NM706 Exam 4 Study Materials: Key Terms and Definitions in Maternal and Neonatal Medicine

· Intermittent asthma

o Symptoms less than 2 days/nights/week

o Doesn't interfere with daily life

o PEF or FEV1 >80% predicted

· Mild-persistent asthma

o Symptoms >2 but not daily or nightly

o Minor limitation to daily life

o PEF or FEV1 >80%

Moderate persistent asthma

o Symptoms daily but not continual, >1 night weekly, but not nightly.

o Moderate limitation to daily life

o PEF or FEV1 60-80%

· Severe persistent asthma

o Symptoms throughout the day and frequently at night

o Extreme limitation to daily life

o PEF or FEV1<60%

Management of mild intermittent asthma in pregnancy

o No daily medications

o Albuterol PRN

Management of mild persistent asthma in pregnancy

o Low dose inhaled corticosteroid

Management of moderate persistent asthma in pregnancy

o Low dose inhaled corticosteroid + Advair

o Or medium-dose inhaled corticosteroid

· Management of severe persistent asthma in pregnancy

o High-dose inhaled corticosteroid + Advair

o Oral corticosteroid if needed

Management of intermittent asthma in pregnancy

o Short-acting-beta-agonists PRN (albuterol sulfate/Proventil)

o If use more than 2 days/week, consider persistent asthma

· Peripartum cardiomyopathy (PPCM)

o Rare complication during pregnancy or postpartum period

o New onset heart failure that cannot be attributed to any other cause during the last weeks of pregnancy or first five months PP

o Recovery occurs 3-6months PP, can take as long as 48mo

Peripartum cardiomyopathy symptoms

o Presents with respiratory symptoms

o SOB, fatigue, edema, cough, tachycardia and heart palpitations

Peripartum cardiomyopathy management goals

o Prevent fluid from accumulating in the lungs and support the heart in recovery

o Diuresis and fluid restriction are essential

· Superficial thrombophlebitis

· Superficial thrombophlebitis

o Increased leg pain, localized edema, erythema, and warmth over the thrombotic site

o Physical exam reveals an enlarged and hard cord-like structure

o Managed with NSAIDs, leg rest, elevation, and support stockings

Factors that contribute to the risk of VTE in pregnancy

o Gravid uterus pressing down on the lower extremity blood vessels

o Increased clotting factors during pregnancy from estrogen

o Increased thrombin

o Venous stasis increases d/t progesterone

· Diagnosing DVT in pregnancy

o D-dimer is usually used, but pregnancy decreases specificity

o D-dimer can be used as a good negative predictive value

o imaging for DVT and PE with CUS of lower extremity veins is standard

· s/s of PE in pregnancy

o dyspnea, abrupt onset of chest pain, cough

o tachypnea, crackles, and tachycardia

o syncope, hypotension, PECA, death

· Diagnosing PE in pregnancy

o Imaging with chest radiography

o Ventilation/perfusion scanning

o Spiral computed tomography pulmonary angiography (CT-PA)

· Managing VTE in pregnancy

o Indirect thrombin inhibitors: heparin

o Direct thrombin inhibitors

o Vitamin K antagonists

· Amniotic fluid embolism

o Happens when there is an exchange of amniotic fluid or fetal material between birthing person and fetus, may cause obstruction and/or anaphylactoid reaction

o Rare, life-threatening perinatal emergency

o May occur anytime from the onset of labor to within 30 minutes of placenta

o Unpredictable and hard to prevent

· Risk factors for AFE

o Operative vaginal birth

o C/S

o Placenta previa

o Multi gestation

o Trauma

o Abruption or rupture

· AFE presentation

o Sudden cardiorespiratory arrest that may include

o Hypotension, dyspnea, and cyanosis

o Triad of symptoms: hypoxia, hypotension and coagulopathy

o DIC and massive hemorrhage

· Five cardinal signs of respiratory distress in a newborn

o Flaring of the nares

o Grunting

o Tachypnea

o Retracting

o Cyanosis

· Retractions in the newborn

o Neonatal chest wall is very elastic, retractions are very visible

o Assists the diaphragm as it mechanically expands during inspiration

· Flaring in the newborn

o Results from increased inspiratory pressure

o Enlarges the nostrils, decreasing any nasal resistance to airflow

· Grunting in the newborn

o Expiration through partially closed vocal cords

o By closing the glottis during expiration, the infants holds in air, maintaining lung expansion, and preserves oxygenation for a few seconds

o Elevates pressure at the end of respiration

· Tachypnea in the newborn

o Most efficient way to temporarily increase ventilation and compensate for hypoxia and hypercarbia

· Cyanosis in the newborn

o Looking for central cyanosis in mucous membranes more than skin

o Oxygenated blood is shunted to the heart, brain, lung, and adrenals

o Not visible until the sPO2 decreases to 80-85%

o May be a sign of respiratory or cardiac problems

· Transient tachypnea of the newborn (TTN)

o Prolonged period of transitioning from fluid filled to air filled lungs

o Lasts 48-72 hr and resolves spontaneously

o May need supplemental O2 and feeding assistance

o Usually monitored until condition resolves

· Birth asphyxia

o Causes a downward spiral of events which block the changes from fetal to neonatal respiration and circulation

o Goal of resuscitation in a compromised newborn is to reverse the cardiovascular and acid-based chain of events

