Effects of Regional Anesthesia and Local Anesthesia 
      Local Anesthetics
      Regional Anesthesia   
   Maternal and Fetal Considerations 
   Maternal and Fetal Trauma During Pregnancy
       Motor Vehicle Accidents 
       Pelvic Features in Pregnancy 
       Other Trauma 
   The Injury Severity Score
       Diagnostic Peritoneal Lavage and other Assessment Methods 
       used in Traumatized Pregnant Women      
   Assessment of Fetal Well-Being
   Perinatal Mortality and Prevention of Preterm Labor 
   Recommendations for Anesthetic Management 
   References    

Effects of Regional Anesthesia and Local Anesthetics

     When selecting regional anesthesia for trauma surgery on a gravida, the anesthesiologist must consider the relative risks and benefits for both mother and fetus.

Local Anaesthetics

     There are few local anesthetic agents that cannot be used for regional anesthesia.  All of them block nerve action potentials by altering conduction through ion channels in the membrane.  The basic structure of a local anesthetic is a tertiary amine bound to an aromatic ring by either an amine or ester linkage.  The type of linkage determines how the drug is metabolized.  Esters are enzymatically hydrolyzed by either plasma or liver cholinesterases, whereas amines are metabolized in the liver by microsomal enzymes.

      Enlarging the alkyl substitutions on the aromatic ring or tertiary amine increases lipid solubility and protein binding of the agent.  In general, the more lipophilic an agent, the greater is its potency and duration of action.  For example, intermediate-acting lidocaine is transformed to long-acting etidocaine by the addition of an ethyl and a methyl group.

     All local anesthetic agents used today cross the placenta.  Local anesthetics usually cross the placenta by passive diffusion; the greater the maternal blood level, the higher the gradient pushing the drug across the placenta to the fetus.  The extent of transfer of a local anesthetic to the fetus is also a function of its physical characteristics(16).  For example, mepivacaine is 39% unionized, whereas procaine is only 3% unionized.  Therefore, at equivalent maternal levels, more mepivacaine than procaine is available to cross the placenta.

     When maternal blood levels are high, protein binding decreases, which permits more local anesthetic to diffuse through the placental membranes.  Fetal protein binding capacity is approximately 50% to 60% of the maternal capacity and probably does not significantly limit fetal blood levels and toxic reactions(17).  The amount of local anesthetic available for perfusion is further limited by maternal metabolism.  Esters are rapidly metabolized and at one time were thought rarely to attain sufficient maternal plasma levels for transfer to the fetus.  However, it has been shown in normal patients receiving chloroprocaine epidural anesthesia for obstetric delivery, no detectable levels of the anesthetic were found in either maternal or cord blood at delivery(18).

     However, if amides of shorter duration are used, frequent redosing can lead to maternal blood accumulation, resulting in higher fetal drug levels than when longer acting amide anesthetics are used(19).  Once the local anesthetic crosses the placenta, its effects are determined by fetal uptake, distribution and metabolism.

Regional Anesthesia

     Epidural and subarachnoid blocks are the regional anesthetic techniques most frequently used for surgery on pregnant patients.  The fetus may benefit by the ensuing decrease in maternal catecholamine levels and by the lessening of uterine artery vasoconstriction.  This could increase uterine blood flow.

     Aortic and vena caval compression by the enlarging uterus occurs by the second trimester.  There is engorgement of blood vessels with reduction in the size of the epidural and subarachnoid spaces.  Local anesthetic drug requirements for epidural and subarachnoid anesthesia are less for these patients and failure to recognize this can result in anesthetic overdosage and undesirable side effects such as hypotension, cardiorespiratory depression and central nervous system toxic reaction.

     Uterine blood flow is at maximum levels.  Decreases in placental perfusion for whatever reason, e.g., hypoxia, hypotension, or peripheral vasoconstriction can lead to fetal hypoxia.

