Thread: British student who disappeared after a beach party on a Cambodian island

Originally Posted by Seekingasylum

Are you totally stupid? If you are going to extrapolate a thesis from a comparison with data from another country citing indigenous victims then you must apply the same parameter in referencing data from the country with which you are making the comparison.
If you were to do this with reference to Cambodia and, say, Thailand then I think you will agree that not only are they dangerous but that the rape and murder rates suggest the offences are a fucking rite of passage.

Poor old SA, he feels cheated by the fact she wasn't raped and murdered.

The post mortem was completed some hours ago and no doubt some lab analyses are awaited but none of those involved in the autopsy is making any comment in the interim.

If it were a straightforward case of accidental drowning then one might have reasonably expected an official response sooner but of course it may be they are awaiting results that might shed light on whether or not she was intoxicated when she decided to take hr swim, ...... with her clothes on and alone. The report I read indicated that officials need to discuss "next steps" with the relatives before any announcement is made.

I have no idea what you mean by implying I will feel cheated if it transpires the girl did not die as a consequence of foul play. But then, you are a dribbling incoherent idiot after all.

To call you obsessive would be an understatement. You probably typed all this rabid nonsense one-handed. Your disappointment is palpable, and you're still whinging that because they aren't meeting your particular standards for doing autopsies then something sinister must have happened, thus feeding your over-excited blathering. All this from one thread with not a shred of evidence as to what happened (and even after there was).

Originally Posted by Seekingasylum

There seems to be a suspension of disbelief among the British middle classes, and Europeans for that matter, who believe that SE Asia isn't a third world destination where the populations comprise a significant strata of society who, given the opportunity, will kill, rape and steal on no more than a passing whim and give it no more thought than they would to eating a bowl of rice.

Originally Posted by Seekingasylum

"Wise after the event " has fuck all to do with it Cecilia, western women have been mugged, raped and murdered over the past two decades in "these circumstances" but as we all know not one of the victims ever believes it would happen to her.

Originally Posted by Seekingasylum

If she had gotten into difficulties while swimming then her body would have washed up somewhere by now, one would have thought. Abduction is the Occam's choice and they simply missed the bag leaving it in situ.

Originally Posted by Seekingasylum

The irony of Thai fishermen raping and killing a westerner in Cambodia would certainly be a twist of fate.

Originally Posted by Seekingasylum

If you were to do this with reference to Cambodia and, say, Thailand then I think you will agree that not only are they dangerous but that the rape and murder rates suggest the offences are a fucking rite of passage.

Perhaps this will calm your frayed nerves.

On Friday, Cambodian National Police told CNN that they had completed an autopsy overseen by a British consular official. Police found that Bambridge died by drowning and said there were no signs of foul play.

https://edition.cnn.com/2019/10/31/a...intl-hnk-scli/

Originally Posted by harrybarracuda

Poor old SA, he feels cheated by the fact she wasn't raped and murdered.

only a frigging loon like yourself could think of it that way

Police found that Bambridge died by drowning and said there were no signs of foul play.

after a week drifting in the warm polluted waters of the gulf of siam, i would imagine that decomposition would have ravaged the corpse to such an extent that a post mortem conducted in cambodia would reveal very little, other than she is dead and has been in salt water for a week.


Not every individual, whose body is recovered from water, has drowned.

When a body is recovered from water, the significant issues raised are frequently:

Is the estimated post mortem interval consistent with witness evidence?
Is there any pathological evidence to indicate cause of death?
Is there any pathological evidence of natural disease, ante mortem injury or assault capable of providing an explanation for how the deceased came to find himself/ herself in, or fail to remove himself/ herself from, the water?

An additional problem for those investigating the deaths of those recovered from water is identification; frequently a body recovered from water is not capable of being identified by visual means, and other forms, such as dental or DNA identification will be required.



the forensic pathological approach to bodies recovered from water - the big picture






post mortem interval.

Estimation of post mortem interval in water is unreliable (Giertsen 2000), but temperature is likely to be the most important factor governing decompositional changes.

There may be signs of immersion (wrinkling of the skin of the palms and soles; loosening of the skin, hair or nails); Polson and Gee (1973) state that maceration of the (exposed) hands and feet is likely to become ‘well established’ during the first week, showing signs of separation of the skin of the digits towards the end of that week. Detachment of skin becomes likely in the second week.

As a matter of interest, research into the process(es) underlying wrinkling of the skin of the fingers following immersion in water in life have hypothesised that water permeates sweat ducts and alters the electrolyte composition, following which autonomic nerve fibres in the digits are triggered. These mediate vasoconstriction, resulting in negative digit pulp pressure (Wilder-Smith and Chow 2002 and 2003).

The epidermis of the digit skin is firmly anchored to the deep dermis via epidermal ridges, which insert every 1mm along longitudinal lines, and this anchoring - which allows us to firmly gripo objects - results in variations in skin tautness (maximal at anchorage sites). Resistance blood vessels in digits are distributed in an inhomogenous manner; large numbers of 'glomus organs/ bodies' are present, which lose volume through vasoconstriction and help create negative digit pulp pressure. A pressure gradient between deep and superficial structures induces a downward pull on the overlying skin. This downward pull is uneven, and leads to the wrinkling seen following immersion.




(a) Evidence of drowning.
Regardless of the composition of water/ fluid, ‘drowning’ (the ‘process of experiencing respiratory impairment from submersion in a liquid’ (van Beeck et al 2005)), may result in pulmonary surfactant insufficiency/ damage, pulmonary oedema, alveolitis, hypoxaemia, and metabolic acidosis (Modell 1993, Pearn 1985, Orlowski 1987).

Extensive experimental (animal) and clinical (human) data exist in the scientific literature, identifying differences between, for example, fresh water and seawater drowning; active respiration of fresh water results in alveolar collapse/ atelectasis, due to the alteration of the surface tension properties of pulmonary surfactant, resulting in intra-pulmonary shunts. Because it is hypotonic with respect to plasma, fresh water is rapidly absorbed into the bloodstream, causing transient (but clinically irrelevant) electrolyte dilution and hypervolaemia. Sea water causes surfactant loss, and because it is hypertonic with respect to plasma, results in fluid shifts into alveoli, plasma electrolyte hyperconcentration and hypovolaemia. (Modell 1993, Pearn 1985, Modell and Davis 1969, Modell et al 1966).

Fresh/ seawater aspiration leads to systemic hypoxaemia causing myocardial depression, reflex pulmonary vasoconstriction and altered pulmonary capillary permeability contributing to pulmonary oedema (Lunetta and Modell 2005).