Periodic breathing in newborns

o Pauses in respirations up to 20 seconds which alternate with breathing

o Common in preterm infants but can occur in term infants as well

o Usually benign but can be induced by hypoxemia

· Apnea in newborns

o Common in preterm infants and associated with respiratory problems

o Pauses are longer and include changes in heart rate (as low as 80bpm)

o Abnormal and may indicate underlying problem (sepsis, hypoglycemia, CNS injury or abnormality, or seizures

· How MAS induces hypoxia

o Airway obstruction

o Surfactant dysfunction

o Chemical pneumonitis

o Pulmonary hypertension

· Intrapartum management of MSAF

o Ongoing eval of FHT, and mec consistency

o Monitor for signs of infection

o Identify and correct cause

o Minimize intraamniotic infection risk

o SDM

o Preparation

· MSAF delivery management

o Presence of team member with neonatal resuscitation skills

o Maintain thermoregulation of infant and clear secretions

o Resuscitate non-vigorous newborns

· Cord blood vessel that reflects maternal/utero-placental status

o Venous

Cord blood vessel that reflects fetal status

o Arterial

· Newborn respiratory acidosis

o Caused by placental perfusion disruption, carbon dioxide cannot get from baby to placenta

o Build up of carbon dioxide in fetus is converted to carbonic acid which lowers serum pH

o If disruption continues, fetus will switch from aerobic metabolism and anaerobic metabolism

· Respiratory acidosis cause

o Can be abrupt (cord compression, prolapse, abruption, epidural hypotension)

o or during initial phase of chronic placental insufficiency (FGR, hypertensive disorders)

· mixed respiratory metabolic acidosis cause

o continued disruption of placental perfusion causing fetus to switch from aerobic metabolism to anaerobic metabolism

o byproducts of anaerobic metabolism, organic acids, can join with carbonic acid and further lower serum pH

· metabolic acidemia cause

o placental perfusion disruption is not corrected, anaerobic metabolism continues

o respiratory component will dissipate

o organic acid levels will continue to increase causing bicarb and pH levels to drop even lower

· type of acidosis effect on infant at time of delivery

o infant with respiratory acidosis suffered an acute event that at delivery will quickly correct itself as the excess carbon dioxide is removed with respiration

o infants with metabolic acidosis take much longer to recover since organic acids are slowly cleared

· Cord gas interpretation for respiratory acidemia

o If PCO2 is high, and bicarb is normal there is respiratory involvement

o pH normal or low

o PCO2 high

o Bicarb normal

o Base deficit normal

· Cord gas interpretation for metabolic acidemia

o If PCO2 is normal and bicarb is low, its metabolic

o pH low

o PCO2 normal

o Bicarb low

o Base deficit high

· Cord gas interpretation for mixed acidemia

o pH low

o PCO2 high

o Bicarb is low

o Base deficit high

· Differentiating normal newborn jitteriness from seizure activity

o Jitteriness is usually stimulus-induced and can be stopped by holding the extremity still

o Seizures occur spontaneously and motor activity is felt when the extremity is held still

· Cause of newborn seizures

o Process in the brain (intracranial hemorrhage, tumor, encephalitis, etc)

o Systemic (metabolic disorders, hypoglycemia, HIE, etc)

o Intracranial hemorrhage is the most common cause in premature infants

o HIE is the most common cause in term babies

· Generalized seizures

o Affect both sides of the brain

· Focal seizures

o Affect just one side of the brain

o Majority of newborn seizures

· Tonic seizures

o Muscles in the body become stiff

· Myoclonic seizures

o Most often occurs in full-term infants

o Lightning-like jerks of extremities

o Rapid isolated jerks

· Clonic seizures

o More common in term infants

o Periods of shaking or jerking parts on the body

o Well-localized

o Infant usually not unconscious

o Signals focal cerebral injury

· Subtle seizures

o Occur in both preterm and full-term

o Eye deviation, blinking, or fluttering eyelids

o Fixed stare in preterm

o Repetitive mouth and tongue movements like smaking, sucking or drooling

o Swimming, rowing, pedaling movements and tonic posturing of limbs

· Generalized tonic seizures

o Primarily in preterm infants, but relatively uncommon

o Tonic extension of upper and lower limbs

o Tonic flexion of upper limbs

· Hypoxic ischemic encephalopathy

o Specific type of neonatal brain dysfunction when the baby's brain does not receive enough oxygen or blood flow for an extended period of time

o Can be antepartum, intrapartum or after delivery

o Length of time the brain was without oxygen usually determines the severity

· Three major signs of HIE

o Neonatal seizures

o Abnormal state of consciousness

o Abnormal tone

o Usually appear within 72 hours of birth and may not be signaled by low Apgars

· Therapeutic hypothermia

o Treatment for moderate to severe HIE

o Neuroprotective strategy to reduce secondary reperfusion injuries for babies at risk for HIE

o Initiate cooling as early as possible, lasts for 72hr

· HIE outcomes

o Vary based on length of time the brain was without oxygen

o A major consequence is cerebral palsy (more common in preterm)

o Term infants have high mortality rates and long term cognitive and motor problems

