Download STUDIES ON POSTMORTEM CHEMISTRY*

STUDIES ON POSTMORTEM CHEMISTRY*
HANS N. NAUMANN, M.D.
From the Department of Pathology, Veterans Administration Hospital, Jackson, Mississippi
It occasionally happens that there are no changes or only minor changes found
at autopsy and the pathologist is pressed for an opinion as to whether diabetes
may have been present, whether a known diabetic may have died from coma, and
whether certain kidney changes were sufficient to cause death from uremia.
These and similar problems can be solved satisfactorily only by a study of postmortem chemistry.
In a previous paper13 simple tests for glucose, urea and acetone in cerebrospinal fluid for the diagnosis of diabetes and uremia at the autopsy table have
been described. In the present study more detailed information will be presented
on quantitative measurements of glucose, urea, creatinine, uric acid, carbon
dioxide and creatine obtained on postmortem cerebrospinal fluid and blood from
the right and left sides of the heart, as well as on acetone tests, urine analysis
and other supplementary examinations. The results are correlated with the postmortem and clinical findings.
TECHNIC
Materials. Cerebrospinal fluid Avas obtained by cisternal puncture, centrifuged
and used only if contamination with blood was less than 1 per cent. Blood was
drawn from the left and right atria or their large vessels and filtered through a
Gooch crucible to remove clots. Urine was obtained by catheterization or puncture of the exposed bladder.
Methods. Blood and cerebrospinal fluid were precipitated Avith tungstic acid
within half an hour after removal from the body. Somogyi's6 zinc filtrates of
cerebrospinal fluid Avere used in a number of cases and the results agreed well Avith
those obtained in tungstic acid filtrates. Glucose Avas determined by Folin-Wu's 8
method, urea by the author's 12 direct nesslerization method, creatinine and
creatine by Folin-Wu's method, 6 uric acid by Folin's direct method, 6 CO2 as
combining poAver in Van Slyke's apparatus. 6 All determinations were performed
in duplicate. The colorimeter used was a Klett Biocolorimeter. A ICAV supplementary tests included Whitehorn's chloride method 6 and Somogyi's amylase
estimation20 adapted to cerebrospinal fluid. Acetone tests Avere performed by
placing a drop of cerebrospinal fluid or urine on "Denco Acetone Test" poAvder.13
Ui'inary albumin was tested Avith sulfosalicylic acid and sugar by Benedict's
qualitative and quantitative methods.
* Presented at the Twenty-Eighth Annual Meeting of the American Society of Clinical
Pathologists, in Chicago, on October 13, 1949.
Published with the permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions
expressed or conclusions drawn by the author.
Received for publication, October 7, 1949.
314
POSTMORTEM CHEMISTRY
315
RESULTS
Since the chemical values obtained on postmortem material cannot be measured with the yardstick of normal values on material obtained from the patient
during life, we have attempted to establish "postmortem normals" from selected
cases in which there were minimal or unrelated lesions. While many cases could
be selected with no abnormality of the carbohydrate metabolism, it was difficult
to find in the present study sufficient material entirely free of renal disease. A
few cases, therefore, were included as functionally normal in which nephrosclerosis was slight, impairment of kidney function during life was absent and
postmortem urine analysis was normal. Table 1 gives high, low and average
"postmortem normals" in cerebrospinal fluid and right and left heart blood as
•compared to normal antemortem values.
The average "postmortem normals" for glucose in cerebrospinal fluid and left
heart blood are about 60 per cent of those during life; that of the right heart blood
is slightly higher but fluctuates over a Avide range. There is also considerable variation of the sugar values in the left heart blood, while the range between high
and low values for all the nitrogenous compounds is higher thamdui;-ing life, most
strikingly that for urea. However, the range between high and low urea values
is much less marked and the agreement between these values for the right and
left heart blood is much closer than in the case of glucose. The postmortem
normals for creatinine are about twice as high and those for uric acid about one
and one-half times as high as the antemortem normals. The COj values after
death are considerably lower than during life. On the average the postmortem
values in cerebrospinal fluid are lower than those in blood. However, there are
many exceptions in individual cases (see Tables 2, 3).
