Forensic Science International 223 (2012) 349352

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Forensic Science International

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Sertraline concentrations and postmortem redistribution

Iain M. McIntyre *, Phyllis Mallett
Forensic Toxicology Division, County of San Diego Medical Examiners Ofce, 5570 Overland Ave., Suite 101, San Diego, CA 92123, USA

A R T I C L E I N F O

A B S T R A C T

Article history:
Received 27 June 2012
Received in revised form 9 October 2012
Accepted 11 October 2012
Available online 3 November 2012

Sertraline is a commonly prescribed selective inhibitor of serotonin uptake used for the treatment of
mental depression and anxiety. Central blood and liver concentrations of sertraline (norsertraline) are
compared to levels in peripheral blood in nine medical examiner cases. Specimens were initially
screened for alcohol and simple volatiles by GC-FID headspace analysis, ELISA for drugs of abuse, and
alkaline drugs by GC/MS. Sertraline, when detected by the alkaline drug screen, was subsequently
conrmed and quantied by a specic GC-NPD procedure. Data suggest that when ingested with other
medications, sertraline may be a contributing factor in death. Sertraline (norsertraline) concentrations
ranged from 0.13 (0.11) to 2.1 (6.0) mg/L in peripheral blood, from 0.18 (0.12) to 2.0 (6.7) mg/L in central
blood, and 21 to 160 mg/kg in liver. Sertraline central blood to peripheral blood ratios averaged
1.22  0.85 (mean  standard deviation). The liver to peripheral blood ratios, on the other hand, were
markedly higher and averaged 97  40 (mean  standard deviation). Given that a liver to peripheral blood
ratio exceeding 20 is indicative of propensity for signicant postmortem redistribution, these data conrm
that sertraline is prone to marked postmortem redistribution.
Published by Elsevier Ireland Ltd.

Keywords:
Postmortem
Sertraline
Norsertraline
Peripheral blood
Central blood
Liver
Redistribution

1. Introduction
Sertraline (Zoloft1) is a commonly prescribed selective inhibitor of serotonin uptake that has been used for the treatment of
mental depression, obsessive-compulsive disorder, anxiety and
premenstrual dysphoric disorder since 1992 [1].
Therapeutic plasma concentrations of sertraline following
chronic daily doses of 100, 200 or 300 mg were reported to
average 32 mg/L (range 2048 mg/L), 91 mg/L (range 40187 mg/L)
and 206 mg/L (range 99309 mg/L), respectively. Plasma norsertraline concentrations averaged 167% of the parent drug concentrations in these patients [2]. Steady-state serum concentrations
averaged 50% higher in patients aged 6579 years and 100% higher
in those aged 8092 years, relative to patients younger than 65
years [3]. Although no signicant differences were found in
pharmacokinetic parameters in patients with renal impairment
[4], cirrhosis resulted in a three-fold increase in half-life of
elimination for sertraline [5]. The estimated half-life of elimination
is generally reported to be 2236 h [6], and therapeutic dosing is
recommended from 50 mg to a maximum of 200 mg a day [1].
Adverse effects have been described as dry mouth, headache,
dizziness, tremor, nausea, diarrhea, fatigue, insomnia and somnolence [1]. Serotonin syndrome has been described when sertraline
is used alone and with concomitant drug treatments [79].

* Corresponding author. Tel.: +1 858 694 2907.

E-mail address: Iain.McIntyre@sdcounty.ca.gov (I.M. McIntyre).
0379-0738/$ see front matter . Published by Elsevier Ireland Ltd.
http://dx.doi.org/10.1016/j.forsciint.2012.10.020

