Ectopic Pregnancy: Etiology, Modern Diagnosis and Treatment
An ectopic pregnancy is an abnormal kind of pregnancy, which occurs outside the uterus or womb (Chen 2008). The term “ectopic” was adapted from the Greek word, ektopos, which means “out of place (Sepilian & Wood 2009). Studies showed that approximately 1-2% of pregnancies are ectopic and 97% of these occur in the fallopian tube (Moeller et al. 2009 as qtd in Kovacs 2010). An ectopic pregnancy develops initially but when there is no more room for it to expand, it can rupture the tube. In rare cases, pregnancy occurs in the ovary, the stomach or the cervix. A condition blocks or slows down the normal travel of a fertilized egg through the fallopian tube to the uterus (Chen). It is seen as an error or flaw of the human reproductive physiology, which allows the fertilized egg to implant itself and grow outside the uterus, its natural location (Sepilian & Wood 2009). Most experts believe that the fertilized egg gets stuck on its way to the uterus and the fallopian tube is scarred, damaged or misshapen (Mayo Clinic Staff 2010). The specific cause remains a mystery. The embryo draws blood supply from the site of implantation. As it enlarges and expands, the site can no longer accommodate it and ruptures. Only the uterine cavity has the natural capacity to expand. The embryo thus ultimately dies. It can also result in massive internal hemorrhage that threatens the mother’s life unless promptly and correctly diagnosed and treated (Sepilian & Wood).
History, Incidence and Frequency
Ectopic pregnancy was first recognized in the 11th century and considered fatal until the 18th century (Sepilian & Wood 2009). John Bard holds the distinction of being the first to successfully treat ectopic pregnancy through surgery in New York City in 1759. The survival rate was very low up to the 19th century at 5 out of 30 by surgery. By the 20th century, great scientific improvements, such as anesthesia, antibiotics and blood transfusion, decreased maternal mortality rate due to ectopic pregnancy. There were 200-400 recorded deaths per 10,000 people from ectopic pregnancy in the early part of the 20th century. The Centers for Disease Control and Prevention reported 17,800 in 1970 and this increased to 108,800 in 1992 (Sepilian & Wood).
A gradual increase in the rate of ectopic pregnancies has been observed in the last three decades (Selway 2006). Many of these are outpatient clients, but roughly 19-20 per 1000 persons are documented (Selway). The incidence has risen six times since 1970, and at present, 2% of all pregnancies are ectopic ( Sepilian & Wood 2009). There were approximately 108,800 cases reported in 1992 and more than 58,000 of these were hospitalized and cost approximately $1.1 billion. It is the leading pregnancy-related cause of death during the first trimester in the country at 9%. Long-term adverse effect is the woman’s ability to reproduce (Sepilian & Wood).
Certain factors are believed to contribute to the risk of ectopic pregnancy (Sepilian & Wood 2009, Chen 2008). These are pelvic inflammatory disease, history of prior ectopic pregnancy or pregnancies, tubal surgery, conception after tubal ligation, fertility drugs or assisted reproductive technology, the use of intrauterine device or IUD, increasing age, smoking, salpingitis isthmica nodosum, exposure to diethylstilbestrol, a T-shaped uterus, prior abdominal surgery, failure with progestin-only contraception, and a ruptured appendix. Theoretically, anything that impedes the transfer of the fertilized egg to the endometrial cavity or uterus can lead to an ectopic gestation or pregnancy. Previous pelvic infection offers the most logical explanation to the increased frequency of ectopic pregnancies. However, most patients have no identifiable risk factors (Sepilian & Wood, Chen).
Pelvic Inflammatory Disease or PID
The most common cause is of a broad range of PIDs from cervicitis to salpingitis and florid PID is the infective agent Chlamydia Trachomatis (Sepilian & Wood 2009). More than 50% of those infected are not aware of the exposure. Other infective agents are Neisseria Gonorrhea and salpingitis. Salpingitis increases the risk of ectopic pregnancy to as many as four times. Successive PDIs also increasingly raise the probability of tubal damage (Sepilian & Wood).
