Clarkes analytical forensic toxicology, 2e pdf download attachment

Originally published as special issue of Contemporary Social Science. YALE H. JOHN L. IGR Publications, ISBN: paperback. TYSON, ed. Nova Science Publishers, Routledge, , pp, ISBN: hardcover ; paperback. PAUL I. LINSK, eds. Guilford, , pp, ISBN: hardcover ; paperback. Springer, , pp, ISBN: paperback. DALEY, eds. MEHTA, eds. TODD F. SAGE, , pp 6 vol. KUHAR, eds. READ, eds. David C. KELLY, eds. LISA M. HART, eds. MARY H. NEIL P. ANNE J. ESSAU, ed. Bill W. Jeremy P. FROST, eds. Academic Press, Norton, , pp.

McGraw-Hill, , pp. ALAN G. HUNT, eds. Springer, , pp, ISBN: paperback version of edition. KENNY, eds. Springer, , ISBN: paperback , reprint of original edition. Future Medicine Ltd. RILEY, eds. HUGH T. Published since by the Society for the Study of Addiction. Editor-in-Chief, Robert West. New Books on Addiction. Bottoms Up: Surrendering to God, Not to booze! Glass and Gavel: The U. Ganja Dictionary K. Fentanyl Inc. Challenging the U. Prohibition: A Concise History W.

Fetal demise was not reported in a limited 3-day follow-up. It has been questioned why women are using medical abortifacients when abortion is legal and accessible in many countries. The answer is thought to be the general movement away from traditional health care and toward herbal remedies [56]. The dangers to women are the toxic effects of the agent on themselves, teratogenic effects if the fetus is carried to term, and complications from delaying a physician-assisted abortion when the abortifacient fails.

Table 4 continued Agent Mistletoe — Phoradendron falvescens, P. Ripe fruit is nontoxic Thujone, tanacetin, boneol, camphor Herbaceous plant, quinazoline alkaloids vasicine and casicinone are most likely abortifacients.

If the pregnancy test is positive, the possibility of abortifacient usage should be addressed. Women who present with vaginal bleeding and pregnancy also should be questioned as to whether the vaginal bleeding was self-induced by an abortifacient. Acetaminophen is contained in many other over-thecounter preparations. As a result, the chance of acetaminophen toxicity is increased in a polydrug overdose. Human and animal studies have shown that acetaminophen crosses the placenta [59—61]. The fetus begins to have cytochrome P activity at approximately 14 weeks of gestation [62].

As with nonpregnant patients, Nacetylcysteine NAC is the prophylactic treatment for maternal acetaminophen overdose with possible hepatotoxicity. Pregnancy outcome is affected by time from ingestion until NAC administration. Spontaneous abortion was increased in pregnancies in which NAC was delayed in treating acetaminophen overdose [62]. One study in sheep showed that little NAC was able to penetrate the placenta [64]. However, NAC later was shown to cross the placenta in rats. IV NAC has been detected in the umbilical cord blood both in poisoned and nonpoisoned patients.

Fetal cord blood concentrations of NAC were measured in four newborns with mothers who overdosed on acetaminophen alone. The average NAC concentration was 9. The outcomes of the mother and fetus are generally good after an acetaminophen overdose. Even a massive g ingestion at 15 weeks of gestation resulted in a good outcome [74], whereas in the third trimester fetal infratentorial hemorrhage, fetal demise, and maternal and fetal death have been documented [68—70].

Two large studies of women exposed to acetaminophen during all trimesters found no correlation between toxicity and malformations or miscarriages [75—77]. There appears to be no indication for a mother to terminate pregnancy if she overdosed on acetaminophen. Although most acetaminophen ingestions result in recovery in the mother with a resultant normal delivery, heroic measures have been suggested in extreme cases of toxicity.

Liver transplantation was attempted in one mother who developed fulminant hepatic failure after a repeat supratherapeutic overdosed on acetaminophen at 19 weeks gestation [78]. The fetus appeared to do well immediately postoperative from the transplant. On postoperative day 14, the fetus began K. Some authors advocate emergent delivery of the fetus in the third trimester if the mother has documented toxic levels of acetaminophen, but there is little to support this approach in the absence of hepatic failure [29].