Although there are reports that sertraline is less sedating and

results in fewer cardiovascular effects than the tricyclic antidepressants on overdose [10], there are reports of fatal intoxications [1116]. Despite such cases however, Kassner and Woolf [17]
(studying 31 overdoses) reported, with an average dose of 1109 mg
and plasma sertraline concentrations averaging 245 mg/L at a
mean time of 4.8 h post-ingestion, that all patients survived the
incident; symptoms of vomiting, lethargy and ataxia were
described. Despite these reports, however, few published studies
have presented tissue (liver) sertraline concentrations.
The study described herein examined nine postmortem cases in
which peripheral blood, central blood and liver were available to
sample from known positive sertraline cases. This study presents
an investigation of postmortem distribution, and provides further
insight on how liver concentrations may correlate with those of
blood, and assist with the interpretation of the drugs propensity
for postmortem redistribution.
2. Experimental
2.1. Sample collection and storage
Sertraline positive cases detected with sufcient appropriate samples were
selected for this study. Cases identied or suspected to be decomposed (as
described in the Medical Examiner Investigation report, or at the time of autopsy)
were not included. All specimens analyzed were collected at autopsy at the San
Diego County Medical Examiners Ofce. Autopsies were performed within 2448 h
after the reported time of death. Peripheral blood was drawn from the iliac veins
(blood returning from the leg and visually identied in the pelvis at autopsy) and
stored in standard glass tubes containing sodium uoride (100 mg) and potassium
oxalate (20 mg). Central blood was collected from the heart or adjacent great

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350

vessels and placed in identical tubes. A section of the upper right lobe of liver was
collected and stored in a sterile four ounce container without preservative. When
available, gastric contents were collected and stored in a sterile four ounce
container without preservative. All samples were stored at 4 8C until analyzed.
2.2. Screening
Drug screening for all cases included, at least, blood alcohol and simple volatiles
by GC-FID headspace analysis, ELISA (Immunalysis Inc., CA) for drugs of abuse (in
blood) (cocaine metabolites, methamphetamine, opiates, benzodiazepines, fentanyl and cannabinoids), and alkaline extractable drugs by GCMS following solid
phase extraction of a blood sample. Sertraline/norsertraline, when detected by the
alkaline drug screen, was subsequently conrmed and quantied by a specic GCNPD procedure.
2.3. Materials
Sertraline and norsertraline standards and controls were purchased from Alltech
(State College, PA) and Ceriliant (Austin, TX) in methanol dissolved stock at a
concentration of 1 mg/mL, and separate lot numbers were used for calibrators and
controls. The internal standard used was cyclizine (Burroughs-Wellcome, Kirkland,
QC, Canada). Cyclizine was prepared in 1.0 mg/mL stock in methanol. Working stock
solutions of sertraline and norsertraline were prepared in deionized (DI) water at a
concentration of 1.0 mg/L for both the standard and control. The cyclizine was
diluted with DI water to make 5.0 mg/L working solution. 1-Chlorobutane, and
ethyl acetate were manufactured by OmniSolv (VWR International, Radnor, PA).
Concentrated hydrochloric acid was manufactured by Aristar (VWR International,
Radnor, PA) and the concentrated ammonium hydroxide was from EMD (VWR
International, Radnor, PA). Sodium sulfate (anhydrous, granular ACS grade) was
obtained from SigmaAldrich Chemical (St. Louis, MO).
2.4. Extraction
Sertraline was rst detected in an alkaline drug screen by gas chromatography
mass spectrometry (GCMS) using a solid-phase extraction of blood. Sertraline and
norsertraline were then quantitated on a gas chromatograph with a selective
NitrogenPhosphorous Detector (NPD). Five point calibration curves were obtained
by making calibrators from the working sertraline and norsertraline solutions in the
concentrations of 0.10 mg/L, 0.25 mg/L, 0.50 mg/L, 1.0 mg/L and 2.0 mg/L. Two
controls were made from a separate working stock with a different lot number than
the calibrators in concentrations of 0.5 mg/L and 1.5 mg/L. A blood curve was used
for blood and gastric samples containing blank porcine blood as the matrix. A liver
curve was constructed using porcine liver homogenate for the matrix of liver
specimens; norsertraline was not determined in the liver homogenates. (Liver
homogenates were prepared by making a 1:1 dilution with deionized water and
homogenized using either a commercial blender or dispersion mixer.)
Samples were all extracted using a method modied after that of Forster et al.
[18]. For all samples a minimum of two separate unknown sample dilutions of
different volumes were used and placed in separate tubes. Volumes used were
those that would bring sample response into the calibration curves response range.
Any sample added that was less than 1 mL had its difference in volume made up
with DI water. Liver specimens were homogenized by taking 1520 g of liver
specimen and blending it with an equal amount of DI water to create a 0.5 g/mL
homogenate. 1 mL of this homogenate was then pipetted into a tube and diluted to
10 mL with DI water to create a 0.05 g/mL liver homogenate. All blood specimens
were run on a blood curve with its own calibrators, controls, blank and negative, and
all liver samples were run with their matching matrixes as well. To each tube 1 mL
of their respective matrix (porcine blood or porcine liver) was added. Each tube was
diluted to 5 mL with DI water and vortexed for 10 s. 50 mL of cyclizine working
solution (0.5 mg/L) was added to each tube except blanks and the tubes were
vortexed again for 10 s. Fresh concentrated ammonium hydroxide (1 mL) was then
added to each tube, and tubes were vortexed again for 10 s. Tubes then had 6 mL of
1-chlorobutane added, were capped, and then extracted by rotation for 30 min.