A selection of diabetic and nondiabetic hyperglycemias is presented in Table 2.
In Case 1 no history and clinical data were available, and death might easily have
been attributed to bronchopneumonia and arteriosclerosis, were it not for the
chemical examination, which revealed a very high value for glucose, the presence
of acetone and a low C0 2 value, indicative of coma due to diabetes which was
corroborated by the anatomic finding of a markedly fibrotic pancreas and confirmed by the urinary findings. Case 2, on the other hand, illustrates that urinalysis alone may be insufficient to detect the severity of diabetes which here,
likewise, was the obvious cause of death. The simultaneous hyperglycemia and
uremia in Case 3 compete for the primary cause of death although the nitrogen
retention, as shown by the comparatively low creatinine, appears less severe and
may be a concomitant finding in diabetic coma. Cases 4 and 5 demonstrate by
their low glucose levels that the diabetes was well controlled and could be excluded as the cause of death.
Of nondiabetic disturbances of the carbohydrate metabolism, acute pancreatitis
may cause considerable elevation of the postmortem cerebrospinal sugar as shown
in Case 6 and to a lesser degree in Case 7. The true nature of such glycorrhachia
is revealed by the increase of amylase activity which, in clear postmortem cerebrospinal fluid, Avas found normally to be less than 15 units and in the presence
of blood contamination less than 30 units. These values are much higher than
316
NATJMANN
TABLE 1
COMPARISON OF POSTMORTEM AND ANTEMORTEM V A L U E S * OP G L U C O S E , U R E A , C R E A T I N I N E ,
U R I C ACID AND CON I N N O N D I A B E T I C S WITH M I N I M A L R E N A L D I S E A S E
EXAMINATION"
Glucose
Postmortem
Cerebrospinal fluid
Right heart blood
Left heart blood
Antemortem
Cerebrospinal fluid
Blood
Urea
Postmortem
Cerebrospinal fluid
Right heart blood
Left heart blood
Antemortem
Cerebrospinal fluid
Blood
Creatinine
Postmortem
Cerebrospinal fluid
Right heart blood
Left heart blood
Antemortem
Cerebrospinal fluid
Blood
Uric Acid
Postmortem
Cerebrospinal fluid
Right heart blood
Left heart blood
Antemortem
Blood
HIGH
94
4S0
344
13
19
20
90'°
110'4
40io
197
179
165
S
24
27
2S"
3214
7014
8"
17'4
AVERAGE
40
102
67
NO.
CASES
75
59
59
AVERAGE
AGE
AVERAGE
HOURS
POSTMORTEM
63
10
|
6S
9i
6519
9014
89
101
102
12
11
11
].
si
14"
26'4
3.6
4.2
4.1
0.9
1.6
1.6
3.0
3.0
1.2"
2.014
0.5"
1.0'4
1.1"
1.5'4
6.7
S.7
8.4
0.7
0.7
0.6
2.6
5.5
5.3
2.8"
5.0'4
0.4"
2.5'4
1.7"
3.514
Carbon Dioxide
Postmortem cerebrospinal fluid. . . 5S
Antemortem cerebrospinal fluid. . . 75'
:
LOW
2.4
10
21
551
651
11
10
10
9
S
S
14
|
62
10
65
6
57
11
Values in mg. per 100 m l . ; values of CO,., in volumes per cent.
those found during life by Kaplan, Cohen, Levinson and Stern. 9 Adrenal hemorrhage as a cause of a moderate increase of glucose is illustrated in Case 8, although anoxia due to severe bronchopneumonia may serve as an alternative
explanation. This latter condition was obviously responsible for the elevated
317
POSTMORTEM CHEMISTRY
cerebrospinal sugar of 134 mg. per 100 ml. in Case 10 as well as of 143 mg. per
100 ml. in Case 2 of Table 4. The increase of sugar in Case 9 is apparently due
to stimulation of the sugar center at the floor of the fourth ventricle according
to the mechanism of Claude Bernard's piqiire.2 The clinical observation of
TABLE 2
POSTMORTEM HYPERGLYCEMIC VALUES IN DIABETICS AND NONDIABETICS
GLUCOSE, MG./100 ML.
