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Linezolid

By U. Sobota. Grace College. 2019.

No increase in adverse maternal or fetal effects discount linezolid 600mg without a prescription, includ- ing no significant differences in birth weight discount linezolid generic, were reported in 120 women treated with atenolol or placebo during pregnancy (Rubin et al generic linezolid 600mg line. Similarly, no adverse fetal effects or pregnancy outcomes associated with metoprolol or metprolol/hydralazine treat- ment in second and third trimesters of pregnancy were noted (Sundstrom, 1978). Breastfeeding is allowed during maternal therapy with either metoprolol or atenolol (American Academy of Pediatrics, 1994), despite a case report of toxicity in a neonate whose mother was receiving atenolol while breastfeeding (Schmimmel et al. Neonatal hemodynamic adaptation failure occurred in five of 11 infants whose mothers were treated with aceb- utolol during pregnancy (Yassen et al. It seems unlikely that this drug is associ- ated with an increased risk of congenital anomalies. Among 51 women with pregnancy-induced hypertension randomized to Antihypertensives 61 hydralazine, hydralazine and propranolol, or hydralazine and pindolol, pindolol was associated with fewer maternal and fetal side effects (Paran et al. However, infants born to mothers who received propranolol had smaller birth weights. In a com- parative study of atenolol or pindolol on uterine/fetal hemodynamics and fetal cardiac function, investigators found that pindolol was preferable to atenolol for the treatment of pregnancy-induced hypertension based upon maternal and fetal cardiovascular func- tion (Rasanen and Jouppila, 1995). No increase in congenital malformations was noted in the offspring of pregnant mice who received up to 150 mg/kg. Also, no increase in the frequency of malformations was found among the offspring of rats, rabbits, and hamsters that had received nadolol in doses several times higher than the usual human dose (Sibley et al. No increased frequency of adverse fetal effects was found in the offspring of mice treated with penbutolol (Sugisaki et al. No epidemiologic studies of the frequency of congenital anomalies and cloni- dine use during early pregnancy have been published. Anecdotal case reports of clonidine use during pregnancy suggest no adverse fetal effects (Horvath et al. Head size and neurologic examination of 22 children whose mothers received clonidine during pregnancy were normal (Huisjes et al. One rat teratology study found no increased frequency of birth defects (Angelova et al. Clonidine is probably not associated with an increased risk of congenital anomalies when used therapeutically. An oral form of this drug (Proglycem) is also used to treat hypoglycemia secondary to hyperinsulin- ism. An anecdotal case report of abnormalities of body and scalp hair, including alopecia, in four neonates of women who received oral diazoxide during the last trimester of pregnancy has been published (Milner and Chonskey, 1972). Maternal diazoxide therapy was also reportedly associated with hyperglycemia in the neonate (Milsap and Auld, 1980). Pancreatic islet cell damage was found in the offspring of sheep and goats treated with intravenous diazoxide (Boulos et al. It is also used to induce hypotension during certain types of 62 Cardiovascular drugs during pregnancy Box 3. No epidemiological studies of congenital anomalies in association with nitroprusside use during pregnancy have been published. Nitroprusside was reported to be associated with cyanide toxicity in animals (Lewis et al. Nonetheless, it is prudent to avoid use of nitroprusside during pregnancy because of the theoretical accumulation of cyanide in the fetal liver. Chronic use of sodium nitroprus- side is logically associated with a much higher risk than acute usage. Three basic categories of diuretics are: (1) loop diuretics; (2) potassium-sparing diuretics; and (3) thiazide diuretics. Loop diuretics Loop diuretics act primarily by inhibiting sodium and water reabsorption by the loop of Henle. No increase in malformations was found in offspring of animals receiving several times the usual adult human dose of bumetanide (McClain and Dammers, 1981). Diuretics given after the