When nished, tubes were centrifuged at 3200 RPM for 5 min. Any emulsions still
present after centrifugation was eliminated by the addition of sodium sulfate in
necessary quantities. All tubes were centrifuged for 5 more minutes at 3200 RPM
and then the top organic solvent (1-chlorobutane) phase was extracted by pipette
into a clean glass tube. Extracted organic layers were put into screw cap tubes and
3.5 mL of 1 N HCl was added to each tube. Tubes were capped and extracted by
rotation for 30 min. Following extraction by rotation and centrifugation at
3200 RPM for 5 min, the organic 1-chlorobutane layer was aspirated to waste. A
1 mL aliquot of concentrated ammonium hydroxide was added to the remaining
acid layer of each tube and vortexed for 10 s. Then to each tube 3 mL of 1chlorobutane was added, tubes were capped and extracted by rotation for 30 min.
The tubes were then centrifuged for 15 min at 3200 RPM and the top organic layer
was extracted carefully to clean culture tubes. The culture tubes solvent was
evaporated off at room temperature under nitrogen to dryness. Dry extract were
reconstituted with 100 mL of ethyl acetate and vortexed for 10 s. Extracts were then
transferred to autosampler vials tted with glass volume inserts.
Calibrators were back calculated to original known concentrations and were
within 20% of target value. Calibration curves were constructed from a minimum of
four non-zero points. The calibration curves used a linear regression t (r2  0.99).
Both positive control samples were back calculated to known value of 0.5 mg/L or
1.5 mg/L. All specimen tubes (blood and liver homogenates) were diluted so the
concentration would fall within the range of the calibration curve.
2.5. Instrumentation
Sertraline specimens were analyzed using a HP 5890 Series II Plus Gas
Chromatograph using a DB-1 (15 m  0.252 mm  0.25 mm) column from Agilent
and a nitrogenphosphorous bead detector from Agilent. Helium was the carrier gas
and had a ow rate of 1.2 mL/min. For all samples the inlet temperature was set to
250 8C and the detector set at 280 8C. For blood and liver samples, 1 mL of sample
was injected on the column and after 30 s the GC started its oven ramp. The oven
started at 50 8C, and the ramp was an increase of 35 8C/min for 4.5 min. After
4.5 min the oven temperature remained constant at 275 8C until the end of the run.
Total runtime after injection was 13.5 min. The cyclizine internal standard was seen
at about 5.8 min. Sertraline had a retention time of about 6.9 min within a window
of 1% and a relative retention time of 1.18. Norsertraline had a retention time of
about 6.99 min within a window of 1% and a relative retention time of 1.20.
2.6. Accuracy and precision
Accuracy of the method for the analysis of sertraline in blood was established
over 2 years and was 99% at 0.50 mg/L and 92% at 1.5 mg/L. Precision was
established over the same period with sertraline having a coefcient of variation of
18% and 7.4% for concentrations of 0.50 mg/L and 1.5 mg/L, respectively over 14
analyses. For liver, the accuracy was 94% at 0.50 mg/kg and 99% at 1.5 mg/kg.
Precision was established over the same period with sertraline having a coefcient
of variation of 8.4% and 13.7% for concentrations of 0.50 mg/kg and 1.5 mg/kg,
respectively over 11 analyses.

