Journal of Analytical Toxicology, Vol. 30, May 2006
ICase Report
Distribution of Orally Ingested Hydrochloric Acid
in the Thoracoabdominal Cavity After Death
Kei Yoshitome1, Satoru MiyaishP,*, Takaki Ishikawa2, Yuji Yamamoto1, and Hideo Ishizu1
7Departmentof LegalMedicine, OkayamaUniversityGraduateSchoolof Medicine, Dentistry,andPharmaceuticalSciences,
Okayama,Japanand 2Departmentof LegalMedicine, OsakaCity UniversityMedicalSchool, Osaka,Japan
Abstract I
The authors encountered a case of hydrochloric acid (HCI)
poisoning, thought to be caused by oral ingestion of concentrated
HCI. Coagulation of the surface of the tongue and the mucosa of
the pharynx, esophagus, and stomach were observed at forensic
autopsy. An overabundance of CI- was found in the gastric
contents, corresponding to 8.19 mL of concentrated HCI. This was
suggested to be a lethal oral dose of concentrated HCI, and the
cause of death was determined to be HCI poisoning. Measuring the
pH and concentrations of various ions in body fluids and contents
of the alimentary tract enabled postmortem diffusion of HCI to be
determined.
Introduction
Hydrochloric acid (HCI) poisoning is relatively rare. To the
best of the authors' knowledge, no cases of fatal HC1 poisoning
diagnosed by forensic autopsy have been reported, and only
two clinical cases have been documented in the last 20 years
(1,2). It is very difficult to diagnose fatal HCI poisoning at autopsy because this acid is secreted physiologically in the
stomach. Moreover, qualitative analysis and observation at a
macroscopic level cannot determine whether ingestion of a
fatal dose of HCl has occurred. Quantitative toxicological analysis must, therefore, be performed in order to diagnose HCI poisoning as a cause of death. In this article, the authors report an
autopsy case in which poisoning resulted from oral intake of
highly concentrated HCI. Quantitative analysis of the ionic concentration and the pH of autopsy materials led to the autopsy diagnosis of fatal HC1 poisoning. Postmortem diffusion of HCI
from the gastric contents is also discussed.
Case History and Autopsy Findings
The slightly decomposed body of an unidentified woman was
found in a thicket in mid-July. Although no personal identifi* Author to whom correspondence should be addressed: Satoru Miyaishi, 5-I Shikata-cho,
2-chome, Okayama, 700-8558, Japan, E-maih [email protected].
278
cation or suicide note were identified at the scene, a bottle of
concentrated HCI was found near the corpse, and it was suspected that she had ingested the contents.
The woman was 150 cm in height and 53 kg in weight. Skin
exfoliations and white discoloration were found on the lips and
at the left angle of the mouth. No mechanical injuries were
noted on external examination. On internal examination, the
soft tissues of the left inferior aspect of the chest had been discolored a dirty brown. The ribs in this area were softened, and
the left eighth rib was fractured, with no accompanying
bleeding evident in the surrounding tissue. The left thoracic
cavity contained a 220-mL effusion; however, the right thoracic and abdominal cavities were empty. The stomach wall
was hardened and thinned in places, and the adipose tissue
around the stomach was partially dissolved. From the pharynx
to the small intestine, the mucosa was dark brown with small
white solidified and exfoliated patches. The stomach contained
around 180 mL of liquid with some undigested food. Both sides
of the heart contained partially coagulated blood, and the thoracic and abdominal aorta contained completely coagulated
blood. However, blood in the femoral veins had not coagulated.
No other significant pathological changes were found in the
organs and tissues.
Toxicological Analysis
Materials
The contents of the stomach, duodenal bulb, horizontal part
of duodenum, and jejunum were collected, avoiding cross-contamination. Samples of cardiac and femoral venous blood, bile,
and pleural effusion were also obtained. All materials were
stored at -20~ until analysis.
Determination of pH
The pH-value of autopsy materials was determined directly
using an F-12 pH meter (HORIBACo. Ltd., Kyoto, Japan). For
the confirmation of measured pH, an ion-sensitive field-effect
transistor pH meter (KS 501, Shindengen Co. Ltd., Tokyo,
Japan) was used. These instruments were calibrated at three
points (pH 4.01, 6.86, and 9.18).