AGE
SKX
POSTMORTEM
Cerebrospinal
Fluid
Right,
Heart
Blood
Left
Heart
Blood
OTHER TESTS*
CLINICAL AND ANATOMIC DIAGNOSIS
Cerebrospinal
Fluid and Urine
In Diabetics
93
F
10
510
615
230
72
M
J 3*
405
415
250
67
F
12
222
710
777
69
M
69
F
7
S3
SO
143
29
150
31
•
10
C 0 2 9%, acetone 2 + ;
urine: sugar 6.5%, acetone 4 +
C O : 5 % , acetone 2 + ;
urine: sugar ± , acetone 2 +
Acetone 2 + ; urea 26S,
creatinine 3.6
Acetone 0
Diabetes, pancreatic fibrosis, nephrosclerosis,
bronchopneumonia
Diabetes, arteriosclerosis,
fatty liver
Diabetes,
pyonephrosis,
cholecystitis,
arteriosclerosis
Diabetes, gastroenteritis,
prostatic h y p e r t r o p h y
Diabetes, ncphrosclcrosis,
bronchopneumonia
In Nondiabetics
33
M
2
20
M
i
250
—
—
C0 2 20%, acetone
amylase 49 units
149
—
—
C0 2 15%, acetone + ,
amylase 65 units
Acetone 0
SO
F
3
146
202
1S3
67
M
in
143
122
125
S4
F
i
134
200
134
50
M
3
112
—
—
+,
Acetone ± ; urine: alb.
2+, sugar ± , acetone
2+
Acetone 0; urine: alb. + ,
casts, red cells
Acetone 0; urine: alb.
3 + , sugar 0, pus cells
Laceration of stomach,
duodenum,
pancreas;
fat necrosis
Acute hemorrhagic pancreatitis, fatty liver
Bronchopneumonia, adrenal hemorrhage, fatty
liver, thrombophlebitis
Cerebral hemorrhage, gastric ulcer, nephrosclerosis, arteriosclerosis
Bronchopneumonia,
nephrosclerosis, thrombosis, femoral vein
Coronary thrombosis, arteriosclerosis
'Data not preceded by "urine" apply to cerebrospinal fluid.
glycosuria and hyperglycemia in recent coronary thrombosis is borne out by
Case 11 with slight elevation of the postmortem cerebrospinal sugar.
Table 3 shows selected cases of uremia, extrarenal azotemia and normal kidney
function. T h e high urea and creatinine values combined with urinary findings of
318
NAUMANN
granular casts, red cells and pus cells in Cases 1, 2, and 3 indicate that the kidney
changes were severe enough to cause fatal renal failure. The same conclusion can
be drawn in Case 4 on the basis of the marked rise of creatinine rather than that
of urea. On the other hand, the low urea and creatinine values and scant urinary
TABLE 3
R E S U L T S OF POSTMORTEM T E S T S OF K I D N E Y F U N C T I O N IN S U B J E C T S WITH K I D N E Y D I S E A S E ,
E X T R A R E N A L AZOTEMIA, AND N O R M A L K I D N E Y F U N C T I O N
UREA*
Cerebrospinal
Fluid
CREATININE*
Left CerebroHeart spinal
Blood Fluid
III
HOURS
POSTMORTEM
III
AGE
SEX
OTHER TESTSf
Left
Heart
Blood
Cerebrospinal
Fluid and Urine
CLINICAL AND ANATOMIC
DIAGNOSIS
Kidney Diseases
27
M
1
670
—
73
M
1*
42S
356
317
5.3
9.2
8.7
S7
M
53
M
S4
F
4:
300
2S9
27S
5.0
8.6
9.9
13
20S
—
—
S.5
9
30
34
34
2.7
11.0
—
—
3.1
—
—
3.1
CO» 10%, acetone 0;
urine!: alb. 2 + ,
casts, red cells
Glucose 143; urine!:
alb. 2 + , casts, pus
cells
Urine:
alb.
