5 JClin Pathol 1992;45:654-659

Bodies recovered from water: a personalapproach and consideration of difficulties

W Lawler

IntroductionFor the pathologist providing a routine nec-ropsy service to the local coroner, examinationof bodies recovered from water can generatethe most difficult of interpretational problems,and this is probably the prime context whereappropriate historical and circumstantial evi-dence is vital to interpretation and overallconclusions,' 2 although such collateral evi-dence should always be available before anycoroner's necropsy is undertaken.3

It must be appreciated, at the outset, thatnot all persons whose bodies are recoveredfrom water will have died from its inhalation,although they may show features reflectingimmersion in water. Such bodies should there-fore be particularly carefully examined, bothexternally and internally, to catalogue (andsubsequently to explain satisfactorily) all inju-ries present, to determine whether deathindeed followed immersion in the water, and tosee whether any natural disease, such asischaemic heart disease, cerebrovascular dis-ease, and hypertension, may have contributedto, precipitated, or even caused death. It is alsoimportant to determine whether the deceasedwas under the influence of alcohol or otherdrugs at the time of death (although inter-pretation of laboratory results should be influ-enced by the knowledge that, as discussedbelow, classic fresh water drowning mayincrease the blood volume by as much as30-35%). Finally, the pathologist has a vitalrole in determining, from all pathological andcircumstantial evidence available, whether theoverall findings are consistent with, or evenpoint directly towards accident, suicide, orhomicide.

Unfortunately many bodies recovered fromwater will have been there for several days, anddecomposition may have obscured ordestroyed features of drowning; nevertheless,careful examination may elicit sufficient pos-itive or negative findings to allow reasonableconclusions to be drawn.For the pathologist to interpret accurately

the necropsy findings, it is necessary briefly toconsider the mechanisms of death after sub-mersion in water and to appreciate the resultsof immersion in water, including artefactualinjuries.

Mechanisms of death after submersionin waterThese are well documented in severalstandard textbooks of forensic medicine andpathology.48

It has been reported that about 85-95% ofthose dying from water inhalation presentfeatures of drowning,59 although in most, notall the typical features are seen9; the remainderdie from vagal inhibition (sometimes, inaccu-rately, known as "dry drowning", and oncedesignated "hydrocution"), or the postimmersion syndrome; perhaps, rarely, laryn-geal spasm may be important.At this stage, it is worth remembering that

hypothermia can supervene very quickly inindividuals swimming or trying to remainafloat in cold water, and that it may be animportant factor contributing to theirdeath'0 "; indeed, hypothermia may be themain cause of death after shipwreck in theopen sea.1 12

DROWNINGMechanisms for death from drowning aremultiple, complex, and, in part, still incom-pletely understood. Although drowning ismuch more than simple asphyxia followingmechanical airway obstruction by water, thisprocess probably does at least contribute.Major factors, however, seem to be osmoticand perhaps also hydrostatic effects of theinhaled fluid once it reaches alveolar spacesand gains access to semipermeable alveolarmembranes; here, water and electrolyteexchanges take place, the nature of which isinfluenced by the tonicity of the inhaled fluid-fresh or salt water.

Fresh water This is hypotonic relative toplasma. Therefore, when present in alveoli, it israpidly absorbed into the pulmonary circula-tion; this causes pronounced haemodilution(the blood volume may be increased by up to30-35%) which, in turn, soon produces localhaemolysis. Although haemodilution will leadto hyponatraemia, circulatory overload, and,ultimately, high output cardiac failure, hae-molysis is probably more important, as itcauses hyperkalaemia and consequent cardiacarrhythmias, particularly with concomitantgeneralised hypoxia. These changes candevelop very rapidly-over a few minutes,supporting the view that drowning in freshwater tends to occur more quickly than in seawater.5 6

Salt water is hypertonic relative to plasma.Therefore, when present in alveoli, it attractswater into the airways from the pulmonarycirculation, causing local haemoconcentrationand severe pulmonary oedema. Haemocon-centration increases blood viscosity and pro-

Department ofPathological Sciences,The Medical School,Stopford Building,Oxford Road,Manchester M13 9PTW LawlerCorrespondence to:DrW LawlerAccepted for publication20 December 1991

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duces acute hypernatraemia, while severe

pulmonary oedema causes clinically import-ant hypoxia/hypercapnoea; all these factorsadversely affect the heart, with bradycardiaand, ultimately, asystole.