Experimental evidence (Modell and Moya 1966, Modell et al 1967) shows that there is an inverse relationship between survival and the volume of aspirated fluid (sea water being twice as lethal as fresh water), but even small quantities (i.e. as little as 30 mL) caused arterial hypoxaemia.

Autopsy findings ascribed to drowning (‘external’ foam (i.e. visible at the mouth or nostrils), frothy fluid in the airways and lung ‘hyper-expansion’ reflect the pathophysiology of submersion and aspiration of the drowning medium; none of these, however, is diagnostic of drowning or present in all ‘verified’ drownings. (Lunetta and Modell 2005, Saukko and Knight (2004), Modell et al 1999).

In a series of 1590 bodies recovered from water, Lunetta et al (2002) found external foam in 29%, froth in the airways in 70.6% and overlapping of the lung margins in 64.1% of ‘fresh bodies’ of ‘verified drownings’; the combination of all three was present in only 8.8% of cases, but was said to be ‘100% specific for drowning’.

Suggested ‘signs of drowning’ reported in the literature include;
(i) External foam/ froth and frothy fluid in the airways reflects an admixture of bronchial secretion/ mucus, proteinacious material and pulmonary surfactant with the aspirated liquid (Lunetta et al 2002), which may persist for several days after death, and has been described as being ‘different in quality’ – more tenacious and persistent - from pulmonary oedema produced by other conditions (including cardiac failure, for example)(Modell et al 1999). Frothy secretions may be ‘washed away’ by flowing water during the submersion or recovery period, or may be absent due to the length of time spent immersed.

(ii) ‘Emphysema aquosum’ is the term used to describe hyperexpanded and ‘waterlogged’ lungs, whose medial margins ‘meet in the midline’, and which do not collapse on removal from the body. There may be ‘rib imprints’ on their pleural surfaces, and copious frothy fluid may exude from their cut surfaces (Giertsen 2000, Saukko and Knight 2004). See Magdeburg University's Virtual Pathology website for a 'pot specimen' of emphysema aquosum which can be rotated using your mouse wheel.

Combined lung weight of over 1Kg are comparable with ‘normal’ lung weights (de la Grandmaison et al 2001), but overlapping with that seen in fresh water drownings in Copeland’s series (Copeland 1985). However, Lunetta et al (2002) argue that lung weight alone is of ‘limited value’ for the diagnosis of drowning.

(iii) Pleural fluid accumulation. It has been stated (Morild 1995) that there is an association between drowning, post mortem submersion/ immersion interval and pleural fluid accumulation. However, data to the contrary has been presented by Yorulmaz et al (2003).

(iv) Sub-pleural haemorrhages (‘Paultauf’s spots’). These probably reflect haemolysis within intra-alveolar haemorrhages, and have been described in 5-60% of drownings (Lunetta and Modell 2005).

(v) Additional (morphological) ‘signs’ of drowning - ‘middle ear congestion and haemorrhage’, bloody/watery fluid in the sinuses and engorgement of solid organs, including the liver, reduction in the weight of the spleen, and muscular haemorrhages in the neck and back, are non-specific (Lunetta and Modell 2005).

(vi) Microscopy (particularly of the lungs) in the diagnosis of drowning has been described as yielding ‘nothing conclusive’(Giertsen 2000) and is ‘unreliable’ (Saukko and Knight 2004); there may be distension and/ or rupture of alveolar walls, alveolar haemorrhage and ‘narrowing of pulmonary capillaries’ (Lunetta and Modell 2005).

(vii) Diatom testing. Samples of major organs, and bone marrow, are often retained for diatom testing (eg. Kidney, liver, brain). The utility of such testing is ‘controversial’ (Peabody 1980); diatoms have been said to be ubiquitous in food and the environment, in non-drowning deaths, and absent in ‘known cases of drowning’. (Saukko and Knight 2004, Hendy 1973, Foged 1983).

(viii) Blood chloride content/ specific gravity analysis is considered to be ‘of no practical utility for the diagnosis (of drowning)’ (Lunetta and Modell 2005); analysis of blood strontium (Azaparren et al 1998) has also been suggested as a means with which drowning may be diagnosed.



(b) Evidence of an alternative mechanism(s)?
Drowning without evidence of liquid aspiration (‘dry drowning’) has been reported in up to 15% of cases, although in a series of 578 adults presumed to have drowned (Lunetta et al 2004), only 1.4% had lungs of ‘normal weight’ and no macroscopic signs of over-inflation.

Rather than represent true ‘drowning’, these deaths may be due to an alternative mechanism such as trauma, the effects of intoxication, arrhythmia, laryngospasm, or some other neurologically mediated mechanism (Modell et al 1999, Saukko and Knight 2004).

Stimulation of trigeminal nerve receptors by immersing the face (and laryngeal/ pharyngeal mucosa) in water has been shown to elicit reflex apnoea, bradycardia and peripheral vasoconstriction in humans- the so-called ‘diving response’ (Suzuki 1996, De Burgh Daly et al 1979), which is augmented by anxiety/ fear (Wolf 1966), a water temperature of less than 20 ºC (Pearn 1985) and, possibly, alcohol (Pearn 1984), increasing the likelihood of the development of a fatal arrhythmia. Cardiac arrest has also been documented following entry of water into the nose (Datta and Tipton 2006).

The ‘cold shock response’ - initiated by peripheral subcutaneous receptors - causes respiratory effects (inspiratory gasp and uncontrolled hyperventilation, respiratory alkalosis, cerebral hypoxia and possibly ventricular fibrillation) and cardiovascular effects (tachycardia, increased cardiac output, hypertension and ‘heart strain’, potentially leading to cardiac irritability and ventricular fibrillation), which appear temperature dependent (Tipton 1989, Datta and Tipton 2006). Co-stimulation of both diving and cold shock responses may precipitate supraventricular arrhthmias (Golden et al 1997).









why was the deceased in the water, and why could they not get out?

(a) Intoxication.
Despite evidence that alcohol is frequently found in the blood of adult drowning victims (Howland and Hingson 1988, Quan and Cummings 2003, Wintermute et al 1990), a causative role between alcohol and drowning has not been proven.

Lunetta et al (2004) found that the strongest association between drowning and alcohol was in relation to ‘fall-related’ cases (82.8%), and it is possible that an individual, whose body is recovered from water, came to be in the water because of an accidental fall due to alcohol intoxication. It is also an individual may have suffered a fatal alcohol-related concussive head injury, for example (Milovanovic and Di Maio 1999, Ramsay and Shkrum 1995).

