2. PENDAHULUAN
• Toksikologi forensik dapat dimengerti sebagai pemanfaatan atau
penerapan ilmu toksikologi untuk kepentingan peradilan.
• = Science Forensic :
• ”the application of science to law”
3. • Ilmu toksikologi :
• ilmu yang menelaah tentang kerja dan efek berbahaya zat
kimia atau racun terhadap mekanisme biologis suatu
organisme.
• ilmu yang mempelajari sumber, sifat serta khasiat racun,
gejala-gejala dan pengobatan pada keracunan serta kelainan
yang didapatkan baik pada korban hidup maupun meninggal
• mendeteksi, mengisolasi, memisah, mengukur secara
kuantitatif dan kualitatif cara dan daya kerja racun dalam
tubuh korban,tentang dosis lethalis, temuan-temuan dalam
otopsi, penentuan sebab kematian korban dan juga tentang
terapi dan antidotumnya.
• Secara singkatnya toksikologi adalah ilmu yang mempelajari
racun, suatu senyawa yang merugikan kesehatan atau
organisme hidup.
4. • Toksikologi forensik mencangkup
• Terapan ilmu alam dalam analisis racun sebagai bukti
dalam tindak kriminal,
• Mendeteksi dan mengidentifikasi konsentrasi dari zat racun
dan bentuk metabolitnya dari materi biologi,
• Menginterpretasikan temuan analisis dalam suatu
argumentasi tentang penyebab keracunan dari suatu kasus.
5.
6.
7.
8. • Racun
• Menurut Taylor :
• Suatu zat yang dalam jumlah relatif kecil, apabila atau mengenai
tubuh seseorang akan menyebabkan timbulnya reaksi kimiawi yang
besar yang dapat menyebabkan sakit atau bahkan kematian.
• Menurut Grandwohl :
• Substansi yang tanpa kekuatan mekanis kalau mengenai atau masuk
ke dalam tubuh seseorang akan menyebabkan gangguan fungsi
tubuh, kerugian bahkan kematian.
• Menurut Seinen :
• Substansi yang diberikan secara berlebihan
• “Toxicology is the knowledge of too much”
9. • Berdasarkan sumber :
• tumbuhan-tumbuhan (misal opium, kokain, kurare, aflatoksin)
• hewan (misal toksin ular, laba-laba, hewan laut)
• mineral (misal arsen, timah hitam)
• sintetik (misal heroin).
• Berdasarkan tempat di mana racun berada,
• alam bebas (misal gas racun di alam),
• rumah tangga (misal detergen, disinfektan, insektisida,
pembersih, pemutih)
• pertanian (misal insektisida, herbisida, pestisida)
• industri dan laboratorium (misal asam dan basa kuat, logam
berat)
• makanan (misal sianida, toksin botulinus, bahan pengawet)
• obat yang beredar dalam kalangan medis (misal hipnotika,
sedatif, transquilizer, antidepresan, narkotika).
Penggolongan racun:
10. • Berdasarkan mekanisme kerja racun dalam tubuh :
• racun yang bekerja lokal (seperti zat bersifat korosif, iritan
maupun anestetik),
• racun yang bekerja secara sistemik (misal narkotika,
barbiturat, alkohol, digitalis, asam oksalat, karbon
monoksidan, sianida, insektisida golongan chlorinated
hydrocarbon dan fosfor organik, striknin, cantaridhes)
• racun yang bekerja secara simultan lokal dan sistemik (misal
asam oksalat, asam karbol, arsen, garam Pb)
11. Faktor yg mempengaruhi kerja racun :
• Cara pemberian
• Keadaan / kepekaan tubuh
• Umur
• Kesehatan
• Kebiasaan
• Hipersensitif & idiosinkrasi
• Faktor racun
• Dosis
• Konsentrasi
• Bentuk & kombinasi fisik
• Susunan kimia
• Addisi & sinergisme
• Antagonisme
12. Kriteria diagnostik akibat racun
• Anamnesis
• Pemeriksaan fisik :
Periksa luar dan atau dalam (otopsi)
• gejala,
• tanda,
• kelainan tubuh korban
• Pemeriksaan penunjang :
• Analisa kimia sisa bahan beracun & metabolit dalam jaringan tubuh
13. Anamnesis
• Pada umumnya anamnesa tidak dapat dijadikan pegangan sepenuhnya sebagai
kriteria diagnostik
• Hal yang diperlukan :
• Jenis racun
• Cara masuknya racun
• Kebiasaan & kepribadian korban
• Status psikiatri korban
• Keadaan kesehatan
• FR peningkatan efek lethal spt RPD, alergi, idiosinkrasi atau drug abuse
14. Pemeriksaan fisik
• Tanda mencurigakan :
• Bau dari mulut & saluran nafas
• Warna muntahan, cairan/sekret
• Tanda kekerasan, al : needle mark, luka sekitar mulut, hidung dll.