History of Prior Ectopic Pregnancies or Pregnancy
A single prior history of ectopic pregnancy increases the likelihood of another from 7 to 13 times, a 50-80% intrauterine gestation and 10-25% future tubal pregnancy (Sepiilian & Wood 2009, Chen 2008).
History of Tubal Surgery and Conception after Tubal Ligation
Records showed that prior tubal surgery increases the risk of ectopic pregnancy according to the degree of damage and bodily change (Sepilian & Wood 2009, Chen 2008). These surgeries include salpingostomy, neosalpingostomy, fimbrioplasty, tubal reanastomosis and lysis of peritubal or periovarian adhesions. Pregnancy after tubal ligation also raises the risk of ectopic gestation at 35-50%, reports said. These reports also said that ectopic pregnancies follow tubal sterilizations 2 or more years after rather than immediately (Sepilian & Wood, Chen).
Fertility Drugs or Assisted Reproductive Technology
The use of clomiphene citrate or the injectable gonadotropin to induce ovulation has been blamed for the increased risk of ectopic pregnancy up to four times, a recent study found (Sepilian & Wood 2009). The study implied the enhancement of multiple eggs and high hormone levels to ectopic pregnancy. Another study found that infertile patients with luteal phase defects are more highly prone to developing ectopic pregnancy than those whose infertility is caused by anovulation. On the other hand, the use of assisted reproductive techniques can increase the risk of ectopic pregnancy and heterotopic pregnancies in different parts of the body. Examples of these techniques are in vitro fertilization and gamete intrafallopian transfer. This was the conclusion of a study of 300 clinical pregnancies through in vitro fertilization wherein ectopic pregnancy rate was 4.5%. Other studies also showed that pregnancies achieved through in vitro fertilization or gamete intrafallopian transfer can result in heterotopic gestation at 1%. The incidence occurs in 1 out of 30,000 pregnancies from normal spontaneous conceptions (Sepilian & Wood).
Use of Progesterone IUD
The presence of this device has always been suspected as a risk factor of ectopic pregnancy (Sepilian & Wood 2009, Chen 2008). The modern copper IUD does not entail this risk. Nonetheless, the probability of ectopic pregnancy remains when the women gets pregnant at a 3-4% risk (Sepilian & Wood, Chen).
Ectopic pregnancy occurs mostly in women aged 35-44 years old at a three-to-four times the risk among those aged 15-24 (Sepilian & Wood 2009). The myoelectrical activity in the fallopian tube responsible for tubal motility may slow down with age and lead to abnormal gestation (Sepilian & Wood).
Studies showed an elevated risk of ectopic pregnancy at 1.6 to 3.5 times among smokers as compared to non-smokers (Sepilian & Wood 2009). Laboratory research on both human and animal subjects identified several mechanisms by which smoking contributes to ectopic pregnancies. These include delayed ovulation, altered tubal and uterine motility and altered immunity (Sepilian & Wood).
Salpingitis Isthmica Nodosum
These are microscopic substances of tubal epithelium fund in the myosalpinx or below the tubal serosa (Sepilian & Wood 2009). Studies of the fallopian tubes of 50% of patients who underwent salpingectomy for ectopic pregnancy had these microscopic substances. Their origin or cause is not clear. But their assumed mechanisms include post-inflammatory and congenital and acquired tubal alterations (Sepilian & Wood).
Other Risk Factors
These include previous exposure to diethylstilbestrol, a T-shaped uterus, previous abdominal surgery, failure of progestin-only contraception and ruptured appendix (Sepilian & Wood 2009).