3+ ,
casts, pus cells
U r i n e ! : alb. 2 + , feured and pus cells
Urine: alb. 0, few
casts
Chronic glomerulonephritis
Nephrosclerosis
P r o s t a t i c hypertrophy
Malignant
nephrosclerosis, edema
Nephrosclerosis, severe
Extrarenal Azotemias
65
F
12
255
3S
M
5
230
—
—
2.3
—
1.5
—
—
NaCl 420, acetone
2 + ; urine: alb. ± ,
few pus cells
C 0 2 32%; acetone 2 +
Meningioma (excessive vomiting)
Duodenal ulcer, hemorrhage
Normal Kidney Function
24
M
25
M
13
197
12
23
2.7
—
—
2.1
Urine!: alb. ±
—
—
U r i n e ! : alb. 2 +
Rheumatic
mitral
stenosis
Skull fracture
"Determinations in nig. per 100 ml.
f D a t a not preceded by " u r i n e " appl}' to cerebrospinal fluid.
{Contaminated with seminal fluid.
findings in Case 5 rule out nephrosclerosis as the cause of death; probably death
resulted from generalized severe arteriosclerosis in an aged person. Case 6 illustrated extrarenal azotemia due to excessive vomiting as confirmed by low
chlorides, low creatinine and increased acetone, a condition incidental to greatly
increased intracranial pressure caused by a large meningioma. The high urea in
319
POSTMORTEM CHEMISTRY
Case 7 Avas obviously due to intestinal hemorrhage in accordance with observations first reported by Schiff and Stevens.18 In Cases 8 and 9 the kidneys were
normal, the values of creatinine were normal and the urinalysis gave positive
albumin tests because of admixture with seminal fluid. In both cases the age, the
sex, the time elapsing between death and autopsy and the general state of nutrition were almost identical but the lesions were not the same. The postmortem
cerebrospinal fluid in the patient who died suddenly by accident with short
agony showed a low urea of 23 mg. per 100 ml., while that of the patient who
TABLE 4
COMPARISON OF ANTEMORTEM BLOOD AND POSTMORTEM C E R E B R O S P I N A L C H E M I C A L V A L U E S
GLUCOSE,
MG. PER
100 ML.
Antemortem 1 hour. . . .
Postmortem 2 hours. . .
UREA,
MC. PER
100 ML.
CREATININE,
MG. PER
100 ML.
392
225
Antemortem 6-S hours.
Postmortem 11-13 hours
5S
57
3.0
2.1
Antemortem 1 day
Postmortem 10-22 hours
210
47
113
119
2.0
1.9
Antemortem 1 day
Postmortem 7-18 hours.
154
72
45
57
l.S
2.1
Antemortem 1 day
Postmortem 3-14 hours.
105
25
54
15S
2.5
2.0
Antemortem 2 d a y s . . . .
Postmortem 4-9J hours.
150
35
131
60
5.0
5.1
Antemortem 2 days. . . .
Postmortem 2-J—11 hours
150
173
4.S
5.5
Antemortem 2 days. . . .
Postmortem 5-9 hours. .
51
134
3.4
2.S
died of cardiac failure Avith prolonged agony showed a high urea of 197 mg.
per 100 ml.
In the preceding paragraphs the chemical Aralues obtained on postmortem
material have been correlated Avith the anatomic and clinical findings. An
attempt will noAv be made to correlate postmortem and antemortem chemical
findings in those cases in Avhich the interval between examinations before and
after death Avas short enough to alloAv a comparison. As seen from Table 4, there
is no agreement between postmortem and antemortem glucose levels. It can be
assumed that a hyperglycemia of at least 300 mg. per 100 ml. Avould have to be
present at the time of death in order to result in a detectable elevation of the
postmortem glucose of more than 100 mg. per 100 ml. Postmortem and ante-
320
NAUMANN
mortem urea levels show much less discrepancy especially in the first three cases.