3. Results and discussion

A total of nine cases were collected where central blood (C),
peripheral blood (P) and liver (L) were available. Sertraline (and
norsertraline) concentrations, and ratios for central to peripheral
blood (C/P) and liver to peripheral blood (L/P) (where available) are
shown in Table 1. Norsertraline was not determined in the liver
homogenates.
Cause and manner of death and the other drugs detected in each
case are shown in Table 2. Most cases (except cases 2, 3 and 9) were
determined to be accidental drug related deaths. Case 2 was a
gunshot homicide, and case 3 was a driver involved in a fatal motor

Table 1
Peripheral blood, central blood, liver and gastric sertraline (norsertraline) concentrations and ratios.
Case number

PB (mg/L)

CB (mg/L)

Liver (mg/kg)

Total gastric
contents (mg)

Sertraline
C/P ratio

Norsertraline
C/P ratio

Sertraline
L/P ratio

1
2
3
4
5
6
7
8
9

0.13 (0.11)
0.20 (0.43)
0.34 (0.66)
0.57 (1.2)
0.92 (3.0)
1.0 (0.90)
1.0 (1.0)
1.1 (1.7)
2.1 (6.0)

0.19 (0.12)
0.38 (1.1)
0.95 (2.0)
0.55 (1.2)
0.29 (1.0)
0.18 (0.64)
1.0 (1.4)
1.6 (2.6)
2.0 (6.7)

22
21
36
41
160
79
47
68
140

ND
<1
<1
<1
NA
58
<1
NA
3

1.44
1.9
2.79
0.96
0.32
0.17
1.03
1.46
0.95

1.16
2.51
3.08
0.98
0.35
0.71
1.40
1.54
1.12

170
105
106
72
174
76
47
60
67

PB, peripheral blood; CB, central blood; L, liver; NA, specimen not available; ND, not detected.

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351

Table 2
Cause and manner of death and other drugs detected.
Case
number

Cause of death

Other drugs detected

Manner of death

Acute alcohol, hydrocodone, sertraline and

diphenhydramine intoxication
Perforating gunshot wound
Multisystem blunt force injuries (motor
vehicle driver)
Acute morphine, methamphetamine and
sertraline toxicity
Acute sertraline and oxycodone
intoxication
Morphine, sertraline, zolpidem, trazodone,
quetiapine and lorazepam intoxication

Alcohol 0.39, hydrocodone 0.35, dihydrocodeine 0.04,

diphenhydramine <0.10
Mirtazapine <0.10
Lamotrigine detected

Accident

2
3
4
5
6

8
9

Acute sertraline, oxycodone, alprazolam,

carisoprodol and diphenhydramine
intoxication
Mixed alcohol, sertraline, zolpidem and
diphenhydramine intoxication
Acute citalopram, amitriptyline, sertraline,
oxycodone and gabapentin intoxication

Homicide
Accident

Methamphetamine 0.14, morphine 0.17, acetaminophen 8.0,

theophylline 10, nordiazepam trace
Oxycodone 0.40, alprazolam 0.09

Accident

Morphine 0.81, 70 (G), lorazepam 0.12, quetiapine 1.0, trazodone

0.79, zolpidem 0.09, carisoprodol detected, meprobamate detected,
solifenacin detected
Oxycodone 0.30, <1 (G), alprazolam 0.11, nordiazepam trace,
carisoprodol 12, 19 (L), 82 (G), meprobamate 7.3, 12 (L),
diphenhydramine 0.51, acetaminophen 33
Alcohol 0.20, zolpidem 0.10, diphenhydramine <0.10, ibuprofen <2.0

Accident

Citalopram 1.1, 1 (G), amitriptyline 1.2, 3 (G), nortriptyline 0.30,

oxycodone 0.21, acetaminophen 4.2, diltiazem 0.25, gabapentin 27,
hydroxyzine detected

Accident

Accident

Accident
Suicide

All blood concentrations were determined in peripheral blood.

