ACUTE INFECTIOUS HiEMOGLOBINiEMIA OF THE 
NEWLY BORN. 
By T. Grange Simons, M. D., Charleston, S. cby 
Mrs. , a healthy primipara was delivered of a vig- 
orous female infant on the 10th May, ’91, at 4:30 A. M. The 
rupture of the membranes without pain was followed by 
three or four strong expulsive pains, and the infant was 
born before the arrival of the nurse or myself. The peri- 
neum was deeply torn and was immediately repaired with 
deep silver wire sutures and dressed with Iodoform. The 
infant cried strongly and all seemed well, urination and 
defecation from the infant attracted no attention as in any 
way being abnormal. On the night of the 12th and morn- 
ing of 13th, inst the child was restless and declined to 
nurse, bowels confined, abdomen distended somewhat. 
01. olivae was given and two dark mucous discharges, ac- 
companied with tenesmus occurred, a carminative of 
R.—Tinct. Assafoetid gtts. viii. 
Tinct. Lavandul. Comp. . . m x. 
Spts. Ammon. Arom. . . m. viii. 
Sod. Bi-Carb grs xx. 
Aq. Anis. Ft %\. 
M. S —Take a tea-spoonful every hour or two. 
The child seemed in a state of apathy—it would not nurse 
nor cry, it would take the mother’s milk from a spoon and 
no trouble in swallowing existed. The discharges from the 
bowels dark, of a tarry hue, with great tenesmus. At 11.30 
A. M., May 13th, the child became cyanosed, cold extremi- 
ties, convulsive or choreic twitchings of face and limbs, 
especially marked on the left side. Thinking I had a case 
with congenital cardiac disturbance, directed the right pos- 
tural position on a pillow with dry warmth. 4.30 P. M.the 
discharges from the bowels of dark mucus, respiration and 
pulsation not materially affected, temperature normal, skin 
moist, hot, suffused with a dark pink color, the convulsive 
l Q Acute Infectious Hxmoglobinsemia—T. Grange Simons, M. D. 
movements constant. I now directed Bromide of Soda gr. ii 
to be given every two or three hours, with the carminative 
already prescribed. This seemed to influence the convulsive 
movements, yet the facial contortions were still apparent at 
times. The jaws were not contracted, nor closed in a tetanic 
manner, the tongue appeared to be too large for the mouth 
and was often protruded in a restless, uncomfortable way. 
Careful examination failed to detect any lesion or injury to 
neck or spinal column, a slight glairy discharge from 
vagina and rectum was observed. The condition of the 
child impressed you as one of great discomfort rather than 
of danger. The apathy or inability to nurse or cry was 
very evident. It continued to take its nourishment from 
the spoon and was well supported and continued to grow. 
Early on the night of the 14th May, the urine became dark 
and apparently bloody. The dusky hue of the skin became 
of a tawny or icteric tinge, the coujunctivae showing the 
icteric condition most markedly, the faeces also became 
more dark, tarry and mucoid, the choreic movements were 
still observed but not intensified. 
The urine under the microscope showed the presence of 
dark granular masses, no blood corpuscles, nor tube casts, 
albumen in small quantity, or a condition of Haemoglobi- 
naemia. The diagnosis was now made as “ Acute Hsemoglo 
binaemia,” or Winkel’s disease. 
Tinct. Ferri Chloridi gts. iii. in water was directed to be 
given every six hours, the child to be kept quiet, warm 
and free from disturbance, noise and exposure to the bright 
light (electric) as its eyes were very sensitive to such influ- 
ences. The Haemoglobinuria continued for two days, then 
the urine became occasionally clear, but this condition fluc- 
tuated for three or four days longer. The convulsive 
movements ceased. The apathy and inability to cry 
continued, nor would she nurse; would allow the nipple 
to remain in her mouth, but could not make traction 
upon it. On May 16th, the sixth day since her birth, 
the face, neck, legs and arms showed an eruption of 
vesicles or bullae of various sizes, some sudaminal, others 
quarter of an inch in diameter, all filled with a turbid 
serum, the lips and eyelids swollen from the presence of the 
eruption, no areolae, or inflamed base surrounded the vesi- 
cles. Warm baths with borax dissolved in them were now 
employed and 
R—Ungt. Zinc. Oxid. 
