Significantly less variability in heart rate usually occurs during tachydardia episodes Tachycardia (2 of 2) : Tachycardia (2 of 2) Can occur secondary to: Transient fetal hypoxia Fetal anemia Maternal fever Maternal or fetal infections Maternal smoking Sympathomimetic drugs Terbutaline Chorioamnionitis Sinusoidal Wave Pattern : Sinusoidal Wave Pattern Frequent, wave-like pattern of regularly occurring increases and decreases of FHR over a range of 5–20 beats from baseline May be appreciated in cases of fetal anemia, erythroblastosis, or hypovolemia Indicates severe fetal hypoxia Maternal use of narcotics may also cause sinusoidal wave pattern but does not indicate fetal distress Variability (1 of 4) : Variability (1 of 4) Variability in baseline FHR is normal and indicates an adequately oxygenated and normally functioning autonomic nervous system Associated with normal oxygenation status at delivery Variability occurs as the sympathetic and parasympathetic nervous systems alternately influence the fetal heart rate Can be described as short- or long-term Variability (2 of 4) : Variability (2 of 4) Short-term variability Beat-to-beat changes in FHR Usually irregular in rate and frequency Greatly influenced by the parasympathetic branch More susceptible to hypoxia than sympathetic branch Cessation of normal, short-term variability may be first indicator of fetal hypoxia Long-term variability Broad “waviness” of FHR tracing over time Can range from 5 to 25 beats above and below the baseline Fewer than 5 beats over 1 minute is considered short Differs from the sinusoidal wave pattern in that its waves occur with much less frequency or over a longer period Influenced by the sympathetic nervous system Variability (3 of 4) : Variability (3 of 4) Absent or minimal variability, long and short term, can result from: Fetal hypoxia Maternal narcotic use Smoking Administration of magnesium sulfate Extreme prematurity Fetal neurologic insult Normal fetal sleep cycles Variability (4 of 4) : Variability (4 of 4) Increased variability can be early sign of hypoxia or the result of ultrasound (US) transducer use US transducers are notorious for erroneously high variability readings in critical care transport The most likely measuring devices used by transport team due to their noninvasive nature If true evaluation of FHR short-term variability is required, a physician should place a fetal scalp electrode Long-term variability is accurate with an ultrasound transducer and should be monitored and recorded during transport Periodic Changes in FHR : Periodic Changes in FHR Acceleration (1 of 3) : Acceleration (1 of 3) Defined as obvious, abrupt increase (fewer than 30 seconds from onset to peak rate) in FHR with a peak rate 15 bpm above baseline that lasts for more than 15 seconds and fewer than 2 minutes from onset to return to baseline Over 2 minutes acceleration is considered prolonged, over 10 minutes is considered change in baseline Accelerations are usually benign Acceleration (2 of 3) : Acceleration (2 of 3) Can occur secondary to uterine contractions or fetal movement and indicate that the fetus has intact central nervous system and normal pH Accelerations strongly suggest normal fetal pH Can also indicate developing fetal hypoxia, occurring before pH has changed Acceleration (3 of 3) : Acceleration (3 of 3) Critical care transport team should ensure that fetal movement or contractions accompany all accelerations Ask the mother if movement or contractions are occurring Palpate the uterus during the acceleration Identify contractions on a tocodynamometer Decelerations (1 of 3) : Decelerations (1 of 3) Defined as obvious, gradual (more than 30 seconds from onset to nadir) decrease and return of FHR from baseline during a uterine contraction Considered normal during uterine contraction Nadir of the deceleration occurs simultaneously with the peak of the uterine contraction Decelerations (2 of 3) : Decelerations (2 of 3) In most cases, deceleration mirrors the contraction Can be classified as early, late, or variable Early decelerations are not associated with fetal hypoxia or acidosis and need no intervention Late decelerations are more serious sign than early ones Decelerations (3 of 3) : Decelerations (3 of 3) Indicate hypoxia and acidosis secondary to uteroplacental insufficiency Variable decelerations can occur any time during a contraction or independent of contractions Caused by umbilical cord compression and occlusion secondary to uterine contraction or fetal movement Late Decelerations (1 of 3) : Late Decelerations (1 of 3) Begins at the peak of a uterine contraction and returns to FHR baseline after the contraction concludes Causes of uteroplacental insufficiency include: Abruptio placentae and previa Uterine hypertonicity secondary to oxytocin administration Maternal hypotension and smoking Late Decelerations (2 of 3) : Late Decelerations (2 of 3) Diabetes Postmaturity Degree of deceleration is proportional to contraction strength Two mechanisms are responsible for late decelerations: Central nervous system induced reflex bradycardia secondary to hypoxia Metabolic acidosis resulting in myocardial depression Late Decelerations (3 of 3) : Late Decelerations (3 of 3) Hon E, (1976). An introduction to fetal heart rate monitoring (Second Ed., p. 29). Los Angeles: University of Southern California School of Medicine. Variable Decelerations (1 of 4) : Variable Decelerations (1 of 4) Characterized by abrupt decrease in FHR below baseline more than 15 bpm and lasting between 15 seconds and 2 minutes Morphology may be in the shape of an inverted V or an M Short accelerations on either side of the deceleration are termed “shoulders” Their appearance is thought to be caused by a partial, rather than complete, cord occlusion Variable Decelerations (2 of 4) : Variable Decelerations (2 of 4) “Smoothing” of the decelerations or loss of shoulders indicates fetal distress Can occur any time during a contraction or independent of contractions Caused by umbilical cord compression and occlusion secondary to uterine contraction or fetal movement Variable Decelerations (3 of 4) : Variable Decelerations (3 of 4) Most common decelerations seen in labor, and while not an ominous when isolated, should raise concern when: They are deep and long and accompanied by decreased FHR variability They are slow to return to baseline Baseline FHR increases or becomes tachycardic Variable Decelerations (4 of 4) : Variable Decelerations (4 of 4) Hon E, (1976). An introduction to fetal heart rate monitoring (Second Ed., p. 29). Los Angeles: University of Southern California School of Medicine. Changes in FHR Trending Patterns (1 of 3) : Changes in FHR Trending Patterns (1 of 3) Questions to rule in/out fetal distress Is FHR baseline within normal range? If the baseline is between 110 and 160 bpm, the fetus is maintaining an adequate cardiac output and metabolic acidosis is not present Is variability adequate? If it is, the fetus is being adequately oxygenated Changes in FHR Trending Patterns (2 of 3) : Changes in FHR Trending Patterns (2 of 3) Questions to rule in/out fetal distress If hypervariabilty presents, may be due to the ultrasound transducer Are accelerations present? Accelerations can only occur absent metabolic acidosis, so their presence is reassuring Is the event an early deceleration? If so, it is a normal, benign event that can be expected to occur with each uterine contraction Changes in FHR Trending Patterns (3 of 3) : Changes in FHR Trending Patterns (3 of 3) Questions to rule in/out fetal distress If tachycardia or bradycardia present, have accelerations and adequate variability presented? If so, metabolic acidosis is not present If late or variable decelerations present, have accelerations and adequate variability presented? If so, the fetus is tolerating the events well and metabolic acidosis is not present Signs of Fetal Distress : Signs of Fetal Distress Signs the fetus may be developing hypoxia and acidosis Gradual, significant, uncorrected decrease in baseline FHR over time A fluctuating baseline over time Tachycardia or bradycardia with reduced short- and long-term variability Reduced variability as labor progresses Late decelerations that “smooth out” over time Management of Fetal Distress (1 of 2) : Management of Fetal Distress (1 of 2) Ensure patient is breathing adequately and has a pulse Administer 100 percent oxygen via NRM Place patient in left lateral recumbent position If hypotension presents, consider repeated fluid boluses until hypotension corrects Perform an external vaginal exam to ensure there is no vaginal hemorrhage, prolapse Especially if the patient was high-risk for abruptio placentae or previa Management of Fetal Distress (2 of 2) : Management of Fetal Distress (2 of 2) If the fetal distress occurs secondary to hypertonic contractions resulting from oxytocin infusion, discontinue the infusion immediately Consider tocolytic agent like terbutaline 0.25 mg subcutaneous or 0.125–0.25 mg intravenous to relax the uterus Consider need for amnioinfusion When fetal distress is suspected, intrauterine resuscitation measures must be taken to improve uterine blood flow and increase fetal oxygenation Pathophysiology, Assessment, and Management of OB/GYN Emergencies : Pathophysiology, Assessment, and Management of OB/GYN Emergencies Vaginal Hemorrhage during Pregnancy : Vaginal Hemorrhage during Pregnancy Abruptio Placentae (1 of 12) : Abruptio Placentae (1 of 12) Abruptio Placentae (2 of 12) : Abruptio Placentae (2 of 12) Epidemiology Incidence about 0.83 percent (1 in 120) of all deliveries Fetal death occurs in 0.4 percent of all abruptions Approaches 100 percent when 50 to 100 percent of the placenta is involved Abruptio Placentae (3 of 12) : Abruptio Placentae (3 of 12) Pathophysiology Premature separation of a normally implanted placenta from the uterine wall Begins with arterial hemorrhaging into the deciduas basalis Hematoma formation and progression can cause expanding abruption As abruption continues, more vessels become involved, further contributing to the expanding retroplacental hematoma Deciduas is rich in thromboplastin Abruptio Placentae (4 of 12) : Abruptio Placentae (4 of 12) Pathophysiology Rapid clot formation may help attenuate the hemorrhage Uterus will often contract during an abruptio episode Separation of the placenta can be partial (marginal) or complete Abruption with vaginal bleeding is termed an external hemorrhage (90 percent of all abruptions) If no vaginal bleeding is appreciated on physical exam, the abruption is said to be concealed (10 percent of all abruptions) Abruptio Placentae (5 of 12) : Abruptio Placentae (5 of 12) Pathophysiology Blood loss is impossible to estimate based on external observation alone Significant amounts of blood can remain in the uterus, trapped behind the placenta Most blood loss