first trimester of pregnancy may inter- fere with normal plasma volume expansion. An adverse effect on plasma volume, no improvement in perinatal outcome (Sibai et al. Furosemide also displaces bilirubin from albumin, increasing the risk for fetal hyper- bilirubinemia (Turmen et al. In animal studies, furosemide exposure in preg- nancy was associated with an increase in fetal loss and skeletal anomalies in offspring (Godde and Grote, 1975; Mallie et al. Furosemide crosses the placenta and assists in assessing fetal urinary tract obstruction and fetal urine production (Barrett et al. Potassium-sparing diuretics Potassium-sparing diuretics include amiloride, spironolactone, and triamterene, and result in sodium and water loss while sparing potassium. Spironolactone is a competi- tive inhibitor of aldosterone, while ameloride and triamterene function at the level of the collecting tubules. No increase in malformations in offspring of pregnant hamsters that received small doses of ameloride was found (Storch and Layton, 1973). Spironolactone was not associated with an increased frequency of malforma- tions in offspring of rats (Miyakubo et al. This diuretic is not recommended for use dur- ing human pregnancy because of the theoretical risk of feminization of male genitalia. Spironolactone for the treat- ment of pregnant women with Bartter’s disease (Groves and Corenblum, 1995; Rigo et al. None of the three male infants or two female infants had any demonstrable adverse effects, including undervirilization of the male infant. Of 271 pregnant women included in the Collaborative Perinatal Project who were treated with this diuretic (Heinonen et al. The frequency of congenital malformations was not increased in the offspring of these women; neither was the frequency of malformations increased in the offspring of animals who received triamterene (Ellison and Maren, 1972). Thiazides function by pre- venting reabsorption of sodium at the distal renal tubules. No increase in frequency of congenital anomalies in the offspring of over 500 women who took thiazide diuretics in the first trimester of pregnancy was noted (Kraus et al. In a study of diuretics to prevent preeclampsia, no increase in the frequency of malformations or stillbirths was found in the offspring of over 1000 women who received this diuretic after the first trimester. No increased fre- quency of congenital anomalies was found among offspring of rats given hundreds of times the usual human dose (Stevens et al. The frequency of congenital anomalies was not increased over the expected rate reported among offspring of 63 women who took this diuretic in early pregnancy and of over 5000 women who took this drug after the first trimester of pregnancy (Heinonen et al. Neonatal thrombocytopenia was reported in the offspring of several mothers who received chlorothiazide during pregnancy (Rodriguez et al. An increased frequency of hyper- tension was reported in the offspring of rats treated with chlorothiazide at doses 30 times those employed in humans (Grollman and Grollman, 1962). No increase in mal- formations in offspring of rats treated with this agent in doses up to 12 times that used in humans was found by another group of investigators (Maren and Ellison, 1972). Birth defects were not increased in frequency among offspring of more than 200 women who received this diuretic in early pregnancy (Heinonen et al.

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It has been estimated that 2 there are 600 cases of Wilson’s disease in the United entity that now bears his name purchase cheapest linezolid. Many other individuals 14 have embellished and expanded our understanding of States and that 1% of the population are carriers buy generic linezolid 600mg online. Kayser in 1902 and Fleischer in 1903 5 and 1912 described the rings of corneal pigmentation that are characteristic of Wilson’s disease buy linezolid. The number 7 8 of specific mutations that have been identified is now Mandelbrote et al and Cumings in 1948 that the 20 disturbance of copper metabolism in Wilson’s disease approaching 300. Ceruloplasmin deficiency in most frequent, deletions, insertions, nonsense, and splice 21 Wilson’s disease was documented independently by site mutations all occur. Most affected