Suicide by drowning is rare (and not usually associated with alcohol intoxication); reports in the literature estimate 4.5% (Copeland 1987) to 8.9% (Avis 1993) of all suicides.



(b) Natural disease.
Had the deceased any history of cardiovascular disease, or seizure disorder, capable of providing an explanation for falling into a body of water, or for their inability to get out of the water, following an arrhythmia/ seizure?



(c) Ante mortem injury/ assault.
The ‘vast majority of homicidal drownings’ involve forms of violence such as ‘beating’ and stabbing etc (Lunetta and Modell 2005). Careful evaluation of any injuries present is required in order to determine whether any could have been caused by assault during life. Injuries to the facial skeleton, neck (including larynx) or ulnar borders of the arms (suggestive of ‘defensive’ injuries), for example, should be excluded. It is not always possible, due to the effects of immersion, confidently to determine whether all or some of the injuries present are ante/ peri or post mortem in origin. Marine animals/ fish may cause skin, soft tissue or skeletal damage that may sometimes cause interpretation difficulties (Rutty 2001), and injuries caused by contact between the body and submerged objects, structures, rocks, gravel etc are frequently seen. In some bodies of water, damage may be caused by propeller blades, resulting in severe ‘chopping injuries’ and amputations.









cause/ manner of death
‘Classical’ anatomical signs of drowning are frequently absent, and this may be a reflection of post mortem interval; their absence does not exclude the diagnosis.

On the pathological/ toxicological findings alone, it is not always possible to be certain about the most likely cause of death in the case of a body recovered from water. A ‘diagnosis’ of drowning may be possible, but in some cases where a range of possibilities exist, it may be considered appropriate (Davison and Leadbeatter 1996) to give the medical cause of death as; 1a Indeterminate.

The manner of death is frequently accidental, but suicidal drowning has been described (Copeland 1987, Avis 1993), and disposal of bodies in water is well recognised following homicide (Copeland 1986).

references
Avis SP. Suicidal drowning. Journal of Forensic Sciences 1993; 38: 1422-1426
Azaparren JE, Vallejo G, Reyes E et al. Study of the diagnostic value of strontium, chloride, haemoglobin and diatoms in immersion cases. Forensic Science International 1998; 91: 123-132
Copeland AR. An assessment of lung weights in drowning cases – the Metro Dade County experience from 1978 to 1982. The American Journal of Forensic Medicine and Pathology 1985; 6(4): 301-304
Copeland AR. Homicidal drowning. Forensic Science International 1986; 31: 247-252
Copeland AR. Suicide by drowning. The American Journal of Forensic Medicine and Pathology 1987; 8: 18-22
Datta A, Tipton MJ. Respiratory responses to cold water immersion: neural pathways, interactions, and clinical consequences awake and asleep. Journal of Applied Physiology 2006; 100: 2057-2064
Davison AM, Leadbeatter S. Confession of ignorance of causation in coroners’ necropsies – a common problem?. Journal of Clinical Pathology 1996; 49:439-443
De Burgh Daly M, Angell-James JE, Elsner R. Role of carotid-body chemoreceptors and their reflex interactions in bradycardia and cardiac arrest. The Lancet 1979; 1(8119): 764-767
de la Grandmaison GL, Clairand I, Durigon M. Organ weight in 684 adult autopsies: new tables for a Caucasoid population. Forensic Science International 2001; 119: 149-154
Foged N. Diatoms and drowning – once more. Forensic Science International 1983; 21: 153-159
Franks CM, Golden FS, Hampton IF, Tipton MJ. The effect of blood alcohol on the initial responses to cold water immersion in humans. European Journal of Applied Physiology and Occupational Physiology 1997; 75: 279-281
Giertsen JC. ‘Drowning’, Chapter 16 In: ‘The pathology of trauma’, Mason JK, Purdue BN (Eds), 3rd Edition, Arnold Publishing 2000, London UK
Golden F St C, Tipton MJ, Scott RC. Immersion, near-drowning and drowning. British Journal of Anaesthesia 1997; 79: 214-225
Hendy NI. The diagnostic value of diatoms in cases of drowning. Medicine, Science and the Law 1973; 13: 23-34
Howland J, Hingson R. Alcohol as a risk factor for drownings: a review of the literature (1950-1985). Accident Analysis and Prevention 1988; 20: 19-25
Lunetta P, Penttila A, Sajantila A. Circumstances and macropathologic findings in 1590 consecutive cases of bodies found in water. The American Journal of Forensic Medicine and Pathology 2002; 23(4): 371-376
Lunetta P, Modell JH, Sajantila A. What is the incidence and significance of ‘dry lungs’ in bodies found in water?. The American Journal of Forensic Medicine and Pathology 2004; 25: 291-301
Lunetta P, Smith GS, Pentilla A, Sajantila A. Unintentional drowning in Finland 1970-2000: a population-based study. International Journal of Epidemiology 2004; 33: 1053-1063
Lunetta P, Modell JH. Macroscopical, microscopical, and laboratory findings in drowning victims – A comprehensive review. Chapter 1. In: ‘Forensic Pathology Reviews – Volume 3’, Tsokos M (Ed), Humana Press 2005, Totowa USA
Milovanovic AV, Di Maio VJM. Death due to concussion and alcohol. The American Journal of Forensic Medicine and Pathology 1999; 20: 6-9
Modell JH, Gaub M, Moya F et al. Physiological effects of near drowning with chlorinated fesh water, distilled water and isotonic saline. Anesthesiology 1966; 27: 33-41
Modell JH, Moya F. Effects of volume of aspirated fluid during chlorinated fresh water drowning. Anesthesiology 1966; 27: 662-672
Modell JH, Moya F, Newby EJ et al. The effects of fluid volume in seawater drowning. Annals of Internal Medicine 1967; 67:68-80
Modell JH, Davis JH. Electrolyte changes in human drowning victims. Anesthesiology 1969; 30: 414-420
Modell JH. Current concepts: Drowning. New England Journal of Medicine, 1993; 328(4): 253-256
Modell JH, Bellefleur M, Davis JH. Drowning without aspiration: is this an appropriate diagnosis?. Journal of Forensic Sciences 1999; 44: 1119-1123
Morild I. Pleural effusion in drowning. The American Journal of Forensic Medicine and Pathology 1995; 16: 253-256
Orlowski JP. Drowning, near-drowning, and ice-water submersions. Pediatric Clinics of North America 1987; 34: 75-92
Peabody AJ. Diatoms and drowning – a review. Medicine, Science and the Law 1980; 20: 254-261
Pearn J. Drowning and alcohol. Medical Journal of Australia 1984; 141: 6-7
Pearn J. Pathophysiology of drowning. The Medical Journal of Australia 1985; 142: 586-588
Polson CJ, Gee DJ. Drowning. Chapter 11. In: ‘The essentials of forensic medicine’, Polson CJ and Gee DJ (3rd Edition), Pergamon Press 1973, Oxford, UK
Quan L, Cummings P. Characteristics of drowning by different age groups. Injury Prevention 2003; 9: 163-168
Ramsay DA, Shkrum MJ. Homicidal blunt head trauma, diffuse axonal injury, alcohol intoxication, and cardiorespiratory arrest: a case report of a forensic syndrome of acute brainstem dysfunction. The American Journal of Forensic Medicine and Pathology 1995; 16: 107-114
Rutty GN. Post-mortem changes and artefacts. Chapter 4. In: ‘Essentials of autopsy practice – Volume 1’, Rutty GN (Ed), Springer-Verlag London Limited 2001, UK
Saukko P, Knight B. Immersion deaths. Chapter 16. In: ‘Knight’s Forensic Pathology’, 3rd Ed Saukko P, Knight B (Eds), Arnold Publishing 2004, London UK
Suzuki T. Suffocation and related problems. Forensic Science International 1996; 80: 71-78
Tipton MJ. The initial responses to cold-water immersion in man. Clinical Science 1989; 77: 581-588
van Beeck EF, Branche CM, Szpilman D et al. A new definition of drowning: towards documentation and prevention of a global public health problem. Bulletin of the World Health Organisation, Volume 83 Number 11 November 2005
Wilder-Smith E, Chow A. Water immersion and EMLA cause similar digit skin wrinkling and vasoconstriction. Microvascular Research 2003; 66:68-72
Wilder-Smith E, Chow A. Water-immersion wrinkling is due to vasoconstriction. Muscle and Nerve 2003; 27:307-311
Wintemute GJ, Teret SP, Kraus JF, Wright M. Alcohol and drowning: an analysis of contributing factors and a discussion of criteria for case selection. Accident Analysis and Prevention 1990; 22: 291-296
Wolf S. Sudden death and the oxygen-conserving reflex. The American Heart Journal 1966; 71: 840-841
Yorulmaz C, Arican N, Afacan I et al. Pleural effusion in bodies recovered from water. Forensic Science International 2003; 136: 16-21