Early vaginal or cesarean delivery may avoid potential complications if the mother becomes encephalopathic and coagulopathic. If there is fetal demise, emergent delivery also may be indicated if the fetus is retained and the mother has evidence of disseminated intravascular coagulation [68].

Treatment of pregnant patients for acetaminophen toxicity should be the same as that for nonpregnant patients, with some differences as noted previously Grade III. Salicylates Similar to acetaminophen, salicylates can be found in combination with other drugs in many preparations [79—81].

There is potential harm from salicylates taken therapeutically during pregnancy. Because of effects on neonatal coagulation and premature closure of the ductus arteriosus, salicylates are contraindicated in the third trimester of pregnancy [29].

Salicylates freely cross the placental membrane [82—85]. There are some variations from adult pharmacokinetics in the way the fetus reacts to the burden of a maternal salicylate overdose. Aspirin is hydrolyzed rapidly to salicylate. A small amount is excreted in the urine unchanged, whereas the remainder is metabolized to salicyluric acid, salicyl phenolic glucuronide, salicyl acyl glucuronide, and gentisic acid Fig. The largest fraction is converted to salicyluric acid, and the other pathways follow Michaelis-Menten kinetics.

The percentage values refer to the dose. Oxidation produces a mixture of ortho- and para relative to original OH group isomers metabolism slows after a switch to zero-order kinetics. The mother and the fetus metabolize salicylate at a decreased rate after overdose. The metabolism of salicylate was studied in the newborn of a mother who ingested 6. The neonate metabolized a relatively larger fraction to salicyluric and gentisic acids, with little glucuronidation.

As a result, salicylate elimination by the infant was much slower than that in the adult. The fetus is especially vulnerable to salicylate toxicity in the third trimester of development. In an overdose, the measured serum fetal salicylate level is greater than the maternal concentration [86].

A greater proportion of salicylate enters the fetal brain than the maternal central nervous system. The fetus also has decreased capacity to buffer salicylate-induced metabolic acidosis. Lastly, metabolism and excretion of salicylate are decreased in the fetus, as discussed earlier [29, 87]. Therefore, logic dictates that treatment of the mother should be initiated at lower serum salicylate concentrations than one would initiate for a nonpregnant patient Grade III.

Salicylate ingestion just before delivery can lead to maternal and fetal platelet dysfunction. After delivery, these neonates can have petechiae, purpura, cephalohematoma, GI bleeding, and intracranial bleeding [90, 91]. Other effects on the fetus from maternal salicylate use are hyperbilirubinemia resulting from displacement from albumin, lower birth weight, and increased mortality [92].

Increased risk of congenital abnormalities and hypoglycemia are uncommon. It is believed that the antiprostaglandin effects of salicylates can cause complications in the mother as well [93]. The maternal effects of chronic salicylate ingestion include longer gestational periods, prolonged labor, increased risk of hemorrhage, and higher rates of cesarean [86]. Treatment of pregnant patients with salicylate toxicity should be the same as that for nonpregnant patients, with the caveat discussed previously Grade III.

In acute toxicity, GI decontamination should begin with AC, which is effective in binding salicylate. Multiple determinations of serum concentrations of salicylate are needed to monitor for continued absorption and hence dictating the need for further activated charcoal. Because of the high toxicity of salicylate to the fetus, fetal monitoring may be needed to assist in the determination of the need for emergent delivery in a fetus of potentially viable gestational age.

Emergent delivery is considered optimal treatment by some [29]. If the time of maternal overdose approximates the expected delivery date, the neonatologist should be alerted about the increased risk of platelet dysfunction. Iron Although accidental iron overdose has decreased substantially in the pediatric population because of changes in iron supplementation packaging, intentional overdose in the adult remains a serious ingestion. Iron is readily available to the pregnant woman because it is prescribed routinely during the prenatal period.

As a result, it is a concern for potential overdose in pregnancy. Iron toxicity injures the human body through multiple mechanisms: peroxidation of biologic membranes, inhibition of oxidative phosphorylation, and formation of free hydrogen ions as a by-product of the change from the ferrous to the ferric state, causing metabolic acidosis [94, 95].

Iron seems to have little direct toxicity to the fetus. It does not diffuse passively across biologic membranes but acts through a receptormediated endocytosis. A study of iron toxicity in pregnant sheep showed that elevated maternal serum iron concentrations are not reciprocated in the fetal circulation [21]. Iron does not affect the fetus directly but does so indirectly through poisoning of the mother.

