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Respiratory Complications

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Respiratory Complications Dr. Yuma S, SpOG 

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Both prostaglandins and ergometrine (methergine) can cause bronchospasm and therefore should be avoided if possible. Hemabate, a PGF2α, should be avoided . Physiologic Adaptations of the Respiratory System  Administer stress doses of corticosteroids in women on steroid During pregnancy: treatment within previous 6 months (empirical recommendation  the diaphragm rises by 4 cm, without data).  the transverse diameter of the thoracic cage increases by 2 cm  Complications  the subcostal angles increase from 68 degrees to 103 degrees at  Poorly controlled asthma is associated with increased risks of term. preeclampsia, prematurity, and low birth weight. Increased oxygen demands of pregnancy are met by deeper ventilation rather than more frequent respiration. The respiratory rate and the Influenza  Influenza A and B are the two types of influenza that can cause total lung capacity are unchanged epidemic human illness Progesterone stimulates hyperventilation Because the fetal hemoglobin has a higher O2 affinity compared to  Influenza is airborne with an incubation period of 1 to 4 days. maternal hemoglobin fetal O2 delivery is not reduced until the  It is usually a self-limited respiratory illness lasting a few days, but maternal PaO2 drops to 65 mm Hg, corresponding to a maternal O2 women in the last two trimesters have an increased risk of Sat of less than 90%. complications.  Evaluation Asthma Signs and symptoms Background  fever,  Asthma affects 5% to 9% of pregnant women (3).  myalgia,  Severity is unchanged in 50%, improved in 29%, and worse in 22%  headache, (4).  malaise, Definition  nonproductive cough,  Asthma is a chronic inflammatory disease of the airways that  sore throat, and rhinitis. causes exaggerated bronchial smooth muscle contraction, mucus  Treatment hypersecretion and edema, and airway wall remodeling.  Inactivated influenza vaccine is preferred and may be given in any Bronchoconstriction  IgE-dependent release of histamine, tryptase, trimester , postpartum, and during breast-feeding. . leukotrienes, and prostaglandins from the mast cells.  The intranasal live attenuated influenza vaccine, marketed as Atopy is the strongest identifiable predisposing factor FluMist, should not be used during pregnancy. Evaluation  The effects of influenza antiviral agents (amantadine, rimantadine,  History of Precipitating Factors zanamivir, and oseltamivir) on pregnant women and their fetuses  Inhalant allergens: Animal allergens, house-dust mites, cockroach are unknown; therefore, they should be used only if the potential allergens, indoor molds, outdoor allergens benefit justifies the potential fetal risk (7).  Occupational exposures  Complications  Irritants: Tobacco smoke, pollution, and irritants  Exacerbation of underlying medical conditions (e.g., pulmonary or  Others: Rhinitis/sinusitis, gastroesophageal reflux, aspirin, other cardiac disease). nonsteroidal anti-inflammatory drugs, sulfites (a common  Secondary bacterial pneumonia or primary influenza viral preservative for processed food), and viral respiratory infections. pneumonia. Physical Evaluation  Coinfection with other viral or bacterial pathogens.  Physical findings: Pneumonia  poor air entry,  Background  expiratory wheezing,  Pregnancy does not predispose to pneumonia. The pathogens in  prolonged phase of forced exhalation, pregnancy are the same as those affecting nonpregnant women of  use of accessory muscles, reproductive age:  nasal secretion,  Bacterial: Streptococcus pneumoniae, Haemophilus influenzae,  mucosal swelling, Legionella  nasal polyp, and atopic dermatitis/eczema.  Viral: Influenza A, varicella  Spirometry  Mycoplasma  Decreased FEV1 and FEV1/FVC  Diagnosis  increase of 12% or greater and 200 ml in FEV1 after inhaling a  Typical symptoms are cough, dyspnea, sputum production, and short-acting bronchodilator. pleuritic chest pain.  Arterial blood gases (performed with severe exacerbation or poor Signs include fever, tachypnea, rales, dullness to percussion, and response to initial treatment) show hypoxemia associated with an  bronchial breath. elevated PaCO2. This should be interpreted as a sign of severe  Chest x-ray may reveal single lobar infiltrate typical of bacterial respiratory compromise pneumonias or patchy multilobular infiltrates typical of Treatment Mycoplasma or viral infections. Antepartum Management  Monitor asthma with spirometry or peak expiratory flow  Treatment  Hospitalization for intravenous hydration, oxygen supplementation, measurements. and empirical antibiotic treatment is indicated.  Monitor fetal growth with ultrasound examinations if asthma is  Erythromycin monotherapy is effective in most communitysuboptimally controlled. acquired pneumonias.  Reduce exposure to allergens.  Cefotaxime or ceftriaxone should be added for:  Pharmacotherapy .  Staphylococcal or Haemophilus pneumonia (suspected or  Theophylline levels should be monitored (serum concentration of 5 documented) to 12 mcg per ml) due to its decreased clearance in the last  Coexisting chronic conditions trimester.  Respiratory rate of 30 per minute or faster, hypotension, pulse of  Treatment of exacerbating factors is paramount: 125 bpm or faster, temperature of <35 or >40 degrees Celsius,  Intranasal corticosteroids are the most effective medications for altered mental status chronic rhinitis.  Extrapulmonary disease, sepsis, coagulopathy, or anemia  Loratadine and cetirizine are the preferred nonsedating  WBC <4,000 per µl or >30,000 per µl antihistamines.  PaO2 of 60 mmHg or less and/or CO2 retention  Influenza vaccination is recommended .  Elevated serum creatinine Labor Management  Multilobar involvement, cavitation, or pleural effusion.  Continue prenatal asthma medications. Penicillin can be used if pneumococcal disease is strongly  Inhaled β2-agonists do not delay the onset or slow the progress of  suspected. labor.  Pneumococcal polysaccharide vaccine (PPV-23) is not recommended in the healthy pregnant women.