Read more: bodies recovered from water :: www.forensicmed.co.uk

I think you can leave the family in peace now, rather than continue to post this idiotic conspiratorial nonsense.

She drowned. She probably went out too far and lost her bearings in the dark.

It's very sad, and it definitely doesn't need the insane ramblings of a bunch of paranoid whackjobs frankly.

Originally Posted by harrybarracuda

I think you can leave the family in peace now, rather than continue to post this idiotic conspiratorial nonsense.

She drowned. She probably went out too far and lost her bearings in the dark.

It's very sad, and it definitely doesn't need the insane ramblings of a bunch of paranoid whackjobs frankly.

Its still a mystery on what actually happened.

I dont think its very common for ppl to wade out into the water with their cloths on at full moon parties.

^ Unless they have taken too much acid - which people take quite frequently at full moon parties. But doing it fully clothed is not what you think would be the norm, I agree....... but if she was really tripping ??

Originally Posted by Wally Dorian Raffles

^ Unless they have taken too much acid - which people take quite frequently at full moon parties. But doing it fully clothed is not what you think would be the norm, I agree....... but if she was really tripping ??

Yeah maybe. And the acid will be long gone from her system. As would ketamine and other party drugs. They are out of the system in 1 day.

So the only way to get to the bottom of that is to see what kinds of drugs were on offer around there at the time.

They are out of the system in 1 day.

for those with a background in physiology this article on the breakdown of drugs in the body after death is interesting.
dont be put off by the length of the article.



Interpreting postmortem drug analysis and redistribution in determining cause of death: a review

Received 14 April 2015

Accepted for publication 11 June 2015

Published 3 August 2015 Volume 2015:7 Pages 55—62

DOI https://doi.org/10.2147/PLMI.S65245



Editor who approved publication: Dr Paul Zhang

Article has an altmetric score of 1

Michael Kennedy

Department of Clinical Pharmacology & Toxicology, St Vincent's Hospital, University of New South Wales, Sydney, NSW, Australia

Abstract: Multiple interacting factors alter the measured concentration of almost all drugs after death. The ratio of centrally to peripherally collected samples provides an indication of this redistribution. At present, there are no reliable markers from which to accurately predict how much an individual drug has redistributed. Knowledge of antemortem factors is essential for the interpretation of the effects of any measured drug or toxin.

Keywords: postmortem drugs, drug redistribution

Introduction

Correct interpretation of postmortem drug concentrations is becoming increasingly important in forensic pharmacology and as an adjunct to clinical toxicology. The finding of drugs in a dead body can raise important questions – and may sometimes provide immediate answers – about cause of death and antemortem events. This in itself is not new. Postmortem assaying of drugs and toxic agents commenced in the mid-nineteenth century with chemical analysis being used to detect arsenic and antimony. At the time, this new technology resulted in some spectacular murder convictions that would have previously gone undetected.1,2 Technology today is of course far superior to the classical quantitative methods of 150 years ago, and detecting a drug in a dead body is only the first step in a long and sophisticated process of measurement and interpretation of drug concentrations. Nevertheless, McBay’s summation of the process made in 1973 is still highly relevant: “In the absence of an autopsy or an enlightening medical history, it is difficult to determine how the amount of a specific poison in a person might be interpreted”.3

Coming to the right conclusion about levels of pharmacological agents found after death is important. Various interested parties such as relatives of the deceased, clinical review processes, and judicial bodies receiving the results will act on these conclusions. The case of the Dr Harold Shipman, now estimated to have murdered 220 patients during his practicing life, serves as an example of getting it right. Vital evidence resulting in his conviction and subsequent imprisonment for murder was drug analysis and interpretation of the morphine concentrations found in nine exhumed bodies.4 Similarly, not reaching a wrong conclusion about levels of pharmacological agents found after death is essential to avoid gross miscarriages of justice.5

Most analytical work is performed by mass spectroscopy with subsequent ability to interpret very low concentrations of a larger number of drugs. The databases have grown considerably, and these advances have resulted in a number of areas relevant to forensic science. The overlap between “therapeutic”, “toxic”, and “lethal” concentrations has largely made these terms obsolete.6 The mechanisms and predictions of drugs that alter their concentrations after death is now better understood.