"VAGAL INHIBITION" ("REFLEX CARDIAC ARREST")

This is a well recognised and accepted mech-anism, particularly since Simpson's widelyquoted review. '3 Vagus nerve branches may bestimulated in several ways, with a direct andperhaps almost instantaneously fatal cardiacinhibition. Following submersion, it may beinitiated by the sudden and unexpected entryof water into the larynx, nose, or naso-

pharynx4 4 16; concurrent emotional statesmay act as a contributing sensitising factor.'6Vagal inhibition seems to be more commonwhen the submersion is total and unantici-pated, when the victim is under the influenceof alcohol and/or other drugs, when the wateris cold, and when the individual enters it feetfirst.

LARYNGEAL SPASM

This probably occurs, at least to some extent,in most individuals following submersion, as itpresumably represents a normal reflex to fluidentering the larynx.6 15 In most, however, itseems to be transient, and a true asphyxialdeath from laryngeal spasm, if it occurs at all,is probably extremely rare. Gardner reportshaving seen only one fatal case-in a boy aged8 who sank into water immediately afterjumping in, and whose body showed asphyxialchanges and no features of drowning. '5 Thismechanism is discussed by Polson, Gee, andKnight,6 who quote Gardner's case but do notoffer any of their own; they do, however, statethat laryngeal spasm is "a rare mode of deathfrom submersion." Several reviews9 12 16 donot mention it at all; some, illogically, link itwith vagal inhibition as a mechanism foralmost instantaneous death, and do not refer toasphyxial features.4 My views, and, I believe,those of many colleagues involved in forensicpathology, are well summarised by Donald, 7

who says "previous literature would suggestthat a number of human beings are drownedwith dry lungs owing to glottic spasm, but littleconvincing evidence has been produced".Recently, Knight has stated "another mechan-ism that is often postulated as a cause of non-drowning immersion death is 'laryngealspasm', leading to a hypoxic death fromclosure of the airway.8 The evidence for such a

condition is tenuous, as such closure wouldhave to operate for a considerable time forhypoxia to kill, all the time keeping the larynxclosed to prevent entry of water."

POST IMMERSION SYNDROME (SECONDARY

DROWNING)

Occasionally, individuals survive the immer-sion and are recovered alive from the water,only to die later from delayed effects or othercomplications. Such deaths are usually pulmo-nary, reflecting surfactant loss following fluidinhalation; some represent prolonged, pro-found hypoxia.'8"1

Findings and interpretations in deathsafter submersion in waterIt is important to distinguish changes directlyattributable to death following submersion(discussed here) from those which purelyreflect immersion (discussed later). The chan-ges described here, which are well documentedin standard textbooks4 ' and review art-icles,'8 20 are those encountered in fresh bod-ies-that is, those removed from the waterbefore decomposition becomes established;once a lengthy delay has occurred, positivediagnosis may be difficult.

DROWNING

Externally, although a range of changes may beidentified, there may be nothing specific todrowning. Sometimes, however, firm, tena-cious foam is present at the mouth or nostrils.Typically, it is white or blood tinged, andreappears after wiping away. It is thought torepresent an admixture of air, fluid, mucus andsurfactant, and therefore an ante mortemphenomenon.Internally, the foam, even if not apparentexternally, is often found in major airways orsecondary bronchi and bronchioles. The air-ways may also contain water and such extrinsicmaterials as silt, weeds, or sand. Similarsubstances (particularly water) may be swal-lowed and thus identified within the stomach.Pulmonary changes vary according to thedrowning fluid, although they are often not asdistinct as suggested by differences in causativemechanisms and as implied in some text-books.

Fresh waterTypically, the lungs are almost twice theirnormal weight, and present an appearancesometimes still designated "emphysema aquo-sum"-they are bulky and overdistended (suchthat they may well overlap the pericardial sacand meet in the midline), with a very charac-teristic doughy texture which causes them topit on digital pressure and sometimes to showprominent rib markings. Classic petechialhaemorrhages are uncommon, but larger sub-pleural and intrapulmonary haemorrhages maybe identified. Section releases frothy, oftenblood tinged fluid. Elsewhere, haemodilutioncauses the blood to appear rather "watery";haemolysis may produce intimal staining ofmajor vessels.