PPV-23 should be given to pregnant women with immunosuppression, diabetes mellitus, asplenia, tobacco use, and renal and cardiopulmonary diseases  Complications Severe pneumonia is associated with an increased risk of preterm labor and acute respiratory distress syndrome. However, there is a high probability of a good outcome. 

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Low molecular weight heparin (LMWH) is replacing unfractionated heparin in nonpregnant women. Treatment should be continued for the duration of pregnancy and for 6 to 12 weeks postpartum. After delivery, anticoagulation with oral warfarin

Renal Complications  Anatomic Alterations Pulmonary Edema Renal size increases approximately 1 to 1.5 cm. These changes are Pulmonary edema in pregnancy is usually secondary to: secondary to:  Preeclampsia  Increase in renal vascular volume  Tocolytic therapy  Increase in capacity of the collecting system  Massive fluid resuscitation  Glomerular hypertrophy.  Amniotic fluid embolism  Renal volume increases 30% (1)  Sepsis  Ureteral dilation:  Cardiac disease (peripartum cardiomyopathy, mitral stenosis,  Changes begin in the first trimester myocardial infarction)  Normal pregnancy measurement Diagnosis  Renal pelvicalyceal dilation  Symptoms of dyspnea and orthopnea.  Physiologic Changes  hypoxemia.  Renal blood flow (RBF) may increase up to 75%  Chest x-ray reveals fluffy infiltrates or Kerley B lines.  Glomerular filtration rate (GFR) is increased by approximately 50% Treatment  Potassium is retained to support fetal-placental development .  similar to that in nonpregnant women:  Identification and reversal of underlying cause.  lasix (diuresis), morphine (to dilate airways), Na2+ and water Urinary Tract Infections  UTI:Minimum of 1000 per ml of a single organism in the presence of restriction, oxygen, and position patient upright. symptoms  Consider management in an ICU setting.  Etiology  Antibiotics and inotropic support if indicated  Normal vaginal flora. Tuberculosis  Most common organisms Background  Escherichia coli 70% of cases  The acid-fast bacillus Mycobacterium tuberculosis is transmitted  Klebsiella 3% of cases from person to person through an airborne route. Infectivity is  Proteus 2% of cases associated with cavitary pulmonary disease,  Gram positive cocci ,group B streptococcus 10%  sputum smear-positivity, and frequency of cough.  Evaluation Diagnosis UTI  The Mantoux tuberculin skin test  Urinalysis and urine culture  chest x-ray  Follow up culture two weeks after treatment to assess for  sputum test for acid-fast-bacilli smear eradication.  culture for M. tuberculosis Pyelonephritis (Characterized by fever of >38°C, chills, flank pain, costovertebral angle tenderness, nausea, emesis, anorexia, &either  Drug susceptibility should always be obtained from the initial 20 bacteria per high-power field or pyuria ) isolates because the proportion of multidrug-resistant TB is 1%.  Urinalysis, urine culture, blood cultures, basic metabolic panel to Treatment assess creatinine, and electrolytes  The first-line regimen consists of isoniazid (INH), rifampin (RIF), and ethambutol daily for 2 months, followed by INH and RIF daily  Treatment  UTI or twice weekly for 7 additional months.  Streptomycin should be avoided due to possible fetal ototoxicity.  oral antibiotics for 3 to 7 days  The fetal risks of using pyrazinamide are unknown;  Complicated UTI or recurrent UTIs  Asymptom. is treated with daily INH 300 mg for 9 months after the  oral antibiotics for 10 days. first trimester (12 months if HIV-infected).  Pyelonephritis  INH therapy can be started during pregnancy.  Admission for inpatient treatment  INH should be supplemented with pyridoxine (vitamin B6), daily  Antibiotics for 24 hours after resolution of flank pain and fever tablets of 50 mg, to decrease neurotoxicity.  Combined IV and oral course for 10 to 14 days after clinical  The mother should be separated from the infant at delivery if improvement active TB is suspected.  Medications  Antituberculosis medications are not contraindicated during Adjust antibiotics based on culture/sensitivity results. breastfeeding. UTI  Vaccination with BCG is not recommended due to unproven  Macrobid 100 mg po bid efficacy Avoid if past medical history of G6PD deficiency to avoid hemolytic Complications crisis.  