Pulmonary Disorders During Pregnancy PDF

956 CHAPTER 54 Pulmonary Disorders ASTHMA...................................... 956 3. Prgesterne-driven respiratry stimulatin raises tidal vol- ume apprximately 40 pe...

956 CHAPTER 54 Pulmonary Disorders ASTHMA...................................... 956 3. Prgesterne-driven respiratry stimulatin raises tidal vol- ume apprximately 40 perent. ACUTE BRONCHITIS............................ 961 4. Minute ventilation inreases 30 t 40 perent due t higher PNEUMONIA.................................. 961 tidal vlume. As a result, arterial partial pressure  xygen (Pao2) rises rm 100 t 105 mm Hg. TUBERCULOSIS................................ 965 5. Expanded metabli demands ause a 30-perent inrease in carbon dioxide (CO2) production. But, beause  its n- SARCOIDOSIS................................. 967 mitantly greater diusin apaity and hyperventilatin, CYSTIC FIBROSIS............................... 968 the Paco2 is redued rm 40 t 32 mm Hg. 6. Residual volume diminishes apprximately 20 perent rm CARBON MONOXIDE POISONING................. 969 1500 mL t 1200 mL. 7. An expanding uterus and higher intraabdminal pressure REFERENCES................................... 970 lwer chest wall compliance by ne third. Tis auses a 10- t 25-perent redutin in unctional residual capacity—the sum  expiratry reserve and residual vlumes. Beginning at 14 t 16 weeks’ gestatin orced vital capac- ity and peak expiratory ow prgressively inrease (Grindheim, During pregnany, pulmnary disrders are requently 2012). Te result  these pregnany-indued hanges is sub- enuntered. In ne study, asthma and mmunity-aquired stantively greater ventilatin due t deeper but nt mre re- pneumnia aunted r almst 10 perent  nnbstetri- quent breathing. Tis is thught t be stimulated by basal al antepartum hspitalizatins (Gazmararian, 2002). Preg- xygen nsumptin, whih inrementally rises rm 20 t nant wmen, espeially thse in the last trimester, tlerate 40 mL/min in the send hal  pregnany. lung disease prly beause  imprtant pregnany-indued hanges in ventilatry physilgy (Han, 2018). Lung vlumes ASTHMA and apaities are signiantly altered. In turn, these shit gas nentratins and aid-base values in bld. Tese Pathophysiology imprtant and smetimes marked hanges are reviewed in Asthma is a hrni inammatry airway syndrme with a Chapter 4 (p. 66), and nrmal values r bld gas an be majr hereditary mpnent. Plymrphism genes n hr- und in the Appendix (p. 1232). Sme  these an be sum- msme 5q that inlude ytkine gene lusters, β-adrenergi marized as llws: and glurtiid reeptr genes, and the -ell antigen reep- 1. Vital capacity and inspiratory capacity inrease by apprxi- tr gene are assiated with greater airway respnsiveness and mately 20 perent by late pregnany. persistent subaute inammatin (Barnes, 2018). Raial di- 2. Expiratory reserve volume delines rm 1300 mL t apprxi- erenes are seen, and mrbidity rates are disprprtinately mately 1100 mL. higher in blak mpared with white wmen (Kdadhala,  Pulmonary Disorders 957 2018). Asthma is etilgially and linially hetergeneus, and an envirnmental allergi stimulant suh as inuenza r igarette smke serves as a prmter r suseptible individuals. CHAPTER 54 Te hallmarks  asthma are reversible airway bstrutin rm brnhial smth musle ntratin, vasular nges- tin, tenaius muus, and musal edema. Stimuli ause aute inltratin  esinphils, mast ells, and  lymph- ytes. Inammatry mediatrs prdued by these and ther ells inlude histamine, leuktrienes, prstaglandins, ytkines, immunglbulin E (IgE), and many thers. F-series prstaglan- dins and