• Tanda fisik lain
• Gejala :
• Kejang, pin point pupil, gejala gagal nafas, dll.
15. Pendekatan pemeriksaan korban keracunan
• Berdasarkan tempat ditemukan korban
• Shower, dapur CO
• Kamar tidur Rape, drug, hipnosis
• Jalan raya alkohol, benzodiazepin, drug abuse
• Garasi Parathion, CO, cleaner
• Pesta designer drug, ethanol,
16. • Berdasarkan penampakan fisik
• Kebiruan sianosis, aspirasi
• Biru ujung ektremitas vasokonstriksi, ergotamin
• Darah kecoklatan Met-Hb, Nitrat, Dapson
• Kuning/ikterik sulphonamide, hepatitis
• Hitam nekrosis, alkali kuat, asam kuat,
iodine
• Lebam mayat
• pucat/hampir tidak ada anemia, hemolisa intravasa, racun
hemolitik
• Cherry red CO, sianida
• Kelabu sianotik pembentuk Met-Hb (potasium klorate,
nitrobenzene, asetanilide, quinine atau aniline)
18. • Gejala menyerupai keracunan
• Koma hipoglikemia
• Cerebrovasculer accident
• Trauma otak dan brain death
• Meningitis
• Idiosinkrasi dan rekasi hipersensitifitas
• Shock neurogenic
• Gejala tak terduga dari penyakit tertentu, misal tumor otak
19. DD Berdasarkan gejala
DD Keracunan Penyakit
Sakit kepala CO, CO2, alkohol, narkotika Depresi, meningitis, tumor
otak, hipertensi, migrain dll
Muntah, sakit
perut, pusing
Garam logam berat, racun
makanan
Gastritis, enteritis, uremia dll.
Gangguan
kesadaran, koma
Akohol, hipnotika, sedativa,
CO
CVD, eklamsia, uremia
Miopia Opium, morfin, pilokarpin,
organosphospat
Penyakit SSP.
Midriasis Belladona, alkohol, acontin Syok, koma
Delirium Belladona, alkohol, hasis,
LSD
Penyakit jiwa, psikosa
Kejang Striknin, ergotamine,
garam amonium
Uremia, eklamsia, tetanus
Sianosis Anilin, nitrit, fenasetin,
parakuat
Bronxhopenumonia, COPD,
peny.jantung
20. Zat Korosif Perubahan warna pada
kulit atau mukosa
Asam karbol (phenol) Abu-abu keputih-putihan
Asam oksalat Abu-abu kehitam-hitaman
Asam sulfat, asam klorida Abu-abu kemudian menjadi hitam
Asam nitrat Kuning
Asam fluorida merah kecoklatan, pendarahan
Kaustik alkali Abu-abu keputih-putihan
Zinc klorida keputih-putihan
Merkuri klorida biru keputihan, pendarahan
21. Pemeriksaan penunjang
• Pengambilan sampel
• Sisa zat yang digunakan (obat / cairan / makanan, dll.)
• Cairan / jaringan tubuh (sisa muntahan, sekret mulut dan hidung, darah, urin)
• Analisa sampel :
• Penginderaan : visual, bau
• Toksikologi analitik : kualitatif / kuantitatif
22. Pengambilan & pengiriman sampel
• Kasus hidup :
• Sebelum tindakan terapi diberikan
• Jenis & volume bahan tgt cara & dugaan racun
• Umumnya : seluruh urin, muntahan / bilasan lambung; darah (20-50 cc)
• Pengawet yang sesuai (alkohol absolut, NaF, Na-benzoat, phenyl merkuri
nitrat)
• Pengemasan, penyegelan & berita acara
23. • Kasus mati (otopsi)
• Sebanyak mungkin organ ??
• Minimal seperti orang hidup, ditambah :
• Sebagian organ sesuai racunnya, misal
• Hepar 100 grram keracunan insektisida
• Seluruh empedu keracunan gol. morphin
• Ginjal, kedua ginjal logam, Ca oksalat, sulfonamide.