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Journal of Analytical Toxicology, Vol. 30, May 2006
Ion analysis
Quantities of CI-, PO43-, Na +, K +, Mg2+, and Ca2+ in autopsy
materials were analyzed by ion chromatography using a DX-500
chromatography system (Dionex Co. Ltd., CA). For anion analysis, the ASRS-ULTRA4-mm suppressor and IonPac| AS15 (4 x
250 mm) were selected, and 28 mmol/L KOH was used as the
eluent (1.2 mL/min). Cations were analyzed using an CSRSULTRA-4 mm suppressor, the IonPac CS15 (4 x 250 ram), and
20 mmol/L methane sulfonic acid (1.2 mL/min). All instruments were rinsed with ion-free water before use. Under the described conditions, correlation coefficients of more than 0.997
were obtained from calibration curves constructed using mixed
standard solution of ions. Limits of detection and quantitation
for this apparatus are summarized in Table I. Samples for analysis were prepared from the supernatants of centrifuged autopsy materials (3,000 rpm for 5 rain) by diluting 10 to 3000
times with ion-free water. After filtration (pore size 0.45 tim), 50
]JL of each sample was injected.
Results
Hydrogen ion concentrations of autopsy materials
The pH of the gastric contents was 0.24, and the pH of the intestinal contents ranged from 0.72 to 1.36. The pH of blood
samples was as follows: left cardiac, 3.62; right cardiac, 3.51; left
Table I. Limits of Detection (LOD) and Quantitation
(LOQ) of the Present Ion Chromatogram
Ion
LOD (nmol/L)
LOQ (nmol/L)
ClPO43-
8.0 x 101 nmol/L
4.5 x 102 nmol/L
1.5 x 102 nmol/L
9.0 x 102 nmol/L
Anions
femoral vein, 4.95; and right femoral vein, 5.08. All pH-values
examined are shown in Table II.
Ion concentrations
CI-, Na§ K+, Mg2+, and Ca2+were detected in the gastric contents (Figure 1). Cl- concentration was 7.1 x 102 retool/L, and
the total cation equivalent concentration was 1.6 x 102 mEq/L
(Table III). C1- concentration was 2.0 x 102 mmol/L in the left
cardiac blood, 1.8 x 102 mmol/L in the right cardiac blood, 1.3
x 102 mmol/L in the left femoral venous blood, and 1.5 x 102
mmol/L in the right femoral venous blood (Table IV). The left
pleural effusion contained 1.3 x 101 mmol/L of PO43- and 9.8
mmol/L of Ca22+.
Discussion
HCI is known to cause white or ash-colored necrosis in the
oral region and dark brown discoloration of the gastrointestinal
mucosa. These signs are considered macroscopic evidence of
HC1 poisoning (3), and death from this cause was, therefore,
suggested in the present case. Nonetheless, although macroscopic findings may indicate oral intake of this substance, they
provide almost no information regarding the dose ingested and
are, therefore, insufficient grounds for diagnosing fatal HC1
poisoning. Qualitative analysis of HC1 is also insufficient to diagnose the cause of death because HC1 is physiologically secreted in the stomach. The authors, therefore, determined pH
and ionic concentration in various autopsy materials.
In the present case, C1- concentration in the gastric contents
was determined as 7.1 x 102 mmol/L. This revealed that the deceased had swallowed a huge amount of CI- because normal gastric juice contains HC1 at a concentration about 1.0 x 102
CI"
2.OC
Cations
NA§
K+
Ca2+
Mg2§
1.5 x
2.5 x
2.0 x
2.5 x
102 pmol/L
102 pmol/L
102 pmol/L
102 pmol/L
3.0 x 102 pmol/L
5.5 xl 02 pmol/L
4.0 x 102 pmol/L
5.0 x 102pmol//L
Table II. pH Values of Autopsy Materials
A
~1.0C
r,,)
O
5,OO
I O.OO
15.00
20.00
25.00
Retention time (min)
Material
pH
Na+
Gastric content
Duodenal content (bulb)
Duodenal content (horizontal part)
Jejunum content
Bile
0.24
1.00
0.72
1.36
3.66
Left heart blood
Right heart blood
Left femoral blood
Rightfemoral blood
3.62
3.51
4.95
5.08
Pleura[ effusion
0.99
I
1.00
.~ 0.50
-O.50
-I .00
B
4+
l
2,00
4,00
M 2+
,2
6.00
8.00
Ca2+
I
A
10.00
12.00
14.00
Retention time (rain)
Figure I. Ion analysis of the gastric contents: anions (A) and cations (B).