L, liver; G, gastric.
Concentrations in mg/L (blood), mg/kg (liver), mg (gastric), % (w/v) alcohol.

vehicle accident. Interestingly, these two cases showed the highest

C/P ratios, which may be a reection of the traumatic nature of
these deaths. Case 9 was determined to be a mixed drug suicide
and exhibited the highest peripheral 2.1 mg/L (6.0 mg/L) and
central blood 2.0 mg/L (6.7 mg/L) sertraline (norsertraline) concentrations.
Based on these cases, it seems that when ingested with other
medications (particularly alcohol, opioids and other antidepressants); sertraline may be a contributing factor in death. Case 1, for
example, involved a therapeutic concentration of sertraline
(0.13 mg/L peripheral blood; 22 mg/kg liver) together with a
signicant alcohol of 0.39% and a hydrocodone concentration of
0.35 mg/L. Similarly, case 4 exhibited therapeutic sertraline
concentrations (0.57 mg/L peripheral blood; 41 mg/kg liver) but
involved morphine 0.17 mg/L and methamphetamine 0.14 mg/L.
Given that the blood to plasma ratio for sertraline is about 1.11.2
[6], the two cases in which there was a competing cause of death
(sertraline was not directly involved; cases 2 and 3), had peripheral
blood concentrations that correspond to in vivo therapeutic serum
concentrations (0.20 mg/L and 0.34 mg/L). The liver concentrations
were also not substantially elevated (21 mg/kg and 36 mg/kg).
Clearly, at least for these cases presented, sertraline was not found
to be the cause of death in its own right; it was always combined
with other medications.
Postmortem drug concentrations in blood may not always
reect antemortem drug concentrations in blood due to the
movement of the drugs after death. The mechanisms involved in
postmortem redistribution (PMR) are both complicated and
poorly understood. However, postmortem drug concentrations
in blood do follow some generally accepted trends that aid with
interpretation. Generally speaking, the characteristics of the drug
itself can be used to predict if a drug is subject to PMR; large
changes in blood drug concentrations are predicted for basic,
lipophilic drugs with a high volume of distribution (>3 L/kg).
When PMR occurs, blood specimens drawn from the central body
cavity and heart generally will have higher drug concentrations
postmortem than specimens drawn from peripheral areas, most
commonly the femoral region. The diffusion of drugs from organ
tissue into the blood may explain the observed phenomenon [19].
To compensate for PMR, postmortem blood specimens are
frequently recommended to be collected from at least two areas

of the body at autopsy; a peripheral area and a central area (often

the heart), so that a comparison can be made.
Prouty and Anderson [20] rst provided detailed information
about blood drug concentrations attained from different sites for
over fty drugs. Then Dalpe-Scott et al. [21] presented a tabular list
of the drug concentrations from both cardiac and peripheral blood
samples expressed as a ratio of cardiac to peripheral blood (C/P) for
over one hundred drugs. The C/P ratio became the accepted
benchmark with the accepted guideline that high ratios were
associated with potential for redistribution [21].
In this investigation, only ve of the nine cases had greater
concentrations of sertraline in the central blood when compared to
the peripheral blood. The highest difference was 2.79 times that of
peripheral blood. For the nine cases studied, the central blood to
peripheral blood concentration (C/P) ratios averaged 1.22  0.85
(mean  standard deviation), with a range of 0.172.79. Norsertraline
exhibited analogous results; the C/P ratio averaging 1.43  0.91
(mean  standard deviation), with a range of 0.353.08. These results
are consistent with the small number of publications which have
described C/P ratios ranging from 0.56 to 1.4 for sertraline and 0.55 to
2.2 for norsertraline, and that there is essentially no difference
between peripheral and central blood concentrations [16,22]. Based
upon the C/P ratio model these numbers suggest, arguably, only a
minimal propensity for sertraline PMR; although the possibility of
some degree of PMR occurring in the peripheral blood cannot be
discounted.
Limitations of the C/P model, however, have been documented. While drug properties such as volume of distribution,
protein binding, and pKa are thought to contribute to PMR, a
relationship between C/P and drug properties has not been
established [23]. In addition, there has been little agreement as
to what ratio actually denes that a compound is prone to PMR,
or not [24]. Reports of a C/P ratio greater than 1.0 have been
published for salicylate and tramadol, which are not prone to
redistribution [24,25]. Arterio-venous differences, anatomic
variability within individuals, and statistical chance may result
in a C/P ratio greater than 1.0 in drugs that do not redistribute.
In addition, resuscitation attempts may result in a C/P ratio less
than 1.0 [26]. Inaccurate ratios may also be obtained as an
artifact of sampling when the cardiac blood volume is depleted
by the collection of blood from connected blood vessels, from