• Otak, jaringan lipoid yang terdapat dalam otak keracunan CHCl3, CN.
• Perlakuan : = kasus hidup + lampirkan hasil otopsi
• Kasus ekhumasi :
• Organ sisa tertentu sesuai indikasi
• Isi lambung
• Tanah di bawah lambung dan tanah “normal” di sekitar makan
24. PRINSIP PENTING
• Dalam rantai proses pemeriksaan penunjang, CARA
PENGAMBILAN SAMPEL merupakan prosedur yang
sangat utama!
• Sampel yang ada, diambil, dikirim ke laboratorium,
kemudian diperiksa tosikologi.
• Pre analisis sangat menentukan post analisis. Petugas
medis hanya bergerak di pre analisis.
25. ALUR PROSEDUR PRE ANALISIS
KELOMPOK SAMPEL
DIAMBIL
ASPEK LEGAL
LABORATORIUM TOKSIKOLOGI/POM
26. KELOMPOK SAMPEL
1. Berasal dari makanan dan minuman atau sesuatu
yang dapat dimakan atau diminum.
2. Berasal dari manusia (berupa cairan, jaringan atau
organ).
3. Berasal dari lingkungan.
27. DASAR PEMILIHAN SAMPEL
ORGAN TUBUH?
1. Cerita kasus
2. Gejala klinis
3. Tanda-tanda patologi jenazah
4. Barang bukti di TKP
ADAKAH RACUN?
Bagaimana afinitas dan perjalanannya?
SAMPEL
29. PENGAMBILAN SAMPEL
Dalam pengambilan sampel, sering
dilakukan pengawetan.
Hal yang penting dalam pengambilan
sampel adalah:
1. Wadahnya apa dan bagaimana?
2. Yang mana sampelnya?
3. Berapa banyak sampel yang harus diambil?
30. WADAH
• Prinsip dapat menjamin bahwa sampel tidak berubah secara kualitatif
dan kuantitatif ketika dibawa dari TKP sampai ke Laboratorium.
• Syarat: bersih, kering, kuat, mulut lebar, tidak berpengaruh dari
lingkungan, tertutup rapat, steril (khusus pemeriksaan bakteriologis &
DNA).
32. SEBERAPA BANYAK SAMPEL?
DIAMBIL SEBANYAK-BANYAKNYA!
1. Ada kesempatan mengulang pemeriksaan
+
2. Metode kromatografi lapis tipis perlu banyak sampel. Makin banyak
sampel, makin banyak racun yang terekstraksi.
34. AFINITAS RACUN?
• Zat volatyl paling kuat dengan otak
• Zat non volatyl paling kuat dengan hepar
• Kelompok logam paling banyak
berhenti di ginjal
35. SAMPEL LAMBUNG
• Cara memotong? Ikatan dan potongan?
• KCN + HCl KCl + HCN
• Sianida lebih cenderung deteksi positif.
• Sebagian besar racun masuk dari mulut melewati
lambung.
• Racun di lambung yang ada masih utuh, paling mudah
diidentifikasi.
36. PERHATIAN!!
1. Hepar merupakan sampel yang harus disertakan
pada pemeriksaan toksikologi, karena organ
tersebut merupakan tempat detoksifikasi.
2. Sianida setelah masuk ke darah kemudian akan
cepat hilang.
38. SETELAH DIKEMAS?
1. Pemberian label dan segel.
2. Disertakan dengan surat pengantar.
3. Disertakan dengan berita acara penyegelan.
4. Disertakan dengan keterangan peristiwa termasuk
riwayat medisnya.
39. ISI BERITA ACARA
1. Hari dan Tanggal
2. Identitas Saksi
3. Uraian Proses
4. Tanda Tangan
40. Analisa pemeriksaan toksikologi
• Penginderaan curiga / dugaan adanya racun
• Analisa kualitatif ada / tidak
• Mendeteksi racun
• Racun (+), kadar ?? kematian akibat keracunan diduga dari
:
• Mati mendadak/tidak jelas sebabnya
• Riwayat kontak dengan zat yang dicurigai
• Gejala dan tanda sesuai racun yang dipakai
• Terjadi pada orang yang berhubungan dengan racun/obat
• Lebih dari satu orang mati dgn gejala yg hampir sama/sesuai
• Kesimpulan V et R :
• Ditemukan zat racun berupa…… dalam tubuh korban yang
berhubungan dengan kematian korban
41. • Analisa kuantitatif kadar
• Mendeteksi dan mengetahui kadar
• Kesimpulan V et R :
• Sebab mati korban adalah karena racun ….. yang ditemukan dalam tubuh
korban dalam kadar yang mematikan
• Hasil analisa kualitatif/kuantitas yang negatif, tidak identik
tidak ada racun
• Racun telah dimetabolisme atau diekskresi
• Racun telah rusak/hilang karena perubahan pasca kematian
• Tidak dapat ditentukan dengan metode yang dipakai
• Pengambilan sampel yang tidak tepat
• Dugaan keracunan yang salah, pemeriksaan tidak mencakup
Kesimpulan V et R :
Sebab kematian korban karena …….., pada tubuh korban tidak
ditemukan racun……..