     Blockade of the sympathetic innervation by major techniques usually produces hypotension unless prevented or treated promptly.  If the block should rise above the T1-T2 dermatome, the heart may be depressed by stopping the accelerator fibers and allowing a vagal effect to predominate.  The degree of hypotension is related to the height of the block and the fluid balance status of the patient.  The pregnant patient is more susceptible to hypotension from regional anesthesia.

     Regional anesthesia would be preferable to general anesthesia for various reasons.  Using short acting, rapidly metabolized ester anesthetics, one avoids high maternal blood levels and increased fetal risks.  If a subarachnoid block rather than an epidural block is used, fetal exposure is even less.  In addition, because the pregnant patient is more prone to acid aspiration by week 20 of gestation, a regional technique should reduce the chance for aspiration(5).  Whichever anesthetic technique is chosen, careful attention to maintenance of maternal blood pressure, oxygenation and acid base status is mandatory to optimize fetal outcome.

Maternal and Fetal Considerations

     A relatively controversial situation regarding the use of nitrous oxide for surgery during pregnancy stems from nitrous oxide and DNA synthesis.  Some authorities believe nitrous oxide should not be used during the first two trimesters of pregnancy(20).  Nitrous oxide is deleterious to vitamin B12 formation, the essential cofactor for the enzyme methionine synthetase.  Alteration of methionine synthetase activity interferes with folate metabolism and the conversion of uridine to thymidine and may impair DNA synthesis.  In the non-pregnant patient this does not seem to be significant; however, in the pregnant patient, there is worry that the use of nitrous oxide may be deleterious to the developing fetus.  Christensen et al(21) showed that in rodents maternal exposure to nitrous oxide yielded a significant drop in fetal methionine synthetase activity in less than an hour.  The decreased methionine synthetase activity persisted for up to 72 hours.  It has been suggested that this possible nitrous oxide problem can be prevented by pretreatment with folinic acid(20).  This substance is a naturally occurring compound that is necessary in the production of thymidine from deoxyuridine.  However, this method of treatment is still not proven.

     Halothane in low concentrations for several hours caused many rat fetus anomalies.  In mice that were given 3 hours of halothane (1.5%) there was an increase of foot anomalies and cleft palates(22).  In hamsters, 3 hours of halothane (0.6%) in the middle of pregnancy increased the number of abortions(23).  Some investigators using rats, rabbits and mice have not shown any teratogenic effects of halothane(24).

     Studies in humans have usually dealt with epidemiologic surveys retrospectively carried out.  These surveys are concerned with reproductive outcomes in groups consistently exposed to low levels of anesthetic gases or in women who have undergone surgery during their pregnancy.  These approaches have important limitations.  Investigation of the adverse affects of persistent exposure to waste anesthetic gases are not accurate due to lack of comparable control groups, lack of detailed reporting, and the reporting of misinformation.  The problem with surveys of women that have undergone surgery during pregnancy includes many of the above limitations as well as few cases having been reported.  The use of many anesthetic agents and the effects of the surgery and the disease process on anesthetic teratologic causation are often ignored.  The most consistent finding is the increased risk of spontaneous abortion in female personnel exposed to waste anesthetic gases.  The incidence of miscarriage among the exposed women is approximately 25% to 30% greater than in non-exposed women.

     There has been no anesthetic pinpointed as a teratogen in women undergoing surgery during pregnancy.(13,14)  A retrospective study investigated the results in 67 women who had undergone surgery during pregnancy.  Eleven of these women received an anesthetic during the first trimester.  No congenital anomalies were found(13).  Shnider and Webster(14) reviewed the records of about 150 women who received anesthesia for surgery during pregnancy:  47 during the first trimester, 58 during the second, and 42 during the third.  They compared these women to 8,926 women who delivered during this period.  There was no statistical difference in these two groups.  These investigators also reviewed the statistics from 61,000 patients who participated in the National Collaborative Study.  They found that the "incidence of birth defects in women who had not undergone surgery during pregnancy (60,000 women) was 5.02% compared with 6% in the 50 women undergoing appendectomy, a statistically insignificant difference."