Perinatal complications include low birth weight and, rarely,  Bactrim DS one tab po bid neonatal tuberculosis. Avoid in first trimester as trimethoprim is an antifolate agent wit theoretical risk of neural tube defects  Congenital infection may occur via hematogenous spread (an Avoid in the third trimester due to risk of kernicterus. active placental infection), amniotic fluid, or at the time of delivery.  Amoxicillin 500 mg po tid Pulmonary Embolism  Ampicillin 250 mg po qid Venous thromboembolic disease (pulmonary embolism [PE] and deep  Keflex 500 mg po qid. vein thrombosis [DVT]) is the leading obstetric cause of maternal Pyelonephritis mortality.  Intravenous antibiotics Etiology Ampicillin 2 gm every 6 hours plus gentamicin (dose depends on  Pregnancy is a thrombogenic state. Thromboembolic events are selection of daily versus. three times daily dosing regimen) fivefold more common in pregnant women than in nonpregnant Cefazolin 2 gm every 8 hours women. Ceftriaxone 1 gm every 24 hours.  Other predisposing factors include trauma (surgery), infection,  Oral antibiotics to complete course of treatment obesity, and underlying thrombophilia. Selection based on sensitivities Avoid nitrofurantoin (Macrobid) for completion of antibiotic Treatment regimen due to poor tissue penetration.  Unfractionated heparin is the treatment of choice for acute thromboembolism. Chronic Renal Disease

 Definition  Mild renal insufficiency is defined by a serum creatinine of 1.4 mg per dl or less. Associated with few maternal or fetal complications. Underlying renal disease is not irreversibly worsened by pregnancy.  Moderate renal insufficiency is defined by a serum creatinine of 1.5 to 2.4 mg per dl  Severe renal insufficiency is defined by a serum creatinine of 2.5 mg per dl or greater (14).  Chronic renal failure is characterized by oliguria or anuria requiring dialysis (2).  Etiology Most common causes are:  Diabetes mellitus 33%  Hypertension 24%  Glomerulonephritis 17%  Polycystic kidney disease 5%.  Evaluation  Baseline 24-hour urine collection for protein and creatinine clearance  repeated monthly (16).  Baseline blood pressure  monitoring.  Prenatal visits at least twice monthly.   Targeted ultrasound at 18 to 20 weeks followed by monthly sonograms to assess for fetal growth restriction.  Antepartum fetal testing with biophysical profiles twice weekly.  Treatment  Medical management of comorbidities of renal insufficiency should be addressed. Hypertension Anemia.  Delivery for: Uncontrollable hypertension Preeclampsia Decreasing renal function once viability is reached Standard fetal indications.  Medications  Hypertension calcium-channel blockers, hydralazine.  Anemia Maintain hematocrit at 25% or greater with  Ferrous sulfate   Erythropoietin  Transfusion of packed red blood cells.  Systemic Lupus Erythematosus (SLE)  Background  Autoimmune disorder occurring primarily in women.  Definition  Lupus glomerulonephritis is characterized by: hematuria, proteinuria, thrombocytopenia, hyperuricemia, and hypocomplementemia  Evaluation  Laboratory Tests  screened at initial visit with baseline 24-hour urine collections for total protein and creatinine clearance ,every trimester if both blood pressure and disease status remain stable.  Serum creatinine should be obtained at initiation of prenatal care and then every trimester or more frequently if there is concern for  progression of disease.  Treatment  Management should be undertaken by a rheumatologist with nephrology consultation as needed for concomitant renal disease.  Patients should be seen in the office at least every two weeks.  monthly sonograms to assess for fetal growth restriction.  Fetal heart rate assessment by auscultation, nonstress test (NST),  or ultrasound/ echocardiogram should be undertaken to exclude fetal heart block.  Antepartum fetal testing should begin at 28 weeks  Acute Renal Failure  Definition  Impairment of renal function characterized by progressive azotemia accompanied by oliguria developing over hours to days  Oliguria is defined as production of 400 mL or less of urine in 24  hours.  Etiology  Abruptio placenta  Placenta previa.   Septic abortion.