is maternal, although the fetus can hemorrhage, as well Risk factors associated with abruptio placentae include: Chronic or gestational hypertension (most common factor) Cocaine use Smoking Abruptio Placentae (6 of 12) : Abruptio Placentae (6 of 12) Pathophysiology Trauma increasing maternal age (over 35) Multiparity Uterine scarring from surgeries Past curettage Infection Past incidence of abruptio placentae Complications Fetal complications include hypoxia, anoxia, anemia, and CNS compromise Maternal complications include the development of hemorrhagic shock, the development of disseminated intravascular coagulation (DIC), and end-organ failure Abruptio Placentae (7 of 12) : Abruptio Placentae (7 of 12) Assessment Classic signs are considered: Presence of abdominal pain (50 percent) Uterine contractions (90 percent) Vaginal bleeding (90 percent) Except in cases of concealed abrupto Uterine tenderness to palpation Fetal demise Abruptio Placentae (8 of 12) : Abruptio Placentae (8 of 12) Assessment Severe cases may present with: Rigid, board-like abdomen upon palpation Signs and symptoms of hemorrhagic shock Diagnostic imaging Ultrasound cannot diagnose abruptio placenta, although it can demonstrate a placental hematoma that is consistent with abruption Recognized in 2 to 25 percent of all abruptions Ultrasound can, however, rule out placenta previa as a cause of vaginal bleeding by determining the location of the placenta Abruptio Placentae (9 of 12) : Abruptio Placentae (9 of 12) Labs Labs ordered should include a CBC, type and crossmatch, coagulation profile, and renal function studies Patients should also be assessed for signs associated with DIC, which include bleeding from IV or catheter sites, hypotension, and increased ventilatory resistance Abruptio Placentae (10 of 12) : Abruptio Placentae (10 of 12) Management Oxygenation and perfusion is a priority in abruptio placenta treatment Especially in cases with signs and symptoms of shock 100 percent oxygen should, at minimum, be supplied at 15 lpm via a nonrebreather mask Give assisted ventilations with a BVM or endotracheal intubation as required Abruptio Placentae (11 of 12) : Abruptio Placentae (11 of 12) Management IV access Two large bore IVs Central line Volume replacement Volume resuscitation with crystalloid solution in cases of mild abruptio If hemorrhagic shock is present, aggressive volume replacement should be initiated with a crystalloid and packed red blood cells Critical care paramedic should procure additional packed red blood cells from the transporting facility for infusion during transport Abruptio Placentae (12 of 12) : Abruptio Placentae (12 of 12) Management Foley catheter Monitor of urinary output 0.5 ml/kg/hr is desired Tocolytic agents May help prevent a developing abruption from expanding Placenta Previa (1 of 7) : Placenta Previa (1 of 7) Placenta Previa (2 of 7) : Placenta Previa (2 of 7) Epidemiology Incidence at 18 weeks is about 5 to 15 percent About 90 percent of these cases resolve by gestation’s end 0.5 percent (1 in 200 deliveries) still present at delivery About 20 percent of all cases of vaginal bleeding occurring in the second half of pregnancy result from placenta previa Placenta Previa (3 of 7) : Placenta Previa (3 of 7) Pathophysiology Occurs when the placenta implants and develops in the lower third of the uterus, totally or partially covering the cervical os Three presentation types are possible: Complete previa occurs when the cervical os is completely covered Marginal previa occurs when the edge of the placenta lies adjacent to, but does not cover, the cervical os Partial previa is characterized by a placenta that partially covers the cervical os Placenta Previa (4 of 7) : Placenta Previa (4 of 7) Pathophysiology Complete previa completely covers the cervical os Risk factors contributing to placenta previa include: Advanced maternal age (35 years) Smoking (doubles risk of nonsmokers) Cocaine use Placenta Previa (5 of 7) : Placenta Previa (5 of 7) Pathophysiology History of previa Multiparity Multifetal gestations Previous cesarean section or curettage Maternal complications associated with previa include need for cesarean delivery, postpartum hemorrhage, and the development of hemorrhagic shock Fetal complications include hypoxia, anoxia, and death Placenta Previa (6 of 7) : Placenta Previa (6 of 7) Assessment Hallmark of previa is the acute onset of painless, bright red bleeding in the late second or third trimester History of recent vaginal exam, sexual intercourse, or onset of labor should increase suspicion but is not needed for previa to occur Abdominal exam is usually benign, although uterine contractions may be present Digital or speculum examination is to be avoided in all cases of suspected placenta previa Diagnosis of previa is confirmed with transabdominal ultrasound Accurate from 93 to 98 percent Placenta Previa (7 of 7) : Placenta Previa (7 of 7) Management For Barker, R.K., Fields, D.H., & Kaufman, S.A. (1990). Quick reference to OB-GYN procedures (3rd ed.). New York: Lippencott/Harper & Row. Complications of Labor and Delivery : Complications of Labor and Delivery Preterm Labor (1 of 2) : Preterm Labor (1 of 2) Epidemiology Preterm labor occurs in about 10 to 15 percent of all pregnancies Complicates 10 to 12 percent of all births Responsible for about 85 percent of all neonatal deaths not due to genetic or congenital abnormalities Most neonatal mortality occurs in infants delivered before 28 weeks gestation Preterm Labor (2 of 2) : Preterm Labor (2 of 2) Pathophysiology Defined as frequent uterine contractions resulting in progressive cervical dilation or effacement between the 20th and 37th weeks of gestation Numerous physiologic factors can contribute to the development of preterm and premature labor Physiologic Factors Leading to Preterm Labor : Physiologic Factors Leading to Preterm Labor Hormonal influences Prostaglandin release High oxytocin levels Decreased uteroplacental blood flow Maternal dehydration Maternal hypertension Overdistension of the uterus Smoking, cocaine use Cardiovascular disease Placental abruption or previa Anatomic/physiologic abnormalities affecting the cervix or uterus Preterm Labor Risk factors : Preterm Labor Risk factors Premature rupture of membranes (PROM) Smoking Cocaine use Poor nutritional status Maternal age 35 or 20 Previous preterm delivery, abruptio placentae or previa Infection Dehydration Uterine abnormalities Cervical incompetence STDs like chlamydia, gonorrhea, and syphilis Complications of Preterm Labor : Complications of Preterm Labor Maternal complications of premature labor include endometritis, septicemia and septic shock secondary to PROM, and chorioamnionitis Fetal consequences of premature labor include preterm birth Accounts for about 100 neonatal deaths for every 100,000 live births in the United States Assessment (1 of 2) : Assessment (1 of 2) Assess for evidence of the numerous etiologies of preterm labor, including fever, dehydration, vaginal hemorrhaging, and PROM Patient history will identify risk factors like age, history of preterm labor, and social history Cervical exam should be performed by an appropriately trained health care provider to assess for cervical dilation or membrane rupture Assessment (2 of 2) : Assessment (2 of 2) Identification of suspected amniotic fluid Tested with nitrazine paper pH 6.5 is positive for amniotic fluid Swabbed on a glass slide and inspected for ferning, indicating amniotic fluid Presence of blood renders both tests useless In addition, the fundal height should be determined, fetal weight estimated, and FHR and contractions monitored via electronic fetal monitoring (EFM) Lab Studies to Be Evaluated : Lab Studies to Be Evaluated Include: CBC to evaluate for leukocytosis and low hematocrit Urinalysis to assess the degree of dehydration and rule out infection Cervical cultures for chlamydia, gonorrhea, and group B streptococcus Urine toxicology screen Consider when substance abuse is suspected Determine serum glucose and potassium before initiating -adrenergic agonists for tocolysis Physical Assessment : Physical Assessment Pay attention to the pattern of contractions, status of membranes, and the degree of cervical dilation to determine the stage of labor Allows for an informed decision on the part of the transport crew as to whether the transport should be delayed to allow delivery at the transporting facility Management : Management Management goals during transport include maintaining uteroplacental perfusion and suppressing labor Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Ensure IV access Initiate volume replacement if dehydration is suspected Give tocolytic agents Breech Presentation (1 of 6) : Breech Presentation (1 of 6) Breech Presentation (2 of 6) : Breech Presentation (2 of 6) Epidemiology Breech presentations occur in 3 to 4 percent of all term pregnancies Higher incidence before 34 weeks gestation Morbidity rate three to four times that of cephalad presentations Breech Presentation (3 of 6) : Breech Presentation (3 of 6) Pathophysiology Breech presentation is term used to describe the situation in which the fetus’s buttocks or legs present first Frank breech presentation Most common type Occurs when both legs are extended upward, with both hips flexed and both knees extended Complete breech Occurs when the buttocks descend first, both hips are flexed, and one or both knees are flexed, resulting in one of both feet presenting with the buttocks Breech Presentation (4 of 6) : Breech Presentation (4 of 6) Pathophysiology Maternal complications Maternal trauma is common Fetal complications Prolapsed cord, cord compression, and cord entanglement are common complications, and birth trauma is likely Breech fetus is at higher risk of hypoxia, acidosis, and anoxia than infant delivered in cephalad position Breech Presentation (5 of 6) : Breech Presentation (5 of 6) Management Allow fetus to deliver on own Apply no traction to fetus Once umbilical cord has delivered, help free the legs, if needed Wrap the fetus in a towel and rotate so the shoulders are in an anterior-posterior position Breech Presentation (6 of 6) : Breech Presentation (6 of 6) Management As the shoulders become visible, either: Use a finger to hook each arm and apply gentle downward traction to remove each one Apply upward traction to facilitate the delivery of the posterior shoulder and downward traction for the anterior shoulder After the shoulders have been delivered, rotate the body so the back is anterior Maintain flexion of the head by placing the index and middle fingers over the fetus’s maxilla With the body resting on the forearm of the same arm and the opposite hand supporting the head and shoulders, apply upward traction to the body while an assistant applies suprapubic pressure to encourage the delivery of the head with as little