individuals are 9 10 actually compound heterozygotes, having inherited dif- Scheinberg and Gitlin and by Bearn and Kunkel in 1952, and the presence of impaired biliary excretion of ferent mutations from each parent. The large number of 11 mutations has made commercial genetic testing for copper by Frommer in 1974. Recent years have brought dramatic advances in both the characterization Wilson’s disease impractical. Copyright # 2007 by Thieme Address for correspondence and reprint requests: Ronald F. As many as and clinical presentation, which suggests that additional 5 to 15% of individuals with Wilson’s disease may have factors are also operative. For example, recent reports normal or slightly reduced ceruloplasmin, whereas 10 to propose that methionine homozygosity at codon 129 of 20% of heterozygotes who are clinically asymptomatic 13,14,33 the prion-related protein gene may influence the onset of have reduced ceruloplasmin. Although the fundamental pathogenetic defect of Wil- However, the development of depression and parkinson- son’s disease lies within the hepatobiliary system, the ism, recently described in three elderly sisters who were consequences of the relentless copper accumulation are found to be heterozygotes for a nucleotide deletion at the played out on a multisystemic battlefield. To cope with this, elegant systems In 40 to 50% of individuals with Wilson’s disease, have evolved that bind the copper molecule to ensure hepatic dysfunction is the initial clinical manifesta- 14,34 safe transport of necessary copper to intended sites and tion. The average age of onset for those who present 35 safe elimination of excess copper through the biliary with hepatic symptoms is 11. Hepatic presentation beyond age 40 years is the incorporation of six copper molecules into apocer- also unusual; however, in a report from one center, 17% 29 uloplasmin, forming ceruloplasmin. In the liver and spleen may occur, sometimes with elevation individuals with Wilson’s disease, mutation in the of liver enzymes. Although this may be mistaken for progressively accumulates within the hepatocytes. Not viral hepatitis by the unwary, the presence of hemolytic only does this progressive copper accumulation ulti- anemia in conjunction with the hepatic dysfunction, or mately compromise hepatic function, the hepatic stor- elevation of unconjugated (indirect) bilirubin, should 14 age capacity is also eventually exceeded and unbound alert the clinician to the possibility of Wilson’s disease. As the excess copper escapes from the that ceruloplasmin, as an acute-phase reactant, may rise 14,39 liver, urinary copper excretion rises dramatically, but transiently into the low normal range. Wilson’s is unable to compensate fully for the defect in biliary disease can also make its appearance as acute fulminant excretion. The mortality rate with mentioned in reviews of Wilson’s disease, autonomic this mode of presentation is alarmingly high; individuals dysfunction is noted by some investigators to be present 52,53 typically are younger than 30 years and two-thirds are in 26 to 30% of persons with the disease. A severe Coombs-negative hemolytic anemia, Seizures are an infrequent component of Wilson’s 54 presumably due to intravascular hemolysis triggered by disease, but may occur in up to 6% of patients. Partial the sudden release of massive amounts of copper into the seizures occur most frequently, and benign epilepsy of 42 bloodstream from the failing liver, is often present. Wilson’s disease, however, is the development of pro- Headache or seizure may occur in the setting of Wilson’s gressive cirrhosis. The cirrhosis has no Wilson’s disease– disease and may be the initial neurological symptom in 13 specific features. Neither upper motor presentation that Wilson’s disease can assume, any in- neuron nor lower motor neuron dysfunction is typically dividual younger than age 50 years with unexplained present in Wilson’s disease. However, peripheral sensor- 14 liver disease should be screened for Wilson’s disease. Olfactory impair- Neurological Manifestations ment has recently been reported in persons with Wil- 58 Neurological dysfunction constitutes the initial clinical son’s disease who have neurological dysfunction. The manifestation in 40–60% of