279
Journal of Analytical Toxicology, Vol. 30, May 2006
mmol/L. The C1- concentration can be increased by swallowing
metal chlorides (e.g., in the case of sodium chloride poisoning).
However, if this were the case, an increase of the cation paired
with C1-would be seen and no change of pH would occur. In the
present case, as total cation concentration was 1.6 x 102 mEq/L
(Na§ K+, Mg2§ and Ca2+),an overabundance of 5.5 x 102 mEq/L
(retool/L) of C1-was observed in the gastric contents. The pH of
the gastric contents was 0.24, which was markedly lower than
normal (about 1.0) and close to the pH theoretically calculated
from the overabundant C1- (0.26). Moreover, a very similar pH
(0.21) was calculated from an additional titration study of the
gastric contents using NaOH, which demonstrated an acid normality of 0.62 (data not shown). From the previously mentioned analysis, the high level of Cl- ions in the gastric contents
was determined to have originated from the ingested concentrated HCl.
The secondary issue to be solved in this case was whether the
ingested HC1 had caused death. When the volume of intake
was calculated from the overabundant C1- in the gastric contents, it corresponded to 8.19 mL. This is in accordance with the
previously described fatal doses of HC1, which have been reported at 4-18 mL (4-5). In addition, no evidence of mechanical injuries or internal disease were found at autopsy. Hence,
the cause of death was determined to be HCl poisoning.
Blood pH has been reported to fall to 6.73 during the first 12
h postmortem and to 6.43 during the second 12 h (6). The authors have also confirmed fall in blood pH (6.58-5.75) in four
autopsy cases at 48-72 h after death. In the present case, however, blood pH in both sides of the heart was much lower (3.62
Table III. Ion Concentrations in the Gastric Contents
Ion
Concentration(mmol/L)
CINa§
K+
7.1 x 102
1.2 x 100
1.2 x 102
4.0 x 101
Ca2+
Mg2+
9.5 x 10-1
4.1 x 10-1
PO43-
Table IV. CI- Concentrations in Blood Samples
CI- Concentration
Sample
280
(retool/L)
Heart blood
Left
Right
2.0 x ] 02
1.8 x 102
Femoral venous blood
Left
Right
1.3 x 102
1.5 x 102
on the left and 3.51 on the right). Although the pH of the
femoral venous blood also fell to 4.95 on the left and 5.08 on the
right, these values remained higher than those of the cardiac
blood. This could be explained by postmortem diffusion of HCI
into the blood from the gastric contents, a well-known phenomenon affecting chemical substances contained in the
stomach (7-9). Comparing with the C1- concentration in
normal postmortem blood (10), those in the present case were
much higher, especially in the cardiac blood (Table IV). This
phenomenon also could be explained by the same mechanism.
This interpretation is also supported by the respective distance from the stomach of the heart, femoral veins, and the remainder of the gastrointestinal tract, explaining the degree of
blood coagulation, blood concentration of CI-, and pH of the intestinal contents and bile.
The non-hemorrhagic fracture of the left 8th rib could also be
explained by the effect of HCI exuding from the stomach after
death, which was confirmed by the low pH (0.99) and high
concentration of Ca2+ and PO43- (9.8 mmol/L and 1.3 x 101
mmol/L, respectively) determined in the left pleural effusion.
Diffusion of HC1 appeared to have caused discoloration of the
left lower part of the chest and weakening of the ribs in this
area. It is likely that the fracture occurred during transportation
of the deceased.
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Manuscript received July 8, 2005;
revision received October 3, 2005.