Asfiksia

Judicial Hanging
 ETIOLOGI :
1. ALAMIAH :
- PENYAKIT SAL NAFAS.
2. MEKANIK :
- TRAUMA
- SUMBATAN SAL. NAFAS.
3. KERACUNAN :
- CNS DEPRESANT.
 FASE PADA ASFIKSI :
1. DYSPNOE
2. KONVULSI
3. APNOE / AKHIR
TANDA-TANDA ASFIKSI PADA
JENASAH :
1. CYANOSIS.
2. LEBAM MAYAT :
– LEBIH GELAP
– LEBIH LUAS
– LEBIH CEPAT TERBENTUK.
3. BUSAH HALUS :
- DEPAN HIDUNG MULUT
- SALURAN NAFAS
TRIAS ASFIKSIA :
busa halus
perbendungan
(kongesti)
warna darah lebih gelap
CYANOSIS
LEBAM MAYAT :
lebih gelap
lebih luas
lebih cepat terbentuk
TRIAS ASFIKSIA :
busa halus
perbendungan
(kongesti)
warna darah lebih gelap
CYANOSIS
LEBAM MAYAT :
lebih gelap
lebih luas
lebih cepat terbentuk
TRIAS ASFIKSIA :
busa halus
perbendungan
(kongesti)
warna darah lebih gelap
CYANOSIS
LEBAM MAYAT :
lebih gelap
lebih luas
lebih cepat terbentuk
 TANDA-TANDA ASFIKSI
(Cont.)
4. PELEBARAN PEMBULUH DARAH
BINTIK2 PERDARAHAN/TARDIEU
SPOT/PETECHIAEL HEMORRHAGE.
5. PERBENDUNGAN / KONGESTI.
6. OEDEM PULMONER.
7. DARAH LEBIH ENCER 8 GELAP.
Pelebaran Pembuluh
Darah
Oedem Pulmonum
 ASFIKSIA MEKANIK
1. PEMBEKAPAN/SMOTHERING.
2. GAGGING & CHOKING.
3. PENCEKIKAN.
4. PENJERATAN / STRANGULASI.
5. GANTUNG / HANGING.
6. TRAUMATIC ASFIKSIA.
Mekanisme Kematian Pada Asfiksia
Anatomi leher
 GANTUNG / HANGING
• JEJAS JERAT ;
1. MENGARAH KEATAS KE SIMPUL.
MENGHILANG PADA B.RAMBUT.
2. DIATAS RAWAN GONDOK.
3. SIMPUL HIDUP.
• LEBAM MAYAT PD UJUNG EXT. DAN
--GENITALIA EXTERNA.
• POSISI GANTUNG :
1. KOMPLIT HANGING
2. INKOMPLIT HANGING ;
A. DUDUK/ BERLUTUT
B. BERBARING TERLUNGKUP.
• LETAK SIMPUL :
1. TYPICAL HANGING: BLK KEPALA
2. ATYPICAL HANGING :
- SAMPING LEHER KIRI,KANAN
- DEPAN.
 SEBAB KEMATIAN
(GANTUNG)
1. ASFIKSIA.
2. ANOKSIA JARINGAN OTAK.
JERAT KECIL&KERAS,
LETAK SIMPUL, POSISI GANTUNG
3. VAGAL REFLEX.
4. FRAKTUR OS CERVICAL.
--- KASUS HUKUM GANTUNG.
Lidah Menjulur atau Tidak?
Soft Ligature?
Atau
Hard Ligature?
Hard Ligature
Soft Ligature atau Hard Ligature?
Typical atau atypical?
How can someone hang oneself in sitting,
kneeling, or lying down positions?
The amount of pressure necessary to
compress :
 The jugular veins is 4.4 lb;
 The carotid arteries, 11 lb; and
 The vertebral arteries, 66 lb.
 The trachea requires 33 lb of pressure.
And weight of the head (10-12 lb) is sufficient to
occlude the carotid arteries and cause of death.
Tehnik Otopsi
Tehnik Otopsi
Decomposed body
PENJERATAN /STRANGULASI