individuals with Wilson’s severity of the olfactory deficit parallels the severity of 14,34 disease. Tremor, which may be resting, postural, or ki- Psychiatric Manifestations netic, is the most frequent initial neurological feature of The frequency with which Wilson’s disease makes its Wilson’s disease. Proximal upper extremity tremor may clinical appearance in the form of psychiatric dysfunction take on a coarse, ‘‘wing-beating’’ appearance, but Wil- is unsettled. Although most reports indicate a frequency son’s disease tremor may also be distal and quite small in in the range of 20%, some investigators have noted that amplitude. The many psychiatric features were evident at the time of initial guises that Wilson’s disease tremor may assume make it presentation in 65% of individuals with Wilson’s disease, important to consider and exclude the possibility of and that these symptoms had been sufficiently severe to Wilson’s disease in any individual, but especially young warrant psychiatric intervention in almost 50% before 59 persons, with tremor. Psychiatric Dysarthria is also common in persons with Wil- symptoms appear at some point in time in most indi- son’s disease and may possess either an extrapyramidal or viduals with Wilson’s disease, and most frequently in 45 a cerebellar character. A peculiar ‘‘whispering dysphonia’’ has been disturbances of mood, particularly depression, are the 46 60 described in Wilson’s disease, as has a laugh in which most frequent behavioral features of Wilson’s disease. Depression may be severe, and in one study almost 16% 61 A variety of other neurological features may of patients had a history of suicide attempts. Anti- velops in 25% of individuals with neurological Wil- social or criminal behavior has been reported in Wilson’s 48 63 son’s disease. Dystonia may be present in almost disease, as has sexual preoccupation and disinhibi- 49 13,59 40%. Never- oclonus are unusual, although severe generalized myo- theless, cognitive difficulties including impairment of clonus associated with extensive white matter lesions has frontal-executive ability, visuospatial processing, and 50 64 recently been described. A range legs and moving toes syndrome has also been reported in of abnormalities on formal neuropsychological testing 51 65 a person with Wilson’s disease. They which the psychiatric features of Wilson’s disease can consist of copper deposition in the lens that assumes a present, Wilson’s disease should be considered and sunburst or sunflower appearance, with a central disc and 68,75 excluded in any young person who develops unexplained radiating petal-like spokes. Poor school performance, especially if coupled with abdominal symp- Other Manifestations toms, should prompt consideration of Wilson’s dis- Bone and joint involvement are under-recognized com- 66 ease. Radiographic evidence of be considered in young persons suspected of drug abuse, osteoporosis is present in up to 88% of persons with 14,67 76,77 because the symptoms can be similar. Joint involvement, especially at the knees, is also com- mon and joint pain may be the presenting symptom of 77 Ophthalmological Manifestations Wilson’s disease. Radiological evidence of vertebral 3 4 The description by Kayser and Fleischer of pigmented column abnormalities is evident in 20 to 33% of indi- 76,78 corneal rings antedated Wilson’s description of Wilson’s viduals with Wilson’s disease. Kayser-Fleischer rings are formed by dep- initial manifestation of Wilson’s disease in 10 to 15% of 79–81 osition of copper within Descemet’s membrane. In the setting of fulminant hepatic failure, the copper is actually deposited throughout the cornea in presence of concomitant hemolytic anemia may be an 14 Wilson’s disease, but it is only in Descemet’s membrane important diagnostic clue for Wilson’s disease. A recent almost always bilateral, but unilateral formation has been report describes a patient with thrombocytopenia and 70 reported. The color of the rings can range from gold to the combination of Wilson’s disease and antiphospholi- 83 brown to green; consequently, they can be difficult to see pid antibody syndrome. Ring formation first Renal involvement may also occur in Wilson’s becomes visible in the superior aspect of the cornea, disease.