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I.M. McIntyre, P. Mallett / Forensic Science International 223 (2012) 349352

trauma, or in cases of acute overdose where the drug has not

undergone complete absorption and/or distribution.
The liver to peripheral blood ratio has been recently proposed as a
marker for PMR, with ratios exceeding 20 indicative of a propensity
for signicant PMR, and ratios less than 5 indicating little to no
propensity toward PMR [24,27]. The sertraline liver concentrations
reported in this investigation were markedly greater than both
peripheral and central blood concentrations for all cases. The liver to
peripheral blood (L/P) ratio averaged 97  40 (mean  standard
deviation). This ratio is greater than that reported in four cases in which
the cause of death was not related to sertraline intoxication (36  17;
mean  standard deviation [22]). Elevated liver concentrations as a
result of acute oral ingestion have been suggested as a possible
explanation, however, the ratios in cases considered therapeutic (cases
2 and 3), were higher than that of a probable overdose case (case 9).
Nevertheless, sertraline clearly demonstrates a L/P ratio exceeding 20
(similar in magnitude to that reported for tricyclic antidepressants)
which according to the model, suggests that it is prone to signicant
PMR. Additionally, sertraline is a basic, lipophilic compound with a
volume of distribution (Vd) reported to be 2050 L/kg [6], which is
consistent with reports that such drugs with a Vd greater than 3 L/kg
maybe prone to PMR. Using these criteria, sertraline is indeed expected
to demonstrate marked PMR.
Acknowledgement
The authors would like to thank the San Diego County Chief
Medical Examiner, Dr. Glenn Wagner, for making available case
details described in this manuscript.
References
[1] Physicians Desk Reference, 62nd ed., Thompson Healthcare Inc., Montvale, NJ,
2008.
[2] R.N. Gupta, S.A. Dziurdzy, Therapeutic monitoring of sertraline, Clin. Chem. 40
(1994) 498499.
[3] J. Lundmark, M. Reis, F. Bengtsson, Therapeutic drug monitoring of sertraline:
variability factors as displayed in clinical setting, Ther. Drug Monit. 22 (2000)
446454.
[4] S.J. Warrington, Clinical implications of the pharmacology of sertraline, Int. Clin.
Psychopharmacol. 6 (Suppl. 2) (1991) 1121.
[5] J.L. Demolis, P. Angebaud, J.D. Grange, P. Coates, C. Funck-Brentano, P. Jaillon,
Inuence of liver cirrhosis on sertraline pharmacokinetics, Br. J. Clin. Pharmacol.
42 (1996) 394397.