Ungt. Aq. Ros. a a 3 ss. Acute Infectious Hsemoglobinsemia—T. Grange Simons, M. D. 
3 
The vesicles dried up in 36 to 48 hours, but a crop of 
smaller size succeeded them, some of the larger bullae were 
punctured at their bases, and the serous fluid allowed to 
exude. After desication of the bullae there were left dark 
pink spots covered with branny scales, but no ulcerative 
process at any time was shown. The mixture with the 
Bromide of Soda was discontinued when the cutaneous lesions 
were shown. The Tinct. Ferri Chloridi was still continued, 
with an increase of one drop, or four drops every 6 hours. 
The urine was now normal, and the fecal discharges natural 
as to consistency, but showing the color from the iron. The 
child cried and nursed, but not with avidity, the tongue 
seemed to embarrass it and was still frequently thrust out 
between the lips as if in the way when the nipple came in 
contact with it. Such is the clinical history of the case. 
The literature of this disease is not voluminous, nor is 
the etiology or pathology clearly defined. The best article 
that I have had access to is by J. P. Crozer Griffiths, of 
Philadelphia, in Encyclopedia of Diseases of Children, 
Keating, vol. iii. I shall freely use this article. The 
varied synonyms collected by him nearly all have allied 
nomenclature. It is needless to repeat them. The defini- 
tion given is : “An acute and usually epidemic affection of 
the blood, developing in the new born, characterized by 
cyanosis, icterus and haemoglobinuria running a rapid 
course.” 
Griffith states that in 1871, Pollack, of Vienna, first 
reported 12 sporadic cases. In 1873, Larroyenne described 
an epidemic in the Lyons Maternity Hospital. Bigelow 
reported in the Boston Lying-in Hospital 10 cases, and pub- 
lished his cases in the Boston Medical and Surgical Journal, 
March 11th, 1875. In 1877, Herz reported two cases of 
acute fatty degeneration of the new born that appeared to 
be identical with the disease now developed. Winkel, in 
1879, described more fully the history of twenty-four cases 
in the Dresden Maternity Hospital, these cases occurred 
within one month. He called it “ a hitherto undescribed 
endemic disease among the new-born. From this account 
his name has been linked with the disease, Birsch-Hirch- 
field made some publication about this period with a patho- 
logical report of autopsies of these cases. Some few other 
cases have been described by other observers. 
The Etiology is not well understood. In the case now re- 
ported, all sanitary conditions were good, so as to exempt 
the mother from any source of danger or discomfort. At 4 
Acute Infectious Heemoglobimernia—T. Grange Simons, M. I). 
first the rapid delivery was adjudged a factor that might 
have produced profound centric disturbance, and that a 
case of " Trismus” was to be dealt with. Toxic influences 
could hardly have had any effect as to cause. Creolin was 
used in the vaginal douche employed for the mother, and 
the torn perineum was dusted with iodoform, but I never 
omitted the use of either agent, so little did I regard them 
as a source of danger to the infant. 
Vaso-motor disturbances produced by cold or heat, as 
causing haemoglobinsemia is adduced by Ponfick and others. 
The child was born at 4 30 A. M., on a mild May morning, 
and all care was used by a competent, trained nurse in 
dressing it. Tyson on Haemoglobinuria, page 52G, Vol. I, 
Annals of Medical Science, 1888, refers to this condition 
occurring in malarial subjects, especially after severe mus- 
cular exercise, followed by sudden chilling of the body. 
Bankerstein also alludes to like causes, especially when 
much gastric disturbances occur. When we have the mala- 
rial dyscrasia an additional factor presents itself in pro~ 
ducing liaemoglobinaemia, although Baker, of North Caro- 
lina, thinks that another additional factor exists in the so- 
called malarial haemoglobinuria besides the malarial miasm, 
and regards the destruction of the red blood corpuscles as 
due to a special bacillus. 