ergnvine exaerbate asthma, and these mmnly used utertnis are avided i pssible. Clinical Course Asthma maniestatins range rm mild wheezing t severe brnhnstritin, whih bstruts airways and dereases airw. Tis lwers the red expiratry vlume in 1 send/ red vital apaity (FEV1/FVC) rati and the peak expiratry w rate (PEFR). Te wrk  breathing prgressively inreases, and patients nte hest tightness, wheezing, r breathless- ness. Subsequent wrsening  xygenatin primarily reets ventilatin–perusin mismathing. Tis results rm an uneven distributin  airway narrwing. Varied maniestatins  asthma have led t a lassiatin FIGURE 54-1 Clinical stages of asthma. FEV1 = forced expiratory volume in 1 second. system that nsiders severity, nset, and duratin  symp- tms (Table 54-1). With persistent r wrsening brnhial bstrutin, linial stages prgress as shwn in Figure 54-1. asthma stages may be dangerus r the pregnant wman and Hypxia initially is mitigated by hyperventilatin, whih main- her etus. Tis is beause diminished untinal residual apa- tains the Pao2 within a nrmal range but lwers Paco2, reating ity and greater pulmnary shunting render the gravida mre respiratry alkalsis. As airway narrwing wrsens, the degree suseptible t hypxia and hypxemia.  ventilatin–perusin deets is aentuated, and arterial hypxemia ensues. With severe bstrutin, atigue auses early Effects of Pregnancy on Asthma CO2 retentin and impairs ventilatin. Beause  hyperventi- Chrni asthma r an aute exaerbatin aets up t 8 latin, this may nly be seen initially as the Paco2 returning perent  gravidas (Baghla, 2019; Flres, 2020; Mazurek, t the nrmal range. With ntinuing bstrutin, respiratry 2018). Pulmnary untin hanges in pregnany are mre ailure llws. prnuned in asthmatis mpared with healthy wmen Tese hanges are generally reversible and well tlerated (Zairina, 2015). Despite this, pregnany has an unpredit- by the healthy nnpregnant individual. Hwever, even early able eet n underlying asthma. In a review  mre than TABLE 54-1. Classification of Asthma Severity Severity Persistent Component Intermittent Mild Moderate Severe Symptoms ≤2 d/wk >2 d/wk, not daily Daily Throughout day Nocturnal awakenings ≤2×/mo 3–4×/mo >1×/wk, not nightly Often 7×/wk Short-acting β-agonist for ≤2 d/wk ≥2 d/wk, but not Daily Several times daily symptoms >1×/d Interference with normal activity None Minor limitation Some limitation Extremely limited Lung function Normal between exacerbations FEV1 >80% predicted ≥80% predicted 60–80% predicted 5% FEV1 = forced expiratory volume in 1 second; FVC = forced vital capacity. From National Heart, Lung, and Blood Institute, 2007.  958 Medical and Surgical Complications 2000 gravidas, apprximately a third eah imprved, remained (2013) nted that the inidene  spntaneus abrtin may unhanged, r learly wrsened (Gluk, 2006). Exaerbatins be slightly greater in wmen with asthma. are mre mmn with severe disease (Ali, 2013). In a study Sme evidene suggests that severe disease, pr n- Section 12 by Shatz and assiates (2003), baseline severity rrelated trl, r bth is linked t higher mrbidity rates. In a study with asthma mrbidity during pregnany. With mild disease, by the Maternal-Fetal Mediine Units (MFMU) Netwrk, 13 perent  wmen had an exaerbatin and 2.3 perent delivery bere 37 weeks’ gestatin was nt mre requent in required admissin; with mderate disease, these numbers pregnanies  wmen with asthma mpared with ntrls were 26 and 7 perent; and r severe asthma, 52 and 27 per- (Dmbrwski, 2004). Hwever, r wmen with severe asthma, ent. Others have reprted similar ndings (Charltn, 2013; the