Salt waterTypically, the lungs are slightly, but not alwayssignificantly, heavier than in fresh waterdrowning,2' and although overdistended, clas-sic emphysema aquosum is less pronounced;on section, greater quantities of frothy fluidtend to be released. Pleural effusions may alsobe present.

VAGAL INHIBITION

This is really a diagnosis of exclusion based notonly on negative pathological and toxicologicalfindings, but also on appropriate circum-stantial evidence; necropsy shows no foam inthe airways, no emphysema aquosum, no

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petechial haemorrhages and no clinically rele-vant natural disease.6 '

LAYRNGEAL SPASM

Here, presuming the existence of this entity,the features are those of classic mechanicalasphyxia, including cyanosis, congestion, andwidespread petechial haemorrhages; there islittle or no water in the airways (although somemay be present in the stomach), no or minimalairway froth, and no emphysema aquosum.' 5Such findings indicate the possibility of anasphyxial death before entry into the waterwhich must be actively and seriously con-sidered, as this mechanism for death followingsubmersion is extremely rare, if it exists atall.

POST IMMERSION SYNDROME (SECONDARYDROWNING)With short term survival, lungs develop haem-orrhagic, desquamative bronchopneumonia,with intra-alveolar hyaline membranes; later,abscesses may develop, and granulomatousreactions to inhaled foreign particles may beidentified.'8 19 Simultaneously, there may behypoxic damage elsewhere, particularly in cer-ebrum, brain stem, and renal tubules.

"Confirmatory" tests for drowningTwo are often quoted as providing evidence fordrowning. In practice, both are difficult toperform and to interpret, with many falsepositive and false negative results.2

DIATOMS

This subject has generated much debate andcontroversy, with strong arguments in favour ofand against diatom identification as a helpfuldiagnostic test; review articles are avail-able,22 25 26 and the subject has been discussedin standard textbooks.' 5 8 Diatoms (Bacillar-iophyceae) are unicellular algae with hard silica-ceous exoskeletons resistant to decomposition,heat, and acids strong enough to destroy softtissues. Over 10 000 species and types exist,about half in fresh water and half in brackish orsea water; unfortunately, they are not found insubstantial numbers all year round, the peaksbeing spring and autumn. In theory, drowningshould allow diatoms to enter not only thelungs, but also, via the circulation, otherorgans. Therefore, in the drowned, diatomsshould be extractable, after tissue digestion instrong acids, from such remote sites as bonemarrow, liver, brain and kidneys. Unfortu-nately, two main problems exist: first, theremay be insufficient or even no diatoms in thedrowning fluid-from seasonal variations asnoted above or following pollution by efflu-ent-second, when identified, they may repre-sent "contamination", such as during nec-ropsy, from tap water, from reagents, fromfood via the deceased's gastrointestinal tract oreven from the atmosphere. At best, despitestrict, proper techniques and appropriate con-trols23 27 the diatom test can only providesupportive evidence of drowning.25 Such reser-vations probably apply even when experienced

diatomologists undertake taxonomic analysesand comparisons of test and controlsamples.26 27

ELECTROLYTES

The haemodilution of fresh water drowning orthe haemoconcentration of salt water drowningmay be reflected in different electrolyte (partic-ularly chloride ion) concentrations and plasmaosmolarity or specific gravity between thedifferent sides of the heart,28 29 although mostworkers find these tests unreliable and quiteunhelpful2 8 12 16 30; furthermore, as both areinvalidated by decomposition, they can only beof any possible value in bodies recovered soonafter death.4 6 22

Effects of immersion in waterThese, reviewed in standard texts,459 areobviously influenced by duration and watertemperature, but other factors, such aswhether the water is still or flowing, fresh orsalt, clean or polluted, are also relevant.Immersion modifies most changes after

death. Body cooling will relate directly to thewater temperature. In the United Kingdomcooling in water is roughly twice that in air, andis accelerated in flowing rivers and streams.Onset and duration of rigor mortis are alsoaffected by water temperature: in cold wateronset is delayed and duration prolonged.Drowning is a well recognised context in whichcadaveric spasm (instantaneous rigor) may beencountered ("the drowning man clutching atstraws"). As most submerged bodies floatprone, with arms and legs hanging downwards,hypostasis (lividity) is usually maximal on face,neck, upper anterior chest, forearms, hands,lower legs and feet. In Caucasians it may beappreciably pink, perhaps because immersionfacilitates oxygenation through the wet skinafter death,7 9 12 or perhaps merely the result ofcold.8 With fast flowing water, the constantmovement may impair, if not inhibit com-pletely, development of hypostasis.