42. Penyebab keracunan yang populer
• Sianida
• Karbonmonoksia
• Insektisida
• Drug abuse
• Narkoba & psikotropika
• Alkohol
• Zat korosif & iritatif
• Logam berat (arsen)
Patofisiologi
Gejala & tanda klinik
Ciri khas
43. Zat Korosif
• Asam :
• Asam mineral/anorganik : asam hidroklorida, sulfat, nitrat,
dan fluorida.
• Asam organik : asam karbolat, oksalat, dan asetat.
• Basa :
• kaustik alkali : NaOH, KOH, CaOH dan NH4OH.
• Garam logam berat : HgCl2, ZnCl, KCN
44. Patofisiologi Zat Korosif Asam
• Daya kerja :
• Konsentrasi lemah : merangsang
• Konsentrasi agak kuat : iritasi
• Konsentrasi kuat : korosif
• Reaksi umum :
1. Ekstraksi air & jaringan sekitar
2. Koagulasi protein albuminat
3. Hemoglobin asam hematin
Makroskopik kelainan lokal :
1. Kering
2. Kasar
3. Gambaran luka bakar pada kulit/mukosa
45. Zat Korosif Perubahan warna pada
kulit atau mukosa
Asam karbol (phenol) Abu-abu keputih-putihan
Asam oksalat Abu-abu kehitam-hitaman
Asam sulfat, asam klorida Abu-abu kemudian menjadi hitam
Asam nitrat Kuning
Asam fluorida merah kecoklatan, pendarahan
Kaustik alkali Abu-abu keputih-putihan
Zinc klorida keputih-putihan
Merkuri klorida biru keputihan, pendarahan
46. Keracunan Asam mineral/anorganik
• Apabila peroral dapat menimbulkan gejala :
• Luka bakar mulut, tenggorokan, esofagus sampai lambung
• Muntah yang mengandung darah, mukosa dan bagian membran
mukosa (tidak terjadi pada volume asam yang banyak)
• Rasa nyeri dan kembung
• Sudut mulut mengalami korosi
• Gigi berwarna putih kapur
• Lidah mengalami korosi
• Suara serak kareda edema laring
• Bisa disertai perforasi (misal racun asam sulfat)
• Konstipasi usus, kadang disertai diare bercampur darah dan membran
mukosa
• Disfagi
• Oliguri dan dysuria
47. Keracunan Asam mineral/anorganik…….
• Penyebab kematian :
• Kematian segera :
• Syok
• Gagal nafas karena spasme dan edema glotis
• Perforasi lambung peritonitis
• Kematian lambat :
• Sepsis, misal pada kasus aborsi
• Lemas dan malnutrisi sikatrik/stenosis pada esofagus/pylorus
• Dispepsia berat
48. • Gambaran postmortem :
• Tergantung :kepekatan asam, volume, durasi kontak.
• Pada kematian segera :
• Tanda-tanda korosi dan kerusakan pada mulut sd lambung. Dapat
berupa sedikit erosi hingga bercak kerusakan luas.
• Bisa terdapat perforasi lambung isi lambung masuk cavum
abdomen
• Kematian lambat :
• Terdapat proses penyembuhan/sikatrik
Keracunan Asam mineral/anorganik…….