The concentrations of most drugs alter after death as a result of numerous mechanisms. These and other factors identified as changing the concentration of a drug postmortem are presented in Table 1.


Table 1 Factors affecting drug concentrations reported after death

Evidence base

The largest database of pharmacodynamic and pharmacokinetic parameters of most drugs is based on live subjects, most of whom are normal healthy volunteers. Correlations between plasma concentrations and therapeutic responses and toxicity have been obtained from patients and always need to be interpreted in relation to the individual clinical case. As clinical use of any particular drug expands, a larger database becomes established. This in turn expands on earlier data.

The database for the living is considerably larger than what is established in the area of forensic pharmacology. Most data in this area, sometimes termed necropharmacology, have been obtained from samples obtained from forensic autopsies. Each month, there are additions to the world literature in the form of case reports or small series reporting drug concentrations in varieties of circumstances. There are a number of comprehensive tabulations of postmortem drug concentrations that are valuable sources of information. In 1990, Prouty and Anderson tabulated the concentrations of 69 drugs from numerous vascular sites and solid organs obtained from hundreds of individuals who died under various conditions.7 Druid and Holmgren’s examination of 15,000 samples, collected from medico-legal autopsies conducted in six laboratories in Sweden between 1992 and 1995, remains one of the most comprehensive retrospective reports. The authors tabulated the femoral concentrations of 83 drugs in relation to whether 1) the drug exclusively caused death on its own, 2) the drug caused death in combination with other substances, 3) the drug was associated with death due to other causes, and 4) a group was associated with suspected drug-related driving deaths.8 In 2012, Schulz et al compiled a comprehensive tabulation of almost 1,000 drugs and xenobiotics from various sources.9 The percentile distributions of postmortem concentrations of the top 25 drugs in Sweden serves as a guide to concentrations causing death and is useful in “flagging” a drug-related death.10

Baselt’s Disposition of toxic drugs and chemicals in man is a standard reference text. It includes details of individual pharmacokinetic, binding properties and physicochemical and stability properties on a very large number of drugs and poisons.11 Repetto and Repetto compiled a reference table of 103 drugs with the proviso: “Although these data may be useful they should not be taken as absolute. Precaution must be taken when interpreting these values and relating them to a particular case.”12 In other words, each case is subject to its own characteristics. With increased analytical sophistication and ever-growing interest from clinical, media, and legal areas, the database is slowly increasing, but there remain large areas that still require extensive research.

Drug concentrations measured in deceased individuals will rarely be the same as they were at the time of death. This was not fully appreciated until the 1970s, at which time, Bailey and Shaw reported considerable variations in amitriptyline concentrations in various organs.13 Later, in a much referenced article, Jones and Pounder describe the considerable variations in the concentrations of imipramine, desipramine, diphenhydramine, codeine, and paracetamol at different sites within the body of a female aged 25 who had died as a result of the polydrug overdose.14 These differences in concentrations are not due to any single factor. In most cases, it is the sum of multiple factors combining to alter the concentration of a drug after death. The relative importance of these factors will differ considerably between an individual who dies almost immediately after receiving a single dose of a drug and one who is in a pharmacokinetic steady state with the drug at the time of death. The resulting changes are sometimes grouped together and named “postmortem redistribution”. This term was coined by Pounder and Jones in 1987. In 1990, Pounder further described it as “toxicological nightmare”.15 Both terms continue to be used to the present day.

The relative contribution of the various processes presents an everyday challenge to scientists and clinicians interpreting the analytical results obtained from autopsy samples.

The considerable technical complexities associated with the processing and analysis of collected samples have been reviewed by Drummer and Gerostamoulos and will not be discussed in this review.16

The body

Complete information as to the circumstances surrounding death is essential. In some cases, such as suicide by a complex task such as self-hanging, it may be irrelevant to cause of death. However, if an antidepressant or antipsychotic medication is detected, it may be important in ascertaining the mental state of the individual, irrespective of the concentration measured.

Some drugs such as paracetamol and Paraquat will have caused death long after the drug could be detected in samples of blood.17,18 Drug screening is an important part of standard protocols for diagnosing brain death, but once the diagnosis has been made, concentrations of drugs such as propoxyphene may rise considerably when respiratory support is maintained but hepatic necrosis is continued.19 Bodies are usually stored at 4°C, and autopsies are usually conducted within a few days of death. Often these ideal conditions are not met with numerous factors coming into play that will have a major effect on the concentrations of drug(s) assayed.

The sample

Almost all baseline pharmacokinetics and plasma concentration monitoring have been undertaken on plasma samples collected from venous blood. Antemortem samples are extremely important in ascertaining a cause of death but are a rare occurrence outside of hospitals. Forensic samples are usually blood collected from a femoral site, but at times, blood may be collected from central veins, the subclavian vein, or cardiac chambers in cases where femoral samples are unavailable such as in decomposed or burnt bodies. Blind stick collection of femoral samples are probably as reliable as samples obtained from a cut-down and ligated vein, which also allows samples to be collected prior to the formal autopsy.20 The use of whole blood complicates the interpretation of some results, where the red blood cell/partition ration is less or greater than one. For example, phenytoin has a partition ratio of 0.5–0.6, and may in part, account for lower concentrations being found postmortem, while chloroquine concentrations are three to ten times that of plasma due to binding to platelets and granulocytes.21,22

Urine samples are easy to collect and contain either parent drug or metabolite(s). Collection of gastric contents will give information and to very recent ingestion of drug, vitreous humor is of particular value in cases involving alcohol, and samples of solid organs such as liver, brain, adipose tissue, hair, and bone may also be collected under special circumstances. To ensure the chemical stability of the drug is maintained, it is essential that correct collection procedures be used for collection, transport, and short- and long-term storage of samples.

