Module 7 Unit A Flashcards
Describe mild intermittent asthma?
Symptom frequency
Two days per week or less
Nightime awakenings
Two times per month or less
Interference with normal acitivity
None
FEV1 or peak flow
More than 80%Describe mild persistent asthma.
Symptom frequency
More than 2 days per week but not daily
Nightime awakenings
More than twice per month
Interference with normal acitivity
Minor limitation
FEV1 or peak flow
More than 80%Describe moderate persistent asthma.
Symptom frequency
Daily symptoms
Nightime awakenings
More than once per week
Interference with normal acitivity
Some interference
FEV1 or peak flow
60% to 80%Describe severe persistent asthma.
Symptom frequency
Throughout the day
Nightime awakenings
4 times per week or more
Interference with normal acitivity
Extremely limited
FEV1 or peak flow
Less than 60%What are the maternal implications of asthma?
Sig relationship b/w decreased FEV1 during pregnancy and ↑risk of LBW and prematurity
Even early asthma stages may be dangerous d/t smaller functional residual capacity and increased pulmonary shunting→ susceptibility to hypoxia and hypoxemia
Slight increase (studies not consistent) - stillbirth, preeclampsia, PTL, FGR, perinatal mortality, abruption, previa, PROM, GDM
Morbidity more linked to severe disease, poor control, or both
Status asthmaticus can → morbidity, muscle fatigue, resp arrest, pneumothorax, pneumomediastinum, acute cor pulmonale, cardiac arrhythmias
What are the fetal implications of asthma?
Fetal implications
Fairly uncommon, if any risk it is slight and studies are not consistent
SAB
PTL/PTB
FGR - with increased asthma severity
Abruption/previa
PROM
Fetal response to maternal hypoxemia → ↓umbilical blood flow, ↑systemic and pulmonary vascular resistance, ↓cardiac output
Possible teratogenic or adverse effects of meds
Slight risk for abnormalities - cleft lip and palate, autism spectrum disorders
How does pregnancy affect asthma severity?
Variable - 23% improved symptoms, 30% became worse
Pregnant who have asthma, even mild or well-controlled disease, need monitoring w/ PEFR and FEV1 testing as well as tracking symptoms throughout pregnancy
What are the differential diagnoses for a patient with asthma?
Dyspnea of pregnancy
GERD
Chronic cough from postnasal drip
Bronchitis
How should the nurse midwife assess for asthma in pregnancy?
Asthma symptom review - onset, duration, time of day, severity, recurrence
Chest tightness, SOB, difficulty w/respiration or wheezing, nonproductive cough
Relief measures used and their effects
Medical and surgical hx
Allergies, meds (quick and long-acting for asthma), asthma hx, chronic diseases
Exposure to triggers - allergens, irritants, pets, drugs, mold, air, exercise
Social hx - race/ethnicity, smoking or exposure, air quality, living conditions
Risk for development - atopy, rhinitis, hay fever, eczema, indoor air exposure
Physical ex - VS, general appearance, skin, color, pallor, cyanosis, pale nasal mucosa
Respiratory eval - breathing, auscultation, hyperinflated chest, prolonged expiratory phase, accessory muscle use, retractions, upright breathing easier, percussion
Evidence of resp distress - nasal flaring, retractions, peripheral cyanosis, ↑pulse or resp rate, grunting or wheezing
What non pharmacologic approaches can the nurse midwife use to manage asthma in pregnancy?
Control of triggers
Herbal remedies - NOT in place of asthma meds
Licorice, ginkgo Biloba, coltsfoot, hops
Fish oil, vitamin C
Yoga, acupuncture, biofeedback
What pharmacologic methods should the nurse midwife use to manage Intermittent asthma?
For mild - SABAs are usually enough
What pharmacologic method should the nurse midwife use to manage my who managed mild persistent asthma?
Low-dose ICS + SABA
What pharmacologic methods should the nurse midwife use to manage moderate persistent asthma?
High dose ICS + LABA + SABA
What pharmacologic methods should the nurse midwife use to manage severe persistent asthma?
High dose ICS + LABA + OCS + SABA
What is the clinical presentation of superficial thrombophlebitis?
Inflammation at the site
Leg pain
Localized heat
Palpation of a knot or cord, tenderness
What is the management of superficial thrombophlebitis?