These include abnormal vaginal bleeding, amenorrhea or lack of menstruation, breast tenderness, low back pain, mild cramps on one side of the pelvis, nausea, and pain in the pelvic area (Chen 2008). When the site ruptures and bleeds, symptoms include fainting, pain in the shoulder area and sharp and sudden pain in the lower abdomen. Shock may follow internal bleeding from rupture. It is the first symptom of almost 20% of ectopic pregnancies (Chen). Quite often, there will be no symptoms or indication of pregnancy (Mayo Clinic Staff 2010). If any, they resemble those of any pregnancy, such as a missed period, breast tenderness, nausea and fatigue. But a pregnancy test will yield positive results. The first signs of an ectopic pregnancy can be light vaginal bleeding, pain in the lower abdomen and cramps on one side of the pelvis. Symptoms of a ruptured fallopian tube include sharp and stabbing pain in the pelvis, abdomen, shoulder or neck; dizziness; and lightheadedness (Mayo Clinic Staff).
Only about 50% of all patients display the typical symptoms of ectopic pregnancy (Sepilian & Wood 2009). Instead, they report symptoms common to early pregnancy. These include nausea, breast fullness, fatigue, low abdominal pain, heavy cramps, shoulder pain and dyspareunia. In addition, only 40-50% of them report or exhibit vaginal bleeding, palpable adnexal mass at 50%, and abdominal tenderness at 75%. About 20% of those with ectopic pregnancies are hemodynamically compromised. This suggests rupture. Modern diagnostic techniques can now diagnose most ectopic pregnancies before rupturing (Sepilian & Wood).
An exploratory pelvic exam by a health care provider will call attention to pain in the pelvic area (Chen 2008). Initial tests may be culdocentesis, hematocrit, a pregnancy test, a qualitative HCG blood test, a transvaginal ultrasound or pregnancy ultrasound and a white blood count test. An ectopic pregnancy can be distinguished from a normal intrauterine pregnancy through a rise in quantitative HCG levels. Declining B-hCG levels is indicative of an ectopic pregnancy (Kulp & Barnhart 2008). AD & C, laparoscopy and laparotomy tests will confirm the diagnosis (Chen).
An early diagnosis of ectopic pregnancy with transvaginal ultrasound scan or TVS provides the clinician with conservative options (Madani 2008). Methotrexate may be prescribed if the ectopic pregnancy is small. TVS also reduces chances of mortality. Laparoscopy can be reserved for use as treatment rather than for diagnosis (Madani).
Differential diagnosis includes appendicitis, salpingitis, ruptured corpus luteum cyst, or ovarian follicle, spontaneous or threatened abortion, ovarian torsion, and urinary tract disease (Sepilian & Wood 2009).
An ectopic pregnancy can neither be treated nor saved to continue to full term
(Chen 2008). It must be eliminated to save the mother’s life. Emergency medical help for the mother is needed in case of rupture, which can lead to shock. Treatment for shock includes blood transfusion, fluids given intravenously, oxygen, keeping the woman warm and raising her legs. In case of rupture, laparotomy is performed to stop blood loss. At the same time, it confirms an ectopic pregnancy, removes it and repairs any damage tissue. The fallopian tube may need to be removed. If there is no rupture, a minilaparatomy and laparoscopy are often performed. If the doctor does not think a rupture will occur, he may prescribe methotrexate and monitor the patient’s condition. He may also direct the patient to undergo blood and liver function tests (Chen).
Medical therapy has become the preferred approach for ectopic pregnancy in place of surgical removal in many instances (Lipscomb 2007). It has a high success rate of 88-92% and even higher on patients with relatively low hCG levels. Methotrexate is a folic acid analog, which works to interfere with DNA synthesis. It is currently used in multiple doses, alternately with citrovorm or as a single planned dose. Which of these is the superior protocol is still unclear (Lipscomb). Certain factors must be considered in prescribing methotrexate (Sepilian & Wood 2009). The patient must be hemodynamically stable, without signs or symptoms of active bleeding or hemoperitoneum. She must be dependable, compliant and capable of following up. The gestation should not be more than 3.5 cm by ultrasound measurement. And there should be no contraindications to the use of methotrexate (Sepilian & Wood).