Finally, the concentration measured must be as close as possible to the true concentration present at the time of collection. Some drugs such as olanzapine are inherently unstable; hence, concentrations measured will be lowered as time progresses and will underestimate the degree of postmortem redistribution.23 In Australia, the Victorian Institute of Forensic Medicine is authorized to obtain femoral blood samples from a body on arrival at the morgue prior to the formal autopsy being undertaken at which time a second femoral sample is collected often days later. In the investigation of antipsychotic drugs in 273 paired blood samples, haloperidol, quetiapine, and risperidone showed little change but up to 112% increases were found for chlorpromazine and decreases of up to 43% in the case of 9OH-risperidone.23 While plasma samples collected for routine analysis in the clinical situation pose few technical problems, in the forensic area, tissue samples are sometimes obtained from numerous organs. Analytical procedures need to ensure the results have not been altered by matrix effects caused by substances present in the tissue sample and also involve hemolyzed stored blood in the case of valproate.24,25

Alterations in concentrations after death

Multiple biochemical changes such as rapid elevations in potassium to very high concentrations occur in the immediate postmortem period due to failure of the Na ATPase pump before hemolysis occurs.26 Oxidative phosphorylation ceases, synthesis of adenosine triphosphate stops, and cellular metabolism changes to anaerobic glycolysis. These result in changes such as lactate levels plateauing at 9 hours, reaching maximal levels at 32–48 hours, and pH falling to maximal levels at 96 hours.27 Details of multiple biochemical changes and their forensic implications, such as the relationship to the time of death and other factors, have been comprehensively reviewed elsewhere.28 The conditions of body storage and the time since death are also critical in relation to processes altering the concentrations of drugs.

Continuing metabolic activities within the body

Numerous differing processes continue the transformation of drugs within the body after death. Cocaine concentrations will be lowered by continuing spontaneous hydrolysis to benzoylecgonine and also enzymatic conversion to ecgonine methyl ester. Very recent dosing may be determined by the ratio of benzoylecgonine to cocaine in a sample, where a very elevated cocaine concentration and low concentration of benzoylecgonine may represent very recent consumption.29

Bacterial invasion of the body commences almost immediately after death and metabolizes numerous sulfur-containing antipsychotics such as chlorpromazine, nitrobenzodiazepines such as clonazepam, and the benzisoxazole derivative risperidone at times, with only metabolites of the parent drugs being detected.30–32 Concentrations of physiological compounds such as, for example, gamma-hydroxybutyrate may rise as a result of continuing metabolism.33,34 Ethyl alcohol can rise to quite high concentrations as a result of bacterial metabolism, which is of considerable importance in determining the sobriety of the driver of a transport vehicle involved in an accident. In a study of decomposed bodies, Zumwalt et al found concentrations ranged from 10 mg/dL to 130 mg/dL in cases where ethyl alcohol was not detected in the vitreous.35 Other compounds such as formaldehyde rise in lesser concentrations. The quantitation of nonethanol compounds, such as n-propanol, is rarely undertaken but may assist in determining whether ethanol is the result of bacterial synthesis.36 Culture of collected samples for bacterial contamination is rarely undertaken in routine forensic work.

Drug diffusion from the gut and other reservoirs

Drug diffusion from the gut and other reservoirs must be differentiated from diffusion from sites of high drug concentrations such as heart, lung, and liver. These are considered in the area of drug redistribution from sites of high tissue concentrations.

Human cadaveric studies using various concentrations of instilled ethyl alcohol and methanol into the stomach showed time-dependant diffusion into the pericardial fluid and lesser diffusion into the surrounding vessels. The same investigators infused ethanol into the ligated esophagus and found similar aortic blood ethanol concentrations, and so concluded that postmortem esophageal reflux will cause elevations in this area.37 Further studies using gastric instillations of amitriptyline, paracetamol, and lithium show extensive diffusion from the stomach and upper small bowel into the base of the left lung, the left lobe of the liver and spleen and less diffusion into the gall bladder, aorta, inferior vena cava, kidneys, and psoas muscles.38

Continued absorption of pharmaceutically formulated slow-release drugs would also be expected to occur from more distal areas of the gut well after a dose had been ingested and departed from the stomach. Overdoses of carbamazepine, a drug with profound anticholinergic effects, has slow and erratic absorption with maximal concentrations occurring up to 70 hours after ingestion. In this example, large amounts of drug would remain in the bowel for later local diffusion if death occurs early in the course of an overdose.39 Unusual cases including high concentrations of drug diffusion from other sites include diphenhydramine and dihydrocodeine diffusing from the bladder to the femoral vein, resulting in higher concentrations than that were found at other sites,40 and similar findings were found in fatal cases of intravaginal methamphetamine.41

Movement of drugs within the body

After death, the integrity of cell membranes is lost, and multiple complex processes of drug transport metabolism and storage within vesicles and other structures are destroyed over varying periods of time.

From sites with high organ concentrations

Drugs vary greatly in their tissue distribution, and many of the published data have been obtained from forensic cases. For example, digoxin is concentrated in myocardium and amitriptyline in liver, resulting in elevated concentrations of these drugs if samples are collected from nearby vessels.

Effect of volume of drug distribution

Body density is approximately 1 kg/L, so a uniformly distributed drug will have a volume of drug distribution (Vd) of 70 L.42

Numerous physicochemical factors contribute to a drug’s Vd, including its lipid solubility, protein binding in plasma, and its pKa. In addition to these factors, a drug’s uptake into and out of tissues is also dependent on numerous transport processes. The hypothesis that postmortem redistribution can be predicted by a drug having a Vd of >3 L/kg does not hold for all drugs as there are numerous outliers. A similar circumstance applies to prediction in relation to lipid solubility as measured by the octanol/water partition coefficient.42

Time durations

The quantity of drug measured postmortem will not remain the same over time. Movement of morphine from areas of high concentration into cardiac blood occurs within minutes after death in rats.43 While similar data are of course not available for humans, field samples of cardiac blood showed lower concentrations of amitriptyline, nortriptyline, thioridazine, diphenhydramine, chlorpromazine, doxepin, methadone, ethchlorvynol, pethidine, phentermine, phencyclidine, methamphetamine, and amphetamine than samples collected later at autopsy.7 Some drugs have now been shown to have time-related changes occurring in the days after death even allowing for factors such as continuing endogenous and bacterial metabolism and chemical instability. For example, the concentrations of clozapine rose by >70% at 4 days and promethazine by >170% at 3 days with subsequent falls to low concentrations at 6 days and 5 days, respectively, indicating that there are still a number of unknown and unpredictable factors altering postmortem concentrations.23

Markers of postmortem redistribution

The term redistribution presents a problem as it implies that a drug will disseminate itself within the body without alteration. This is not the case for most drugs or toxic agents. Traditionally, it has been considered that, as a general rule, drugs with a large Vd are most likely to undergo redistribution because of their wide distribution into body tissues with a figure of 3–4 L/kg being a relative threshold for this to occur, as well as the presence of a high central to peripheral drug ratio.44

The ratio of central to peripheral blood concentrations

The ratio of central to peripheral blood concentrations (C/P ratio) assumes considerable prominence when opinions are given in relation to postmortem drug concentrations. A ratio is often referred to as a means of estimating, or at least deciding, that postmortem assayed result is going to be higher or lower than the antemortem concentration. There are considerable variations in the C/P ratio within individual drugs as seen in Table 2. Dalphe-Scott et al published the C/P ratios for 113 drugs obtained from 320 cases of which only six (ephedrine, hydrocodone, hydroxyzine, metoprolol, procyclidine, and trifluoperazine) had a maximal C/P ratio of 1 or <1 and almost all others having values of >1 up to a maximal of 21 in the case of diphenhydramine. This indicates that in almost all cases, there will be a difference between central and peripheral samples with the central sample being higher.45


Table 2 Central peripheral ratios of some common drugs
Note: Data from Baselt.11
Abbreviation: C/P, central to peripheral blood concentrations.