49. Patofisiologi Zat Korosif Basa
• Daya kerja :
• Konsentrasi encer : iritasi
• Konsentrasi kuat : korosif
• Reaksi umum :
1. Menembus membran sel dan
mengikat protoplasma
alkaline dan sabun
2. Hemoglobin alkali hematin
Makroskopik kelainan lokal :
1. Basah
2. Lunak
3. Odematous
4. Merah coklat
5. Teraba licin (penyabunan)
50. Keracunan Basa Anorganik
• Gejala hampir sama dengan keracunan asam mineral
• Gambaran khususnya :
• Basa mempunyai rasa pahit dan seperti sabun, sehingga
pasien akan merasakan ini
• Bahan yang dimuntahkan bersifat basa, berwarna hitam,
campur darah dan bagian membran mukosa
• Diare lebih sering terjadi
51. Keracunan Basa Anorganik…………
• Gambaran post mortem
• Tanda-tanda korosi tidak begitu menonjol
• Warna mukosa coklat (hematin alkali)
• Membran mukosa sistem pencernaan mengalami nekrosis
dan inflamasi
• Mukosa mengalami necrosis liquifactip (colliquation
necrosis) : mukosa lembek, basah dan membengkak,
karena terjadi ikatan alkali albuminyang dengan adanya air
yang berlebihan akan melarut kembali.
• Isi lambung biasa berdrah dan sering berwarna coklat
kehitaman seperti kopi
• Perforasi sangat jarang terjadi, kecuali akibat amoniak
52. Zat Iritan
• Penggolongan :
• Anorganik
• Non logam : fosfor, organofosfor, klorin, bromine
• Logam : arsen, antimon, air raksa, tembaga, timah, seng, bismuth
• Organik :
• Racun tumbuhan
• Racun hewan
53. Keracunan zat iritan
• Gejala umum apabila keracunan peroral :
• Perasaan terbakar
• Perasaan tercekik pada tenggorokan
• Disfagia
• Mual dan muntah
• Haus
• Nyeri abdomen disertai diare
• Disuria
54. Arsenikum
• Termasuk golongan logam berat
• Arsennya sendiri tidak beracun
• Senyawa / garam arsen beracun, al :
• Arsenikum oksida : misal warangan mengandung 40-90% As2O3
• Arsenit potasisum atau sodium
• Copper arsenit
• Arsenik sulfida dan chlorida
• Hydrogen arsenikum
55. Arsen…
• Sifat fisik arsen (As2O3) tidak berwarna, tidak berbau,
bentuk seperti bubuk, kelarutan lebih mudah di air
panas dibandingkan air dingin
• Dosis fatal 250 mg, sejumput bisa membunuh 6-7
orang
• Mekanisme kerja :
• Mengaggu metabolisme seluler akibat enzim sulfidril
terhambat
• Racun kapiler sebagai vasodilator vasa
57. Gejala akut paralitik :
• Timbul mendadak
• Nadi cepat dan lemah
• Nafas dangkal dan sukar
• Kesadaran menurun
• Kejang dan mati dlm 24 jam
58. Gejala gastrointestinal :
• Amat haus
• Rasa terbakar pada traktus digestivus disertai mual, muntah, diare.
Muntah berak seperti kolera
• Bisa disertai perforasi
• Tenesmus, feses hitam akibat banyak darah.
• Pembuluh darah submukosa usus halus robek disertai transudasi
kapiler
• Korban mati dalam beberapa jam
59. Gejala Sub akut
• Timbul gejala lebih lamban
• Gejala gangguan syaraf lebih nyata
• Neuritis perifer multipel
• Nyeri otot betis dan paralise otot
• Nyeri abdomen, muntah, diare, feses coklat
• Ikterik
60. Kronis
• Atropi dan paralise otot ekstremitas akibat neuritis perifer, atrofi otot,
foot drop/wrist drop, bila mengenai myocardium dapat mematikan
segera
• Kulit hiperkeratosis dan hiperpigmentasi di sekitar mulut, mata,
papilla mamae dan perut
• Kuku terdapat garis melintang putih (Mee’s line)
• Berat badan menurun, gizi jelak, anemia
61. Gambaran postmortem
• Pemeriksaan luar :
• Tanda-tanda dehidrasi : mata cekung, penonjolan tulang
• Pemeriksaan Dalam :
• Mukosa biasanya normal atau inflamasi
• Mukosa saluran cerna mengalami inflamasi, berwarna merah disertai
perdarahan submukosa. Membran mukosa mempunyai lekukan dan diantara
lekukan (rugae) terdapat lendir yang kental dan mengikat partike racun.
• Isi lambung berwarna gelap.
62. Alcohol
• No. 1 Abused drug with more related deaths per year than
any other.
• In the United States, nearly 17,500 automobile deaths, 40
percent of all traffic deaths, are alcohol related, with a rate
of injury requiring hospital treatment exceeding two million
people per year.
• 5,000 to 10,000 years ago first prepared (guess).