· Managing chronic htn in pregnant people

o Refer to MD

o Encourage exercise

o Antihypertensives like labetalol and nifed

o Serial growth u/s, biweekly fetal testing

o Pregnant individuals who have cHTN and are not on meds should be delivered between 38-39 weeks

· Chronic hypertension with superimposed PEC

o Pt with chronic HTN AND

o Sudden increase of BP previously controlled

o Need to escalate antihypertensives therapy to control BP

o New onset proteinuria

o End organ dysfunction after 20 weeks gestation

· Gestational hypertension

o Pt does not have proteinuria or meet other diagnostic criteria for PEC

o No proteinuria

o Resolves by 12 weeks after birth

o Increased risk of developing PEC

· Management of gestational HTN

o Weekly in-office BP, twice weekly home BP

o Monitor urine protein

o Twice weekly antenatal fetal surveillance

o Encourage 30 minutes of moderate exercise several days/week

· Diagnosing PEC

o ≥140/90 on two occasions, at least 4hr apart after 20 wks

o WITH protein in urine: PCR ≥0.3, 300mg on 24hr urine, or 1+ urine dipstick

o OR platelet count <100,000, creatinine >1.1, or elevated AST/ALT

· Antepartum PEC management

o Fetal monitoring with daily kick counts, NST twice weekly, and growth US q3 weeks

o BP monitoring 2x weekly, PIH labs weekly

o Monitor proteinuria

o Educate to report s/s

· Intrapartum PEC management

o Labor and deliver in hospital

o Recommend epidural

o Mag sulfate infusion

o Deliver at 37 weeks without SF

o Deliver at 34 wks w/ SF

o Antihypertensives for any severe range BP

· PEC patient warning signs

o Persistent and/or severe headache

o Visual abnormalities

o New onset swelling of face or sudden weight gain

o New N/V in second half of pregnancy

o Unrelenting epigastric pain or RUQ pain

o New onset dyspnea or orthopnea

· HELLP syndrome

o Continuum of severe preeclampsia

o Hemolysis, elevated liver enzymes, low platelet count

o Pt may feel malaise, or flu like symptoms

o Onset and progression may be rapid, immediately refer

o No definitive cure, management focuses on stabilization of fetus and pregnant persons BP

· HELLP symptoms

o Elevated bp

o RUQ pain

o Persistent headaches

o Visual disturbances

o Malaise

o Dyspnea

o N/V

· Postpartum preeclampsia management

o Normal for BP to decrease for first 48hr after birth then increase and peak at 3-6 days PP

o Check bp for a minimum of 72hr after birth, then again 7-10 days or earlier if symptomatic

o Refer/collab with MD for medication management

· Cerebral edema in PEC

o Secondary to disruption of blood-brain barrier from hypertension capillary damage and immune-mediated endothelial dysfunction

o Clonus is a warning sign of cerebral irritation secondary to cerebral edema - shows you need to start mag

· Magnesium toxicity

o Absent or depressed DTR

o Significant hypotension

o Respiratory depression

o Oliguria

o Heart block

· Antihypertensive management of PEC

o Hydralazine - 5mg q20min. Max dose 20mg

o Labetalol - 20mg, then 40-80 q10 minutes. Max dose 300mg

o Nifedipine - 10mg PO q20 minutes. Max dose 50

· Atrial septal defect

o Deficiency of the interatrial septum

o Allows communication between left and right atria

o amount of blood crossing is very limited until several months after birth

· ASD and VSD risks

o Can produce CHF because they often involve pressure overload from the left ventricle associated with obstruction and volume overload of the right ventricle

· Ventricular septal defect

o An opening in the interventricular septum resulting in direct communication between left and right ventricles

o Flow depends on reduction in pulmonary vascular resistance, which occurs 3-6 weeks after birth

o Causes volume overload of the right ventricle

· Patent ductus arteriosus

o Normal tubular structure that connects the underside of the descending aorta to the pulmonary artery

o Normal and usually disappears shortly after 24hr

· Acrocyanosis (peripheral cyanosis)

o Normal finding seen in healthy newborns, may persist 24-48hr

o Refers to the cyanosis found in extremities, may also be seen on skin around the lips

o Doesn't involve mucus membranes (the remain pink)

· Central cyanosis

o Cyanosis of the "central" body parts: mouth, head, torso

o Associated with lower amounts of oxygen in the blood

o Normal for 5-10 minutes after birth

o Persistent is always abnormal and should be evaluated

· Cyanosis without respiratory disease in the newborn

o Sign of heart disease

o Be suspicious if cyanosis with feeds, poor feeding, tachypnea, poor weight gain, edema, or sweating