The central component is more easily understood as there are often large reservoirs of drug in lung, liver, heart, or gastrointestinal tract, so diffusion across concentration gradients raises concentrations in central veins. The peripheral component relies on transport out of striated muscle, connective and adipose tissues. When factors such as chemical instability and bacterial invasion as discussed previously are excluded, the P part of the ratio assumes that the venous site has only received redistributed blood from surrounding tissue, largely striated muscle, in the thigh or less frequently upper arm. A number of factors determine the peripheral component of the C/P ratio, including the postmortem circulation of blood, and transport in and out of myocytes and other tissues, as well as the time over which the drug had been administered. While there are exceptions to this assumption, such as the case of diffusion of dihydrocodeine from the bladder, such cases are very unusual.40

Postmortem blood circulation

Body movement after death, prolonged cardiopulmonary resuscitation, and changes caused by advanced putrefaction may result in movement from areas of high central concentration to the peripheral sites of sampling.7

Drug uptake processes

Drug uptake into muscle is very complex and depends on numerous transport systems. For example, among the most studied group of drugs in relation to muscle are the lipid-lowering HMG-CoA inhibiting statins, atorvastatin, and rosuvastatin. The muscle concentration is dependent on uptake by OATP2B1 (human organic anion transporting polypeptide 2B1) and efflux transporters MRP1, MRP4, and MRP5. These systems are subject to the interacting effects of co-administered drugs, as well as genetic polymorphism.46

Assuming that redistribution will occur across a concentration gradient when transporting systems cease to function after death, there will be differing muscle concentrations between patients if the transporting systems were altered by interacting drugs before death. The concentration in muscle, and hence, the C/P ratio will also depend on the duration of therapy and individual differences in cellular uptake. While the myotoxicity of statins has been the subject of intensive research, there are at present no available data on the postmortem C/P ratios of statins.11

Duration of therapy

Maximal drug distribution throughout the body will occur after approximately four to five half-lives when a drug has reached a pharmacokinetic steady state. If a steady state has not been reached, then there may be considerably less drug to redistribute from peripheral tissues into venous blood. Unfortunately, the duration of drug therapy is often unknown in many forensic cases. This factor probably accounts for some of the wide spread of central to peripheral ratios for individual drugs found in tables and reference books. Time intervals are therefore critical for any meaningful interpretation of a C/P ratio. Consider the theoretical case of a sudden death resulting from a sudden cardiac arrest occurring within minutes of the administration of the now very commonly used cardiostimulant drug methamphetamine. The offending drug will not have equilibrated with peripheral or probably cardiac tissue, so the C/P ratio should be approximately 1. From a series of 20 methamphetamine caused and associated methamphetamine deaths, peripheral methamphetamine concentrations ranged being 0.3–4.10 μg/mL, central blood from 0.04 μg/mL to 8.95 μg/mL, and C/P ratios from 1.3 to 5.0.47 Unfortunately, the times of death were not individualized but varied between 12 hours and 36 hours. When cardiac blood has been collected “in the field” by cardiac puncture prior to autopsy, methamphetamine concentrations have been reported to rise by a factor of up to 2.4 times by the time of autopsy, though in the same publication, there is one case of a methamphetamine-associated death due to trauma where the heart/femoral ratio at autopsy was 1.0.7 It can be concluded that there is considerable variation in C/P ratios, and central (cardiac) blood increases with time after death.

Expert opinions are often requested in cases of methamphetamine-associated deaths. From these data, it can be concluded that the cases with lower ratios probably had shorter time intervals after death. It would not be possible to accurately determine the blood concentration in an individual case from a peripheral sample at the time of death. Consider the case of a sudden cardiac-related death occurring shortly after taking methamphetamine. If there is no evidence of intercurrent pathology and methamphetamine is detected in a sample of peripheral blood, then methamphetamine can be considered to be the triggering agent, irrespective of the measured concentration.

Newer approaches to predicting drug redistribution

Alterations in blood/liver concentration ratios were considered a possible means of determining the time of death with a liver/blood ratio of >4 indicating death occurred within 5 hours of ingestion. Curry and Sunshine were unable to confirm this hypothesis when they reviewed 52 cases, where the time of death was known. Their work has been a stimulus to investigate mechanisms for determining alterations in postmortem drug concentrations.48

Investigations undertaken by Vorpahl and Coe in 1978 showed increases in digoxin concentrations after death.49 In 1990, Pounder and Jones reported the differing tissue concentrations of doxepin, desmethyldoxepin, three barbiturates, clomipramine, desmethylclomipramine, imipramine, desipramine, and flurazepam. Their assessment of redistribution of drugs after death has been called a “toxicological nightmare”.15 Langford and Pounder later undertook a very detailed biochemical and toxicological examination of a single case of a female aged 34 who died as a result of an overdose of amitriptyline. In this investigation report, they measured numerous hepatic enzymes, bilirubin, creatine kinase amino acids, glucose, and lactic acid, as well as concentrations of amitriptyline and nortriptyline from 19 blood samples collected from various central and peripheral sites, fluid samples from vitreous, pericardium, bile, ascitic fluid, urine, stomach, and duodenal contents, and solid organ samples from both lobes of the liver, apex and posterobasal lung, right dome of the diaphragm, left and right rectus abdominus, and right gastrocnemius muscle.