Clostridium welchii or Streptococcus pyogenes are the causative organisms. Thirty percent mortality rate  Hyperemesis gravidarum  Preeclampsiadue to diffuse endothelial swelling, which may result in ischemia.  Acute fatty liver of pregnancy is frequently accompanied by renal failure..  Amniotic fluid embolism  Idiopathic postpartum renal failure known as postpartum hemolytic uremic syndrome May occur days to months after delivery History of a preceding viral illness Attributed to circulating toxins.  Retained fetus  Obstructive uropathy due to compression of the ureters by: Leiomyomata Polyhydramnios Multiple gestation Presence of a solitary kidney Presence of congenital renal abnormalities.  Medications Specifically NSAIDs. Evaluation  History and Physical  Laboratory Tests  Urinalysis: ketonuria, and cells and casts  Urine culture  Complete blood count anemia / infection.  Peripheral smear for schistocytes and burr cells  postpartumhemolytic uremic syndrome.  Blood cultures if there is concern for sepsis or infection.  evaluate renal function and to assess for electrolyte abnormalities.  Liver function tests to assess for acute fatty liver of pregnancy and HELLP.  Renal biopsy for worsening function or no improvement in function with unclear etiology  Imaging Renal arteriogram with findings of patchy blood flow or an absent nephrogram support the diagnosis of renal cortical necrosis. Diagnosis  Made by findings of azotemia (increasing creatinine and decreased clearance electrolytes) with decreasing urine output. Treatment  largely supportive.  Oral fluid restriction.  Hydration with normal saline to maintain sodium and to correct hypovolemia of hyperemesis gravidarum.  Antibiotics as needed for sepsis.  Transfusions and volume replacement for acute renal failure associated with profound anemia.  Delivery in cases associated with preeclampsia, HELLP, and acute fatty liver of pregnancy.  Medications cleared by the kidneys should be dosed to compensate for renal insufficiency to avoid further complications and toxicities. Cardiovascular Disease Antenatal Cardiovascular Changes Blood volume.  Blood volume increases on average by 40% to 60%  The expansion in plasma volume is greater than the expansion of red cell mass  With multiple fetuses, the increase 500 ml more than in a singleton gestation. Cardiac output.  Cardiac output increases on average by 40% to 50%  supine positioning will decrease cardiac output by 25% to 30% because of compression of the vena cava by the gravid uterus. Blood pressure  decrease in diastolic blood pressure beginning in the TS I & maximal in TS II  decrease in systolic blood pressure in TS II  returns to prepregnancy levels in TS III Heart size. Ventricular chamber size is increased with wall thickness maintained. Intrapartum Cardiovascular Changes First-stage labor.

each contraction increase in circulating blood volume of 300 to 500 ml increases maternal cardiac output and blood pressure.  the cardiovascular effects of labor is dependent on maternal position and pain management.   supine positionthe baseline cardiac output between contractions  will rise progressively to a maximum increase of 15%.   lateral position, the increase will be less (approximately 5%).   Most of the increase is caused by maternal pain and anxiety  Second-stage labor  bearing-down efforts  will be diminished venous return causing  decreased stroke volume & increased heart rate to maintain  cardiac output.  Shortening of the second stage for patients with significant cardiac disease Postpartum.   Immediately postpartumincrease in circulating blood volume and  an increase in cardiac output.  there is mobilization of extravascular fluid into the vascular system increases circulating blood volume.  hazardous time for the cardiac patient sensitive to an increase in preload. Evaluation  Physical Examination  Cardiac physical examination.   There is an increase in intensity of the first heart sound with exaggerated splitting. A third heart sound is not commonly  heard, but the presence of a fourth heart sound should not be attributed to pregnancy.   Systolic ejection flow murmurs are commonly heard, but diastolic murmurs are rare and should prompt further evaluation  Diagnostic Evaluation:  Chest x-ray.  Electrocardiogram  Echocardiogram.  Pulmonary artery catheterization.