     Brodsky et al(15) reported the occurrence of deformities in the fetuses of women having general anesthesia for surgery during pregnancy.  These authors surveyed 187 women having surgery and anesthesia during the first trimester and 100 women having surgery during the second trimester.  The control group consisted of 8,654 women who had neither surgery during pregnancy or occupational exposure to waste anesthetic gases.  No association could be found between surgery during early pregnancy and congenital anomalies in live-born offspring.  An increase in the incidence of spontaneous abortions did occur.  In the first trimester the incidence of miscarriage was 8% in anesthetized women and 5.1% in control women.  In the second trimester, the incidences were 6.5% for women having had anesthesia and surgery and 1.4% for women in the control group.

     Duncan et al(25) reviewed the incidence of congenital anomalies and spontaneous abortions in 2,565 women who had surgery during gestation.  These women were matched to a similar number of control pregnancies by maternal age and area of residence.  There was no significant difference in the rate of congenital anomalies between study and control groups.  There was a significant increase (2.0 times) in spontaneous abortions in women undergoing surgery in the first or second trimesters.

     A conclusion from the above data seems to be that there is no increase in anomalies, but a possible increase in the risk of abortions.  It is important to realize that the number of women receiving an anesthetic during their pregnancy is in fact too small to state absolutely that anesthetics are not teratogenic.

Maternal and Fetal Trauma during Pregnancy

Motor Vehicle Accidents

     Road traffic accidents are the leading cause of hospitalized trauma during pregnancy.  Maternal injury puts the fetus at great risk, yet little is known about the incidence, risks, and characteristics of pregnant women.  Recent reports suggest that about 8% of all pregnancies are exposed to hospital treated injury, but the incidence of motor vehicle trauma is not known(28).  Restraint systems, such as air bags and seat belts effectively reduce the risk of serious injuries to car occupants.  However, this equipment may have adverse effects on pregnant women.  Various intra-abdominal and chest injuries have been reported to result from improper use of seat belts(29).  In a frontal air bag deployment the cushion expands with a speed of about 200 km/h towards the driver.  A person within the expansion zone, that is to say within 20 cm from the steering wheel hub, may experience a considerable injury risk.  Short people, pregnant women or people out of normal position are especially at risk.  The air bag gases may provoke an asthmatic attack in sensitive individuals and a few will experience a hearing loss.  Pre-hospital concerns, such as the care and transport between the accident site and hospital may contribute markedly to the safety of the mother and her fetus.

Pelvic Fractures in Pregnancy

     Pelvic and acetabular fractures during pregnancy were associated with a high maternal (9%) and a higher fetal (35%) mortality rate.  Automobile-pedestrian collisions had a trend toward a higher maternal mortality rate, and vehicular collisions had a trend toward a higher fetal mortality rate compared with falls.  Injury severity influenced both maternal and fetal outcomes.  Fracture classification (simple vs. complex), fracture type (acetabular vs. pelvic), or the trimester of pregnancy, did not influence mortality rates(32).

Other Trauma

     Intimate partner violence (IPV), is a common trauma related risk and pregnant women are no exception.  In fact it appears to be more common during pregnancy.  A careful history taking during antenatal visits or in the Emergency Department together with the use of the Abuse Assessment Screen will help to elucidate these cases.  The majority are unsupported mothers, young, single or without a family.  Firearm injury in pregnant women is reported in the literature; however no forensic analysis of the wound sustained by the fetus is available(30).  Often the fetus fares worse than the mother in these instances.  Self-inflicted injuries among women in advanced pregnancy are uncommon.  Attempted suicides or criminal abortions are usually reported in the first or less commonly in the second trimesters(31,32).

The Injury Severity Score

     The Injury Severity Score (ISS) is the standard for injury severity assessment in the general population, but has been rarely validated in pregnant women. Recent investigations found that the ISS was not accurate in predicting placental abruption and fetal death.  Moreover, relatively minor injuries were associated with adverse pregnancy outcomes.  There is a need to evolve a new assessment tool that can accurately predict adverse outcomes in the pregnant trauma population(33).  Ultrasonography is probably the most valuable tool in initial assessment of the injured abdomen.