Concentrations of amitriptyline ranged from 42.1 μg/mL in bile to 1.8 μg/mL in femoral blood. While there were correlations between concentrations of the aminoacids, glycine, leucine, methionine, and serine and valine with blood concentrations, hepatic enzymes were poorly correlated with drug concentrations. The authors concluded that amino acids, and particularly, methionine may be useful as marker of pulmonary drug redistribution.50 More recently, McIntyre conducted a comprehensive review from the published literature of 13 drug concentrations (tramadol, carisoprodol, venlafaxine, mirtazapine, methadone, lamotrigine, quetiapine, citalopram, paroxetine, olanzapine, amitriptyline, clomipramine, and sertraline) measured at various sites and reported by various laboratories.51 Allowing for these difficulties, he concluded that a liver/peripheral blood ratio of <5 means that there is little propensity to postmortem redistribution and if >20–30 redistribution was likely to take place. The same author has further expanded this hypothesis to include an “F” factor (antemortem concentration = postmortem concentration/F) as a means of identifying drug redistribution.52 Application of this factor will require the acquisition of a larger database than is available at present, particularly as measurement of liver concentrations is not without difficulties such as matrix effects. It is also not measured as a routine test in many laboratories.

The application of advanced computer modeling using quantitative structure–activity relationship methodology has been applied to predict the potential for drugs to undergo postmortem redistribution. At present, it has had limited success, but this approach may have potential in the future.53

Conclusion

Passive diffusion from sites of high concentration such as the intestinal tract and liver is easily understood, but the biochemistry causing other changes is clearly more complex. It is less individually predictable on the basis of Vd, lipid solubility, pKa, protein binding, and C/P ratio than was previously thought. The widely used C/P ratio shows considerable alterations after death with few drugs having a ratio of 1.0 or <1.0. Accurate interpretation is possible only when the time of death is known. Prolonged cardiopulmonary resuscitation may complicate the issue by transporting drugs in central areas to the peripheral veins. There is at present no definite marker to predict whether or by how much drug will undergo postmortem redistribution. The recent liver/peripheral blood ratio study serves as a guide for further research. When interpreting the results of drug concentrations after death, it remains essential to have a complete knowledge of the case and to review the known data available on the particular drug.

Disclosure

The author has provided expert evidence in numerous forensic cases. He has no conflicts of interest relevant to this work.

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Re: The discussion on females travelling alone. This poor woman lived in Beirut and called an Uber, the driver of which raped and murdered her (and has been sentenced to death for it thankfully).

She'd probably done it many times before, and the driver must have been retarded to think he wouldn't be the first one pulled in for it.

https://nypost.com/2019/11/01/uber-d...tish-diplomat/

Originally Posted by OhOh

^

But all her fartbuck hi-so friends send her tweets every day, showing how easy it is. Her being a exceptional, white, prosperous, female, she know how to treat those ignorant brown savages, how to be abused.

Alternatively move onto a more exclusive area.

Take advantage of new technology, expensive willing flexible gender dolls, expensive variable electronic devices, teledildonics - groundbreaking new technology that allows you to do things like operate someone's butt plug, via the expensive internet, from halfway across the world ....

Get into the Expensive VR world and live your dream/obsession.

Who is to be tonight, the Butterfly, Luig, LD, MK, FKT, 'arry, Nev?

On top or your need to be dominated?

You stupid, irrelevant wanker.

Originally Posted by OhOh

^

But all her fartbuck hi-so friends send her tweets every day, showing how easy it is. Her being a exceptional, white, prosperous, female, she know how to treat those ignorant brown savages, how to be abused.

Alternatively move onto a more exclusive area.

Take advantage of new technology, expensive willing flexible gender dolls, expensive variable electronic devices, teledildonics - groundbreaking new technology that allows you to do things like operate someone's butt plug, via the expensive internet, from halfway across the world ....

Get into the Expensive VR world and live your dream/obsession.

Who is to be tonight, the Butterfly, Luig, LD, MK, FKT, 'arry, Nev?

On top or your need to be dominated?

That has to be one of the most stupid posts I've read. Misogynist much?

Originally Posted by panama hat

That has to be one of the most stupid posts I've read. Misogynist much?

No, he's just a fucking cretin.

Forgets to take his meds.

Originally Posted by harrybarracuda

No, he's just a fucking cretin.

Forgets to take his meds.

are we talking about you here?

Originally Posted by taxexile

WALL

OF

TEXT

Nic3 cut n paste

^ Tax is being over-hopeful about the mental and reading capacity of many here on TD, and you are the perfect example

Originally Posted by Latindancer

over-hopeful

Terrible grammar.

Originally Posted by AntRobertson

Terrible grammar.

overly hopeful works

Originally Posted by Latindancer

^ Tax is being over-hopeful about the mental and reading capacity of many here on TD, and you are the perfect example

I can read fine, you spasticated twit. Just don't need a complete cut and paste when a link would have worked fine.

The horrified family of British backpacker Amelia Bambridge, who was found dead in Cambodia after a five-day search, say pictures of the 21-year-old’s corpse have surfaced on Instagram.

Her grief-stricken brother Harry posted a message on the social media platform begging followers to report the accounts of twisted trolls who had shared the images.

Shockingly, Facebook – which owns Instagram – initially said the disturbing images did not breach its rules and refused to remove them.

https://www.news.com.au/travel/trave...33a5eb97680bed

Originally Posted by Wally Dorian Raffles

https://www.news.com.au/travel/trave...33a5eb97680bed

I saw that. I wish the parasitic vultures that do that shit a slow and painful death.

Facebook has stressed it has “clear rules against posting graphic content” on its platform after images believed to show the body of British backpacker Amelia Bambridge were circulated online.
Miss Bambridge’s family had urged people not to share distressing images of the 21-year-old, whose body was found at sea a week after she disappeared on a Cambodian island.
It is understood that the social media giant took action to remove offending images after being alerted to them.
A Facebook spokesman said: “We’re saddened by the news about Amelia Bambridge and our thoughts go out to her family and friends.
“We have clear rules against posting graphic content, when we are made aware of this content we remove it.
“People often use Facebook and Instagram to share stories in the news and this can result in content appearing that some may find upsetting.”
In Facebook’s community standards for violence and graphic content, the platform said it bans content which includes images of dying, wounded or dead people who are dismembered, burned or the victims of cannibalism.
The policy said: “We remove content that glorifies violence or celebrates the suffering or humiliation of others because it may create an environment that discourages participation.
“We allow graphic content (with some limitations) to help people raise awareness about issues.”
It is understood Facebook will remove photographs of dead people if asked by a family member or authorised person.
In an Instagram post on Saturday, Miss Bambridge’s brother Harry urged people not to share the distressing pictures.
Miss Bambridge, from Worthing, West Sussex, was last seen on the Cambodian island of Koh Rong late on October 23.
On Thursday, her family confirmed that her body had been found in the sea following days of searching, approximately 60 miles from the island where she disappeared.

https://www.belfasttelegraph.co.uk/news/uk/facebook-stresses-clear-rules-on-content-as-missing-backpacker-pictures-shared-38656527.html