Decomposition (putrefaction) is also influ-enced by water temperature. In the UnitedKingdom time intervals associated with thevarious standard changes are about twice aslong as those in air, but may be prolongedfurther in flowing water and reduced in heavypollution. In tropical waters decompositionmay be established by 24 hours, whereas nonemay be apparent after several weeks in waterconstantly below 40°F (5°C). With advancingdecomposition, gas formation increases buoy-ancy until ultimately (in the United Kingdomafter about three to 14 days, depending on theseason),9 and providing it is free to do so, thebody will float, often, because of intestinalputrefactive gases, belly upwards.4 Inter-estingly, once a submerged body is exposed toair after recovery, decomposition often pro-ceeds very rapidly, and this may well continuedespite apparently adequate refrigera-tion.469'2 With prolonged immersion, adipo-cere will form.

Maceration, the skin change which charac-terises immersion, is due to water absorp-

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tion.6 ' ' It first appears on finger tips, and theninvolves the palm followed by the back of thehand; similar changes soon affect feet and skinelsewhere. The skin becomes whitened, sod-den, thickened and wrinkled (an appearancesometimes designated "washerwoman's skin").With time, the epidermis becomes loose andpeels; finally, nails and hair become detached.Maceration is accelerated in warm water(where it may appear within minutes), but, ingeneral, it takes about eight to 24 hours forearly changes to become apparent outdoors intemperate climes. By about seven to 10 days,epidermal separation may have started, and byabout three to four weeks, the skin and nailsmay be sufficiently loose to allow removal likea glove. Clothing, including footwear, delaysmaceration, perhaps by up to 50%.

Following the above observations and com-ments, it is obvious that considerable variationexists between the different changes; conse-quently, it is extremely difficult to estimate theduration of immersion, and great care needs tobe exercised when trying to draw reasonableconclusions.4

Artefactual injuries during immersionin waterThese are common, and may provide inter-pretational difficulties. ' 4 7-9 As most sub-merged bodies float prone, with arms and legshanging downwards, contact with the roughbed of the stream, river, lake or sea willproduce abrasions maximal over forehead,backs of hands, knees and toes. Tides orcurrents may crush the body against fixedobjects, such as rocks, bridges, quays, weirs,wharfs and piers or ships; propellers may alsoinflict considerable damage.Exposed skin may be bitten or chewed by

fish, shellfish, and other marine life includingaquatic mammals, and some creatures are ableto gain access to skin below loose clothing.Occasionally, such large marine animals assharks cause extensive lesions.Although not always artefactual, serious

injuries may be sustained either before thewater was reached (on projecting rocks, pierpilings, bridge supports and quaysides) orwhile entering the water, especially after fallingor jumping from a considerable height. Theforce generated by the latter may be sufficientto rupture internal organs.

A personal approach to pathologicalconclusionsAs stated earlier, the pathological examinationof a body recovered from water and thedrawing of reasonable and justifiable infer-ences from the findings can be difficult.2 Eachcase has to be considered on merit, but it isessential that all circumstances-how andwhere the body was found, whether there wereany local factors preventing the deceasedextricating himself from the area involved, themental and physical state of the deceased whenlast seen alive, the deceased's backgroundmedical history and even, perhaps, the

deceased's swimming ability-are known bythe pathologist before starting the necropsy.Indeed, most experienced pathologists wouldagree that this is one of the few areas wherecollateral evidence can be vital when trying toreach the most appropriate conclusions.

I believe that four groups of questions mustbe addressed and answered by the patholo-gist:(1) What injuries are present on and withinthe body? How can each be explained satisfac-torily? Consideration needs to be given to thepossibility of artefactual injuries as discussedabove. The likelihood that some, most, or evenall the injuries identified were deliberatelyinflicted by an assailant must always be bornein mind, and may need appropriate investiga-tion and active exclusion.(2) What natural diseases are present? Maythey have produced sudden collapse and thuseither caused death or precipitated drowning?Here, not only obvious structural abnormal-ities, such as ischaemic heart disease, cerebro-vascular disease, and hypertension, but alsofunctional disorders, the existence of which isonly apparent from the deceased's medicalhistory, such as epilepsy, hypoglycaemia andcardiac arrhythmias, should be considered.(3) What was the cause of death? Althoughmost bodies recovered from water have diedfrom its inhalation, the individual could havefallen into it after collapse and death fromnatural causes. The possibility of death fromthe actions of an assailant followed by immer-sion ("dumping") in water as a means ofdisposal must always be considered.(4) Could the deceased's actions before enter-ing the water or once in it have been modifiedby the influence of alcohol or other drugs?Here, the case for requesting routine toxico-logical analyses is strong-if only to facilitateinterpretation of circumstances surroundingthe death.