The best correlation between postmortem and antemortem values is found in the
case of creatinine, confirming the earlier investigation of Polayes, Hershey and
Lederer.15
The interesting observation of Bolliger and Carrodus3 that creatine in blood
and cerebrospinal fluid shows a marked increase after death was confirmed in the
present investigation. As Table 5 shows, there is a rough relationship between the
creatine increase and the interval after death extending up to a maximum at
about ten hours. However, the variation in individual cases shows that this
enzymatic reaction does not depend on time alone and, therefore, cannot be
used to estimate accurately the number of hours after death.
DISCUSSION
The pioneer work on postmortem chemistry was done by Polayes, Hershey
and Lederer15 who first established the value of postmortem creatinine determinations in 1930. Pozzan and Lenaz16 demonstrated the use of postmortem urea
determinations in 1935 and Hamilton-Patterson and Johnson 5 proved the diagnostic importance of postmortem glucose determinations in 1940.
To interpret postmortem chemical findings it is necessary to take into account
the biochemical changes which occur during the agonal period and after death.
The postmortem period should best be less than 24 hours, for during that time the
influence of bacteria can be excluded, except in cases of septicemia and meningitis.
According to Simpson,19 the cooling of a body progresses at the hourly rate of
2.5° during the first six hours and of 1.5° to 2° thereafter without much influence
by low outside temperatures. Because of this slow cooling of the dead body,
enzymatic reactions continue at near-incubator temperatures during the first
four hours after death, even if the body is refrigerated.
The two basic enzyme reactions influencing the blood glucose after death,
namely glycolysis and glycogenolysis, were first observed by Claude Bernard 2
almost a hundred years ago. The gradual disappearance of glucose from the
blood due to the glycolytic action of blood cells was the reason for Bernard's
erroneous conclusion that there was no glucose in the peripheral blood. On the
other hand, the outpouring of glucose from the liver, which led to Bernard's
discovery of glycogen, results in the accumulation after death of sugar in the
hepatic vein and diffusion to the neighboring inferior vena cava and right heart
blood where high sugar values are frequently found. In order to avoid such misleading results, it is usual 5 ' 6 ' 8 ' 2 1 to use blood from the left side of the heart for
postmortem glucose determinations. In the present investigation high glucose
values were found not infrequently also in blood from the left side of the heart,
possibly because of glycogenolysis of myocardial glycogen. (See Table 2, Case 4.)
However, no unexplained high glucose values were obtained in cerebrospinal
fluid, which is subject only to glycolysis and which, therefore, appears to be the
best material for postmortem glucose analysis.
Urea levels after death, as a rule, are three to six times higher than during
life and discrepancies in the values obtained from the left and right heart blood
POSTMORTEM CHEMISTRY
321
and cerebrospinal fluid are less common. The high postmortem blood urea has
been explained17'22 as the result of agonal changes depending on the length of
the agony. As exemplified before, this was partly confirmed, since in cases of
accidental and sudden death with short agony the urea levels were less than 50
mg. per 100 ml. of blood. However, the reverse did not always hold true. For
instance, in a series of 28 cases of cachexia resulting from malignancy or tuberculosis with prolonged agony urea values of more than 100 mg. per 100 ml. were
obtained in only 4 cases. It would appear that essential conditions for the agonal
accumulation of blood urea are a slowly failing circulation with low renal filtration and persistence of urea formation.
Creatinine is least altered by postmortem and agonal changes. Its postmortem
values are more uniform and more closely approach the antemortem values. In
agreement with Polayes, Hershey and Lederer,15 it may be stated that a postmortem creatinine determination represents the most valuable single indication
TABLE 5
C R E A T I N E V A L U E S IN C E R E B R O S P I N A L F L U I D I N R E L A T I O N TO T I M E A F T E R D E A T H
HOURS POSTMORTEM
1
2
3
4
8
9
10
12
13
17
19
CREATINE VALUES, MG. PER 100 ML.