rate was apprximately twld higher. Te MFMU Net- Hendler, 2006). wrk study suggests als a diret relatinship  baseline preg- Intrapartum exaerbatin rates are ntrversial. In ne nany FEV1 with birthweight and an inverse relatinship with study, 20 perent  wmen with mild r mderate asthma rates  gestatinal hypertensin and preterm delivery (Shatz, had an intrapartum exaerbatin (Shatz, 2003). Mabie and 2006). Kemppainen and wrkers (2018) und that wmen wrkers (1992) reprted an 18-ld greater exaerbatin risk requiring treatment r asthma during pregnany are at greater llwing esarean versus vaginal delivery. Cnversely, Wendel risk r adverse perinatal utmes. and lleagues (1996) reprted exaerbatins at the time  Maternal mrbidity rises markedly with status asthmatius delivery in nly 1 perent  asthmatis. and inludes lie-threatening mpliatins suh as musle atigue with respiratry arrest, pneumthrax, pneummedi- Pregnancy Outcome astinum, aute r pulmnale, and ardia arrhythmias. Nt Asthma remains a ptential risk atr r wrse pregnany surprisingly, maternal and perinatal mrtality rates rise sub- utmes despite ntinued imprvements in treatment. Data stantively when mehanial ventilatin is required. rm tw large studies are shwn in Table 54-2. Te inidenes  small-r-gestatinal-age nenates and perinatal mrtality Fetal Effects als are signiantly greater in wmen with asthma (Kemp- Animal and human studies suggest that develpment  mater- painen, 2018). Hwever, these ndings are nt nsistent nal respiratry alkalsis leads t etal hypxemia well bere the amng all studies. A study  apprximately 3000 pregnan- alkalsis mprmises maternal xygenatin (Rlstn, 1974). ies mpliated by asthma shwed higher rates  maternal Teries hypthesize that the etus is jepardized by dereased pneumnia and esarean delivery but nt  perinatal mrtality uterine bld w, redued maternal venus return, and an (Shaked, 2019). In a Eurpean reprt  37,585 pregnanies alkaline-indued letward shit  the xyhemglbin dissia-  wmen with asthma, the risks r mst bstetrial mpli- tin urve (Chap. 50, p. 886). Te etal respnse t maternal atins were nt inreased (ata, 2007). Blais and assiates hypxemia is lwer umbilial bld w, higher systemi and pulmnary vasular resistane, and dereased ardia utput. Several studies ited abve nrm that etal-grwth restritin TABLE 54-2. Maternal and Perinatal Outcomes in rates rise with asthma severity. Beause the etus may be seriusly Women with Asthma mprmised, aggressive management is neessary. Mnitring the etal respnse is, in eet, an indiatr  maternal status. A Asthmaticsa Odds Ratio (95% CI) return  mderate variability r aeleratins in the etal heart Maternal outcomes rate is an indiatr  imprving maternal xygen status. Hemorrhage 1.09 (1.03–1.16) Pssible teratgeni r adverse etal eets  drugs given t Gestational diabetes 1.10 (1.03–1.19) ntrl asthma are a nern. Several reprts shw a slightly Chorioamnionitis 1.12 (1.09–1.15) greater risk r abnrmalities suh as let lip and palate and Preeclampsia 1.14 (1.06–1.22) autism spetrum disrders, but urther veriatin is neessary Placental abruption 1.22 (1.09–1.36) (Eltnsy, 2016; Gidaya, 2016; Murphy, 2013b; Wang, 2014). Placenta previa 1.30 (1.08–1.56) It is wrrisme that up t hal  wmen disntinue essential ICU admission 1.34 (1.04–1.72) treatment between 5- and 13-weeks’ gestatin (Enriquez, 2006). Pulmonary embolism 1.71 (1.05–2.79) Perinatal outcomes SGA neonates 1.10 (1.05–1.16) Clinical Evaluation Preterm delivery 1.17 (1.12–1.23) Te subjetive severity  asthma requently des nt rrelate Preterm PROM 1.18 (1.07–1.30) with bjetive measures  airway