The placenta provides an effective barrier to iron, leaving the fetus reliant on the well-being of the mother for its survival [97]. Two other components of general iron toxicity are present in pregnant patients. The peak serum iron concentration occurs in the range of 2—4 h, and using the total iron-binding capacity to predict the severity of poisoning is inaccurate [98].

Treatment must focus on the sum of many different data points to determine what is most appropriate. GI decontamination after iron poisoning is controversial.

Some authors support gastric lavage if a pregnant patient presents less than 1 h after ingesting a potentially toxic dose, but the proper equipment and training of staff has made 7 Poisoning in Pregnancy this technique largely unavailable, and should likely be avoided in most circumstances.

Activated charcoal may be used if a coingestant is suspected, but it does not adsorb iron itself. Ultrasound is the imaging modality of choice in pregnant patients because it causes no ionizing radiation, though its ability to identify pills in the setting of overdose remains in question [99, ].

Adverse side effects from the amount of radiation are trivial compared with the potential threat of fetal toxicity after a substantial iron ingestion. Deferoxamine is the antidote for iron poisoning. It chelates free iron and is excreted by the kidneys. The reason for this limit is to avoid hypotension and acute lung injury. Previously, deferoxamine was considered dangerous to give to the pregnant patient because of fears of teratogenicity. There have been reports of skeletal abnormalities in animals exposed to high doses of deferoxamine [96, ].

In contrast, reviews of multiple case studies have shown no direct link between deferoxamine treatment in humans with iron toxicity and teratogenicity [—]. More reassurance of the safety of deferoxamine in pregnancy is provided by the fact that deferoxamine does not cross the placenta in the ovine model [21]. In this overdose, the mother has more potential morbidity than the fetus. This constitutes a classic example of the dictum that the future of the mother and the fetus relies on optimal treatment of the mother.

While no longer the leading cause of poisoning death in the United States, CO was still responsible for 14, calls to poison centers in , with 60 of these cases being fatalities [1]. The clinical signs and symptoms of CO poisoning mimic the presentations of many illnesses, such as viral syndrome or gastroenteritis. The best way to diagnose CO poisoning is to consider it often in differential diagnoses.

It cannot be overstated that one needs a high degree of suspicion to discover CO poisoning. The instigator of this increase is progesterone, which induces the catabolism of hemoglobin by hepatic microsomal enzymes. The minute ventilation also increases during pregnancy.

The baseline increased burden of CO and the increased minute ventilation make the pregnant woman more susceptible to CO poisoning. The pathogenesis of CO toxicity is twofold: CO generates oxidative stress, and it binds to heme-containing proteins, such as hemoglobin, myoglobin, and cytochrome aa3 [].

This binding leads to systemic hypoxia and a shift of the oxygen-hemoglobin saturation curve to the left, with a transformation of the curve to a hyperbolic shape []. There may be direct toxicity to cardiac tissue as a result of the replacement of oxygen with CO in cardiac myocytes.

Uncoupling of oxidative phosphorylation causes an increase in free hydrogen ions, leading to metabolic acidosis. Fetal hemoglobin complicates the situation because its oxygen binding curve is already hyperbola shaped and steep at low pressures of oxygen.

Decreased ability of tissues to extract oxygen from the fetal hemoglobin and increased susceptibility to a precipitous drop in oxygen saturation result. In acute maternal CO exposure, the CO slowly crosses the placenta by passive diffusion []. In acute exposure, death by anoxia occurs well before COHb concentrations increase [].

The CO elimination half-life is 2 h in the mother and 7 h in the fetus. The sum of the effects from fetal hemoglobin, prolonged elimination, delayed peak in fetal COHb concentration, and elevated concentration of COHb in the fetus places the fetus at greater risk for morbidity and mortality than the mother. Similar to the situation in nonpregnant patients, the CO level, expressed as percent COHb, does not correlate well with severity of toxicity.

Fetal COHb levels are not realistically obtainable, making a history of exposure along with clinical signs and symptoms in the K. Teratogenicity varies with the timing of the exposure. Case reports suggest the possibility that exposure in the embryonic stage leads to neurologic, skeletal, and cleft palate deformities.