traction as possible Dystocia (1 of 6) : Dystocia (1 of 6) Epidemiology Shoulder dystocia occurs in 0.6 to 1.4 percent of all vaginal deliveries Dystocia (2 of 6) : Dystocia (2 of 6) Pathophysiology Delivery of the fetal head is followed by impactation of the fetal shoulders against the pubic symphysis and sacrum in the pelvis Risk factors Birth weight over 4,000 grams Maternal diabetes Maternal obesity Operative delivery Contracted maternal pelvis Dystocia (3 of 6) : Dystocia (3 of 6) Assessment Turtle sign Fetal head retracts slightly as it is pulled down against the perineum Dystocia (4 of 6) : Dystocia (4 of 6) Management Once dystocia is recognized, the immediate draining of the urinary bladder and a generous mediolateral episiotomy may facilitate delivery Apply pressure to the fetus’s anterior shoulder to dislodge the anterior shoulder from the pubic symphysis Palpate the anterior shoulder in the maternal suprapubic area Dystocia (5 of 6) : Dystocia (5 of 6) Management Do not apply pressure to the fundal area Doing so will further impact the shoulders on the pelvic rim Apply gentle, downward traction to the fetal head If this maneuver fails, try others McRobert’s Woods corkscrew Rubin Zavanelli Dystocia (6 of 6) : Dystocia (6 of 6) Umbilical Cord Prolapse (1 of 6) : Umbilical Cord Prolapse (1 of 6) Umbilical Cord Prolapse (2 of 6) : Umbilical Cord Prolapse (2 of 6) Epidemiology Occurs about once every 250 deliveries Umbilical Cord Prolapse (3 of 6) : Umbilical Cord Prolapse (3 of 6) Pathophysiology Two types of umbilical cord prolapse Overt Occurs when the cord enters the vaginal canal or presents externally before the fetus Occult Occurs when the cord slips into or near the pelvis and is occluded by a presenting part Not visible or palpable on exam Umbilical Cord Prolapse (4 of 6) : Umbilical Cord Prolapse (4 of 6) Risk factors include: PROM Transverse lie of the fetus in the uterus Breech presentation Large fetus Multiparity Multiple gestations Preterm labor Long cord Major concern with prolapsed cord is cord compression and occlusion Fetal complications can include hypoxia, acidosis, anoxia, and death Umbilical Cord Prolapse (5 of 6) : Umbilical Cord Prolapse (5 of 6) Assessment Assessment findings of an overt umbilical cord prolapse are straightforward, but the occult prolapse can be much more insidious and requires a careful examination on the part of the critical care transport team Clinical signs include evidence of fetal distress, including: Absence of short and long-term variability Fetal bradycardia Recurrent variable decelerations that do not respond to maternal positioning, oxygen administration, or fluid administration Umbilical Cord Prolapse (6 of 6) : Umbilical Cord Prolapse (6 of 6) Management If the umbilical cord presents externally or can be visualized in the vagina, use two fingers of a gloved hand to prevent any presenting part of a delivering fetus from occluding the cord Never pull or re-place a presenting cord in the uterus If the cord retracts spontaneously, let it do so Keep the cord free of pressure throughout transport Use Trendelenburg or knee-chest position to decrease pressure on the cord Administer 100 percent oxygen via nonrebreather mask at 15 lpm Start an IV of normal saline Give a tocolytic agent When prolapse is unresolved, treat with cesarean section Uterine Rupture (1 of 5) : Uterine Rupture (1 of 5) Pathophysiology Defined as complete disruption of all layers of the uterine wall Allows the uterine and abdominal cavities to communicate Usually occurs in women who have had cesarean sections Uterine Rupture (2 of 5) : Uterine Rupture (2 of 5) Risk factors include: Previous cesarean section Overdistension of the uterus Grand multiparity Previous rupture Trauma Fetal complications include: Hypoxia Acidosis Anoxia Death Uterine Rupture (3 of 5) : Uterine Rupture (3 of 5) Assessment Common clinical findings include: Acute onset of sharp, severe abdominal pain Signs and symptoms of hypovolemic shock Rebound tenderness and distension Palpation of extrauterine fetal parts Vaginal bleeding possible Palpation of the uterus can reveal contractions that are: Hypertonic Normal Stopped Uterine Rupture (4 of 5) : Uterine Rupture (4 of 5) Diagnostics Laboratory studies of immediate use include a CBC, type and crossmatch, and coagulation profile When uteroplacental blood flow is compromised, evidence of fetal distress includes: Absence of short- and long-term variability Fetal bradycardia Recurrent variable decelerations that do not respond to maternal positioning, oxygen administration, or fluid administration Uterine Rupture (5 of 5) : Uterine Rupture (5 of 5) Management Definitive treatment is surgical repair Primary goal is to maintain ABCs to preserve uteroplacental perfusion Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Provide IV access Initiate volume replacement if dehydration is suspected Use a Foley catheter Monitor urinary output 0.5 ml/kg/hr is desired Use tocolytic agents Postpartum Hemorrhage (PPH) (1 of 6) : Postpartum Hemorrhage (PPH) (1 of 6) Epidemiology PPH occurs in about 5 percent of all deliveries Implicated in almost 30 percent of all pregnancy-related deaths Most hemorrhages occur within 24 hours of delivery Postpartum Hemorrhage (PPH) (2 of 6) : Postpartum Hemorrhage (PPH) (2 of 6) Pathophysiology PPH is considered: The loss of greater than 500 ml of blood after a vaginal delivery More than 1,000 ml of blood lost after a cesarean section Normally, postlabor platelet aggregation and clot formation in the decidua is complemented by myometrial contraction that constricts and occludes blood vessels torn when the placenta disassociates from the uterine implantation site Because blood flow to the uteroplacental boundary is about 600 ml/min, hemorrhage can be significant if uterine contraction does not occur Because uterine contraction is prevented, blood accumulates and clots in the uterus, further preventing uterine contraction and worsening bleeding Postpartum Hemorrhage (PPH) (3 of 6) : Postpartum Hemorrhage (PPH) (3 of 6) Common causes of PPH Uterine atony Retained placental fragments Birth canal trauma Postpartum Hemorrhage (PPH) (4 of 6) : Postpartum Hemorrhage (PPH) (4 of 6) Risk factors for uterine atony include: Retention of placental fragments Overdistension of the uterus Multiparity Polyhydramnios Chorioamnioitis Prolonged or obstructed labor Use of general anesthesia Magnesium tocolysis Placenta accrete Major risk factor for retained placenta Postpartum Hemorrhage (PPH) (5 of 6) : Postpartum Hemorrhage (PPH) (5 of 6) Assessment Uterine atony can be identified by a lack of uterine contractions and a flaccid uterus upon palpation Vaginal bleeding should be apparent, but external blood loss may not be total blood loss Much blood loss may be sequestered in the uterus Evaluate the patient’s hemodynamic status using signs and symptoms of shock, rather than estimates of total blood loss Helpful laboratory results include: CBC Type and crossmatch Hematocrit Coagulation studies Postpartum Hemorrhage (PPH) (6 of 6) : Postpartum Hemorrhage (PPH) (6 of 6) Management Primary goal is to maintain ABCs to preserve uteroplacental perfusion Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Provide IV access Use large-bore, peripheral IVs Strive for central venous access When hypovolemic shock presents, initiate aggressive volume replacement with a crystalloid and packed red blood cells Foley catheter Monitor urinary output 0.5 ml/kg/hr is desired Give uterine fundal massage Administer carboprost tromethamine (Hemabate) Medical Complications of Pregnancy (1 of 2) : Medical Complications of Pregnancy (1 of 2) Hypertension in pregnancy Four categories of hypertension during pregnancy Chronic hypertension Hypertension that predates pregnancy or is identified before 20 weeks gestation Gestational hypertension Occurs after 20 weeks gestation and is not accompanied by proteinuria Pre-eclampsia Hypertension and proteinuria coexist Chronic hypertension with pre-eclampsia Exists when a female with known hypertension develops worse hypertension and proteinuria A pregnant female is considered hypertensive when she has a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mmHg Medical Complications of Pregnancy (2 of 2) : Medical Complications of Pregnancy (2 of 2) Hypertension in pregnancy Pre-eclampsia is termed mild when findings are present but do not meet the criteria established for severe pre-eclampsia Eclampsia, the most serious manifestation of pregnancy-induced hypertension, is said to be present when the patient has a seizure Medical Complications of Pregnancy (1 of 6) : Medical Complications of Pregnancy (1 of 6) Pre-eclampsia Medical Complications of Pregnancy (2 of 6) : Medical Complications of Pregnancy (2 of 6) Pre-eclampsia Occurs in 6 to 8 percent of all live births Exact cause(s) of pre-eclampsia are unknown Theoretical models include: Immunologic responses Increased sensitivity to endogenous vasoconstrictors Endothelial damage with prostacyclin and thromboxane A2 production Chronic disseminated intravascular coagulation (DIC) Genetic predisposition Common thread of practically all of these models is increased vasoconstriction, peripheral vascular resistance, and subsequent hypertension Medical Complications of Pregnancy (3 of 6) : Medical Complications of Pregnancy (3 of 6) Pre-eclampsia Known risk factors include: Age 35 and 15 Pre-eclampsia in a previous pregnancy Multiparity Pre-existing renal or cardiovascular disease Diabetes Medical Complications of Pregnancy (4 of 6) : Medical Complications of Pregnancy (4 of 6) Pre-eclampsia Known risk factors include: Family history African-American descent Maternal risks include renal failure, hepatic failure, DIC, seizures and strokes, and death Maternal mortality rate is 2 to 4 percent in eclampsia or when hemolysis, elevated liver enzymes, and low platelets syndrome complicates preeclampsia Fetal risks include uteroplacental hypoperfusion, placental infarction, abruptio placentae, inhibited fetal growth, oligohydramnios, and fetal demise Medical Complications of Pregnancy (5 of 6) : Medical Complications of Pregnancy (5 of 6) HELLP syndrome HELLP is an acronym for: Hemolysis Elevated liver function tests Low platelets Thought to be a subcategory of severe pre-eclampsia Patients often experience a rapid, degenerative course, and many physicians elect for prompt delivery before the onset of eclampsia Medical Complications of Pregnancy (6 of 6) : Medical Complications of Pregnancy (6 of 6) HELLP syndrome Assessment Headaches, nausea and vomiting, seizures, visual disturbances, and cerebral edema Decreased urine output, proteinuria, decreased kidney function Decreased liver function Labs Elevated serum uric acid, urea nitrogen, and creatinine Elevated liver function tests Proteinuria Low platelet count (100,000/mm3) Management (1 of 2) : Management (1 of 2) Primary goal is to maintain ABCs to preserve uteroplacental perfusion Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Ensure IV access Use large-bore, peripheral IVs Ensure central venous access Management (2 of 2) : Management (2 of 2) Monitor urinary output 0.5 ml/kg/hr is desired Use urine dipstick to assess for proteinuria Administer magnesium sulfate for seizures Give morphine, furosemide for pulmonary edema Use hntihypertensives for severe elevations in blood pressure Magnesium sulfate, hydralazine, or labatalol Gestational Diabetes Mellitus (GDM) : Gestational Diabetes Mellitus (GDM) Epidemiology Incidence of GDM varies between less than 1 to 15 percent of all pregnancies Pathophysiology of GDM (1 of 2) : Pathophysiology of GDM (1 of 2) Those cases of diabetes, regardless of severity or insulin requirements, that present initially during pregnancy GDM can be a true initial onset of Type I or Type II diabetes, or it may represent a previously unrecognized case, worsened by the increased demand placed on the mother by the developing fetus Pathophysiology of GDM (2 of 2) : Pathophysiology of GDM (2 of 2) The pathogenesis of GDM mimics that of Type II (NIDDM) DM Impaired insulin secretion and increased insulin resistance are present in both Most cases of GDM resolve after pregnancy 32 percent lifetime risk of developing Type II DM after GDM Risk Factors for Developing GDM : Risk Factors for Developing GDM Maternal obesity Previous infant over 4,000 g birth weight History or family history of DM History of pre-eclampsia Maternal age over 30 years Excessive weight gain during pregnancy (40 lbs) Maternal complications include preterm labor, preeclampsia, pyleonephritis, and the need for cesarean section Fetal complications include increased perinatal morbidity and mortality, shoulder dystocia, stillbirth, operative delivery, and macrosomia Assessment : Assessment Determine blood glucose Do so every hour for patients in active labor with GDM Patients with preterm labor being controlled with -adrenergic agonists are at a higher risk for hypoglycemia and should be monitored carefully Management : Management Same as for nonpregnant patients If hypoglycemia is present, administer 25–50 g of dextrose IV If hyperglycemia is present, administer insulin subcutaneously If blood glucose levels drop below 80 dl/mg, can initiate a continuous infusion of D5W, 125 ml/hour For insulin-dependent patients in labor, can also consider a continuous insulin infusion Summary (1 of 2) : Summary (1 of 2) The critical care paramedic must know the anatomy and physiology, pathophysiology, symptomotology, and management techniques appropriate for female patients with high-risk OB/GYN conditions Summary (2 of 2) : Summary (2 of 2) The critical care paramedic should stay abreast of literature on the assessment and management of these patients The medical science used to treat the OB/GYN emergency evolves continually 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Edit Comment Close Premium member Presentation Transcript Chapter 28: High-Risk OB-GYN : Chapter 28: High-Risk OB-GYN Galveston College EMS Critical Care Paramedic 2009 Introduction (1 of 2) : Introduction (1 of 2) Pregnancy complications that mandate critical care transport can have multiple etiologies While some complications may be related to pre-existing medical conditions, others may be precipitated by the pregnancy, still others by the fetus Introduction (2 of 2) : Introduction (2 of 2) The critical care paramedic must be able to: Perform a proper physical assessment of both the mother and fetus Form a differential diagnosis and treatment plan Anticipate the risks and possible complications of any scenario so as to ensure the proper care and best possible outcome of both mother and fetus Anatomy and Physiology : Anatomy and Physiology Anatomy (1 of 4) : Anatomy (1 of 4) Courtesy Wendy Hiller Gee. Anatomy (2 of 4) : Anatomy (2 of 4) Courtesy Wendy Hiller Gee. Anatomy (3 of 4) : Anatomy (3 of 4) Anatomy (4 of 4) : Anatomy (4 of 4) General Information : General Information Female reproductive system consists of: Paired ovaries Paired fallopian tubes Uterus Vagina System functions to produce and secrete sex hormones; yield viable gametes; and support, protect, and deliver a developing fetus After birth, the female reproductive system nourishes the newborn infant Gestation : Gestation Time between fertilization of an oocyte until birth In human averages 266 days Gestation of fewer than 37 weeks is considered premature Gestation of greater than 42 weeks is considered postmature The gestational period is often broken into three trimesters, each 3 months long Fertilization and the First Trimester : Fertilization and the First Trimester Fertilization (1 of 2) : Fertilization (1 of 2) Usually occurs in distal one-third of the fallopian tube Fertilized egg termed a zygote Contains the normal human complement of 46 chromosomes Cell division in the zygote starts immediately Zygote travels down the fallopian tube to the uterus Fertilization (2 of 2) : Fertilization (2 of 2) From Nilsson, L. (1990) A child is born. New York: Dell Publishing. Development and Implantation : Development and Implantation Blastocyst formation Blastocyst adheres to uterine endometrium Differentiation Syncytial trophoblast Implantation Hyaluronidase Functional zone of endometrium Human chorionic gonadotropin (HCG) production Corpus luteum Progesterone Further prepares uterus for pregnancy Prevents start of new uterine cycle By Day 9 (1 of 2) : By Day 9 (1 of 2) Syncytial trophoblast has spread into the surrounding endometrium Surrounds and erodes endometrial capillaries Maternal blood leaking from the eroded capillaries flows through channels, called lacunae, in the syncytial trophoblast By Day 9 (2 of 2) : By Day 9 (2 of 2) Days 9–21 : Days 9–21 Chorionic villi form on the trophoblast and extend into the endometrium Embryonic blood vessels develop in the villi, and circulation in these vessels begins As large endometrial blood vessels become involved, more maternal blood flows through the lacunae First exchange between fetal and maternal blood occurs First steps in placenta creation By End of Week 4 : By End of Week 4 Embryo Is about 5 mm long Weighs about 0.02 g Has a heart beat Has begun to develop trachea, lungs, intestinal tract, liver, pancreas, eyes, and ears Week 5 : Week 5 Days 9–21 : Days 9–21 By the End of Week 8 : By the End of Week 8 Diaphragm, intestinal subdivisions, kidneys, axial and appendicular cartilage, and axial musculature have started to develop At this point, embryo is termed a fetus Week 20 : Week 20 By the End of the First Trimester (Week 28) (1 of 2) : By the End of the First Trimester (Week 28) (1 of 2) Gallbladder, gonads, brain, spinal cord, and appendicular musculature start to develop Fetus about 80 mm long and weighs about 25 g Placenta has fully developed and normally is in the fundal or body region of the uterus Typical human placenta is about 20 cm in diameter and 2.5 cm thick and weighs about 500 g By the End of the First Trimester (Week 28) (2 of 2) : By the End of the First Trimester (Week 28) (2 of 2) Primary functions Facilitate the exchange of nutrients and wastes between mother and fetus Developing fetus places significant demands on the mother Produce hormones needed to maintain pregnancy and fetal development Flow blood between the fetus and placenta via the umbilical cord Cord contains paired umbilical arteries and single umbilical vein Significant amount of maternal blood is redirected to the placenta The Second Trimester (1 of 2) : The Second Trimester (1 of 2) During the second and third trimesters, the placenta acts as an endocrine organ and takes over progesterone-releasing duties from the corpus luteum Placenta also produces the hormones HCG, estrogen, human placental lactogen, and relaxin During second trimester, organ system development nears completion The Second Trimester (2 of 2) : The Second Trimester (2 of 2) Fetus continues to mature rapidly Fetus is moving by the end of week 16 By the end of the second trimester, the developing fetus has taken on distinctive human characteristics Eyebrows and eyelashes are well formed, all eye components are developed Hands and startle reflex are evidents Footprints and fingerprints are forming Alveoli are developing The Third Trimester (1 of 2) : The Third Trimester (1 of 2) Early in the third trimester, most organ systems have matured and become fully functional Baby born at 36 weeks has good chance of survival and is considered full term from weeks 37 through 40 The Third Trimester (2 of 2) : The Third Trimester (2 of 2) Third trimester characterized by rapid growth of fetus Has grown to about 345 mm long and weighs about 3.2 kg at full gestation Exhibits other developmental markers Rapid deposition of body fat Rhythmic breathing movements Lungs are not fully mature, however Fully developed though soft and pliable bones Stores of iron, calcium, and phosphorus Changes in Maternal Physiology : Changes in Maternal Physiology Systems affected in pregnancy include: Cardiovascular Respiratory Reproductive Gastrointestinal Urinary Cardiovascular System Changes (1 of 3) : Cardiovascular System Changes (1 of 3) Increased blood volume and red blood cell production By end of gestation, maternal blood volume has increased by 45 to 50 percent Results in: Increased resting heart rate Increased cardiac output Possible flow murmurs on auscultation Slight decreases in peripheral vascular resistance Causes slight decrease in blood pressure during first and second trimesters Cardiovascular System Changes (2 of 3) : Cardiovascular System Changes (2 of 3) System returns to prepregnancy levels during third trimester Peripheral edema Secondary to intravascular fluid shifts into the intracellular space in dependent areas Supine hypotensive syndrome Not true physiologic change Transient decrease in venous return to the heart and subsequent hypotension can occur when the gravid uterus compresses the inferior vena cava Occurs most often when the pregnant female is supine Cardiovascular System Changes (3 of 3) : Cardiovascular System Changes (3 of 3) Hypercoagulable state Secondary to: Increase of clotting factors Decrease in fibrinolytic activity Increase in platelet activation Venous stasis Respiratory System Changes (1 of 3) : Respiratory System Changes (1 of 3) O2 demand increases 10 to 20 percent increase in O2 consumption Progesterone secretion weakens costal cartilage Greater movement of the rib cage 35 to 40 percent increase in tidal volume Respiratory System Changes (2 of 3) : Respiratory System Changes (2 of 3) Respiratory rate increases mildly This, with the increase in tidal volume, increases minute volume Mild, compensated respiratory alkalosis occurs Creates a greater CO2 gradient and greater diffusion of