Leg rest
elevation of the affected extremity
supportive stockings
nonsteroidal anti-inflammatory drug (NSAID) analgesia as needed.
What is the clinical presentation of deep vein thrombosis?
Abrupt onset with leg pain worsening with motion or when standing
Generalized edema of ankle, leg, or calf
Mild tachycardia and possible slight elevation in temperature
Pain with calf pressure
What is the management of deep vein thrombosis?
leg rest
elevation of the affected extremity
supportive stockings
(NSAID) analgesia as needed.
Anticoagulants for at least 6 months
Ambulation gradually as tolerated.
Supportive stockings .
Physician referral is indicated.
What is the etiology of DVT in pregnancy?
Virchow’s triad:
(1) stasis, (2) hypercoagulable state, and (3) vascular trauma.
Venous-wall relaxation resulting from the effects of progesterone and pressure on the veins by the gravid uterus fosters venous stasis. Pregnancy is also a hypercoagulable state, and this state persists throughout the early postpartum period. Venous-wall inflammation and endothelial damage secondary to distension, in the setting of this hypercoagulable state, predisposes the woman to thrombus formation.
Prolonged venous compression during positioning for labor or birth may contribute to the problem. Cesarean section also is considered a risk factor for thrombosis; thus, mechanical thromboprophylaxis, such as alternating compression devices, is recommended before and after cesarean birth.
What are the risk factors for developing a dvt in pregnancy?
Maternal hx ~ Obesity (BMI>30), smoking, age>35, thrombosis hx, inherited thrombophilias, antiphospholipid antibody syndrome, sickle cell disease, heart disease, diabetes, immobility (paraplegia)
Pregnancy ~ Hypercoagulable state, venous stasis, multiple pregnancy, preeclampsia
Labor and Birth ~ operative vaginal birth, c/s, infection, vascular trauma, immobilization, postpartum hemorrhage, preterm birth, stillbirth
What is the clinical presentation of DVT in pregnancy?
Abrupt onset of pain and edema in leg and thigh, pain worsens w/ motion/standing, pain w/calf pressure
Tenderness - along course of involved vessel(s) w/possible palpable cord
Warmth
Mild tachycardia and possible slight elevation in temp
Occasionally reflex spasm → pale, cool extremity w/diminished pulsations
May be no symptoms at all
What is the 1st line diagnostic testing used to assess for DVT in pregnancy?
Compression US w/ or w/o doppler imaging - remember normal findings for venous US doesn’t always exclude PE
What diagnostic test is non specific for assessing for DVT in pregnancy and why?
D-dimer- positive isn’t really helpful but a negative D-dimer is reassuring.
What complications can DVT in pregnancy lead to?
PE
Post-thrombotic syndrome - chronic leg paresthesias or pain, intractable edema, skin changes, leg ulcers
What is the recommended management for DVT in pregnancy?
Warfarin
What level of interprofessional collaboration is warranted when a DVT is diagnosed in pregnancy
Referral
What is the etiology/cause of pulmonary embolism in pregnancy?
Virchow’s triad:
(1) stasis, (2) hypercoagulable state, and (3) vascular trauma.
Venous-wall relaxation resulting from the effects of progesterone and pressure on the veins by the gravid uterus fosters venous stasis. Pregnancy is also a hypercoagulable state, and this state persists throughout the early postpartum period. Venous-wall inflammation and endothelial damage secondary to distension, in the setting of this hypercoagulable state, predisposes the woman to thrombus formation.
Prolonged venous compression during positioning for labor or birth may contribute to the problem. Cesarean section also is considered a risk factor for thrombosis; thus, mechanical thromboprophylaxis, such as alternating compression devices, is recommended before and after cesarean birth.
What are the risk factors for pulmonary embolism in pregnancy?
DVT - primary risk factor
What is the clinical presentation of pulmonary embolism in pregnancy?
Signs and symptoms
Dyspnea, chest pain, cough, syncope, hemoptysis
Tachypnea, apprehension, tachycardia
Pulmonic closure sound, rales, and/or friction rub
Deceptively nonspecific - s/s and lab testing
What diagnostic testing is used to assess for pulmonary embolism in pregnancy with with and without leg symptoms?