During the fetal phase, anoxic encephalopathy and growth restriction may result. In the third trimester, premature delivery is reported and possibly decreased immunity, right-sided cardiomegaly, and delay in myelin formation [, ].

HBO therapy has been advocated as the treatment of choice for pregnant patients exposed to CO [, ]. HBO therapy can reduce the elimination half-life of CO from 4 to 6 h on room air, to roughly 20 min. Normobaric oxygen and HBO therapy increases dissolved oxygen, accelerates dissociation of CO from hemoglobin, and shifts the oxygen-hemoglobin curve back to the right. If maternal or fetal signs of CO toxicity persist 12 h after initial HBO therapy, a repeat session has been proposed [, ].

High PO2 is known to be teratogenic and to cause retinopathy, cardiovascular defects, and premature closure of the ductus arteriosus []. An animal study showed similar adverse effects [18]. Several human case reports and studies strongly advocate HBO therapy in pregnant patients [18, , , , , ]. The safety of HBO therapy in pregnant patients was studied prospectively in 44 women, all of whom tolerated the procedure well, and no morbidity was seen in the mother or the fetus [].

A prospective French series from to found no difference in early childhood development as late as age 6 years between those who received HBO for CO in utero and unexposed age matched controls, further emphasizing the apparent safety of HBO in pregnant patients []. In addition to the described standard therapy of CO poisoning, fetal heart monitoring is indicated in the late second and third trimesters.

Poor variability and late decelerations are indications of fetal distress. One review article cautioned that immediate delivery of the fetus before HBO therapy carries a high risk of perinatal death. The authors concluded that HBO therapy should be considered before performing an emergency cesarean section []. This recommendation is based solely on theoretical considerations, however, and there are no data to support this from clinical trials. Cyanide Cyanide is a cellular asphyxiant that binds to and inhibits cytochrome oxidase at cytochrome a3 in the mitochondria electron transport chain.

It prevents the conversion of electron energy into the creation of ATP, leading to seizures, dysrhythmias and hypotension, metabolic acidosis and hyperlactatemia from anaerobic metabolism.

The most probable exposure of the pregnant patient to cyanide is in the gaseous form found in smoke inhalation, but ingestion of a cyanide salt, organic compound or nitroprusside infusion are possible as well. Pregnant women exposed to cyanide from smoke inhalation or other sources are not well studied, leaving no guidance about this unique population.

Roderique et al. She was extubated after clinical improvement and delivered a healthy infant. There was no long-term follow-up. Nitroprusside contains cyanide molecules that are released as the drug is metabolized. Because nitroprusside crosses the ewe placenta, this animal model was used to determine if prophylactic sodium thiosulfate could prevent cyanide toxicity in the pregnant ewe.

There was successful reduction in uptake of cyanide in RBCs in the mother and the fetus, despite a follow-up study revealing sodium thiosulfate does not cross the ewe placenta [, ]. Hydroxycobalamin, sodium nitrite, and sodium thiosulfate are antidotes available for the treatment of cyanide toxicity in the pregnant patient Grade III and are considered category C in pregnancy. Cocaine Cocaine is a common drug of abuse in women of childbearing age [].

Smoking crack cocaine is the most common route of exposure, and most pregnant women who use this substance do not receive any prenatal care [, ]. Some women do not realize they are pregnant, whereas others surmise the pregnancy is lost and decide to continue using cocaine [].

Still others falsely think that cocaine speeds labor. Cocaine can increase the length of labor, however, and exacerbates pain sensation []. The manifestations of cocaine toxicity are the same as those in any nonpregnant patient. Hyperthermia, hypertension, tachycardia, agitation, seizures, stroke, myocardial infarction, intracerebral hemorrhage, and aortic dissection are possible results of cocaine use.

The unique complications associated with cocaine use in pregnancy are abruptio placentae, decreased fetal growth, preterm labor, urinary congenital abnormalities, neurobehavioral abnormalities, and fetal demise [—].

The pregnant patient theoretically is at enhanced susceptibility to cocaine poisoning due to reduced cholinesterase levels [], causing her to have decreased ability to metabolize cocaine. Benzodiazepines are the medication of choice to treat the agitated, seizing, or tachycardic patient who is manifesting signs of cocaine toxicity. Diazepam and lorazepam are often considered contraindicated in pregnancy out of concern for teratogenic risks.