CO2 between mother and fetus Reproductive System Changes (3 of 3) : Reproductive System Changes (3 of 3) Uterus enlarges Achieves 30 cm length, 1,000 g weight, 5 liter volume Receives about 15 percent of maternal blood volume by gestation’s end Gastrointestinal System Changes (1 of 2) : Gastrointestinal System Changes (1 of 2) Abdomincal organs are compressed and displaced Peristalsis slows, delaying gastric emptying Bloating, nausea, and constipation are common Maternal nutritional requirements increase 10 to 30 percent Gastrointestinal System Changes (2 of 2) : Gastrointestinal System Changes (2 of 2) Glomerular filtration rate (GFR) increases by about 50 percent As result, glucose may be insufficiently reabsorbed and is subsequently excreted in the urine Urine production increases Glucosuria manifests General OB/GYN Assessment : General OB/GYN Assessment History Medical history should include: Entire medical history Obstetric history Medical history concerns Pregnancy Can exacerbate or complicate history Diabetes Seizure disorders Heart disease Hypertension Neuromuscular disorders Medications and allergies to medications Should be identified and recorded Obstetric History Concerns (1 of 5) : Obstetric History Concerns (1 of 5) Gravida/para (G/P) status Number of living children? Complications with previous pregnancies or deliveries? History of preterm delivery? Gestational age? Outcome? History of lective or spontaneous abortion? D&C performed? Obstetric History Concerns (2 of 5) : Obstetric History Concerns (2 of 5) Have all previous births been vaginal or was cesarean section performed? Has patient delivered vaginally after a cesarean section? When was, and what was length of, last labor? With regard to current pregnancy, what is estimated date of confinement (EDC)? Has patient received adequate, limited (three or fewer visits), or no prenatal care? Obstetric History Concerns (3 of 5) : Obstetric History Concerns (3 of 5) Any problem with pregnancy identified? If so, what? Diagnostic tests like ultrasound done? If so, what were results? Is patient taking any medications for obstetric or nonobstetric reasons? If so, which medication(s), what dose(s), and compliant schedule(s)? Obstetric History Concerns (4 of 5) : Obstetric History Concerns (4 of 5) Drug or alcohol abuse suspected? If so, which substance(s), frequency of use, date of last use? Patient smoking? Pregnancy weight gain normal, or patient malnourished or obese? Is patient having contractions? If so, when did they begin, and what are their frequency and duration? Patient with urge to defecate? Obstetric History Concerns (5 of 5) : Obstetric History Concerns (5 of 5) Has patient’s amniotic sac ruptured? If so, at what time, and was it a trickle or gush? Was meconium in the fluid, or did fluid smell foul? Has patient bled vaginally? If so, accompanied by pain? If pain, is it associated with contractions or constant? Has patient or transporting facility used sanitary napkins or other absorbent devices to soak up blood? If so, how much? Physical Exam (1 of 8) : Physical Exam (1 of 8) Abdominal exam for pregnant patients is basically same as that for nonpregnant patients Displacement and compression of abdominal organs by the gravid uterus makes identifying abdominal landmarks challenging Physical Exam (2 of 8) : Physical Exam (2 of 8) Palpate for pain, tenderness, guarding, masses, and uterine contractions During uterine contractions, palpate the fundus for contraction strength, frequency, and duration Use tocodynamometer Records strength, duration, and time between contractions Records and prints continuously while the patient is hooked to the monitor Physical Exam (3 of 8) : Physical Exam (3 of 8) Measure fundal height (FH) of uterus, in centimeters, from the symphysis pubis to the most superior portion of the fundus Each centimeter of FH corresponds roughly to gestational age in weeks Fetus position can be determined by palpating the uterus for the head and buttocks Fetal spine can often be palpated, as well Physical Exam (4 of 8) : Physical Exam (4 of 8) Fundal height (FH) Physical Exam (5 of 8) : Physical Exam (5 of 8) Examine external genitalia for discharge, blood, mucus, a prolapsed cord, or crowning Evaluate for crowning during a contraction Do not conduct internal vaginal exam Not normally in scope of practice of the critical care paramedic May be justified in doing physician examination of the patient’s cervix before transport Physical Exam (6 of 8) : Physical Exam (6 of 8) External genitalia Physical Exam (7 of 8) : Physical Exam (7 of 8) Assess vital signs every 15 minutes or as often as the situation warrants Pulse Blood pressure Respiratory rate Temperature SpO2 Physical Exam (8 of 8) : Physical Exam (8 of 8) Assess and monitor fetal heart tones (FHT) throughout transport Conduct electronic fetal monitoring Evaluate and monitor uterine contractions and fetal heart rate electronically Intrapartum Fetal Heart Rate Monitoring (1 of 2) : Intrapartum Fetal Heart Rate Monitoring (1 of 2) Intrapartum FHR monitoring was introduced as way to prevent intrapartum fetal compromise, death, and asphyxia-induced brain damage A change in FHR is earliest indication of insult to fetal circulation and developing hypoxia secondary to umbilical cord insult or uteroplacental insufficiency Asphyxia is said to have occurred when hypoxia with a resulting metabolic acidosis presents Intrapartum Fetal Heart Rate Monitoring (2 of 2) : Intrapartum Fetal Heart Rate Monitoring (2 of 2) FHR monitoring has very good rate of detecting fetuses at risk of developing asphyxia (about 90 percent) False negatives are rare In most cases, normal FHR tracings are adequate to conclude clinically that fetal perfusion status is normal FHR monitoring specificity is poor False-positive rates between 50 and 75 percent Most newborns with abnormal FHR records do not present with hypoxia and metabolic acidosis at birth Indications for FHR Monitoring : Indications for FHR Monitoring Antepartum risk factors Multiple gestation, preeclampsia, chronic hypertension, and maternal diabetes Intrapartum risk factors Cases of active or suspected abruptio placentae, placenta previa, meconium staining, prematurity, and the documentation of abnormal FHR patterns FHR monitoring is also suggested in cases of active labor with the use of analgesia, anesthesia, or oxytocin Effective OB/GYN Assessment : Effective OB/GYN Assessment Familiarize with FHR monitoring terminology Know normal FHR parameters Be able to recognize normal and abnormal FHR tracings Baseline FHR : Baseline FHR Defined as average FHR during 10-minute period rounded to the nearest 5 beats/minute For baseline FHR, must be at least 2 minutes of 10 with no: Eisodic changes Periods of significant FHR variability Segments with differences greater than 25 beats/minute Normal baseline FHR is 110–160 bpm Bradycardia (1 of 2) : Bradycardia (1 of 2) Exists when FHR is less than 110 bpm for more than 10 minutes Not uncommon for a term or postmature fetus to have baselines between 100 and 110 bpm Bradycardia occurs secondary to increased fetal parasympathetic tone and causes decreased cardiac output, hypoxia, and, eventually, metabolic acidosis Bradycardia (2 of 2) : Bradycardia (2 of 2) Can occur secondary to: Umbilical cord compression or occlusion Maternal hypotension Uterine hyperstimulation resulting in increased intrauterine pressure during contractions As with the use of oxytocin Chronic hypoxia Fetal bradycardia is late, ominous sign May be inadvertent measure of maternal pulse Tachycardia (1 of 2) : Tachycardia (1 of 2) Defined as FHR greater than 160 bpm for more than 10 minutes Early, immediate compensatory reaction is to increase cardiac output in instances of hypoxia Significantly less variability in heart rate usually occurs during tachydardia episodes Tachycardia (2 of 2) : Tachycardia (2 of 2) Can occur secondary to: Transient fetal hypoxia Fetal anemia Maternal fever Maternal or fetal infections Maternal smoking Sympathomimetic drugs Terbutaline Chorioamnionitis Sinusoidal Wave Pattern : Sinusoidal Wave Pattern Frequent, wave-like pattern of regularly occurring increases and decreases of FHR over a range of 5–20 beats from baseline May be appreciated in cases of fetal anemia, erythroblastosis, or hypovolemia Indicates severe fetal hypoxia Maternal use of narcotics may also cause sinusoidal wave pattern but does not indicate fetal distress Variability (1 of 4) : Variability (1 of 4) Variability in baseline FHR is normal and indicates an adequately oxygenated and normally functioning autonomic nervous system Associated with normal oxygenation status at delivery Variability occurs as the sympathetic and parasympathetic nervous systems alternately influence the fetal heart rate Can be described as short- or long-term Variability (2 of 4) : Variability (2 of 4) Short-term variability Beat-to-beat changes in FHR Usually irregular in rate and frequency Greatly influenced by the parasympathetic branch More susceptible to hypoxia than sympathetic branch Cessation of normal, short-term variability may be first indicator of fetal hypoxia Long-term variability Broad “waviness” of FHR tracing over time Can range from 5 to 25 beats above and below the baseline Fewer than 5 beats over 1 minute is considered short Differs from the sinusoidal wave pattern in that its waves occur with much less frequency or over a longer period Influenced by the sympathetic nervous system Variability (3 of 4) : Variability (3 of 4) Absent or minimal variability, long and short term, can result from: Fetal hypoxia Maternal narcotic use Smoking Administration of magnesium sulfate Extreme prematurity Fetal neurologic insult Normal fetal sleep cycles Variability (4 of 4) : Variability (4 of 4) Increased variability can be early sign of hypoxia or the result of ultrasound (US) transducer use US transducers are notorious for erroneously high variability readings in critical care transport The most likely measuring devices used by transport team due to their noninvasive nature If true evaluation of FHR short-term variability is required, a physician should place a fetal scalp electrode Long-term variability is accurate with an ultrasound transducer and should be monitored and recorded during transport Periodic Changes in FHR : Periodic Changes in FHR Acceleration (1 of 3) : Acceleration (1 of 3) Defined as obvious, abrupt increase (fewer than 30 seconds from onset to peak rate) in FHR with a peak rate 15 bpm above baseline that lasts for more than 15 seconds and fewer than 2 minutes from onset to return to baseline Over 2 minutes acceleration is considered prolonged, over 10 minutes is considered change in baseline Accelerations are usually benign Acceleration (2 of 3) : Acceleration (2 of 3) Can occur secondary to uterine contractions or fetal movement and indicate that the fetus has