Minimally invasive surgery has been the more conservative surgical approach to un-ruptured ectopic pregnancy (Sepilian & Wood 2009). This is to preserve tubal function. Laparoscopy is the choice in most cases. On the other hand, laparotomy is usually performed in hemodynamically unstable patients or those with corneal ectopic pregnancies. It is also used when the surgeon is inexperienced with the procedure and when the use of laparoscopy presents difficulty in a particular patient. And salpingectomy is the choice for a patient who no longer desires fertility, has previous ectopic pregnancy in the same tube or has severely damaged tubes (Sepilian & Wood).
The more popular therapy today is the single-dose injection of methotrexate 50 mg/m2 IM or as a divided dose into each buttock (Sepilian & Wood 2009). Its effectiveness is comparable to that of multiple doses. Smaller doses and fewer injections can result in fewer adverse effects. The patient must be extensively informed about the risks, benefits, adverse effects, and the possibility of failure with the use of injectible methotrexate. Failure of use can lead to tubal rupture, which requires surgery. The patient should be informed about the signs and symptoms of tubal rupture. She should be instructed to contact the physician in case of severe abdominal pain or tenderness, heavy vaginal bleeding, dizziness, tachycardia, palpitations or syncope (Sepilian & Wood).
Most women who suffer a single ectopic pregnancy are able to have normal pregnancies afterwards (Chen 2008). A repeat occurs in 10-20% of cases. Some do not become pregnant again. Deaths from ectopic pregnancy in the United States have declined to less than .1% in the last three decades (Chen).
Internal bleeding, which leads to shock, is the most common (Chen 2008). Death from rupture is rare and infertility is placed at 10-15% (Chen).
A b hCG level of higher than 15,000 IU/L, fetal heart activity and free fluid in the cul-de-sac are the major contraindications to the use of methotrexate (Sepilian & Wood 2009). Documented hypersensitivity to methotrexate, breastfeeding, immunodeficiency, alcoholism, alcohol liver disease or any liver disease, blood dyscrasias, leucopenia, thrombocytopenia, anemia, active pulmonary disease, peptic ulcer and renal, hepatic or hematologic dysfunction are other contraindications to methotrexate (Sepilian & Wood).
Ectopic pregnancy in the cervix, ovary or interstitial or corneal part of the tube is a contraindication to surgical therapy (Sepilian & Wood 2009). Medical treatment with methotrexate becomes the alternative therapy in any of these cases. In case of uncontrolled bleeding and hemodynamic instability, radical surgery is resorted to (Sepilian & Wood).
Smoking as Risk Factor
The Perils of Smoking
Tobacco smoke consists of more than 4,000 chemicals, most of them toxins and carcinogens (Copper and Moley 2008). Some of these are nicotine, tar, polycyclic aromatic hydrocarbons, metals, carbon monoxide, arsenic and hydrogen cyanide. These are related to many diseases and disease states. Other contents still have to be identified. Health care professionals have called massive attention to the danger of active smoking. Yet second-hand or passive smoke is just as dangerous. Second-hand or passive smoke is emitted from the burning end of a cigarette stick, while a smoker emits mainstream smoke. Some experts have called attention and caution to the toxins emitted by side-stream smoke because they dilute quickly through the air. The Environmental Protection Agency or EPA classified second-hand smoke as a carcinogen and deleterious to the health of a smoker’s family. Both active and passive smoke can and does harm almost every body organ. Both types have been linked to leading causes of death, such as cardiovascular disease, cancer, stroke and chronic lung disease. Present data offer enough evidence on the huge impact of smoking on public health. It not only poses great threat on life and health but also a great economic drain from medical expenses and indirect costs on all resources. And smoking affects fertility rates as well. A 2004 Centers for Disease Control and Prevention report said that 44.5 million adults, both men and women, are smokers. This translates to more than 1 out of every 5 adults (Cooper & Moley).