Despite this warning, in the case of a pregnant woman with cocaine toxicity who presents with seizures, agitation, and hyperthermia, benzodiazepines are effective at diffusing cocaine toxicity and may decrease morbidity and mortality []. The teratogenic risk of benzodiazepines is likely minimal except for a small association with oral clefts []. Further, mothers K. Antihypertensives, such as nitroglycerin, may be used for hypertension, and rapid external cooling for hyperthermia is essential.

If chest pain is present, investigation and treatment of possible myocardial ischemia are warranted. This epidemic is also seen among pregnant patients, where 0. Some opioids, particularly codeine, have been associated with birth defects including congenital heart defects []. Chronic heroin risk has been associated with a variety of poor fetal outcomes including fetal growth restriction, preterm labor, and fetal death. In the case of heroin, there is a theory that these effects are from both repeated exposure and repeated withdrawal.

The treatment of opioid withdrawal creates a concern regarding naloxone use in pregnancy. Similarly, pregnant patients who may be dependent on opioids should be observed for signs and symptoms of withdrawal and managed as needed to prevent fetal distress Grade III. At levels of 3. Respiratory muscle paralysis may occur at concentrations of 5—6.

Cardiac conduction disturbances occur at magnesium serum concentrations of 7. Magnesium toxicity affects the mother and the fetus. For the mother, this toxicity typically occurs by an error in the rate of administration []. The mother also is in danger when magnesium therapy is combined with polarizing and nondepolarizing agents because of prolonged respiratory paralysis [].

Hypotension can be a complication when magnesium is used with epidural blocks. Because of their calcium channel—blocking properties, magnesium combined with nifedipine can lead to profound hypotension []. The effect of magnesium on the fetus is variable.

The classic result in the neonate is hypotonicity, which may affect diaphragmatic function. Magnesium toxicity in the mother also increases the rate of perinatal mortality, even when there is little effect on the mother []. Magnesium therapy may be detrimental to the fetus in the scenario of maternal hemorrhage. The magnesium may have inhibited the natural response to hypoxemia in the fetus [].

Another study in pregnant sheep found that magnesium did not impair cardiac output, however, or increase fetal death during maternal hemorrhage []. The treatment of magnesium toxicity involves attention to airway, breathing, and cardiovascular There have been many reports of other poisonings and toxic syndromes in pregnancy.

Some of these cases are summarized in Table 5. All recommendations are Grade III. Toxicity of Pregnancy-Related Medications Magnesium Sulfate The magnesium cation is involved in many physiologic reactions and regulation of ion channels. Magnesium sulfate is used as an anticonvulsant in pregnant patients with eclampsia or severe preeclampsia.

In most cases, magnesium sulfate has been shown to be safe and effective [—]. It affects many different systems, which may contribute to the antiepileptic properties of this medication. Magnesium is a calcium antagonist and causes systemic and cerebral vasodilation. It increases cyclic guanosine monophosphate levels, which may act as a vasodilator by increasing nitric oxide levels and decreasing endothelin Magnesium can slow conduction through the myocardium and decrease inotropy in high doses.

It also can protect neuronal tissues from injury by blocking calcium channels directly in N-methyl-D-aspartate receptors. The major importance of this effect is loss of diaphragm function [, , ]. The toxicity of magnesium probably depends more on its rate of administration than the duration or the total dose, except in extreme circumstances. When magnesium administration exceeds its rate of renal clearance, its serum concentrations increase and may result in toxicity.

There are many different regimens used in pregnancy, including regimens involving the intravenous and intramuscular routes with different K. Table 5 Poisonings in pregnant patients Toxin Methanol [] Editorial: 1. Freely crosses the placenta 2. Caution alcohol known teratogen 2. Blockade of alchohol dehydrogenase with ethanol and hemodialysis 3.

Published before fomepizole 4. Emergent delivery if fetal distress 1. Gastric lavage 2. Fetal death presumed from uterine contractions and arterial spasm 1.