untin r ventilatin. Clin- Anomalies 1.48 (1.04–2.09) ial examinatin als an be an inaurate preditr, but useul signs inlude labred breathing, tahyardia, pulsus paradxus, a Compared with outcomes in 206,468 nonasthmatic prlnged expiratin, and use  aessry musles. Signs  women. a ptentially atal exaerbatin inlude entral yansis and CI = confidence interval; ICU = intensive care unit; altered nsiusness. PROM = premature rupture of membranes; SGA = small Pulmnary untin testing shuld be rutine in the man- for gestational age. agement  asthma. Sequential measurement  the FEV1 r Data from Baghlaf, 2019; Mendola, 2013, 2014.  the PEFR is the best measure  severity (see able 54-1).  Pulmonary Disorders 959 An FEV1 240–480 µg >480 µg Budesonide DPI Pulmicort 90, 180, 200 µg 180–600 µg >600–1200 µg >1200 µg Ciclesonide HFA Alvesco 80, 160 µg 80–160 µg >160–320 µg >320 µg Flunisolide HFA Aerospan 80 µg 320 µg >320–640 µg >640 µg Fluticasone furoate DPI Arnuity Ellipta 100, 200 µg daily 100 µg NA 200 µg Fluticasone propionate Flovent Diskus 50, 100, 250 µg 100–300 µg >300–500 µg >500 µg DPI Fluticasone propionate Flovent HFA 44, 110, 220 µg 88–264 µg >264–440 µg >440 µg HFA Mometasone DPI Asmanex 110, 220 µg 110–220 µg 330–440 µg >440 µg Mometasone HFA Asmanex HFA 100, 200 µg 200 µg 400 µg >400 µg LABA /ICS Inhalerb Budesonide/formoterol Symbicort 80/4.5, 160/4.5 µg 320/18 µg >320/18–640/18 µg >640/18 µg Fluticasone/salmeterol DPI Advair Diskus 100/50, 250/50, 100/50– 350/100–500/100 µg >500/50 µg 500/50 µg 350/100 µg Fluticasone/salmeterol HFA Advair HFA 45/21, 115/21, 100/50–250/50 µg 300/50–500/50 µg >500/50 µg 230/21 µg Fluticasone/salmeterol DPI AirDuo Respiclick 55/14, 113/14, 110/28 µg 226/28 µg 464/28 µg 232/14 µg Fluticasone/vilanterol Breo Ellipta 100/25, 200/25 µg 100/25 µg NA 200/25 µg daily Mometasone/formoterol Dulera 110/5, 200/5 µg NA 400/20 µg 800/20 µg a Agents in each group are arranged alphabetically. b Twice daily dosing unless otherwise stated. DPI = dry powder inhaler; HFA = hydrofluoroalkane (an aerosol propellant); hr = hour; ICS = inhaled corticosteroid; LABA = long-acting beta agonist; NA = not applicable; SABA = short-acting beta agonist. American Academy of Allergy Asthma & Immunology, 2020; National Heart, Lung, and Blood Institute, 2007; Therapeutic Research Center, 2017. Management of Acute Asthma assessment  maternal xygenatin, ventilatin, and aid-base status (see Fig. 54-1). Hwever, Wendel and assiates (1996) Early Treatment und that routine arterial bld gas analysis did nt help t man- reatment  aute asthma during pregnany is similar t that age mst pregnant wmen wh required admissin r asthma r the nnpregnant patient (Figure 54-3). Imprtantly, the ntrl. I used, the results must be interpreted in relatin t threshld r hspitalizatin is signiantly lwer. Intravenus nrmal values r pregnany. Fr example, a Paco2 >35 mm Hg (IV) hydratin may help lear pulmnary seretins, and supple- with a pH 60 mm Hg, and preerably nrmal, alng with pneumnitis is mrbid (p. 962) (errane, 2014). 90- t 95-perent xygen saturatin. Baseline pulmnary un- First-line therapy r aute asthma inludes a shrt-ating tin testing inludes FEV1 r PEFR. Cntinuus pulse ximetry β-adrenergi agnist, suh as terbutaline, albuterl, isetha- and eletrni etal mnitring, depending n gestatinal age, rine, epinephrine, isprterenl, r metaprterenl, whih are may prvide useul inrmatin. Arterial bld gas analysis aides given subutaneusly, taken rally, r inhaled. In severely ill in assessing the severity  an aute attak by prviding bjetive wmen, these drugs an be given intravenusly (Barnes, 2018).  