• 700 BC the Greeks had a thriving wine industry, and by
200 BC the Romans had developed the art of wine
making.
• Wine-making was concentrated around the warmer
Mediterranean lands, while beer was mostly perfected in
the cooler northern lands of Europe where it was too cold
to grow grapes.
63. Diagram of increased driving risk in relation to blood-alcohol concentration.
Courtesy U.S. Department of Transportation, Washington, D.C.
65. Alcohols
• Organic Alcohols (R-OH)
• Ethanol C2H5OH (grain alcohol, EtOH)
• Lethal Dose LD50 (LD to 50% of the people) = 7,060 mg/kg of body weight
• Brain- CNS depressant
• Methanol CH3OH (wood alcohol)
• More toxic than ethanol: LD50 = 428 mg/kg
• Propanol C3H7OH (isopropyl alcohol, rubbing alcohol)
• More toxic than Ethanol (3600 mg/Kg)
66. Ethanol
• Colorless liquid with a burning
taste and a characteristic
odor.
• Ethanol may be produced by
oxidation of ethylene gas or
fermentation of sugars.
• Ethyl alcohol can form
hydrogen-bonds and exhibits
intermolecular associations
the same manner as water.
67. Ethanol
• Distilled alcohol always
contains traces of water from
the distillation mixture (4 to
6%). To obtain 99%+ alcohol,
the water must be removed.
• Ethanol dissolves both in
water and in organic solvents.
68. Ethanol Drinks
• Beverage alcohol is formed through fermentation of products such as
corn, potato mashes, fruit juices, and beet and cane sugar molasses.
• Fermentation is an enzymatically anaerobic controlled transformation of
an organic compound - conversion of sugars to ethanol by microscopic
yeasts in the absence of oxygen. The equation for the fermentation of
glucose is:
C6H12O6 → 2CH3CH2OH + 2CO2
• Absorption of ethyl alcohol into the blood occurs mainly by ingestion
but also can occur through the skin and via the lungs.
• Alcohol is quickly equilibrated through all body water.
69. Beer
• Beer is produced from Barley steeped in
water to make it germinate (called Malt)
which is boiled with hops to produce flavor
and aroma.
• The resultant liquid (called Wort) is then
fermented. Various methods of production
after the fermentation stage produce the
range of different beers we have today.
• Stronger beer is often referred to as Ale.
• Stout is sweeter and is flavored with
roasted grain.
• Lager is a lighter beer that has been
matured over a longer period.
• “Lite” beer has less alcohol.
70. Cider
• Cider comes from apples that are
reduced to a pulp which is then pressed
to release the juice.
• This juice is then placed into vats, often
with yeast added, to allow fermentation
to take place.
• Sweet Cider is filtered to stop
fermentation before all the sugar has
been turned into alcohol.
• Traditional Sparkling Cider is allowed to
continue fermenting in the bottle,
although today, modern production
methods mean that Ciders often have the
'fizz' injected by carbonation.
71. Wine
• Made from Fermented Grapes:
• For red wines the skins are generally left
in the mix after the fruit has been
crushed so that during fermentation color
from the skins seeps deep into the juice.
• For white wines the skins are discarded
after crushing, and the grape solids are
also removed before fermentation.
72. Others Alcoholic Drinks
• Brandy. Brandy is distilled wine made from grapes. Other fruit based
liquors can be used (must be clearly identified. e.g.: Cherry Brandy).
Brandy is aged in wooden casks until it is mature. Once it has been
bottled however, it ceases to mature.
• Gin. Made from malted barley and rye and usually flavored using
juniper and other botanicals. (Occasionally it is made from corn or
molasses).
• Rum. Distilled from fermented sugar cane. Traditionally, Rum has a
distinctive brown color, but Light Rum is also produced by rapid
fermentation.
• Whiskey. Made from fermented grain. Fermentation is started by
adding yeast or the residue from previous fermentation before
distillation.
• Sherry. Sherry is a fortified wine in which Brandy has been added to
increase the alcohol content to 15.5% to 18%. (Sherry can only be
produced in the Jerez Region in the southern Spain, and any similar
products made elsewhere must be called 'Fortified Wine’).
73. Ethanol Metabolism
• Ingested alcohol passes down the esophagus and
into the stomach and on into the small intestine.
• The majority of the ethyl alcohol is absorbed from
the stomach (approx. 20%) and the small intestine
(approx. 80%).
• More alcohol will result in increased blood alcohol
concentrations (BAC). A number of factors can
influence ethyl alcohol absorption from the
gastrointestinal tract.