Fetal death presumed from uterine contractions and arterial spasm 2. Early delivery because of deleterious fetal effects without morbidity to mother 1. Bromocriptine is safe to use in pregnancy 3. No maternal deaths 3. Discharged on hospital day 12 21 days postingestion 2. Fetus delivered term, no fetal hemorrhage, no abruption, no problems at 1-year follow-up 1. No fetal hemorrhagic or teratogenic effects noted 2.

Intubation and vasopressors with aggressive supportive care are the mainstays of treatment. Intravenous calcium may serve as an antidote to the effects of magnesium toxicity. Maternal hemodialysis may be indicated in cases of severe hypermagnesemia. Methotrexate Methotrexate MTX is used to abort ectopic pregnancies and to treat gestational trophoblastic disease. MTX destroys actively dividing cells because it acts as an analogue of folate Fig.

MTX replaces folate at its binding site on dihydrofolate reductase and thymidylate synthetase Fig. The end result is inhibition of DNA synthesis, leading to cell death. MTX exhibits profound dose-dependent toxicity.

It may cause nausea, vomiting, mucositis, pleuritis, pericarditis, peritonitis, liver injury, renal failure, anemia, and leucopenia at therapeutic doses [—].

MTX overdose has followed intravenous, oral, and intrathecal routes. Its dosage depends on the serum MTX concentration. This antidote should not be delayed while waiting for an MTX level. Carboxypeptidase is a antidote that directly deactivates MTX. In a severe overdose, granulocyte-macrophage colony-stimulating factor has been used to treat pancytopenia with apparent success []. Methylergonovine in overdose can cause hypertension, chest pain, myocardial infarction, headache, vertigo, nausea, vomiting, and blurred vision.

Fetal bradycardia may occur and may be treated with terbutaline [9]. Standard treatment for possible myocardial infarction and stroke is the same as that for a nontoxic cause. Oxytocin can cause fetal toxicity manifested by bradycardia, brain damage, neonatal jaundice, retinal hemorrhage, hypoxia, and death. In the mother, cardiac arrhythmias, hypertension, seizures, and the syndrome of inappropriate secretion of antidiuretic hormone SIADH have been reported [9].

Treatments for oxytocin toxicity include ritodrine to reverse oxytocin-induced labor and benzodiazepines for seizures. Because of the K. Tetrahydrofolate polyglutamate [FH4 glu n] functions as a carrier of a one-carbon unit, providing the methyl group necessary for the conversion of 20 -deoxyuridylate DUMP to 20 -deoxythymidylate DTMP by thymidylate synthetase.

This one-carbon transfer results in the oxidation of FH4 glu n to the dihydrofolate form FH2 glu n. Prostaglandins can cause tachycardia, hypertension, hyperthermia, chills, cramping, and possibly hypotension.

These agents include magnesium, terbutaline, nifedipine, ritodrine, and indomethacin. Excluding magnesium, terbutaline is one of the more toxic agents in overdose. When comparing ritodrine, hexaprenaline, betamethasone, and terbutaline in mongrel dogs, terbutaline was found to be the most toxic []. Terbutaline overdose can lead to tremor, dizziness, palpitations, myocardial ischemia, and blood pressure changes [].

Propranolol has been advocated as an antidote in a single case report but has not been studied formally []. Terbutaline can cross the placenta and cause injury to the fetus. Three out of the four newborns in a quadruplet pregnancy developed bradycardia, metabolic acidosis, poor tissue perfusion, and decreased urine output after 50 days of terbutaline therapy total of mg to prevent labor [].

All three neonates responded well to dobutamine administration. Calcium channel antagonists are used widely for control of hypertension and tocolysis. The long-acting preparations seem to be safe and effective when used in these settings. When nifedipine has been administered with magnesium, however, severe hypotension has been described []. This association between magnesium and short-acting calcium channel blockers also has been studied in rhesus monkeys and Sprague—Dawley rats.

Treatment of calcium channel antagonist toxicity is described in detail in the chapter on these agents. Indomethacin may cause gastric irritation, ulcers, heartburn, and GI bleeding in the mother. In the fetus, it may cause premature closure of the ductus arteriosus, neonatal anuria, and bowel perforation [].

There is a case report of maternal toxic epidermal necrosis after treatment with ritodrine, indomethacin, and betamethasone []. Treatment of the mother after indomethacin toxicity is supportive, whereas the treatment of the fetus is primarily preventive.