Death certificationOnce the questions considered above havebeen answered satisfactorily by the pathologist,formal death certification is required. This maybe straightforward (Ia drowning; or Ia vagalinhibition, due to lb submersion in water; orwhen death resulted entirely from naturalcauses). But when drowning is associated withnatural diseases or drugs it may be difficult,and the pathologist needs to appreciate theimplications of using the standard death certif-icate format.3' If it is thought that death fromsubmersion in water was the direct result ofnatural disease or intoxication by drugs itshould be so certified (Ia drowning, due to Ibintracerebral haemorrhage, due to Ic essentialhypertension). But if the pathologist believesthat, given all pathological and circumstantialevidence available, death from submersionoccurred regardless of any natural disease orintoxication present, then only the mechanismresponsible for death should appear on thecertificate.2 It must be remembered firstly thatindividuals can die with and not necessarilyfrom diseases and conditions found at post

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mortem examination. Secondly, at present, thedeath certificate used in the United Kingdomdoes not allow for the inclusion of conditionswhich have not caused or contributed signifi-cantly to death.3'

If the pathological findings are negative,ambiguous, or obscured by advanced decom-position certification as "unascertained" (aterm understood and accepted by coroners32)may be honest, accurate and entirely appro-priate.3' The qualification "appearances hereare entirely consistent with drowning" or"appearances here are entirely consistent withdeath following immersion in water" may behelpful and appreciated by the investigatingauthorities.

Circumstances: accident, suicide orhomicide?In practice, almost all deaths after submersionin water are either accidental or suicidal; only afew are homicidal. These questions have beenaddressed elsewhere' 47 '9 but are worth con-sidering briefly here. Sometimes the questionis more complicated in theory than in practice,as strong collateral evidence may render med-ical data of secondary importance.9Accidental deaths predominate, and occurunder a wide range of circumstances.4 In asubstantial minority, perhaps 20% or evenmore, particularly among the young adult agegroups, the victim is under the influence ofdrugs, especially alcohol4733 38 ("Bacchushath drowned more men than Nepture"35).Here, sudden cooling of skin which is warmerthan normal because of vasodilatation may bean important factor in deaths both fromdrowning and from vagal inhibition. In manyof the remainder precipitation by clinicallyimportant natural disease may be relevant.Suicidal deaths are probably commoner than isappreciated or acknowledged,4 39but returninga verdict of suicide in the absence of confirma-tory or good circumstantial evidence is obvi-ously inappropriate and unfair to survivingrelatives. It is worth remembering that individ-uals who commit suicide may first resort toalcohol or other drugs for "courage" and thatsuicides may have substantial natural dis-eases.Homicidal deaths are uncommon40 as itrequires a considerable physical disparitybetween the assailant and the victim, or for thevictim to be incapacitated by disease, drink, ordrugs, or for the victim to be taken bysurprise.6 Nevertheless, the pathologist mustactively consider and positively exclude thispossibility in every body recovered from water;only then will missed homicides be minimised,although without evidence of violence, thepresumption must be that death was accidentalor suicidal.6 Therefore, it is essential that allinjuries on and within the body are docu-mented and subsequently explained to thecomplete satisfaction of all parties-patholo-gists, investigating police officers and Coroner/procurator fiscal. When any doubts exist, it iswise to engage a specialist forensic pathologistat an early stage.