Diagnostic Peritoneal Lavage and other Assessment Methods used in 
Traumatized Pregnant Women

     Diagnostic peritoneal lavage (DPL) continues to be a safe and reliable method for the assessment of the intra-abdominal bleeding and injuries due to road traffic accidents(34-37).  The only absolute contraindication to the procedure is an existing indication for laparotomy.  Computed tomography (CT) is useful in selected patients, and is a critical test for guiding non-operative management of known intraperitoneal and real trauma.  Routine ancillary tests for potentially occult injuries include nasogastric tube placement for ruptures of the left diaphragm, Gastrographin contrast study for duodenum perforations, and pyelography for ureteral injury.  Ultimately, the most important principle in the management of abdominal injuries during pregnancy is a repeat physical examination and evaluation by a multi-disciplinary team consisting of surgeon, gynecologist and anesthetist.

Assessment of Fetal Well-being

     Fetal heart rate monitoring during surgery and the perioperative period may be helpful in detecting fetal hypoxia.  For example, during surgery to repair a detached retina in a pregnant woman in her third trimester, Liu et al(34) observed a significant change in fetal heart rate and rhythm during a period of inadvertent maternal hypoxemia, a time during which there were only minimal alterations in maternal vital signs.  In a case reported by Mahli et al(35), fetal distress was detected during maternal mitral valvoplasty and was corrected by increasing the rate of blood flow through the extracorporeal pump used for cardiopulmonary bypass.  Most experts now recommend that continuous fetal heart rate monitoring be used when maternal surgery is done after the 16th week of gestation(36).

Perinatal Mortality and Prevention of Preterm Labor

There is concern frequently that surgical intervention during pregnancy may provoke abortion or premature labor.  However, the urgency and severity of surgical disease appears to be more important in determining pregnancy outcome than is the use of anesthesia or surgery(14).

It has been stated that anesthesia and surgery during gestation may produce the onset of preterm labour during the postoperative period(36,37).  Intra-abdominal procedures in which manipulation of the uterus or uterine retraction occurred, frequently resulted in preterm labor.  Ovarian cystectomy, especially in the first trimester, has a high incidence of abortion.  However, in many surgical procedures on the ovary, pregnancies have gone to term.  Neurosurgical, orthopaedic, thoracic, or plastic surgery procedures were not associated with preterm labor.  In a review of the 147 pregnant patients undergoing surgery, Shnider and Webster(14) reported that 8.8% of patients went into labor shortly after surgery.  Gianopoulos' survey(13) showed 40% of patients went into preterm labor postoperatively.  Therefore, it is apparent that preoperative pathology plays a prominent role in cases of preterm labor.

Again, the severity of surgical disease appears to be more important in determining pregnancy outcome than is the use of anesthesia or surgery.  If a delay in surgery increases the risk of maternal hypotension, hypoxia, or sepsis, such a delay can be expected to worsen the prognosis for both the woman and the fetus.  Therefore, when clinical evidence suggests the need for an urgent or emergent operation in a pregnant patient, the pregnancy should not affect the decision to proceed.

Anesthetic agents such as halothane, enflurane, and isoflurane decrease uterine tone and inhibit uterine contractions.  On this basis, it has been recommended that these drugs be used during advanced pregnancy when uterine manipulation is anticipated.  In no study has any anesthetic agent or technique been closely linked with a high or low incidence of preterm delivery.

There are anesthetic agents, such as ketamine in doses greater than 1.1 mg/kg, and some vasopressors that do increase uterine tone and should probably be avoided when possible(37).  Rapid intravenous injection of anticholinesterase agents, such as neostigmine or edrophonium, may directly stimulate acetylcholine release and theoretically could increase uterine tone and stimulate preterm labor.  Neostigmine, when used to reverse the effects of muscle relaxants, should be administered slowly and be preceded by adequate doses of atropine.