Silbermann, as quoted by Guiteras, injected dogs with 
substances causing a solution of haemoglobin. This pro- 
duced venous plethora, with obstruction of the veins by 
deposits, dyspnoea, cyanosis, reflex irritability, high tem- 
perature, convulsions and haemoglobinuria, followed by 
death. 
Haeslin, Munich Medical Wochenscrift, 1890, p. 248, Ameri- 
can Journal Medical Science. August, 1890, in discussing 
the fact of the diminution of haemoglobin in anaemia and 
chlorosis, believes the loss is not due to destruction of 
the red blood corpuscles in the vessels, but simply to 
hemorrhage, especially concealed gastric hemorrhages, and 
claims that autopsies have shown conclusively evidences of 
this in cases with anaemia. The icteric hue of the skin may 
be due to the re-absorption of haemoglobin from the gastric 
or intestinal ecehymoses, as well as by its formation or 
destruction in the blood vessels. The presence of iron and 
haematin was much less in the stools as the anaemia de- 
creased. 
Sherenziss, as quoted by Griffith, states that the blood of 
the new-born is of lower specific gravity as it is deficient Acute Infectious Hxmoglobiruemia—T. Grange Simons, M. I). 
5 
in haemoglobin. Kruger also agrees with this statement. 
Leichtenstern claims that the haemoglobin is greater at birth, 
or soon after, and least from the first to the fifth year, when 
the increase is again noted, the decrease of haemoglobin was 
observed within two weeks after birth. 
Silbermann states that Haemoglobinaemia is physiologically 
present in the new-born, as shown by the bile in the urine 
and the peculiar shadows in the blood under the mi- 
croscope. 
The cause of Hsemoglobinsemia is the presence of an 
agent circulating in the blood that may produce a destruc- 
tion of the red blood cells. Hydraemia is the condition of 
the new born, and cold or other depressing influences may 
tend to produce or intensify the changes in the blood cells. 
Hsemoglobinaemia is a condition of the blood in which 
Haemoglobin is circulating free in the plasma, nor is Hsemo- 
globinsemia always accompanied by Ilaemoglobinuria. 
Ponfiek has shown that the liver converts Haemoglobin 
into bile pigments. Dr. Ralfe, in a paper read at Brighton, 
before the British Medical Association Lancet, Oct. 2o, ’86, 
shows that the blood crystals or coloring matter may not 
appear in the urine, but is converted by the liver into urea 
and urobilin, both of which may be found in the urine to 
excess, that from vaso-motor disturbances, we may have 
destruction of the blood corpuscles. Hence the value of 
Iron and Quinine in such cases, as they diminish nervous 
irritability. He claims in many disturbing states of the 
system, the red blood corpuscles may undergo disintegration 
in the liver, the coloring' matter of the haemoglobin is 
changed into bilirubin, subsequently into urobilin, whilst 
the remainder of the protoplasm of the blood cells is con- 
verted into urea. The anaemic condition that ensues is ow- 
ing to the decrease of the red blood corpuscles. The excre- 
tion of urea was small, but when the anaemia was relieved, 
the excretion of urea increased. 
The question of diagnosis between the morbid conditions 
that simulate Acute Hsemoglobinsemia, may, at first, give us 
some difficulty. The doubt may arise as to its identity with 
the “ Acute Fatty Degeneration of the New Born,” or “ Buhl’s 
Disease.” I quote freely from Griffith here, not following his 
text, but the opinion given: Much similarity may appear, but 
in “ Buhl’s Disease,” the infant is usually born asphyxiated, 
and no appreciable cause exists for this condition. They 
rapidly die or show symptoms of fatty degeneration ; nor 
is Haemoglobinuria found in Buhl’s Disease. Haemorrhages 6 
Acute Infectious Hxrnoglobinxmia—T. Grange Simons, M. I). 