However, to prevent maternal toxicity oral or IV NAC should be started, ideally within 8 h of ingestion.

The role of hyperbaric oxygen therapy is inconclusive. Consultation with a medical toxicologist or, if one is not available, with a poison control center is warranted.

References 1. Clin Toxicol Phila. Cocaine abuse during pregnancy. J Obstet Gynaecol Can. J Forensic Sci. Acute poisoning during pregnancy: observations from the toxicology investigators consortium.

J Med Toxicol. Timing of suicide attempts by self-poisoning during pregnancy and pregnancy outcomes. Int J Gynaecol Obstet. Pregnancy outcome after suicide attempt by drug use: a danish population-based study.

Acta Obstet Gynecol Scand. Content and format of labeling for human prescription drug and biological products; requirements for pregnancy and lactation labeling. Fed Regist. Teratogenicity of recently introduced medications in human pregnancy. Obstet Gynecol.

Leikin JB, Paloucek F, editors. Hudson: Lexi-comp; Lack of effect of selfpoisoning on subsequent reproductive outcome. Mutat Res. Teratologic evaluation of infants born to mothers who attempted suicide by drugs during pregnancy.

A study of the risk of mental retardation among children of pregnant women who have attempted suicide by means of a drug overdose. J Inj Violence Res. Systematic meta-analysis of individual selective serotonin reuptake inhibitor medications and congenital malformations. Aust N Z J Psychiatry. Thorp Jr JM. Management of drug dependency, overdose, and withdrawal in the obstetric patient.

Obstet Gynecol Clin North Am. Homicide and other injuries as causes of maternal death in new york city, through Am J Obstet Gynecol. Fine J. Reproductive and perinatal principles. New York: McGraw-Hill; Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. Transferrin: physiologic behavior and clinical implications. Aisen P, Brown EB. The iron-binding function of transferrin in iron metabolism.

Semin Hematol. An ovine model of maternal iron poisoning in pregnancy. Ann Emerg Med. Valproic acid in the perinatal period: decreased maternal serum protein binding results in fetal accumulation and neonatal displacement of the drug and some metabolites.

J Pediatr. Complete maternal and fetal recovery after prolonged cardiac arrest. Jeejeebhoy F, Windrim R. Management of cardiac arrest in pregnancy. Part cardiac arrest in special situations: American heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Drug disposition and pharmacokinetics in the maternal-placental-fetal unit. Pharmacol Ther. Gimovsky ML, Knee D. Fetal heart rate monitoring casebook. FHR monitoring and imipramine overdose. J Perinatol.

Unrecognized pregnancy in the overdosed or poisoned patient. Am J Emerg Med. Koren G. New York: Marcel Dekker; Position paper update: gastric lavage for gastrointestinal decontamination. Tenenbein M. Ancient therapies. Position paper: single-dose activated charcoal.

Position paper: cathartics. J Toxicol Clin Toxicol. Common poisons. In: Gleicher N, editor. Principles of medical therapy in pregnancy. New York: Plenum Press; Successful therapy of iron intoxication in pregnancy with intravenous deferoxamine and whole bowel irrigation. Vet Hum Toxicol. Whole bowel irrigation during pregnancy. Position paper update: whole bowel irrigation for gastrointestinal decontamination of overdose patients.

Placental transfer of N-acetylcysteine following human maternal acetaminophen toxicity. Spence AG. Lipid reversal of central nervous system symptoms of bupivacaine toxicity. The society for obstetric anesthesia and perinatology consensus statement on the management of cardiac arrest in pregnancy. Anesth Analg. Bailey B. Are there teratogenic risks associated with antidotes used in the acute management of poisoned pregnant women?

Fatal iron poisoning in a pregnant female. Minn Med. Manoguerra AS. Iron poisoning: report of a fatal case in an adult. Am J Hosp Pharm. Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. American academy of clinical toxicology; European association of poisons centres and clinical toxicologists. End-stage renal disease and pregnancy. For students and teachers of forensic science, toxicology, clinical pharmacology and analytical chemistry, this is a crucial resource.

It provides unrivaled coverage of analytical forensic toxicology. This second edition is fully updated to reflect advances in analytical and forensic toxicology. New and extended chapters include :. Save my name, email, and website in this browser for the next time I comment. This site uses Akismet to reduce spam.