3.4 4.9
6.1 9.6
7.1
5.8 6.2 7.4 8.7 12.6
10.6
9.8
10.1 10.S 14.4 16.0
8.6 16.2
10.0
11.3
11.0
AVERACE VALUE
•
4.2
7.9
7.1
S.l
10.6
9.S
12.S
12.4
10.0
11.3
11.0
of the presence or absence of renal failure. Postmortem cerebrospinal COo values
also are greatly lowered by postmortem acidosis due to the formation of lactic
and other acids.
An important aid in diagnosing uremia and diabetes after death is postmortem
urinalysis. The significance of postmortem urinary findings is obviously the same
as during life except that a slightly or moderately positive test for albumin may
be given by desquamation of bladder epithelium, and frequently by admixture
of the urine with seminal fluid in the male.
The interpretation of postmortem chemical findings is summarized in Table 6.
Postmortem cerebrospinal glucose levels of less than 100 mg. per 100 ml. exclude diabetes as the cause of death. A glucose level of more than 200 mg. per 100
ml. will establish the presence of severe diabetes, provided pancreatitis is absent
and intravenous glucose was not given shortly before death. The simultaneous
presence of acetone and less than 10 per cent for volume of C0 2 per 100 ml.
fluid indicates diabetic acidosis which may be accepted as a primary cause of
322
NATJMANN
death. Intermediate values between 100 and 200 mg. glucose may be interpreted
as diabetes after excluding endocrine conditions other than diabetes, anoxia, increased intracranial pressure, coronary thrombosis and intoxication by some
drugs and poisons. 2 ' 7
TABLE 6
I N T E R P R E T A T I O N OP POSTMORTEM CHEMICAL V A L U E S .
V A L U E S I N MG. PER 100
ML.
Average Time After D e a t h , 10 Hours
LOW RANGE
Glucose
Left H e a r t
Cerebrospinal
Fluid
Left Heart
Cerebrospinal
Fluid
Left H e a r t
less than 100
unreliable
100-200
unreliable
more than 200
unreliable
Severe diabetes or
known
diabetes
ruled out as cause
of death
Carbon Dioxide
Less than 100
Renal failure
out
Less than 2.5
Creatinine
HIGH RANGE
Cerebrospinal
Fluid
Less than 100
Urea
MEDIUM RANGE
ruled
less than 3.5
Renal failure
out
ruled
less than 10%
-
Diabetes diagnosed
if nondiabetic hyperglycemias excluded
100-200
|
100-200
Kidney damage possible if confirmed
by creatinine and
urinary findings
3.0-4.5
2.5-4.0
Kidney damage possible if confirmed
by increased urea
and urinary findings
-
Diabetic or uremic
acidosis
Diabetes diagnosed if
pancreatitis and glucose
therapy
excluded; diabetic acidosis
if
acetone
present and COs less
t h a n 10%; acceptable p r i m a r y cause of
death
more than 200
more than 200
Renal
failure
diagnosed if creatinine
more than 4 . 5 ; acceptable
primary
cause of death
more than 4
more than 4.5
Renal failure
diagnosed if urea more
than 200; acceptable
primary cause of
death
more than 20%
-
Diabetic 01 uremic acidosis nil ed out
*Vitlues in nig. per 100 ml.; values of CO2 in volumes per cent.
Postmortem cerebrospinal fluid or blood urea values of less than 100 mg. and
creatinine values of less than 2.5 or 3 mg. respectively exclude renal failure as a
cause of death. When confirmed by a high creatinine value and by urinary findings in the presence of kidney disease, a urea of more than 200 mg. must be taken
as evidence of uremia which may be accepted as the primary or as a principal
contributory cause of death. Intermediate values between 100 and 200 mg. should
POSTMORTEM CHEMISTRY
323
be interpreted by evaluation of creatinine figures, the urinary findings and the
renal lesion.