intact central nervous system and normal pH Accelerations strongly suggest normal fetal pH Can also indicate developing fetal hypoxia, occurring before pH has changed Acceleration (3 of 3) : Acceleration (3 of 3) Critical care transport team should ensure that fetal movement or contractions accompany all accelerations Ask the mother if movement or contractions are occurring Palpate the uterus during the acceleration Identify contractions on a tocodynamometer Decelerations (1 of 3) : Decelerations (1 of 3) Defined as obvious, gradual (more than 30 seconds from onset to nadir) decrease and return of FHR from baseline during a uterine contraction Considered normal during uterine contraction Nadir of the deceleration occurs simultaneously with the peak of the uterine contraction Decelerations (2 of 3) : Decelerations (2 of 3) In most cases, deceleration mirrors the contraction Can be classified as early, late, or variable Early decelerations are not associated with fetal hypoxia or acidosis and need no intervention Late decelerations are more serious sign than early ones Decelerations (3 of 3) : Decelerations (3 of 3) Indicate hypoxia and acidosis secondary to uteroplacental insufficiency Variable decelerations can occur any time during a contraction or independent of contractions Caused by umbilical cord compression and occlusion secondary to uterine contraction or fetal movement Late Decelerations (1 of 3) : Late Decelerations (1 of 3) Begins at the peak of a uterine contraction and returns to FHR baseline after the contraction concludes Causes of uteroplacental insufficiency include: Abruptio placentae and previa Uterine hypertonicity secondary to oxytocin administration Maternal hypotension and smoking Late Decelerations (2 of 3) : Late Decelerations (2 of 3) Diabetes Postmaturity Degree of deceleration is proportional to contraction strength Two mechanisms are responsible for late decelerations: Central nervous system induced reflex bradycardia secondary to hypoxia Metabolic acidosis resulting in myocardial depression Late Decelerations (3 of 3) : Late Decelerations (3 of 3) Hon E, (1976). An introduction to fetal heart rate monitoring (Second Ed., p. 29). Los Angeles: University of Southern California School of Medicine. Variable Decelerations (1 of 4) : Variable Decelerations (1 of 4) Characterized by abrupt decrease in FHR below baseline more than 15 bpm and lasting between 15 seconds and 2 minutes Morphology may be in the shape of an inverted V or an M Short accelerations on either side of the deceleration are termed “shoulders” Their appearance is thought to be caused by a partial, rather than complete, cord occlusion Variable Decelerations (2 of 4) : Variable Decelerations (2 of 4) “Smoothing” of the decelerations or loss of shoulders indicates fetal distress Can occur any time during a contraction or independent of contractions Caused by umbilical cord compression and occlusion secondary to uterine contraction or fetal movement Variable Decelerations (3 of 4) : Variable Decelerations (3 of 4) Most common decelerations seen in labor, and while not an ominous when isolated, should raise concern when: They are deep and long and accompanied by decreased FHR variability They are slow to return to baseline Baseline FHR increases or becomes tachycardic Variable Decelerations (4 of 4) : Variable Decelerations (4 of 4) Hon E, (1976). An introduction to fetal heart rate monitoring (Second Ed., p. 29). Los Angeles: University of Southern California School of Medicine. Changes in FHR Trending Patterns (1 of 3) : Changes in FHR Trending Patterns (1 of 3) Questions to rule in/out fetal distress Is FHR baseline within normal range? If the baseline is between 110 and 160 bpm, the fetus is maintaining an adequate cardiac output and metabolic acidosis is not present Is variability adequate? If it is, the fetus is being adequately oxygenated Changes in FHR Trending Patterns (2 of 3) : Changes in FHR Trending Patterns (2 of 3) Questions to rule in/out fetal distress If hypervariabilty presents, may be due to the ultrasound transducer Are accelerations present? Accelerations can only occur absent metabolic acidosis, so their presence is reassuring Is the event an early deceleration? If so, it is a normal, benign event that can be expected to occur with each uterine contraction Changes in FHR Trending Patterns (3 of 3) : Changes in FHR Trending Patterns (3 of 3) Questions to rule in/out fetal distress If tachycardia or bradycardia present, have accelerations and adequate variability presented? If so, metabolic acidosis is not present If late or variable decelerations present, have accelerations and adequate variability presented? If so, the fetus is tolerating the events well and metabolic acidosis is not present Signs of Fetal Distress : Signs of Fetal Distress Signs the fetus may be developing hypoxia and acidosis Gradual, significant, uncorrected decrease in baseline FHR over time A fluctuating baseline over time Tachycardia or bradycardia with reduced short- and long-term variability Reduced variability as labor progresses Late decelerations that “smooth out” over time Management of Fetal Distress (1 of 2) : Management of Fetal Distress (1 of 2) Ensure patient is breathing adequately and has a pulse Administer 100 percent oxygen via NRM Place patient in left lateral recumbent position If hypotension presents, consider repeated fluid boluses until hypotension corrects Perform an external vaginal exam to ensure there is no vaginal hemorrhage, prolapse Especially if the patient was high-risk for abruptio placentae or previa Management of Fetal Distress (2 of 2) : Management of Fetal Distress (2 of 2) If the fetal distress occurs secondary to hypertonic contractions resulting from oxytocin infusion, discontinue the infusion immediately Consider tocolytic agent like terbutaline 0.25 mg subcutaneous or 0.125–0.25 mg intravenous to relax the uterus Consider need for amnioinfusion When fetal distress is suspected, intrauterine resuscitation measures must be taken to improve uterine blood flow and increase fetal oxygenation Pathophysiology, Assessment, and Management of OB/GYN Emergencies : Pathophysiology, Assessment, and Management of OB/GYN Emergencies Vaginal Hemorrhage during Pregnancy : Vaginal Hemorrhage during Pregnancy Abruptio Placentae (1 of 12) : Abruptio Placentae (1 of 12) Abruptio Placentae (2 of 12) : Abruptio Placentae (2 of 12) Epidemiology Incidence about 0.83 percent (1 in 120) of all deliveries Fetal death occurs in 0.4 percent of all abruptions Approaches 100 percent when 50 to 100 percent of the placenta is involved Abruptio Placentae (3 of 12) : Abruptio Placentae (3 of 12) Pathophysiology Premature separation of a normally implanted placenta from the uterine wall Begins with arterial hemorrhaging into the deciduas basalis Hematoma formation and progression can cause expanding abruption As abruption continues, more vessels become involved, further contributing to the expanding retroplacental hematoma Deciduas is rich in thromboplastin Abruptio Placentae (4 of 12) : Abruptio Placentae (4 of 12) Pathophysiology Rapid clot formation may help attenuate the hemorrhage Uterus will often contract during an abruptio episode Separation of the placenta can be partial (marginal) or complete Abruption with vaginal bleeding is termed an external hemorrhage (90 percent of all abruptions) If no vaginal bleeding is appreciated on physical exam, the abruption is said to be concealed (10 percent of all abruptions) Abruptio Placentae (5 of 12) : Abruptio Placentae (5 of 12) Pathophysiology Blood loss is impossible to estimate based on external observation alone Significant amounts of blood can remain in the uterus, trapped behind the placenta Most blood loss is maternal, although the fetus can hemorrhage, as well Risk factors associated with abruptio placentae include: Chronic or gestational hypertension (most common factor) Cocaine use Smoking Abruptio Placentae (6 of 12) : Abruptio Placentae (6 of 12) Pathophysiology Trauma increasing maternal age (over 35) Multiparity Uterine scarring from surgeries Past curettage Infection Past incidence of abruptio placentae Complications Fetal complications include hypoxia, anoxia, anemia, and CNS compromise Maternal complications include the development of hemorrhagic shock, the development of disseminated intravascular coagulation (DIC), and end-organ failure Abruptio Placentae (7 of 12) : Abruptio Placentae (7 of 12) Assessment Classic signs are considered: Presence of abdominal pain (50 percent) Uterine contractions (90 percent) Vaginal bleeding (90 percent) Except in cases of concealed abrupto Uterine tenderness to palpation Fetal demise Abruptio Placentae (8 of 12) : Abruptio Placentae (8 of 12) Assessment Severe cases may present with: Rigid, board-like abdomen upon palpation Signs and symptoms of hemorrhagic shock Diagnostic imaging Ultrasound cannot diagnose abruptio placenta, although it can demonstrate a placental hematoma that is consistent with abruption Recognized in 2 to 25 percent of all abruptions Ultrasound can, however, rule out placenta previa as a cause of vaginal bleeding by determining the location of the placenta Abruptio Placentae (9 of 12) : Abruptio Placentae (9 of 12) Labs Labs ordered should include a CBC, type and crossmatch, coagulation profile, and renal function studies Patients should also be assessed for signs associated with DIC, which include bleeding from IV or catheter sites, hypotension, and increased ventilatory resistance Abruptio Placentae (10 of 12) : Abruptio Placentae (10 of 12) Management Oxygenation and perfusion is a priority in abruptio placenta treatment Especially in cases with signs and symptoms of shock 100 percent oxygen should, at minimum, be supplied at 15 lpm via a nonrebreather mask Give assisted ventilations with a BVM or endotracheal intubation as required Abruptio Placentae (11 of 12) : Abruptio Placentae (11 of 12) Management IV access Two large bore IVs Central line Volume replacement Volume resuscitation with crystalloid solution in cases of mild abruptio If hemorrhagic shock is present, aggressive volume replacement should be initiated with a crystalloid and packed red blood cells Critical care paramedic should procure additional packed red blood cells from the transporting facility for infusion during transport Abruptio Placentae (12 of 12) : Abruptio Placentae (12 of 12) Management Foley catheter Monitor of urinary output 0.5 ml/kg/hr is desired Tocolytic agents May help prevent a developing abruption from expanding Placenta Previa (1 of 7) : Placenta Previa (1 of 7) Placenta Previa (2 of 7) : Placenta Previa (2 of 7) Epidemiology Incidence at 18 weeks is about 5 to 15 percent About 90 percent of these cases resolve by gestation’s end 0.5 percent (1 in 200 deliveries) still present at delivery About 20 percent of all cases of vaginal