Deaths in the bathThese may present particular problems, andalways require adequate explanation.4 1241 43Such deaths may, of course, be unrelated to

inhalation of bath water-for example fromnatural causes, overdose of drugs or, occasion-ally, electrocution. When water inhalation isconsidered relevant by the pathologist, thedeath may, as discussed above, be accidental,suicidal, or homicidal. Precipitation into thewater by natural disease should always beconsidered, as should the influence of poison-ing, not only by alcohol or drugs, but also bycarbon monoxide from faulty water heaters.With apparently accidental deaths, many

pathologists would agree with Cameron that "anormal healthy conscious person does notdrown accidentally and that the possibility ofsuch an accident occurring from falling asleepis a convenient, but virtually unsubstantiated,myth." 2Some authors believe that adult deaths in the

bath are most likely to be suicidal4 42; othersconsider suicide by self immersion to be rare. 12In infancy and early childhood, although mostdeaths are accidental and reflect inadequateadult supervision, deliberate immersion is welldocumented, and should always be consideredand investigated accordingly.44 45

1 Knight B. The Coroner's autopsy. A guide to non-criminalautopsies for the general pathologist. Edinburgh: ChurchillLivingstone, 1983:251-68.

2 Davis JH. Bodies found in the water. An investigativeapproach. Am Jf Forens Med Pathol 1986;7:291-7.

3 Lawler W The negative coroner's necropsy: a personalapproach and consideration of difficulties. J7 Clin Pathol1990;40:977-80.

4 Giertsen JC. In: Tedeschi CG, Eckert WG, Tedeschi LG,eds. Forensic medicine. Philadelphia: WB Saunders Co,1977:1317-33.

5 Pullar P. In: Mant AK, ed. Taylor's principles and practice ofmedical jurisprudence. 13th ed. Edinburgh: ChurchillLivingstone, 1984:292-303.

6 Polson CJ, Gee DJ, Knight B. The essentials of forensicmedicine. 4th ed. Oxford: Pergammon Press, 1985:421-48.

7 Gordon I, Shapiro HA, Berson SD. Forensic medicine. Aguide to principles. 3rd edn. Edinburgh: Churchill Living-stone, 1988:115-25.

8 Knight B. Forensic pathology. London: Edward Arnold,1991:360-74.

9 Simpson K. In: Simpson K, ed. Taylor's principles and practiceof medical jurisprudence. 12th edn. London: Churchill,1965:368-83.

10 Keatinge WR, Prys-Roberts C, Cooper KE, Honour AJ,Haight J. Sudden failure of swimming in cold water. BrMedJ7 1969;i:480-3.

11 Keatinge WR. Hypothermia at sea. Med Sci Law 1984;24:160-2.

12 Cameron JM. In: Camps FE, ed. Gradwohl's legal medicine.3rd edn. Bristol: John Wright, 1976:349-55.

13 Simpson K. Deaths from vagal inhibition. Lancet 1949;i:558-60.

14 Spilsbury B. Some medico-legal aspects of shock. Medico-Legal and Criminological Review 1934;2:1-13.

15 Gardner E. Mechanism of certain forms of sudden death inmedico-legal practice. Medico-Legal and CriminologicalReview 1942;10: 120-33.

16 Anonymous. Immersion or drowning? [Editorial] Br Med J1981;282:1340-1.

17 Donald KW. Drowning. Br Med J 1955;ii: 155-60.18 Fuller RH. Drowning and the postimmersion syndrome. A

clinicopathologic study. Military Med 1963;128:22-36.19 Pearn JH. Secondary drowning in children. Br Med J

1980;281:1103-5.20 Gordon I. The anatomical signs in drowning. A critical

evaluation. Forens Sci 1972;1:389-95.21 Copeland AR. An assessment of lung weights in drowning

cases. The Metro Dade experience from 1978 to 1982.Am Jf Forens Med Pathol 1985;6:301-4.

22 Timperman J. Medico-legal problems in death by drown-ing. Its diagnosis by the diatom method. Jf Forensic Med1969;16:45-75.

23 Hendey NI. The diagnostic value of diatoms in drowning.Med Sci Law 1973;13:23-34.

24 Peabody AJ. Diatoms and drowning-a review. Med Sci Law1980;20:254-61.

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30 Modell JH, Davis JH. Electrolyte changes in humandrowning victims. Anesthesiology 1969;30:414-20.

31 Knight B. The Coroner's autopsy. A guide to non-criminalautopsies for the general pathologist. Edinburgh: ChurchillLivingstone, 1983:53-60.

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33 Giertsen JC. Drowning while under the influence ofalcohol. Med Sci Law 1970;10:216-19.

34 Plueckhahn VD. The aetiology of 134 deaths due to"drowning" in Geelong during the years 1957 to 1971.Med JAust 1972;ii:1183-7.

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45 Pearn JH, Brown J, Wong R, Bart R. Bathtub drownings:report of seven cases. Pediatrics 1979;64:68-70.

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