• Gastric emptying - the faster gastric emptying, the
more rapid absorption. Food delays gastric
emptying and therefore delays absorption of ethyl
alcohol.
• The type of food does not seem to be a factor.
Physical exercise also delays gastric emptying.
Drugs (e.g. nicotine, marijuana, and ginseng), may
modify physiological factors regulating gastric
emptying.
74. Ethanol Metabolism
• Following ingestion, about 20% of the ethanol is
rapidly absorbed through the stomach wall. At first,
absorption is rapid but then the rate decreases even if
gastric concentrations remain high.
• Absorption of alcohol through the small intestine is
extremely rapid.
75. Ethanol Metabolism
• After absorption, alcohol diffuses throughout the body and
is fairly uniformly distributed in all tissues and fluids.
• Ethanol crosses the placenta and gains free access to fetal
circulation.
• It also crosses the blood brain barrier, thus the CNS
becomes an important target during alcohol intoxication.
• Alcohol can affect many functions: the literature shows
pathological conditions on most body organs from chronic
consumption.
• Alcohol first affects front of brain then moves to back
(neurodepressant).
• The nerve functions that are most resistant, and last to fail,
are centered in the brain’s medulla, which regulates such
vital functions as respiration and heart activity.
76. Alcohol and the Brain
Parietal Lobe - Ability to
discriminate between
sensory stimuli, ability
to locate and recognize
parts of the body,
disorientation of
environment space,
ability to write.
Occipital Lobe -
Primary visual
association area:
Allows for visual
interpretation.
Frontal Lobe-
Cognition and
memory, ability to
concentrate,
judgment, inhibition,
personality and
emotional traits,
language, and motor
speech.
Alcohol affects the brain front to back.
78. Alcohol “Flow”
Esophagus
Stomach
Small Intestines
Blood
Lungs, Urine
and Skin
Body
Organs
Liver for
Oxidation
•Concentration of alcohol in tissues depends
upon amount absorbed in blood.
•Direct relationship between amount of
alcohol excreted and blood alcohol levels.
79. Ethanol Metabolism
• 95 to 98% of the ingested drug is completely oxidized (combined with O2) to CO2
and H2O in the liver. The small amounts that remain are excreted unchanged in
the breath, urine and sweat. This process occurs mainly in the liver:
• CH3--CH2--OH + NAD+ → CH3--CHO + NADH + H+
ethanol acetaldehyde
• Blood levels fall some 0.015 % w/v per hour
(about 7.5 - 8.5 grams/hour)
regardless of initial alcohol
concentration (varies by as much as
30% per individual).
• Nothing you can do will speed this process up...not
exercising, vomiting, or drinking 3 glasses of
espresso.
% w/v is g per 100 mL
80. Alcohol Effects
• Mild Intoxication (BAC = 0.050 %w/v) - Feeling of warmth, skin
flushed, impaired judgment, decreased inhibitions.
• Obvious Intoxication in most people (BAC = 0.100 %w/v) -
Increased impaired judgment, inhibition, attention, slowed reflexes.
• Obvious Intoxication in all "normal" people (BAC = 0.150 %w/v)
- General lack of muscle coordination, slurred speech, double vision,
memory and comprehension loss.
• Extreme intoxication (BAC = 0.250 %w/v) - Reduced
responsiveness, inability to stand, vomiting, incontinence,
sleepiness.
• Coma occurs around 0.350 %w/v and death is likely at 0.500
%w/v.
% w/v is g per 100 mL
81. Alcohol Effects
• Alcohol’s action on the brain produces of a number of
behavioral effects. These effects are dependent upon
the:
1. amount of alcohol taken in.
2. the time period over which the alcohol is drunk.
3. whether other drugs are being taken at the same time.
4. the previous drinking history of the individual.
5. the physical state of the person doing the drinking.
6. the genetic background of the individual (i.e. ethnicity,
gender).
7. the mood and psychological makeup of the individual.
8. the environment when alcohol is taken.
82. Alcohol Effects
• Four “Hangover” effects of ethanol:
• Alcohol upsets your body's water balance. Causes “dry mouth” and
thirst.
• When alcohol is metabolized, it causes your blood to become more
acidic than normal (this is called acidosis). Causes nausea and sweating.
• Alcohol alters the normal daily rhythm of certain body functions (loose
about 6 hours).