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Effect of bronchial asthma on the course of pregnancy order 600mg linezolid, labour and perinatal outcome cheap linezolid amex. Many surgeons are reluctant to perform operative procedures on women known to be pregnant generic linezolid 600 mg mastercard, although emergency procedures are sometimes necessary. In addition, elective or indicated procedures may be carried out on women with an unrecognized pregnancy. General principles that the clinician should be aware of when surgery is anticipated in a pregnant woman are based on physiologic differences between the pregnant and non- pregnant state (Box 6. Virtually all anesthetic agents and 98 percent of medications cross the pla- centa, exposing the fetus to medically significant levels. Even a minimal degree of hypotension and hypoxia is to be avoided because this may result in placental hypoperfusion and fetal hypoxemia. Pregnant women being prepared for surgery should be placed on their left side, adequately hydrated, and preoxygenated prior to induction of anesthesia. Pharmacokinetics of anesthetic agents have been reported for only pancuronium, and its disposition was a pregnancy-associated decreased half-life, and this was probably due to significantly increased clearance (Little, 1999). Increased blood volume is caused by a plasma volume increase of approximately 1000 cc and a 300–500 cc increase in red cells. This usually results in lower hematocrit compared to the nonpregnant woman, and is commonly known as physiologic anemia of pregnancy. Accordingly, the glomerular filtration rate increases (as measured by the endogenous creatinine clear- ance) because of increased blood volume. Serum creatinine and blood urea nitrogen decrease because of dilution by increased plasma volume. Other changes in the renal sys- tem include dilatation of the ureters and a relative stasis of urine, resulting in a ‘relative’ hydronephrosis. The relative hydronephrosis is frequently more pronounced on the right than on the left side. Other cardiopulmonary changes that occur during pregnancy include a slight increase in heart rate, and decreased systolic and diastolic blood pressures in the second trimester. Respiratory rate increases slightly during pregnancy with a decrease in physiologic ‘dead space’ as pregnancy pro- gresses. Tidal volume is increased during pregnancy, but minute ventilation and compli- ance do not change during pregnancy. Gastrointestinal system changes with pregnancy affect pregnant women that require anesthesia and/or surgery. The risk for aspiration pneumonitis in surgery on the gravid patient is increased because of pregnancy-associated decreases in intestinal motility and gastric emptying. This has implications for anesthesia dose man- agement of the pregnant patient; lower doses than in the nongravid patient may achieve the desired anesthetic effect. Serum levels as high as 400 mg percent are not unusual during the third trimester and cause increased red cell sedimentation rate in pregnant women. Hematocrit is decreased during pregnancy accompanied by a relative leukocytosis (white blood cell count greater than or equal to 10 000–12 000 or even higher during labor). Several hema- tologic measures are unchanged during pregnancy: for example, the relative percent of immature forms (i. Whole blood clotting time, prothrombin time, and partial thromboplastin time remain in normal ranges during pregnancy. Surgery should be performed without delay when it is indicated for life-threatening maternal conditions. Indicated laboratory tests and radiologic procedures should be per- formed without hesitation to properly guide life-saving surgical procedures. Anesthetic adjuncts, or other ‘nonanesthetic’ drugs and medications during the pre-, intra-, and post-operative peri- ods may also adversely affect the fetus. Regional techniques (spinal and epidural procedures, paracervical and pudendal blocks) result in physiologically important fetal exposure to clinically significant anesthetic levels. Anesthetic potency is related to protein-bound fraction, and the amount of binding determines the duration of action. Highly protein bound anesthet- ics are lipid soluble and readily cross the placenta (Morishima et al. Malformations were not increased in frequency among offspring of women who used procaine, lidocaine, benzocaine, or tetracaine during the first trimester, and there were no adverse fetal effects when these agents were utilized at any time dur- ing pregnancy (Heinonen et al. No investigations of bupivacaine, chlorprocaine or prilocaine have been published with regard to their teratogenic effects. Transient newborn neurobehavioral changes in infants whose mothers received local anesthetic agents have been reported, and vary from mod- erate for regional blocks (Rosenblatt et al. Following first trimester exposure there was a significantly increased frequency of inguinal hernias in the epinephrine-exposed group (Heinonen et al. However, it is unlikely that 118 Anaesthetic agents and surgery during pregnancy epinephrine is a teratogen. Epinephrine is also used as a test agent to detect intravascu- lar injection of local anesthetics. It has been suggested that bradycardia is second- ary