Women and men smokers face the same health concerns but there are less known health risks women smokers contend with (Cooper & Moley 2008). A recent survey conducted with women health care workers on their awareness of the negative impact of smoking revealed that 95-99% of them were aware about its connection with certain diseases. But only 39% of them connected smoking with miscarriage, osteoporosis at 30%, ectopic pregnancy at 27%, infertility at 22%, and early menopause at 17%. A secondary analysis of the 1995 National Survey of Family Growth identified factors indirectly relating to infertility among 824 women-respondents as increasing age, previous ectopic pregnancy, current smoking, obesity and health status. Other studies pointed to active smoking by either partner as a factor, which delays conception. If the woman is the smoker, the delay tends to be greater than 12 months at 54%. Every cigarette box carries the surgeon general’s warning about smoking and adverse pregnancy, yet pregnant women continue to ignore it. There is present evidence linking smoking with increased miscarriage, low birth weight for infants, premature rupture of membranes, placental abruption, perinatal mortality, sudden infant death syndrome and behavioral disorders. Solid evidence of the connection between smoking and untoward pregnancy is still evolving. But the incidence of couples who smoke and cannot “get pregnant” has been rising. Of the available data linking cigarette smoking with reduced fecundity, two reviews make similar conclusions. The first consisted of 13 observational studies of natural conception, which related smoking negatively with live birth rates. The second was a meta-analysis of similar studies, which compared infertile women who smoked with those who did not smoke (Cooper & Moley).
Some other studies sought to establish the toxicity of the long-acting metabolite of nicotine and its effect on the complex process of conception (Cooper & Moley 2008). With rapid achievements in the field of in vitro fertilization, the process could be observed in every stage. And every stage is a potential stage for assault by toxic and mutagenic compounds from tobacco smoke. A group of researchers discovered that exposure to passive smoke is just as deleterious as active smoke. Some toxic compounds can affect, change or distort gene expression as the embryo develops. And the rest of the data suggest that a female fetus, which gets exposed to tobacco smoke while in the womb, incurs an increased risk of future infertility (Cooper & Moley).
Odds Higher among Heavy Smokers
A population-based study with 803 women-respondents who suffered from ectopic pregnancy in central France identified heavy smoking and history of sexually transmitted disease as main factors (Hollander 2003). Thos who smoked 20 or more cigarette sticks a days had four more times the likelihood of having an ectopic pregnancy than those who never smoked. On the other hand, those who had a sexually transmitted disease or confirmed pelvic inflammatory disease ran the risk three times more than those without STD history. Each factor accounted for almost one-third of ectopic pregnancies. It also established the independent link between increasing age and a higher risk of ectopic pregnancy (Hollander).
The study was conducted in the Auvergne region in 1992 with 803 women, aged 15-44, who were treated for ectopic pregnancy at a health care setting between 1993 and 2000 (Hollander 2003). The respondents received treatment at about the same time and had not used contraceptives. The researchers analyzed the respondents’ risk of ectopic pregnancy by obtaining and assessing their background characteristics; surgical, gynecologic and obstetric histories; STD risk factors and history; the use of contraceptives; and other fertility-related characteristics. Result drew a strong relationship between smoking and the risk of ectopic pregnancy. Women who smoked had a 50% higher risk than those who never smoked. The risk was greater with those who smoked at the time of the study. The rate increases with the number of cigarette sticks used daily. Heavy smokers who used 20 or more cigarette sticks were 3.9 times more at risk than those who never smoked (Hollander).
Those who had pelvic inflammatory disease incurred the risk of developing ectopic pregnancy at thrice that of those who never had STD (Hollander 2003).Tubal surgery was also linked with high risk of ectopic pregnancy. STD-related infection also often warrants tubal surgery. As mentioned by previous studies, the risk of ectopic pregnancy increases with advancing years. Those in the late 30s incurred a 40% higher risk than those in their late 20s. But women aged 40 or older incur thrice the risk of those aged 25-29. Other risks are previous pregnancy terminations; previous IUD use at 30%; reduced risk for previous contraceptive pill users at 30%; experience of infertility at 2.1-2.7% (Hollander).
All the factors combined accounted for 76% of all recorded ectopic pregnancies (Hollander 2003). Smoking and STD history with a history of tubal surgery, would constitute 35 and 33%, respectively. The other factors would account for 18% or fewer of ectopic cases. The researchers concluded that increasing awareness of the role of smoking in public health should be fundamental in formulating ectopic pregnancy prevention policies (Hollander).