Nonetheless, many obstetricians believe that the risk of premature labor after abdominal surgery is sufficient to warrant the use of prophylactic ritodrine hydrochloride, although there are no prospective data confirming the usefulness of this approach.  This  ²-adrenergic agonist, which has a direct relaxant effect on the smooth muscle of the uterus, has been shown to effectively inhibit premature labor, prolong gestation, and improve neonatal outcome.(38)  Adverse effects include tremor, palpitations, restlessness, tachycardia, widening of the pulse pressure, moderate decreases in serum potassium level, and elevations of blood glucose.  Also, pulmonary edema has been reported to occur in pregnant patients receiving ritodrine, glucocorticoids, and parenteral fluids(38).

For these reasons ritodrine is contraindicated in women with hypertension, cardiovascular disease, or hyperthyroidism.  Progesterone has also been administered to pregnant patients undergoing non-obstetric surgery in an attempt to prevent premature labor.  However, there are few data to support the efficacy of such a practice.  Finally, it is advisable to monitor uterine activity immediately after surgery, as early detection of premature labor will enhance the opportunity for successful intervention.

Recommendations for Anesthetic Management

In general, physicians agree that only emergency surgery should be performed during pregnancy.  Based on the aforementioned descriptions of maternal and fetal hazards, a rational approach to anesthesia is always indicated.  It is essential that women of childbearing age scheduled for surgery should always be carefully queried regarding the possibility of pregnancy.

Apprehension should be allayed as much as possible by personal reassurance and empathy from the anesthesiologist during the pre-anesthetic visit, and also by adequate premedication if it is indicated.  Barbiturates should be prescribed in preference to benzodiazepines; belladonna alkaloids may also be used, and it must be remembered that glycopyrrolate, unlike atropine and scopolamine, does not cross the placenta.

Pain should be relieved whenever present.  Avoid aspirin or acetylsalicylic acid since it may stimulate in utero closure of the ductus arteriosus by inhibiting prostaglandin synthesis.  Regional blocks can be very beneficial in this respect if performed by an anesthesiologist in the emergency room.  During pregnancy, patients may be at an increased risk of aspiration and the usual safeguards to prevent aspiration pneumonitis should be performed. Administration of a clear antacid, 15 to 30 mL, within an hour prior to induction of general anesthesia will usually raise the pH of the gastric juices above the critical level.  These clear antacids seem to be better tolerated if aspirated.

Beginning in the second trimester, mothers should not be transported or placed on the operating table in the supine position.  The lateral decubitus position or left uterine displacement will minimize the risk of aortocaval compression.

Emergency surgical operations that cannot be delayed without increasing maternal morbidity or mortality are very often necessary in the first trimester.  These are ideally performed under regional blockade if the contemplated surgery and maternal condition allow for it.  Teratogenicity of local anesthetics in animals or humans has not been reported.  It must be remembered that with spinal anesthesia there is much less fetal exposure to local anesthetic than with other regional blocks.  Hypotension related to spinal or epidural anesthesia should be prevented as much as possible by the rapid intravenous infusion of at least one litre of crystalloid solution prior to induction.  If maternal blood pressure falls more than 15% to 20% despite this pre-treatment, a predominantly  ²-adrenergic vasopressor such as ephedrine should be promptly administered intravenously.

General anesthesia should be preceded by careful denitrogenation to avoid maternal and fetal hypoxemia during induction and intubation.  There is no proof that any well-conducted technique is superior to any other.  If nitrous oxide is selected as an inhalational agent, consideration might be given to pretreating with folinic acid.  Again, adequate oxygenation and avoidance of hyperventilation are mandatory.  The risk of aspiration must be minimized by application of cricoid pressure and rapid endotracheal intubation with a cuffed tube.

To reduce fetal hazards, particularly during the first trimester, it appears preferable to choose drugs with a long history of safety.  These include thiopental, morphine, meperidine, succinylcholine and low concentrations of nitrous oxide.  However, ketamine 0.5 to 0.75 mg/kg might be preferable to thiopental as an induction agent in the face of severe hypovolemia.  In these low doses, ketamine should have a minimal effect on uterine tone, particularly in late pregnancy.  Halothane or enflurane may offer a specific advantage of relaxing the uterus during procedures involving the pelvic organs, particularly the uterus itself.  In order to avoid maternal hyperventilation one should monitor arterial blood gases and end expiratory PCO2.