Pulmonary Disorders 961 Status Asthmaticus and Respiratory Failure Severe asthma  any type nt respnding ater 30 t 60 min- utes  intensive therapy is termed status asthmaticus. Generally, CHAPTER 54 management  nnpregnant patients with status asthmatius in an intensive are setting results in a gd utme. In pregnant wmen, nsideratin shuld be given t early intubatin when maternal respiratry status wrsens despite aggressive treatment (see Fig. 54-1). Fatigue, CO2 retentin, and hypxemia are indiatins r mehanial ventilatin (Chan, 2015). In rera- try ases, venvenus extrarpreal membrane xygenatin (ECMO) has been suessully used r status asthmatius dur- ing pregnany (Clird, 2018; Steinak, 2017). Labor and Delivery Fr the labring patient wh has symptmati asthma, the PEFR r FEV1 is determined n admissin, and serial mea- surements are taken. Maintenane mediatins are ntinued thrugh delivery, and stress-dse rtisterids are nt nees- sary (Sylvester-Armstrng, 2020). Oxytin r prstaglandins E1 r E2 an be used r ervi- al ripening and indutin. A nn-histamine-releasing narti suh as entanyl may be preerable t meperidine r labr, and epidural analgesia is ideal. Fr surgial delivery, ndutin analgesia is preerred beause traheal intubatin an trigger severe brnhspasm. Pstpartum hemrrhage is treated with xytin r prstaglandin E1 (misprstl) r E2 (dinprstne FIGURE 54-3 Protocol for management of acute asthma at Park- [Prstin]). Prstaglandin F2α (Hemabate) is ntraindiated land Hospital. aOf predicted value. bLabor & delivery unit, recovery beause it may ause signiant brnhspasm. area, or intensive care unit. FEV1 = forced expiratory volume at 1 second; PEFR = peak expiratory flow rate (liters per minute). ACUTE BRONCHITIS Systemi rtisterids are given early t all patients with Large airway inetin is maniest by ugh withut pneumni- severe aute asthma. One regimen is ral prednisne r prednis- tis. It is mmn in adults, espeially in winter mnths. Ine- lne r IV methylprednislne in a dse  30 t 45 mg daily r tins are usually aused by viruses, and  these, inuenza A 5 t 10 days withut tapering (Barnes, 2018). At Parkland Hs- and B, parainuenza, respiratry synytial, rnavirus, aden- pital, we use a higher daily IV dse (see Figure 54-3). Beause virus, and rhinvirus are requent islates (Irwin, 2018). Bate- their nset  atin is several hurs, rtisterids are given rial agents ausing mmunity-aquired pneumnia are rarely initially alng with β-agnists r severe aute asthma. I the impliated. Te ugh  aute brnhitis persists r 10 t respnse is unsatisatry, a nebulized antihlinergi drug may 20 days and asinally lasts r a mnth r lnger. Evidene be added. Tese drugs at t relax smth musle and diminish supprting the benets  antimirbial therapy is limited muus. By nebulizer, a 0.5-mg dse  ipratrpium brmide is (Smith, 2017). As supprtive are, ugh suppressants n- prvided every 20 minutes as needed r three nseutive dses. taining dextrmethrphan and expetrants with guaienesin Additinal dses every 6 t 8 hurs an be used (Natinal Heart, appear sae in pregnany (Briggs, 2022). Lung, and Bld Institute, 2007). Als, r severe exaerbatins, IV magnesium sulate r thephylline may prve efaius. Further management depends n the severity and respnse PNEUMONIA t therapy. I initial therapy with a β-agnist is assiated with FEV1 r PEFR imprvement t a level >70 perent  base- Inetin  the lungs is a leading ause  death in the United line, disharge an be nsidered. Fr the wman with bvius States (Hern, 2017). Current lassiatin inludes community- respiratry distress r with an FEV1 r PEFR