Compression ultrasound with leg symptoms
CXR without leg symptoms
ECG - right axis deviation and T-wave inversion in the anterior leads
Chest x-ray - results normal 40% of the time, otherwise may have atelectasis, infiltrate, cardiomegaly, or effusion
Most hypoxemic - normal arterial blood glass does not exclude PE
⅓ have PO2 value of >80mmHg
Alveolar-arterial oxygen tension difference more useful indicator - 86% have alveolar-arterial difference >20mmHg
What is the recommended management for pulmonary embolism in pregnancy?
Immediate full coagulation
May consider vena caval filters - especially if c/s needed soon
Vena Caval Filters
Recent PE and must have c/s- particularly serious problem
Reversal of anticoagulation may be followed by another embolus, and surgery while fully anticoagulated frequently results in life-threatening hemorrhage or troublesome hematomas. In these cases, consider placement of a vena caval filter before surgery
Also indicated - If heparin therapy fails to prevent recurrent PE from pelvis or legs, or when embolism develops from these sites despite heparin treatment, a vena caval filter may be indicated.
Following massive emboli in patients who are not candidates for thrombolysis
Device inserted through either the jugular or femoral vein; can be inserted during labor
Routine filter placement has no added advantage to heparin given alone
Retrievable filters - short-term protection and then removed 1 to 2 weeks later
Thrombolysis
Compared w/heparin, thrombolytic agents provide more rapid lysis of pulmonary clots and improvement of pulmonary hypertension
Embolectomy
Given efficacy of thrombolysis and filters- surgical embolectomy uncommonly indicated
Although the operative risk to mother reasonable, the stillbirth rate is 20 to 40%
What level of interprofessional collaboration liberation is warranted when a pulmonary embolism is diagnosed in pregnancy?
Refer
What is the cause of amniotic fluid embolism?
Previously thought to be amniotic fluid and debris passing into maternal circulation - during normal birth, this is a normal occurrence
Now - Disrupted maternal-fetal interface allows material from fetal compartment to enter maternal circulation→ abnormal activation of proinflammatory mediator systems
This causes initial transient pulmonary vasoconstriction and HTN
Acute right ventricular failure is then followed by hemodynamic collapse from right ventricular infarction coupled w/ interventricular septum displacement to the left and ultimately decreased LT sided output
This is followed by cardiogenic pulmonary edema and systemic hypotension
Concurrently acute respiratory failure develops with severe hypoxemia from shunting.
Results in multiorgan failure.
If woman survives this, a consumptive coagulopathy comes next as the fetal material activates factor VII leading to the development of DIC
What are risk factors for amniotic fluid embolism?
Risk factors
Predisposing conditions -
Rapid labor
Mec-stained fluid
Tears into uterine/other large pelvic veins - permits fluid exchange b/w mother & fetus
Other risks
Older maternal age
Post-term pregnancy
Labor induction or augmentation
Eclampsia
Cesarean, forceps, or vacuum delivery
Abruption or previa
Hydramnios
Fetal - male gender, fetal distress, premature ROM, intrauterine death
Maternal - AMA >35, multiparity, diabetes
Obstetric - c/s, induction, cervical laceration, instrument delivery, uterine rupture
Uterine hypertonus - likely effect rather than cause, hypertonus from oxytocin not implicated
What is the clinical presentation of an amnionic fluid embolism?
Signs and symptoms
Classic triad - hemodynamic compromise, respiratory compromise, DIC
Classic example -dramatic, late stages of labor immediately postpartum start gasping for air
Seizures or cardiorespiratory arrest rapidly follows w/ massive hemorrhage from consumptive coagulopathy
Manifestations can be variable
Diagnostic Criteria for Amniotic Fluid Embolism
Abrupt onset of cardiorespiratory arrest, or both hypotension and respiratory compromise
Documentation of overt DIC - Coagulopathy must be detected prior to the loss of sufficient blood to cause dilutional or shock-related consumptive coagulopathy.
Clinical onset during labor or within 30 minutes of placental delivery.
No fever ≥38°C.
What are potential complications of amniotic fluid embolism?
Death
Neurological impairments
What is the emergency management for amniotic fluid embolism?
Immediate high quality CPR and ACLS