bleeding occurring in the second half of pregnancy result from placenta previa Placenta Previa (3 of 7) : Placenta Previa (3 of 7) Pathophysiology Occurs when the placenta implants and develops in the lower third of the uterus, totally or partially covering the cervical os Three presentation types are possible: Complete previa occurs when the cervical os is completely covered Marginal previa occurs when the edge of the placenta lies adjacent to, but does not cover, the cervical os Partial previa is characterized by a placenta that partially covers the cervical os Placenta Previa (4 of 7) : Placenta Previa (4 of 7) Pathophysiology Complete previa completely covers the cervical os Risk factors contributing to placenta previa include: Advanced maternal age (35 years) Smoking (doubles risk of nonsmokers) Cocaine use Placenta Previa (5 of 7) : Placenta Previa (5 of 7) Pathophysiology History of previa Multiparity Multifetal gestations Previous cesarean section or curettage Maternal complications associated with previa include need for cesarean delivery, postpartum hemorrhage, and the development of hemorrhagic shock Fetal complications include hypoxia, anoxia, and death Placenta Previa (6 of 7) : Placenta Previa (6 of 7) Assessment Hallmark of previa is the acute onset of painless, bright red bleeding in the late second or third trimester History of recent vaginal exam, sexual intercourse, or onset of labor should increase suspicion but is not needed for previa to occur Abdominal exam is usually benign, although uterine contractions may be present Digital or speculum examination is to be avoided in all cases of suspected placenta previa Diagnosis of previa is confirmed with transabdominal ultrasound Accurate from 93 to 98 percent Placenta Previa (7 of 7) : Placenta Previa (7 of 7) Management For Barker, R.K., Fields, D.H., & Kaufman, S.A. (1990). Quick reference to OB-GYN procedures (3rd ed.). New York: Lippencott/Harper & Row. Complications of Labor and Delivery : Complications of Labor and Delivery Preterm Labor (1 of 2) : Preterm Labor (1 of 2) Epidemiology Preterm labor occurs in about 10 to 15 percent of all pregnancies Complicates 10 to 12 percent of all births Responsible for about 85 percent of all neonatal deaths not due to genetic or congenital abnormalities Most neonatal mortality occurs in infants delivered before 28 weeks gestation Preterm Labor (2 of 2) : Preterm Labor (2 of 2) Pathophysiology Defined as frequent uterine contractions resulting in progressive cervical dilation or effacement between the 20th and 37th weeks of gestation Numerous physiologic factors can contribute to the development of preterm and premature labor Physiologic Factors Leading to Preterm Labor : Physiologic Factors Leading to Preterm Labor Hormonal influences Prostaglandin release High oxytocin levels Decreased uteroplacental blood flow Maternal dehydration Maternal hypertension Overdistension of the uterus Smoking, cocaine use Cardiovascular disease Placental abruption or previa Anatomic/physiologic abnormalities affecting the cervix or uterus Preterm Labor Risk factors : Preterm Labor Risk factors Premature rupture of membranes (PROM) Smoking Cocaine use Poor nutritional status Maternal age 35 or 20 Previous preterm delivery, abruptio placentae or previa Infection Dehydration Uterine abnormalities Cervical incompetence STDs like chlamydia, gonorrhea, and syphilis Complications of Preterm Labor : Complications of Preterm Labor Maternal complications of premature labor include endometritis, septicemia and septic shock secondary to PROM, and chorioamnionitis Fetal consequences of premature labor include preterm birth Accounts for about 100 neonatal deaths for every 100,000 live births in the United States Assessment (1 of 2) : Assessment (1 of 2) Assess for evidence of the numerous etiologies of preterm labor, including fever, dehydration, vaginal hemorrhaging, and PROM Patient history will identify risk factors like age, history of preterm labor, and social history Cervical exam should be performed by an appropriately trained health care provider to assess for cervical dilation or membrane rupture Assessment (2 of 2) : Assessment (2 of 2) Identification of suspected amniotic fluid Tested with nitrazine paper pH 6.5 is positive for amniotic fluid Swabbed on a glass slide and inspected for ferning, indicating amniotic fluid Presence of blood renders both tests useless In addition, the fundal height should be determined, fetal weight estimated, and FHR and contractions monitored via electronic fetal monitoring (EFM) Lab Studies to Be Evaluated : Lab Studies to Be Evaluated Include: CBC to evaluate for leukocytosis and low hematocrit Urinalysis to assess the degree of dehydration and rule out infection Cervical cultures for chlamydia, gonorrhea, and group B streptococcus Urine toxicology screen Consider when substance abuse is suspected Determine serum glucose and potassium before initiating -adrenergic agonists for tocolysis Physical Assessment : Physical Assessment Pay attention to the pattern of contractions, status of membranes, and the degree of cervical dilation to determine the stage of labor Allows for an informed decision on the part of the transport crew as to whether the transport should be delayed to allow delivery at the transporting facility Management : Management Management goals during transport include maintaining uteroplacental perfusion and suppressing labor Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Ensure IV access Initiate volume replacement if dehydration is suspected Give tocolytic agents Breech Presentation (1 of 6) : Breech Presentation (1 of 6) Breech Presentation (2 of 6) : Breech Presentation (2 of 6) Epidemiology Breech presentations occur in 3 to 4 percent of all term pregnancies Higher incidence before 34 weeks gestation Morbidity rate three to four times that of cephalad presentations Breech Presentation (3 of 6) : Breech Presentation (3 of 6) Pathophysiology Breech presentation is term used to describe the situation in which the fetus’s buttocks or legs present first Frank breech presentation Most common type Occurs when both legs are extended upward, with both hips flexed and both knees extended Complete breech Occurs when the buttocks descend first, both hips are flexed, and one or both knees are flexed, resulting in one of both feet presenting with the buttocks Breech Presentation (4 of 6) : Breech Presentation (4 of 6) Pathophysiology Maternal complications Maternal trauma is common Fetal complications Prolapsed cord, cord compression, and cord entanglement are common complications, and birth trauma is likely Breech fetus is at higher risk of hypoxia, acidosis, and anoxia than infant delivered in cephalad position Breech Presentation (5 of 6) : Breech Presentation (5 of 6) Management Allow fetus to deliver on own Apply no traction to fetus Once umbilical cord has delivered, help free the legs, if needed Wrap the fetus in a towel and rotate so the shoulders are in an anterior-posterior position Breech Presentation (6 of 6) : Breech Presentation (6 of 6) Management As the shoulders become visible, either: Use a finger to hook each arm and apply gentle downward traction to remove each one Apply upward traction to facilitate the delivery of the posterior shoulder and downward traction for the anterior shoulder After the shoulders have been delivered, rotate the body so the back is anterior Maintain flexion of the head by placing the index and middle fingers over the fetus’s maxilla With the body resting on the forearm of the same arm and the opposite hand supporting the head and shoulders, apply upward traction to the body while an assistant applies suprapubic pressure to encourage the delivery of the head with as little traction as possible Dystocia (1 of 6) : Dystocia (1 of 6) Epidemiology Shoulder dystocia occurs in 0.6 to 1.4 percent of all vaginal deliveries Dystocia (2 of 6) : Dystocia (2 of 6) Pathophysiology Delivery of the fetal head is followed by impactation of the fetal shoulders against the pubic symphysis and sacrum in the pelvis Risk factors Birth weight over 4,000 grams Maternal diabetes Maternal obesity Operative delivery Contracted maternal pelvis Dystocia (3 of 6) : Dystocia (3 of 6) Assessment Turtle sign Fetal head retracts slightly as it is pulled down against the perineum Dystocia (4 of 6) : Dystocia (4 of 6) Management Once dystocia is recognized, the immediate draining of the urinary bladder and a generous mediolateral episiotomy may facilitate delivery Apply pressure to the fetus’s anterior shoulder to dislodge the anterior shoulder from the pubic symphysis Palpate the anterior shoulder in the maternal suprapubic area Dystocia (5 of 6) : Dystocia (5 of 6) Management Do not apply pressure to the fundal area Doing so will further impact the shoulders on the pelvic rim Apply gentle, downward traction to the fetal head If this maneuver fails, try others McRobert’s Woods corkscrew Rubin Zavanelli Dystocia (6 of 6) : Dystocia (6 of 6) Umbilical Cord Prolapse (1 of 6) : Umbilical Cord Prolapse (1 of 6) Umbilical Cord Prolapse (2 of 6) : Umbilical Cord Prolapse (2 of 6) Epidemiology Occurs about once every 250 deliveries Umbilical Cord Prolapse (3 of 6) : Umbilical Cord Prolapse (3 of 6) Pathophysiology Two types of umbilical cord prolapse Overt Occurs when the cord enters the vaginal canal or presents externally before the fetus Occult Occurs when the cord slips into or near the pelvis and is occluded by a presenting part Not visible or palpable on exam Umbilical Cord Prolapse (4 of 6) : Umbilical Cord Prolapse (4 of 6) Risk factors include: PROM Transverse lie of the fetus in the uterus Breech presentation Large fetus Multiparity Multiple gestations Preterm labor Long cord Major concern with prolapsed cord is cord compression and occlusion Fetal complications can include hypoxia, acidosis, anoxia, and death Umbilical Cord Prolapse (5 of 6) : Umbilical Cord Prolapse (5 of 6) Assessment Assessment findings of an overt umbilical cord prolapse are straightforward, but the occult prolapse can be much more insidious and requires a careful examination on the part of the critical care transport team Clinical signs include evidence of fetal distress, including: Absence of short and long-term variability Fetal bradycardia Recurrent variable decelerations that do not respond to maternal positioning, oxygen administration, or fluid administration Umbilical Cord Prolapse (6 of 6) : Umbilical Cord Prolapse (6 of 6) Management If the umbilical cord presents externally or can be visualized in the vagina, use two fingers of a gloved hand to prevent any presenting part of a delivering fetus from occluding the cord Never pull or re-place a presenting cord in the uterus If the cord retracts spontaneously, let it do so Keep the cord free of pressure throughout transport Use Trendelenburg or knee-chest