from stomach, bowels, umbilicus, or extravasations of blood 
under the skin, or mucous surfaces, and a more chronic 
course differentiate it from Acute Infectious Haemoglobinse- 
mia, from poisoning by Chlorate of Potash, Carbolic Acid 
or Phosphorous. The absence of these agents must be consid- 
ered. True, in Chlorate Potash poisoning, we have cyano- 
sis, icterus and the urine also shows the presence of Haemo- 
globin or Methaemoglobin and brownish casts with remains 
of the red blood corpuscles, the blood is of a chocolate brown, 
with many colorless corpuscles. The tubules of the kid- 
neys are filled with casts, echymosis under the mucous mem- 
branes, dyspnoea, vomiting and diarrhoea also occur with 
Chlorate Potash poisoning. The liver also, after death, 
shows an enlargement, with brown detritus, resulting from 
the disintegrated blood corpuscles. The dark or blackish 
green urine of Carbolic acid poisoning when treated 
with Nitric acid, then with Potash, shows a reddish, then a 
pea-green changing to a violet hue; without this chromatic 
test being shown Carbolic acid is not present. Cyanosis from 
congenital malformation of the heart, would not show the 
other symptoms noted- 
Prognosis unfavorable. Of the 71 cases reported in Griffith’s 
article only 5 are recorded as having recovered. Winkel 
reports 24 cases, with 1 recovery; Bigelow 10 cases, with 2 
recoveries; Pollack 12 cases and 2 recoveries. 
The duration of the cases variable, but all short. The 
fatal cases of Pollack died on the second or third day. 
low’s cases averaged five days. Winkel’s averaged 22 hours, 
the shortest 9 hours, the longest four and a half days. San- 
der’s case 0 hours. Strellitz’s case two days. Herz one or 
two days. Most of Winkel’s cases died in convulsions or 
collapse. 
Treatment.—In cases of such short duration, often no 
treatment will avail. In the case reported, carminatives with 
alkalies were given with a view of relieving the gastric and 
intestinal or colicky symptoms. Constipation was relieved 
by oil and also, glycerine enemata. For the convulsive 
disturbance when it became apparent, Bromide of Soda, 
gr. ii, was given with the carminative mixture every 
two or three hours; as soon as the exact nature of the case 
was shown by the icteric condition and the Hamioglobin- 
uria, Tinct. Ferri Chloridi, gtts. iii, in water, every six 
hours, in addition to the Bromide treatment. The Bromide 
was omitted, as soon as the convulsions ceased, and especially 
as the skin lesions became also evident. Acute Infectious IIxmoglobincemia—T, Grange Simons, M. D. 
7 
The administration of Tinct. Ferri Chloridi wTas carried 
out in Bigelow’s favorable cases. I regarded it beneficial 
not only for its haemostatic properties, and for the pur- 
pose of diminishing the loss of Haemoglobin, but also as 
aiding its formation, and for its influence, upon the vaso- 
motor system, as it doubtless, allays or averts morbid 
changes set up by the irritability of the nervous system. 
Quinia may have been indicated in an older subject, but I 
did not care to risk gastric irritation, which Quinine so often 
produces in children. Arsenic was theoretically indicated 
to give stability to the red blood corpuscles, it was not, how- 
ever, administered, as the case improved. The child was 
kept warm and quiet on a pillow. Mother’s milk was given 
regularly from a spoon until the power of nursing was re- 
stored. The cutaneous lesions were treated with warm 
baths, in which Borax was dissolved, these were used night 
and morning, and served to allay the inflammation mate- 
rially. The larger bullae were carefully punctured at their 
bases, with a fine needle and the contents being allowed 
to exude and were wiped off with absorbent cotton. Ungt. 
Zinc. Oxid. and Ungt. Aq. Ros. a a 3 ss was also used as a 
dressing The child convalesced and became vigorous. 
18 Montague street, Charleston, S. C. 
June 6th, ’91.