It is advisable to continuously monitor the fetal heart throughout surgery and anesthesia, providing that placement of the transducer does not encroach upon the surgical field.  Continuous fetal heart rate monitoring should be employed for any surgery after the 16th week of gestation.  This monitoring becomes technically feasible if a directional Doppler apparatus is used and may provide an indication of abnormalities in maternal ventilation as well as uterine perfusion.

Uterine activity should be monitored continuously with an external tocodynamometer if the uterus has grown enough to reach the umbilicus or above.  Uterine activity should also be monitored continuously during the postoperative period to detect the onset of preterm labour.  Tocolytic therapy instituted early may prevent preterm delivery.  More importantly, left uterine displacement should be maintained postoperatively to reduce or prevent aortocaval compression.

Special procedures such as hypothermia, induced hypotension or even the use of cardiopulmonary bypass might be needed to facilitate surgery despite potential fetal hazards.  It is reassuring to know that successful fetal outcome has been reported following use of these procedures.

References

1.  Moll W.  Physiological cardiovascular adaptation in pregnancy - its significance for cardiac diseases.  Z Kardiol, 2001;Suppl 4:2-9.

2.  O Day MP.  Cardio-respiratory physiological adaptation of pregnancy.  Semin Perinatol 1997;21:268-75.

3.  Campbell DC.  Physiological changes of pregnancy.  Semin Anesth Perioperative Medicine and Pain 2000;19:149-56.

4.  Bumm R, Feussner H, Holscher AH, et al.  Interaction of gastroesophageal reflux and esophageal motility.  Evaluation by ambulatory 24-hour manometry and pH-metry. Dig Dis Sci 1992;37:1192-9.

5.  Schneck Hajo, Scheller Michaela.  Acid aspiration prophylaxis and caesarean section.  Curr Opin Anaesthesiology 2000;13:261-65.

6.  Davidson JM.  Renal disorders in pregnancy.  Curr Opin Obstet Gynecol 2001;13:109-14.

7.  Russell JA, Douglas AJ, Ingram CD.  Brain preparations for maternity-adaptive changes in behavioral and neuroendocrine systems during pregnancy and lactation.  An overview.  Prog Brain Res 2001,133:1-38.

8.  Orebaugh SL.  Succinylcholine:  adverse effects and alternatives in emergency medicine.  Am J Emerg Med 1999;17:715-21.

9.  Shepard TH, Lemire RJ.  Teratology, in Quilligan EJ, Kretchner N, (eds): Foetal and Maternal Medicine.  New York, John Wiley and Sons, 1980, pp 403-417.

10. Haas DA, Pynn BR, Sands TD.  Drug use for the pregnant or lactating patient.  Gen Dent 2000;48:54-60.

11. Stanway G.  Potential hazards of trace inhalation of anaesthetic gases:  a risk assessment.  SAAD Dig 2002;19:14-9.

12. Goodman S.  Anesthesia for nonobstetric surgery in the pregnant patient.  Semin Perinatol 2002;26:136-45.

13. Gianopoulos JG.  Establishing the criteria for anesthesia and other precautions for surgery during pregnancy.  Surg Clin North Am 1995;75:33-45.

14. Shnider SM, Webster GM:  Maternal and fetal hazards of surgery during pregnancy.  Am J Obstet Gynecol 1965;92:891-900.

15. Brodsky JB, Cohen EN, Brown BW, et al.  Surgery during pregnancy and fetal outcome.  Am J Obstet Gynecol 1980;138:1165-7

16. Moya F, Smith B.  Uptake, distribution and placental transport of drugs and anaesthetics.  Anesthesiology 1965;26:465-76.