position to decrease pressure on the cord Administer 100 percent oxygen via nonrebreather mask at 15 lpm Start an IV of normal saline Give a tocolytic agent When prolapse is unresolved, treat with cesarean section Uterine Rupture (1 of 5) : Uterine Rupture (1 of 5) Pathophysiology Defined as complete disruption of all layers of the uterine wall Allows the uterine and abdominal cavities to communicate Usually occurs in women who have had cesarean sections Uterine Rupture (2 of 5) : Uterine Rupture (2 of 5) Risk factors include: Previous cesarean section Overdistension of the uterus Grand multiparity Previous rupture Trauma Fetal complications include: Hypoxia Acidosis Anoxia Death Uterine Rupture (3 of 5) : Uterine Rupture (3 of 5) Assessment Common clinical findings include: Acute onset of sharp, severe abdominal pain Signs and symptoms of hypovolemic shock Rebound tenderness and distension Palpation of extrauterine fetal parts Vaginal bleeding possible Palpation of the uterus can reveal contractions that are: Hypertonic Normal Stopped Uterine Rupture (4 of 5) : Uterine Rupture (4 of 5) Diagnostics Laboratory studies of immediate use include a CBC, type and crossmatch, and coagulation profile When uteroplacental blood flow is compromised, evidence of fetal distress includes: Absence of short- and long-term variability Fetal bradycardia Recurrent variable decelerations that do not respond to maternal positioning, oxygen administration, or fluid administration Uterine Rupture (5 of 5) : Uterine Rupture (5 of 5) Management Definitive treatment is surgical repair Primary goal is to maintain ABCs to preserve uteroplacental perfusion Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Provide IV access Initiate volume replacement if dehydration is suspected Use a Foley catheter Monitor urinary output 0.5 ml/kg/hr is desired Use tocolytic agents Postpartum Hemorrhage (PPH) (1 of 6) : Postpartum Hemorrhage (PPH) (1 of 6) Epidemiology PPH occurs in about 5 percent of all deliveries Implicated in almost 30 percent of all pregnancy-related deaths Most hemorrhages occur within 24 hours of delivery Postpartum Hemorrhage (PPH) (2 of 6) : Postpartum Hemorrhage (PPH) (2 of 6) Pathophysiology PPH is considered: The loss of greater than 500 ml of blood after a vaginal delivery More than 1,000 ml of blood lost after a cesarean section Normally, postlabor platelet aggregation and clot formation in the decidua is complemented by myometrial contraction that constricts and occludes blood vessels torn when the placenta disassociates from the uterine implantation site Because blood flow to the uteroplacental boundary is about 600 ml/min, hemorrhage can be significant if uterine contraction does not occur Because uterine contraction is prevented, blood accumulates and clots in the uterus, further preventing uterine contraction and worsening bleeding Postpartum Hemorrhage (PPH) (3 of 6) : Postpartum Hemorrhage (PPH) (3 of 6) Common causes of PPH Uterine atony Retained placental fragments Birth canal trauma Postpartum Hemorrhage (PPH) (4 of 6) : Postpartum Hemorrhage (PPH) (4 of 6) Risk factors for uterine atony include: Retention of placental fragments Overdistension of the uterus Multiparity Polyhydramnios Chorioamnioitis Prolonged or obstructed labor Use of general anesthesia Magnesium tocolysis Placenta accrete Major risk factor for retained placenta Postpartum Hemorrhage (PPH) (5 of 6) : Postpartum Hemorrhage (PPH) (5 of 6) Assessment Uterine atony can be identified by a lack of uterine contractions and a flaccid uterus upon palpation Vaginal bleeding should be apparent, but external blood loss may not be total blood loss Much blood loss may be sequestered in the uterus Evaluate the patient’s hemodynamic status using signs and symptoms of shock, rather than estimates of total blood loss Helpful laboratory results include: CBC Type and crossmatch Hematocrit Coagulation studies Postpartum Hemorrhage (PPH) (6 of 6) : Postpartum Hemorrhage (PPH) (6 of 6) Management Primary goal is to maintain ABCs to preserve uteroplacental perfusion Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Provide IV access Use large-bore, peripheral IVs Strive for central venous access When hypovolemic shock presents, initiate aggressive volume replacement with a crystalloid and packed red blood cells Foley catheter Monitor urinary output 0.5 ml/kg/hr is desired Give uterine fundal massage Administer carboprost tromethamine (Hemabate) Medical Complications of Pregnancy (1 of 2) : Medical Complications of Pregnancy (1 of 2) Hypertension in pregnancy Four categories of hypertension during pregnancy Chronic hypertension Hypertension that predates pregnancy or is identified before 20 weeks gestation Gestational hypertension Occurs after 20 weeks gestation and is not accompanied by proteinuria Pre-eclampsia Hypertension and proteinuria coexist Chronic hypertension with pre-eclampsia Exists when a female with known hypertension develops worse hypertension and proteinuria A pregnant female is considered hypertensive when she has a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mmHg Medical Complications of Pregnancy (2 of 2) : Medical Complications of Pregnancy (2 of 2) Hypertension in pregnancy Pre-eclampsia is termed mild when findings are present but do not meet the criteria established for severe pre-eclampsia Eclampsia, the most serious manifestation of pregnancy-induced hypertension, is said to be present when the patient has a seizure Medical Complications of Pregnancy (1 of 6) : Medical Complications of Pregnancy (1 of 6) Pre-eclampsia Medical Complications of Pregnancy (2 of 6) : Medical Complications of Pregnancy (2 of 6) Pre-eclampsia Occurs in 6 to 8 percent of all live births Exact cause(s) of pre-eclampsia are unknown Theoretical models include: Immunologic responses Increased sensitivity to endogenous vasoconstrictors Endothelial damage with prostacyclin and thromboxane A2 production Chronic disseminated intravascular coagulation (DIC) Genetic predisposition Common thread of practically all of these models is increased vasoconstriction, peripheral vascular resistance, and subsequent hypertension Medical Complications of Pregnancy (3 of 6) : Medical Complications of Pregnancy (3 of 6) Pre-eclampsia Known risk factors include: Age 35 and 15 Pre-eclampsia in a previous pregnancy Multiparity Pre-existing renal or cardiovascular disease Diabetes Medical Complications of Pregnancy (4 of 6) : Medical Complications of Pregnancy (4 of 6) Pre-eclampsia Known risk factors include: Family history African-American descent Maternal risks include renal failure, hepatic failure, DIC, seizures and strokes, and death Maternal mortality rate is 2 to 4 percent in eclampsia or when hemolysis, elevated liver enzymes, and low platelets syndrome complicates preeclampsia Fetal risks include uteroplacental hypoperfusion, placental infarction, abruptio placentae, inhibited fetal growth, oligohydramnios, and fetal demise Medical Complications of Pregnancy (5 of 6) : Medical Complications of Pregnancy (5 of 6) HELLP syndrome HELLP is an acronym for: Hemolysis Elevated liver function tests Low platelets Thought to be a subcategory of severe pre-eclampsia Patients often experience a rapid, degenerative course, and many physicians elect for prompt delivery before the onset of eclampsia Medical Complications of Pregnancy (6 of 6) : Medical Complications of Pregnancy (6 of 6) HELLP syndrome Assessment Headaches, nausea and vomiting, seizures, visual disturbances, and cerebral edema Decreased urine output, proteinuria, decreased kidney function Decreased liver function Labs Elevated serum uric acid, urea nitrogen, and creatinine Elevated liver function tests Proteinuria Low platelet count (100,000/mm3) Management (1 of 2) : Management (1 of 2) Primary goal is to maintain ABCs to preserve uteroplacental perfusion Place patient in the left lateral recumbent position Administer 100 percent oxygen at 15 lpm via NRM Ensure IV access Use large-bore, peripheral IVs Ensure central venous access Management (2 of 2) : Management (2 of 2) Monitor urinary output 0.5 ml/kg/hr is desired Use urine dipstick to assess for proteinuria Administer magnesium sulfate for seizures Give morphine, furosemide for pulmonary edema Use hntihypertensives for severe elevations in blood pressure Magnesium sulfate, hydralazine, or labatalol Gestational Diabetes Mellitus (GDM) : Gestational Diabetes Mellitus (GDM) Epidemiology Incidence of GDM varies between less than 1 to 15 percent of all pregnancies Pathophysiology of GDM (1 of 2) : Pathophysiology of GDM (1 of 2) Those cases of diabetes, regardless of severity or insulin requirements, that present initially during pregnancy GDM can be a true initial onset of Type I or Type II diabetes, or it may represent a previously unrecognized case, worsened by the increased demand placed on the mother by the developing fetus Pathophysiology of GDM (2 of 2) : Pathophysiology of GDM (2 of 2) The pathogenesis of GDM mimics that of Type II (NIDDM) DM Impaired insulin secretion and increased insulin resistance are present in both Most cases of GDM resolve after pregnancy 32 percent lifetime risk of developing Type II DM after GDM Risk Factors for Developing GDM : Risk Factors for Developing GDM Maternal obesity Previous infant over 4,000 g birth weight History or family history of DM History of pre-eclampsia Maternal age over 30 years Excessive weight gain during pregnancy (40 lbs) Maternal complications include preterm labor, preeclampsia, pyleonephritis, and the need for cesarean section Fetal complications include increased perinatal morbidity and mortality, shoulder dystocia, stillbirth, operative delivery, and macrosomia Assessment : Assessment Determine blood glucose Do so every hour for patients in active labor with GDM Patients with preterm labor being controlled with -adrenergic agonists are at a higher risk for hypoglycemia and should be monitored carefully Management : Management Same as for nonpregnant patients If hypoglycemia is present, administer 25–50 g of dextrose IV If hyperglycemia is present, administer insulin subcutaneously If blood glucose levels drop below 80 dl/mg, can initiate a continuous infusion of D5W, 125 ml/hour For insulin-dependent patients in labor, can also consider a continuous insulin infusion Summary (1 of 2) : Summary (1 of 2) The critical care paramedic must know the anatomy and physiology, pathophysiology, symptomotology, and management techniques appropriate for female patients with high-risk OB/GYN conditions Summary (2 of 2) : Summary (2 of 2) The critical care paramedic should stay abreast of literature on the assessment and management of these patients The medical science used to treat the OB/GYN emergency evolves continually High-risk OB/GYN patients should enjoy the same high level of patient care as others using critical care transport systems