New York Heart Association Functional Classification of Heart Disease Class  Description:  Asymptomatic   Symptoms with normal activity  Symptoms with less than normal activity  Symptoms at rest  Treatment General Antepartum Management  Activity level.   Diet.  Rapid treatment of stressors.  Subacute bacterial endocarditis prophylaxis.   Medications  Most medications used in cardiac patients may be continued during  pregnancy CI:  Warfarin (Coumadin), which may cause an embryopathy (nasal  hypoplasia, mental retardation, optic atrophy).   Angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists, which may cause fetal death or intractable neonatal renal failure. General Intrapartum Management  Maternal positionAvoidance of supine positioning  Anesthesia should be used liberally because stress and pain in  labor will greatly increase cardiac demand.   Second-stage labor may be shortened.  Cesarean section should be reserved for normal obstetric  indications.  Hemodynamic monitoring. 

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Hematologic Complications Iron-deficiency Anemia  This is the most common cause of anemia in pregnancy Pathophysiology Oral iron intake inadequate . the loss of iron stores because of increased maternal blood production and fetal growth needs.  Pregnancy requires an increase to 15 to 18 mg per day of elemental  iron In total, pregnancy requires about 1130 mg of elemental iron   450 mg for RBC expansion

 360 mg for fetus-placenta  170 mg for basal loss  150 mg for delivery loss. Bleeding during pregnancy, vaginally or from another source Multiple gestation Iron malabsorption Concurrent antacid use, which may prevent iron absorption Poor dietary habits or pica (an appetite for inedible substances, such as clay or dirt). Evaluation History and physical The symptoms are nonspecific and diagnosis depends on laboratory evaluation. Laboratory studies Treatment Prophylaxis Medications  Ferrous sulfate, 300 mg tablets, contain 60 mg (10 grains) of elemental iron.  Intestinal absorption permits absorption only up to 15 mg of iron without signs of iron intolerance or even toxicity. Anemia Resulting from Folic Acid Deficiency Folic acid deficiency is common in pregnancy. Pathophysiology the recommended daily requirement for folic acid is 0.4 mg; this increases to 0.8 to 1.0 mg during pregnancy. Folate stores are limited and easily depleted within a few months in times of increased demand All supplies of folate must come from external sources: Prime dietary sources are fruits and vegetables, of which the best are  Spinach  Lettuce  Asparagus  Broccoli  Lima beans  Melons  Bananas. Etiology pregnant women may be at risk , those with the following:  Ongoing hemolysis  Seizure disorders on medication interfering with folic acid metabolism  Multiple gestation. Epidemiology Folic acid deficiency is the most common cause of megaloblastic anemia. Evaluation History and Physical The symptoms nonspecific. Deficiencies in either folic acid or B12 can present with glossitis and roughness of skin. Diagnosis Clinical Manifestations associated with such pregnancy complications  Low birth weight  Smaller maternal blood volume  Abruptio placentae  Prematurity. Treatment Medications The daily dose of folic acid is 1.0 mg whether for prophylaxis or treatment. an increased reticulocyte count should be seen within three to four days. If neurologic symptoms are present, a B12 level should be measured because folic acid will correct the anemia but not the neurologic sympt Oral folic acid is sufficient for treatment unless folic acid antagonists are being used, at which time parenteral folic acid is indicated. Anemia from B12 Deficiency Etiology B12 is absorbed in the ileum, bound to intrinsic factor. B12 deficiency is rarely due to inadequate ingestion, except in strict vegetarians. malabsorption syndromes are common causes.  Pernicious anemia (rare in this age group)

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 Previous gastric or intestinal surgery  Inflammatory bowel disease   Helminth infestations.  Evaluation Laboratory Tests  necessary to establish the diagnosis.  A radioimmunoassay is used to measure B12 serum levels. levels below 50 pg per ml are indicative of B12 deficiency.  The Schilling test is used to measure B12 absorption but is  contraindicated in pregnancy because of the use of radioactive cobalt. Neurologic abnormalities are seen, as are elevated serum bilirubin and lactic dehydrogenase levels (4).

Diagnosis Clinical Manifestations Neurologic symptoms Treatment Medications 1 mg B12 is given parenterally weekly5-6 weeks, then 100 mcg monthly. should respond within six weeks. A brisk reticulocytosis should manifest within 3-5 days.

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