17. Tsen LC, Tarshis J, Denson DD, et al.  Measurements of maternal protein binding of bupivacaine throughout pregnancy.  Anesth Analg 1999;89:965-8.

18. Niruthisard S, Somboonviboon W, Thaithumyanon P, et al.  Maternal and neonatal effects of single-dose epidural anesthesia with lignocaine and morphine for cesarean delivery.  J Med Assoc Thai 1998;81:103-9.

19. Dounas M, O'Kelly BO, Jamali S, et al.  Maternal and fetal effects of adrenaline with bupivacaine (0.25%) for epidural analgesia during labour.  Eur J Anaesthesiol 1996;13:594-8.

20. Nunn JF, Chanarin I.  Nitrous oxide inactivates methionine synthetase, in  Eger EI, (ed): Nitrous oxide/N2O.  New York, Elsevier, 1985, pp 211-233.

21. Christensen B, Guttormsen AB, Schneede J, et al.  Preoperative methionine loading enhances restoration of the cobalamin-dependent enzyme methionine synthase after nitrous oxide anesthesia.  Anesthesiology 1994;80:1046-56.

22. Kaufman MH, Chang HH.  Influence of anaesthetic agent on limb abnormalities observed following amniotic sac puncture.  Eur J Morphol 1998;36:217-26.

23. Crawford JS, Lewis M.  Nitrous oxide in early human pregnancy.  Anaesthesia 1986;41:900-5.

24. Kissin I, Morgan PL, Smith LR.  Anesthetic potencies of isoflurane, halothane, and diethyl ether for various end points of anesthesia.  Anesthesiology 1983;58:88-92.

25. Duncan PG, Pope WD, Cohen MM, et al.  The safety of anesthesia and surgery during pregnancy.  Anesthesiology 1986;64:790-4.

26. Weiss HB, Strotmeyer S.  Characteristics of pregnant women in motor vehicle crashes.  Inj Prev 2002;8:207-10.

27. Bjornstig U, Haraldsson PO, Polland W, et al.  Awareness of the risk of air bag associated injuries essential.  Lakartidningen 2002;99:28-9;3022-6.

28. Leggon RE, Wood GC, Indeck MC.  Pelvic fractures in pregnancy:  factors influencing maternal and fetal outcomes.  J Trauma 2002;53:796-804.

29. Catanese CA, Gilmor K.  Fetal gunshot wound characteristics.  J Forensic Sci 2002;47:1067-9.

30. Osuna E, Toucedo MA, Sanchez-Espigares G, et al.  A case of self- inflicted wounding by the introduction of needles through the abdominal wall to induce abortion.  Forensic Sci Int, 2002;128:141-5.

31. Anderson BA, Marshak HH, Hebbeler DL.  Identifying intimate partner violence at entry to prenatal care:  clustering routine clinical information.  J Midwifery Womens Health 2002;47:353-9.

32. Schiff MA, Holt VL.  The injury severity score in pregnant trauma patients:  predicting placental abruption and fetal death.  J Trauma 2002;53:946-9.

33. Liu PL, Warren TM, Ostheimer GW, et al.  Foetal monitoring in parturients undergoing surgery unrelated to pregnancy.  Can Anaesth Soc J 1985:525-32.

34. Mahli A, Izdes S, Coskun D.  Cardiac operations during pregnancy: review of factors influencing fetal outcome.  Ann Thorac Surg 2000;69:1622-6.

35. Levinson G, Shnider SM.  Anaesthesia for surgery during pregnancy, in  Shnider SM, Levinson G, (eds): Anaesthesia for Obstetrics (ed 4). Baltimore, Williams and Wilkins, 1997, pp 188-205.

36. Stone K.  Acute abdominal emergencies associated with pregnancy.  Clin Obstet Gynecol 2002;45:553-61.

37. Eryilmaz R, Sahin M, Bas G, et al.  Acute appendicitis during pregnancy.  Dig Surg 2002;19:40-4.

38. Caughey AB, Parer JT.  Tocolysis with beta-adrenergic receptor agonists.  Semin Perinatol 2001;25:248-55.