Smoking-Related Ectopic Pregnancies on the Rise in the Western World
A population-based study conducted with 9,237 hospitalized Norwegian women from 1991-1997 pointed to a link between smoking and an increased risk of ectopic pregnancy (Aronsen 1999). It also decreases fertility and increases risks for complications. These complications include abortion, placental rupture, low birth weight, perinatal death and SIDS. The women respondents were aged 35-49, chosen at random from the national registry to answer 15,000 questionnaires about their pregnancy, smoking habits and use of birth control. Two out of 3 were current or previous smokers. Of the total, 301 or 3.3% had an ectopic pregnancy or a 50% higher chance among smokers than among non-smokers. Moreover, both ectopic pregnancy and smoking are risk factors for infertility. The overall risk is 15% that ectopic pregnancy would not have occurred if the women did not smoke (Aronsen).
Ectopic pregnancy has become more frequent in the Western world in the last two or three decades (Aronsen 1999). The incidence in the United States was 19.7 per 1000
reported pregnancies in 1992. This was thrice the incidence in 1917. In comparison, the assumption for Norway is that 1200-1500 women are hospitalized every year. A study conducted on Hordaland County in Norway showed an increase in incidence from 11.2 in 1976-81 to 18 in 1988-93. Some hospitals consider this increase in incidence an epidemic. Three deaths occurred in Norway from 1986-95 due to ectopic pregnancy and 20-40% of survivors became infertile. The risk for recurrence is 10-20%. About 30-36% of Norwegian women smoked regularly every day from 1973 to 2000. Approximately 32% of fertile women aged 16-24 and 38% of those aged 35-44 smoked regularly (Aronsen).
The study also yielded other highlights. It found the strongest association between smoking and ectopic pregnancy among women without previous children (Aronsen 1999). With a 32% risk for ectopic pregnancy, which was not dependent on IUD use, the overall conclusion was that ectopic pregnancy would not have occurred if the women were not smoking. The respondents were not asked about genitourinary infections as questions about STD are sensitive ones. An American study conducted to test the link between smoking and ectopic pregnancy includes queries about genitourinary infections. The findings showed no statistical effect on the association and genitourinary infections were, therefore not considered a confounding variable (Aronsen).
Overall findings of the study support the hypothesis that smoking increases the risk of ectopic pregnancy (Aronsen 1999). The study, however, cannot indicate how large or small the increase is. Other studies only on women who smoked at the time of conception provided statistical evidence on that increase. One was a clinical patient-controlled study conducted in Georgia, USA from 1988-90. After certain adjustments on age, previous procedures, infertility and parity were made, it found a 95% probability for women who smoked during the peri-conception period as compared with women who did not smoke (Aronsen).
This study, therefore, offers strong evidence of the association between smoking the increased risk of ectopic pregnancy (Aronsen 1999). It also raises the risk for complications. It recommends that women at fertile age should quit smoking and that this recommendation be adopted as part of consultations with doctors (Aronsen). A lot has been said about tobacco smoke and its effects on health. Yet only few researches have explored the clear association between tobacco smoke and its reproductive consequences, particularly ectopic pregnancy (Cooper & Moley 2008). Nonetheless, whether the exposure to tobacco smoke happens in utero, during pregnancy or throughout a woman’s reproductive years, it adversely affects all facets of fertility. Evolving evidence suggests that its adverse effects include ectopic gestation (Cooper & Moley).
Ectopic pregnancy outside the fallopian tubes is not preventable (Chen 2008). But tubal pregnancy can be prevented by avoiding what may scar the fallopian tubes.
Avoiding pelvic inflammatory disease and its conditions, early diagnosis and treatment of sexually transmitted disease and of salpingitis and pelvic inflammatory disease are preventive measures (Chen).