For routine purpose the simple tests for glucose, urea and acetone in postmortem cerebrospinal fluid13 and postmortem urinalysis may be used as a screening method and quantitative determinations resorted to only if indicated. Such a
procedure will be a valuable adjunct to postmortem examinations and will help
to establish or rule out diabetes and uremia as causes of death especially in those
cases in which autopsy findings are inconclusive and clinical data incomplete.
SUMMARY
1. Postmortem chemical values of glucose, urea, creatinine, uric acid, carbon
dioxide and creatine in cerebrospinal fluid and blood from the right and left sides
of the heart were determined in a series of 170 human subjects.
2. Biochemical changes after death include lowering of blood and cerebrospinal sugar because of glycolysis; increase of glucose in the blood of the right
side of the heart because of glycogenolysis in the liver; frequently increase of
glucose in the blood of the left side of the heart, possibly because of myocardial
glycogenolysis; and agonal increases of urea and decrease of carbon dioxide resulting from postmortem acidosis.
3. Cerebrospinal fluid is preferable to blood for postmortem determination of
glucose because of the greater reliability of results.
4. The following postmortem average normal values were obtained on cerebrospinal fluid one to 22 hours after death in nondiabetics and in subjects with
minimal renal disease: glucose, 40 mg.; urea, 89 mg.; creatinine, 2.4 mg.; uric
acid, 2.6 mg.; and carbon dioxide, 21 volumes per 100 ml. fluid.
5. Postmortem cerebrospinal glucose values of more than 200 mg. are evidence
of diabetes if pancreatitis and administration of glucose intravenously shortly
before death are excluded. The simultaneous presence of acetone and of less than
10 volumes per 100 ml. fluid of C0 2 indicate diabetic acidosis which may be accepted as a primary cause of death. Glucose values of less than 100 mg. per 100
ml. allow us to rule out severe diabetes.
G. Postmortem cerebrospinal urea values of more than 200 mg., if associated
with a creatinine value of more than 4 mg. and with positive urinary findings are
evidence of uremia which may be accepted as a cause of death. Urea values of
less than 100 mg. and creatinine values of less than 2.5 mg. with absence of urinary findings allow us to rule out fatal renal failure.
7. Creatinine in postmortem cerebrospinal fluid or blood from the left side of
the heart is the most reliable single postmortem test of renal function. Its values
closely approach antemortem values.
8. The postmortem creatine values of cerebrospinal fluid increase roughly with
the interval after death, reaching a maximum at about ten hours.
9. Postmortem urinalysis is of value in enabling one to confirm the diagnosis
of diabetes or uremia as a cause of death.
REFERENCES
1. A N D E S , J. E., AND EATON, A. G.: Synopsis of Applied Pathological Choraistrv. St.
Louis: C. V. Mosby Company, 1941 ] p. 262.
324
NAUMANN
2. BANG, I . : D e r Blutzuker. Wiesbaden: J. F . Bergmann, 1013, p p . 4 ff., 103, 113 ff.
3. BOLLIGER, A., AND CORRODUS, A. L.: Creatine retention in blood and cerebrospinal
fluid. M. J. Australia, 1: 69-72, 1938.
4. HAMILTON, R. C.: Postmortem blood chemical determinations: A comparison of chemical analyses of blood obtained postmortem with degrees of renal damage. Arch.
P a t h . , 26: 1135-1143, 1938.
5. HAMILTON-PATERSON, J. L., AND JOHNSON, E . W. M . : Postmortem glycolysis. J. P a t h .
and Bact., 50: 473-4S2, 1940.
6. H A W K , P. B., AND BERGEIM, 0 . : Practical Physiological Chemistry. Philadelphia:
The Blakiston Company, 1943, p p . 426-42S, 433,"437, 458, 499.
7. H I L L , E . V.: Significance of dextrose and non-dextrose reducing substances in postmortem blood. Arch. P a t h . , 32: 452-473, 1941.
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