to vasoconstriction of uterine artery caused by the anesthetic agent (Fishburne et al. Thus paracervical blocking techniques are not recommended in the presence of fetal heart rate abnormalities or compromised uterine blood flow (Carlsson et al. The fetus will be exposed to a variety of agents that include narcotics, paralyzing agents, and inhalational anesthetic agents. Thiopental and ketamine Thiopental and ketamine are narcotic anesthetics, and are given intravenously for rapid induction of anesthesia prior to the intubation and initiation of inhalational anesthetic agents. The frequency of con- genital malformations was not increased in human or animal studies (Heinonen et al. Ketamine is rarely used in obstetrics, except for rapid anesthe- sia in emergency operative vaginal deliveries. Ketamine presents two problems: (1) clin- ically significant increase in blood pressure; and (2) significant maternal hallucinations. Perhaps 20 percent of patients have lowered cholinesterase activity, and pregnancy reduces cholinesterase activ- ity in general. Therefore, pregnant patients probably require a smaller dose of succinyl- choline than nongravid women. Newborns may be exposed to enough drug to experience neuromuscular blockade that requires supportive therapy. Other common agents used for neuromuscular blockade are vecuronium bromide, pancuronium bromide, and atracurium besylate (Box 6. Unlike succinylcholine, which is a depolarizing agent, these three neuromuscular blocking agents are nonpolarizing in action. However, according to its manufacturer, atracurium is potentially teratogenic in animals. Neither ether nor cyclopropane is commonly used in present-day anesthetic techniques, and there have been no adequate human studies regarding potential teratogenicity of either of these agents (Friedman, 1988). Halothane and other halogenated agents Halogenated agents are often used to supplement the standard nitrous oxide, thiopental and muscle relaxant regimens for balanced general anesthesia.

Rapport with the patient is important purchase genuine linezolid online, assuring confidentiality and establishing a basis for the patient’s trust buy linezolid 600mg with amex. The counselor must convey to the patient his or her under- standing of the patient’s concerns linezolid 600 mg discount, and explain that the purpose of the consultation is to deal directly with those concerns by ascertaining the magnitude of the risk for an adverse pregnancy outcome arising from the drug exposure. General principles of counseling Many patients are not satisfied with the counseling they receive for exposure to poten- tial teratogens during pregnancy. Dissatisfaction stems largely from two major issues that both cause patient anxiety. First, the physician is frequently unable to obtain ade- quate information to make meaningful statements regarding the medical risks of whether the pregnancy was adversely affected by the drug exposure. Second, most patients do not understand the difference between an embryo and a fetus. Consequently, patients may not be able to grasp the importance of the concept of ‘critical periods’ unless they have been given a proper briefing during the consultation. It is our policy to explain that there are two distinct phases involved in the growth of a baby, as shown in Fig. The first phase is the embryonic development, and it is dur- ing this period that the structure or architecture for the baby is laid down. Embryonic age should be differentiated from menstrual age, which is 2 weeks greater than embryonic age. Briefly, we explain to our patients that organs take shape and the body assumes the form it will have thereafter by day 58 postconception. All major structures, such as the heart, brain, liver, kidneys, and limbs, have formed by this time. Fetal development dur- ing the remainder of pregnancy, the second phase of development, is primarily devoted to the growth of these organs and structures, and to augmenting their function. It is through this heuristic approach to counseling that the patient understands that most congenital anomalies are caused by early exposures, often before the pregnancy was recognized. This component is included early in the consultation; patients then understand why certain questions are important and having such knowledge increases their cooperation and rapport. Preconceptional counseling Ideally, all counseling regarding drug or medication use during pregnancy should occur before conception, because the opportunity to prevent possible adverse effects is then optimal. Preconceptional counseling should include all the components of a consultation during the pregnancy, with one exception. Recommendations regarding medication or drug use during pregnancy will be prospective for a preventive purpose, and only med- ically indicated drugs and medications known to be safe will be recommended for con- tinued use while attempting to conceive. The concept of background risk for major congenital anom- alies should be explained in a manner tailored to the patient’s level of understanding. This concept is especially important because it conveys to the patient that, even if the drug exposure is harmless, no guarantee can be given that the fetus she carries will