• JERAT--- JEJAS JERAT/SIM PUL

• JEJAS = LUKA LECET TEKAN
1. MENDATAR ,SELURUH LEHER
2. DIBAWAH RAWAN GONDOK.
3. SIMPUL MATI.
• JEJAS JERAT --- TALI PENJERAT
---KERAS, KECIL, KASAR ---JELAS
 PENJERATAN (Cont.)
--HALUS, LEBAR. LUNAK ---- T.JELAS
• ASFIKSIA / VAGAL REFLEX.
• PERBENDUNGAN MUKA JELAS.
• RESAPAN DARAH SUBCUTIS/OTOT
- LEHER DIBWH. JEJAS.
• JEJAS POST MORTAL T. JELAS
Manual Strangulation
(Penjeratan)
Manual Strangulation
 PENCEKIKAN
• LUKA LECET KECIL2 BENTUK BULAN
SABIT DI LEHER --- KUKU.
• LUKA MEMAR – KULIT/OTOT LEHER
• PATAH TULANG LIDAH
• PATAH TULANG RAWAN GONDOK
• PERBENDUNGAN –MUKA/KEPALA.
• ASFIKSIA / VAGAL REFLEX.
Plastic Bag Suffocation
 Smothering
(Pembekapan)
 Smothering
(Pembekapan)
 TENGGELAM / DROWNING

Def. : Suatu proses yg dihasilkan oleh terbenamnya korban dalam air yang
menyebabkan kehilangan kesadaran & dan mengancam jiwa.

Diagnosa / sering sulit bila tak ada tanda khas

Tenggelam dapat seluruh tubuh / muka terbenam

Kematian : dpt. Akibat tenggelam atau sudah mati oleh karena sebab lain.
JENIS2 DROWNING :

1. Wet Drowning
2. Dry Drowning
3. Secondary Drowning
4. Immersion Syndrome
TENGGELAM YANG DI AIR TAWAR : (Hypotonik)

Darah di atrium kiri Hemodilusi hemolysis

Ion K. Fibralasi Ventrikel Tek.darah

Cerebral Anoksi  dalam 5 menit

 TENGGELAM DI AIR ASIN (Hypertonik) :

Tek.osmotik air laut 4X dp plasma air ditarik dari sirkulasi

Pulmonal Ke jaringan Interstitial acute secondary pulmoner

edema---- Haemokonsentrasi ------ Sirkulasi lambat-----------

payah jantung  dlm 8 – 9 menit.

 SEBAB KEMATIAN LAIN AKIBAT TENGGELAM

- Asphyxia akibat Spasme Larynx

Gagging & Choking

- Vagal Reflex
 TUJUAN PEMERIKSAAN JENAZAH

1. Tentukan identitas korban

2. Apakah korban masih hidup waktu tenggelam

3. Apakah sebab kematiannya

4. Faktor2 apa yg berperan pada proses kematian

5. Tempat dimana korban pertama kali tenggelam

Untuk itu perlu pem.teliti

1. Pemeriksaan luar jenazah

2. Pemeriksaan dalam jenazah

3. Pemeriksaan Laboratorium
PEMERIKSAAN LUAR JENAZAH

Tanda2 terendam dalam air

1. Basah, berlumuran pasir, lumpur, dll
2. Telapak tangan & kaki keriput
(Washer Woman Hand)
3.Kulit permukaan kasar Kulit bebek
(Cutis Anserina)
Tanda-tanda Intravital

1. Kaku pada sebagian otot/cadaveric Spasme Posisi &

Kekuatan  Orang hidup.

2. Luka2 lecet  gesekan / benturan dalam air

Luka2 lecet  tempat2 lain  kekerasan pd kasus

pembunuhan

3. Tanda2 aspirasi/infiltrasi air dan asfiksia akut

 PEMERIKSAAN DALAM JENAZAH :

1. Busah halus dihidung, mulut,sal nafas dan benda asing

(pasir, Lumpur,algae) dalam saluran pernafasan.

2. drowning lung/aqueous pulmonary emphysema dan edema

----paru2 membesar (balon) sembab, lebih berat, pyramidal

hemorrhage ----- pengirisan banyak cairan.

3. Bercak perdarahan dibawah pleura paru, (bercak Paltauf)

4. Lambung dapat sangat membesar, isi air, lumpur, dll

 diusus halus.

5. Otak, hati, ginjal, limpa tanda2 perbendungan.

6. bila ditemukan cairan hemolysis dl rongga dada > 100 cc
(beb.hari stl mati)--- D/kemungkinan kematian tenggelam
 PEMERIKSAAN LABORATORIUM :

1. Adanya diatome ganggang bersel satu bila pd.pem. di

paru2 ditemukan 4 –5 diatome berarti orang masih hidup.

a. pemeriksaan sediaan apus getah paru - sediaan langsung

b. pemeriksaan destruksi jaringan

2. Pem.darah jantung bilik kiri dan bilik kanan. Berat jenis & kadar

elektrolitnya Mg, beda > 10% sokong diagnosa.