[6] R.C. Baselt (Ed.), Disposition of Toxic Drugs and Chemicals in Man, 9th ed.,
Biomedical Publications, Foster City, 2011, pp. 15461574.
[7] M.E. Mullins, J. Horowitz, Serotonin syndrome after a single dose of uvoxamine,
Ann. Emerg. Med. 34 (1999) 806807.
[8] A.A. Fisher, M.W. Davis, Serotonin syndrome caused by selective serotonin
reuptakeinhibitorsmetoclopramide interaction, Ann. Pharmacother. 36
(2002) 6771.
[9] D.O. Lee, C.D. Lee, Serotonin syndrome in a child associated with erythromycin
and sertraline, Pharmacotherapy 19 (1999) 894896.
[10] L.B. Myers, B.S. Dean, E.P. Krenzelok, Sertraline (zoloft): overdose assessment of a
new antidepressant, Vet. Hum. Toxicol. 35 (1993) 341.
[11] I.M. McIntyre, C.V. King, V. Staikos, J. Gall, O.H. Drummer, A fatality
involving moclobemide, sertraline, and pimozide, J. Forensic Sci. 42 (5) (1997)
951953.
[12] D.A. Milner, M. Hall, G.G. Davis, R.M. Brissie, C.A. Robinson, Fatal multiple drug
intoxication following acute sertraline use, J. Anal. Toxicol. 22 (1998)
545548.
[13] H.J. Carson, M. Zweigart, N.E. Lueck, Death from asthma associated with sertraline
overdose, Am. J. Forensic Med. Pathol. 21 (3) (2000) 273275.
[14] K.E. Goeringer, L. Raymon, G.D. Christian, B.K. Logan, Postmortem forensic toxicology of selective serotonin reuptake inhibitors: a review of pharmacology and
report of 168 cases, J. Forensic Sci. 45 (3) (2000) 633648.
[15] F. Musshoff, S. Banaschak, B. Madea, Postmortem distribution of sertraline and
desmethylsertraline in a fatality, Arch. Kriminol. 210 (12) (2002) 5156.
[16] K.E. Rodda, O.H. Drummer, The redistribution of selected psychiatric drugs in
post-mortem cases, Forensic Sci. Int. 164 (2006) 235239.
[17] J. Kassner, A. Woolf, Sertraline hydrochloride: correlation of clinical presentation
with plasma concentration, Vet. Hum. Toxicol. 35 (1993) 341.
[18] E.H. Forster, D. Hatchet, J.C. Garriott, A rapid comprehensive screening procedure
for basic drugs in blood and tissues by gas chromatography, J. Anal. Toxicol. 2
(1978) 5055.
[19] D.J. Pounder, G.R. Jones, Post-mortem drug redistribution a toxicological
nightmare, Forensic Sci. Int. 45 (1990) 253263.
[20] B.S. Prouty, W.H. Anderson, The forensic science implications of site and temporal
inuences on postmortem blooddrug concentrations, J. Forensic Sci. 35 (2)
(1990) 243270.
[21] M. Dalpe-Scott, M. Degouffe, D. Garbutt, M. Drost, A comparison of drug concentrations in postmortem cardiac and peripheral blood in 320 cases, Can. Soc.
Forensic Sci. J. 28 (1995) 113121.
[22] B. Levine, A.J. Jenkins, J.E. Smialek, Distribution of sertraline in postmortem cases,
J. Anal. Toxicol. 18 (1994) 272274.
[23] R.E. Ferner, Post-mortem clinical pharmacology, Br. J. Clin. Pharmacol. 66 (2008)
430443.
[24] I.M. McIntyre, J. Sherrard, J. Lucas, Postmortem carisoprodol and meprobamate
concentrations in blood and liver: lack of signicant redistribution, J. Anal.
Toxicol. 36 (3) (2012) 177181.
[25] J. Cook, R.A. Braithwaite, K.A. Hale, Estimating antemortem drug concentrations
from postmortem blood samples: the inuence of postmortem redistribution, J.
Clin. Pathol. 53 (2000) 282285.
[26] A.L. Pelessier-Alicot, J.M. Gaulier, P. Champsaur, P. Marquet, Mechanisms underlying postmortem redistribution of drugs: a review, J. Anal. Toxicol. 27 (2003)
533544.
[27] I.M. McIntyre, C. Meyer Escott, Postmortem drug redistribution, J. Forensic Res. 3
(2012) e108, http://dx.doi.org/10.4172/2157-7145.1000e108.