not have a congenital anomaly. Notwithstanding other risk factors, the risk for major con- genital anomalies is approximately 3. Other identified risks are generally considered to be additive to background risk. A usual component of counseling is the determination of exactly what drugs were taken, the dosage, the timing and duration of the exposure(s), the patient’s health history and present state of health. A thorough physical examination should be used to deter- mined the present state of health. No No further action although Yes ultrasound may reassure Confirm gestational age by ultrasound Drug taken Drug taken during critical outside of period of organogenesis embryogenesis Rule out Refer for Other possible targeted prenatal adverse fetal ultrasound and tests as effects advice indicated Counseling and evaluation of the drug-exposed pregnant patient 17 parents as well as the baby’s father’s parents, brothers and sisters, and nieces and nephews, should be constructed. The current state of health of all people in the pedigree should also be elicited. For those individuals in the pedigree who are no longer living, whether death was due to a birth defect or to a heritable disorder should be determined. It is also important to ask whether the patient’s family or the baby’s father’s family has any member who was mentally retarded, or has a chromosomal abnormality, Down syn- drome, congenital heart disease, spina bifida or another neural tube defect, or any other inherited disease. When such risk factors are discovered, it is important to explore these avenues further. It is desirable to refer the patient for a medical genetic consultation and evaluation when a risk increase above background is other than zero. The next step in the consultation is to determine whether or not the agent(s) has known teratogenic potential. This is the most difficult part of the evaluation because there is insufficient information to make such a determination for more than 60 percent of medications. The Effects of Neurologic and Psychiatric Drugs on the Fetus and Nursing Infant: A Handbook for Health Care Professionals. If it can be documented that the agent has no terato- genic risks or adverse fetal effects associated with its use during pregnancy, then no fur- ther action is required except to document this in the medical record and counsel the patient accordingly. Some patients may benefit from reassurance offered by high-resolu- tion ultrasound to confirm fetal well-being, and this procedure should be offered if the patient’s anxiety is not relieved through counseling. The limitations of diagnostic ultra- sound should also be included in the consultation. If the drug is known not to be safe for use during pregnancy, or if there are reasons to suspect that a drug with unknown risks is associated with congenital anomalies, then gestational age should be confirmed by ultrasound. It is of utmost importance to base the risk assessment and counseling upon embryonic age, not menstrual age. If the expo- sure occurred during embryogenesis, then it is necessary to undertake high-resolution ultrasound in an attempt to detect damage to specific organ systems or structures that were being formed during the time of the exposure. If the ultrasound scan is normal, then it is reasonable to reassure the patient of normal fetal structure within the limits of the sensitivity and specificity of ultrasound, which range from 40 to 90 percent for gross structural abnormalities when the procedure is performed by an experienced sonogra- pher. If the exposure occurred during the fetal period, it is likewise important to evalu- ate the possible fetal effects of the medication. If defects are detected, it is necessary to describe them in detail to the patient and to give a prognosis, as far as available medical knowledge will allow, regarding the out- come of pregnancy and postnatal development. To assist the patient in making a deci- sion on the disposition of the pregnancy, prognostication should include medically doc- umented risk figures. Ethically, pregnancy termination should not be a recommendation made to the patient and her family and significant others. This option should be dis- cussed, but the ultimate decision of whether to continue the pregnancy should be left to the patient and her family and significant others. The role of teratogen counseling is ulti- mately to provide the patient with as much information as possible and encourage her to make her own decision regarding whether to continue the pregnancy. Drug- or chemical-related causes of maternal complications, congenital anomalies, and fetal toxicity are almost unique among adverse pregnancy outcomes because they are potentially preventable, given the window of opportunity to do so. These problems are also exceptional among obstetric complications in that they are often the focus of malpractice litigation. Attorneys recognize that such adverse outcomes could have been prevented, and litigation ensues despite the fact that the window of opportunity to inter- vene prudently may not have existed for the physician and, more importantly, the drug exposure may not be teratogenic at any time during the pregnancy.

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