3. Pem. Keracunan (kalau perlu)

4.Pem. Mikroskopik jaringan.

gambar
 DIAGNOSA KEMATIAN AKIBAT TENGGELAM

Pada mayat segar mudah ditegakkan berdasarkan

pemeriksaan2 tersebut diatas.

Pada mayat busuk pemeriksaan diatome saja.

Asphyxia can literally be translated
from the Greek as meaning 'absence of
pulse', but is usually the term given to
deaths due to 'anoxia' or 'hypoxia'.
The term 'asphyxia' is thought by some
forensic pathologists to be a vague and
confusing term.
In its broadest sense it refers to a
state in which the body becomes
deprived of oxygen while in excess of
carbon dioxide (ie. hypoxia and
hypercapnoea).
The classic sign of `asphyxia`
 Petechial hemorrhages
 Congestion and edema
 Cyanosis
 Fluidity of the blood
Petechiae are often known as `tardieu`s spot`,
and discribed at the first time by the Parisian
Professor Ambroise Tardeu in 1866, in the
bodies of infants who he called had been
`overlain`
A common error is to attribute the petechie to
the rupture of capillaries, whereas they actually
emanate from small venules - capillary bleeding
would be invisible to the naked eye.
Petechiae are caused by an acute rise in
venous pressure that in turn causes over
distension and rupture of thin walled peripheral
venules, specially in lax tissues, such as eyelid,
and in unsupported serous membranes, such
as the viceral plura especially in the interlobar
fissures and epicardium, thymus. In the brain,
petechiae may be larger patches of bleeding in
the subarachnoid space where superficial
vessels have ruptured.
It is traditionally claimed that hypoxia of the
vein wall is an added factor, but there is no
experimental proof of this conjecture, for
example, petechiae can appear almost
instantly after violent sneezing or coughing
before any hypoxia is possible.
Posture also has an affect on the appearance
of haemorrhages. They are commonly seen,
along with larger ecchymoses, on the front or
back of corpses who have died from a variety
of causes in which mechanical asphyxia is
absent.
They are often present in normal post mortem
hypostasis, especially where the mode of death
was congestive as in many types of natural
heart disease.
Another problem in the autopsy interprestation
of petechiae is that not all punctate lesions in
the pleura are petechiae. Zaini and Knight
showed that many such apparent petechiae
were either intravascular venous pools,
subpleural microbullae or pigment foci.
In some types of death where oxygen
deprivation is to be expected (such as
drowning, plastic bag suffocation and entering
an atmosphere devoid of oxygen), petechiae
are seldom demonstrable.
In summary, petechial hemorrhages are highly
unreliable indicators of an asphyxial process,
taking this to mean a hypoxic state.
They are the result of venous engorgement,
usually from mechanical obstruction of venous
return to the heart – or in the thorax from
attempts to inspire against a blocked airway.
 Congestion and edema
Congestion and edema this is even more non specific
than petechiae and once again is the result of
obstructed venous return.
Congestion is often associated with tissue swelling if
the venous obstruction continues. The edema is the
result of rapid transudation through capillary and
venule walls, again mainly a function of back pressure
in the venous system.
Hypoxia of the vascular endothelium is alleged to allow
increased permeability, but generalized hypoxia from
other causes does not produce the tissue swelling
seen in strangulation.
Pulmonary oedema, causing excess fluid to enter the
alveoli, is often found in hypoxic death. Here the
mechanism is more obscure, but it is probably a
combination of hypoxia and raised pulmonary vessel
presure.
 Cyanosis
The bluish color of post mortem lividity does not
have the same connotation as cyanosis produced
during life. The term "cyanosis", which means a
bluish discoloration of the skin or mucous
membranes, should be confined to clinical
descriptions and not used for corpses.
In the living, the cyanotic color of the blood
requires the presence of at least 5 g of reduced
haemoglobin per cent in the capillary blood.
However, in the corpse, oxygen dissociation
continues and there may be reflux of
deoxygenated venous blood into the capillaries.
For these reasons, the blood of a cadaver
becomes purplish-blue, but this is not the result of
a pathophysiological change occurring during life,
e.g. strangulation.
The normal color of areas of post mortem lividity is a
cyanotic hue, but this description should not be used
since it is misleading.

Cyanosis produced during life may be partly or

wholly overshadowed by hypostasis, which may
be a deep purple or blue, and may be mistaken
for true cyanosis – indeed, some pathologist
refuse to use `cyanosis` in respect o the dead,
claiming that it cannot reflect the ante-mortem
situation.
.