Pelvic inflammatory disease or PID is the most common cause of ectopic pregnancy
(Sepilian & Wood 2009, Chen 2008). It is also a common complication of cervicitis (Paavonen 1998). Infections, such as PID, can develop without clinical findings, which suggest it. Hence, silent or atypical PID accounts for many cases or tubal factor infertility and tubal pregnancy. With C. trachomatis as the most common sexually transmitted pathogen and a major cause of PID, earnest efforts should be set in preventing Chlamydia. Suspect cases should, therefore, be tested for cervicitis and C. trachomatis, in particular, for long-term prevention of the consequences of PID. STD prevention and control programs should include diagnostic services with proper quality control, clinician guidelines in diagnosing and managing cervicitis, screening asymptomatic carriers of C. trachomatis, surveillance systems, health care training, periodic monitoring and evaluation of control measures, routine tests of sex partners, and effective patient education on behavioral aspects and contraception (Paavonen).
Ectopic pregnancy cannot be prevented but the risk of developing it can be reduced (Mayo Clinic Staff 2010). A woman can limit the number of her sexual partner or the partner can use a condom to prevent the spread of sexually transmitted disease, such as PID (Mayo Clinic Staff). Preventing disease can be primary, secondary, or tertiary (Paavonen 1998). Primary prevention includes avoiding exposure to and acquiring chlamydial infection through lifestyle counseling and health education. Clinicians should inquire into a patient’s high-risk sexual behavior, encourage her and her partner or partners to be tested if at risk and treated if infected, and then counsel them about safe sex practices. Primary prevention of sexually transmitted disease through health education has not proved to be effective. Health education is slow and quite complicated to implement. Yet health education is quite needed, especially among adolescents (Paavonen).
Secondary prevention is conducted through universal screening in order to prevent PID and its long-term consequences (Paavonen 1998), including ectopic pregnancy. Part of secondary prevention is the early detection of sub-clinical diseases through tests. This is to prevent lower genital tract infections from becoming upper genital infections. A recent and randomized controlled trial offered strong evidence that the selective screening for chlamydial infections could reduce the incidence of PID. Screening included a single-dose therapy of azithromycin, amplification tests, and the first-void urine specimen. But whether the result of the screening would significantly impact the incidence of ectopic pregnancies and tubal factor infertility remained uncertain (Paavonen).
Tertiary prevention of acute and chronic chlamydial infections of the upper genital tract, however, fails (Paavonen 1998). Significant tubal damage has already occurred when symptoms begin to surface. The subsequent delay in care also predicts tubal damage. The risk remains high for tubal-factor infertility or ectopic pregnancy despite the patient’s response to antimicrobial therapy (Paavonen).
The other contributing factor to ectopic pregnancy that prevention measures should effectively address is smoking. Statistics say that smoking kills 430,000 Americans every year and accounts for 20% of all deaths (Bernstein et al. 2006). This is why the Surgeon General, through his 5 a’s, encourages all healthcare providers to inquire into smoking habits and counsel against it at every opportunity. Emergency Departments or EDs treat more than 115 million patients every year. They report that patients’ smoking exceeds the national average. Although EDs are not the front-liners in the massive anti-smoking campaign, it plays a very important role in it. But it is unable to deliver valuable intervention for lack of time, resources and reimbursements (Bernstein et al.).
In response, a comprehensive approach to ED-based services has been initiated. An ED-initiated tobacco control has been enforced, connecting them to a network of interventions (Bernstein et al. 2006). They are encouraged to use a variety of smoking cessation screening tools. These include computerized self-report, traditional verbal evaluations by provides and peer educators. They may adopt and use counseling methodologies, such as video interventions, brochures, verbal reminders, peer education, education by a discharged nurse, a national quite hotline, nicotine replacement therapy, screening and counseling of smoking pediatric patients and caregivers, discouraging the start of smoking, well-designed and strict randomized clinical trials on the effectiveness of these interventions and researches, new curriculum for ED professionals on tobacco-related diseases, and advocacy to increase reimbursement for smoking cessation counseling. ED clinicians should advise smokers to quit in a clear but non-conflicting manner and then referred to treatment centers or national quit lines. Nicotine replacement therapy should be prescribed, especially to heavy smokers (Bernstein et al.).#
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