• Alcoholic drinks contain certain impurities called congeners which can
be toxic. [vodka and gin have few congeners and are supposed to
produce less of a hangover, whereas whisky and red wine, with lots of
congeners are supposed to ensure a big headache. Also a toxic
byproduct of alcohol metabolism (acetaldehyde) builds in the
bloodstream].
• Typical symptoms of hangover include nausea, ringing of the ears,
headache, increased heart rate, excessive thirst, anxiety, insomnia,
unsteadiness, dizziness (bed spins), diaphoresis (sweating), shakiness.
83. Ethanol Testing
• Specimen Acquisition
• Breath Test (alcohol)
• Blood sample (alcohol and drugs)
• Urine sample (alcohol and drugs)
• Collection
• Breath: police officer at the scene
• Blood: must be obtained by a medic (forensic medical
examiner)
• Urine: collection must be observed
84. Ethanol Testing
• FIELD SOBRIETY TESTING
• Portable, roadside breath tester.
• Psychophysical tests:
• Walk and turn and/or one leg stand
(divided attention tasks).
• Horizontal-gaze nystagmus: involuntary
jerking of eye as it moves to the side,
usually when following a penlight – the
more intoxicated the less the eye moves
before jerking.
85. Ethanol Testing
• Breath Testing - direct relationship between BAC
and amount of alcohol vapor in breath.
• Henry’s Law - When a volatile compound is dissolved in
a liquid in equilibrium with the air, there is a fixed ratio
between the concentration of the volatile compound in
the air and its concentration in the liquid (remains
constant for a fixed temperature).
• When alcohol in blood is brought into equil. with
air (lungs), there is a fixed ratio between the
concentration of alcohol in air and the BAC.
• Measuring the concentration of alcohol in alveolar
air tells the BAC quite reliably.
86. Ethanol Testing
Breath Alcohol Testing: collects and measures alcohol content of
alveolar breath.
• Ratio of alcohol in the blood to alcohol in alveoli air is 2,100
to 1 (1 mL of blood to 2,100 mL of alveolar breath).
• Use Henry’s Law to determine BAC.
• Determines BAC in pulmonary artery. May not be the same
as venous blood but is most reflective of alcohol getting to
the brain.
• Spectrophotometer measures absorption of light through
potassium dichromate K2Cr2O7 .
• Alcohol reacts with dichromate so less dichromate means
more alcohol. Indirect Method.
• Some use infrared light to measure alcohol in chamber
directly. Direct Method.
87. Breathalyzer
Exhaled
Breath
Piston
Sample
Chamber
(52.5 mL)
–Ratio of alcohol in the blood to alcohol in alveoli air is 2100 to 1 (1 mL of
blood to 2100 ml of alveolar breath). Alcohol in 52.5 mL of exhaled air is
equivalent amt. In 1/40 mL of blood.
3 mL of 0.025%
K2CrO4
• Alcohol reacts with K2CrO4 to
form acetic acid.
• Amount of K2CrO4 consumed
is related to amount of
alcohol present.
• Spec. determination of
amount of K2CrO4
consumed.
• Determine alcohol content in
sample.
• Calculate BAC.
88. Breathalyzer
–Silver nitrate is a catalyst
–Sulfuric acid removes alcohol from the air
–Reddish-orange dichromate ion changes color to the green chromium ion
when it reacts with the alcohol.
• Alcohol reacts with K2CrO4 to
form acetic acid.
• Amount of K2CrO4 consumed
is related to amount of
alcohol present.
• Spec. determination of
amount of K2CrO4
consumed.
• Determine alcohol content in
sample.
• Calculate BAC.
89. Considerations
• A major consideration is to avoid measuring
“mouth alcohol” resulting from regurgitation,
belching, or recent intake of an alcoholic
beverage.
• The recent gargling of an alcohol-containing
mouthwash can lead to the presence of mouth
alcohol, as well.
• Mouth alcohol has been shown to dissipate
after fifteen to twenty minutes from its
inception.
90. The Analysis of Blood for Alcohol
• Gas chromatography offers
the toxicologist the most
widely used approach for
determining BAC levels
with a high degree of
accuracy.
91. Collection and Preservation of Blood
• Blood must be drawn by a qualified individual.
• It is sealed in an airtight container after adding
an anticoagulant, and a preservative.
• Storage temperature, and time of storage are
important factors also affecting alcohol’s
stability in blood.
• Ethanol may be generated in a deceased
individual as a result of bacterial action.
Therefore in postmortem analysis, it is best to
collect a number of blood samples from
different body sites.
