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BRITISH
MEDICAL
JOURNAL
VOLUME
285
18
SEPTEMBER
1982
777
SHORT
REPORTS
Can
a
cat
smother
and
kill
a
baby?
Whether
a
cat
can
smother
and
kill
a
baby
was
asked
in
the
BMJ
in
1981.1
An
expert
replied
that
it
was
theoretically
possible
but
he
had
never
heard
of
such
a
case
and
considered
it
to
be
an
old
wives'
tale.1
We
describe
such
a
tragedy.
Case
report
A
5-week-old
previously
healthy
baby
girl
was
found
in
her
pram
with
a
cat
lying
over
her
face.
She
was
deeply
cyanosed
and
gasping.
Her
father,
a
doctor,
gave
mouth-to-mouth
resuscitation,
and
her
colour
and
breathing
became
normal
after
about
30
seconds.
A
few
hours
later
she
had
severe
diarrhoea,
fever,
and
poor
peripheral
circulation
and
was
admitted
to
hospi-
tal.
Examination
showed
no
abnormalities
apart
from
her
blue-grey
colour
and
tachypnoea.
There
was
biochemical
evidence
of
slight
dehydration
with
severe
metabolic
acidosis
(pH
7-18),
which
was
corrected.
Lumbar
puncture
showed
no
abnormality,
urine
and
cerebrospinal
fluid
were
sterile,
and
no
pathogenic
bacteria
were
found
in
the
stools.
The
diarrhoea
stopped
after
two
days.
An
electroencephalogram
taken
a
few
days
later
was
abnormal,
with
spikes
and
waves
over
the
frontal
and
temporal
regions.
During
the
next
few
days
she
had
several
convulsions,
which
responded
to
phenobarbi-
tone.
Over
the
subsequent
months
her
psychomotor
development
was
clearly
retarded
and
she
again
had
convulsions
consistent
with
infantile
spasms.
Electroencephalography
showed
hypsarrhythmia.
She
was
treated
with
adrenocorticotrophic
hormone
but
died
at
the
age
of
8
months
from
broncho-
pneumonia.
Postmortem
examination
showed
bronchopneumonia
as
the
immediate
cause
of
death.
The
brain
was
severely
shrunken
and
showed
massive
bilateral
symmetrical
dissolution
of
the
white
matter
of
the
cerebral
hemi-
spheres
and
multiple
cystic
trabeculated
cavities
of
varying
size.
There
was
severe
focal
atrophy
of
the
cerebral
cortex.
Histologically
there
was
massive
loss
of
brain
substance
with
widespread
gliosis.
There
was
loss
of
Purkinje
cells,
and
some
of
the
surviving
ones
had
poorly
demarcated
fluffy
borders.
Ort#--
Section
of
brain
showing
bilateral
symmetrical
loss
of
white
matter,
forming
trabeculated
cystic
cavities,
and
focal
atrophy
of
the
cortex.
Comment
This
case
was
complicated
by
the
fact
that
the
baby
had
both
asphyxia
and
gastroenteritis,
either
of
which
might
have
caused
the
metabolic
acidosis.
The
brain
lesions
were,
however,
typical
of
those
seen
after
severe
hypoxic
damage
in
this
age
group,
resembling
those
seen
after
severe
anoxic
birth
injury,2
and
we
suggest
that
they
can
be
explained
only
by
the
smothering
episode.
We
found
only
one
report
of
a
baby
smothered
by
a
cat
in
the
stan-
dard
textbooks
of
paediatrics
and
forensic
medicine.3
Some
authors
of
popular
books
on
child
care
seem
to
be
fully
aware
of
the
risk,
however,
and
recommend
the
use
of
a
cat
net
to
prevent
a
cat
climbing
into
the
cot
or
pram.4
5
It
is
perhaps
surprising
that
deaths
due
to
smothering
of
a
baby
by
a
cat
do
not
occur
more
often,
but
possibly
they
may
go
undetected.
It
is
interesting
to
speculate
what
might
have
happened
in
this
case
if
the
cat
had
been
disturbed
by
the
baby's
movements
and
had
jumped
out
of
the
pram
before
being
discovered:
if
the
baby
had
died
it
would
have
undoubtedly
been
called
a
cot
death
or
sudden
infant
death
syndrome;
if
she
had
survived
and
then
gone
on
to
develop
a
progressive
nervous
disease
with
severe
psychomotor
retardation
and
convulsions
it
would
probably
have
been
labelled
as
"infantile
encephalopathy
of
obscure
origin."
In
some
instances
children
labelled
with
these
diagnoses
may,
in
fact,
have
been
smothered
by
a
cat.
1
Anonymous.
Is
it
true
that
a
cat
can
smother
and
kill
a
baby
in
its
cot,
or
is
this
an
old
wives'
tale?
Br
MedJ7
1981;282:1679.
2
Blackwood
W,
Corsellis
JAN,
eds.
Greenfield's
neuropathology.
London:
Edward
Arnold,
1976.
3
Polson
CJ.
The
essentials
of
forensic
medicine.
2nd
ed.
Oxford:
Pergamon
Press,
1965.
4
Leach
P.
Baby
and
child.
Harmondsworth:
Penguin
Books,
1979.
5
Jolly
H.
Book
of
child
care.
London:
George
Allen
and
Unwin,
1975.
(Accepted
4
June
1982)
Departments
of
Pathology
and
Paediatrics,
University
Hospital,
Tromso,
Norway
MICHAEL
S
KEARNEY,
MB,
MRCPATH,
consultant
pathologist
LAURITZ
B
DAHL,
MD,
consultant
paediatrician
HELGE
STALSBERG,
MD,
professor
of
pathology
Glaucoma
and
driving
The
presence
of
an
adequate
field
of
vision
is
a
necessary
requirement
for
the
driver
of
a
motor
vehicle.'
Chronic
open-angle
glaucoma
leads
to
erosion
of
the
visual
field.
In
carrying
out
a
survey
in
the
Southampton
area
on
patients
with
this
form
of
glaucoma,
we
asked
patients
if
they
were
drivers
and,
if
so,
whether
they
had
any
visual
problems
while
driving.
Patients,
methods,
and
results
A
total
of
214
patients
were
interviewed.
In
six
cases
the
patients'
glau-
coma
was
diagnosed
as
a
result
of
their
becoming
aware
of
a
field
defect
while
driving.
Two
patients
discovered
an
extensive
field
loss
in
one
eye
when
they
rubbed
the
opposite
eye.
Details
of
the
other
four
patients
are
as
follows:
Case
1-A
74-year-old
man,
who
prided
himself
on
his
driving,
bumped
into
the
kerb
while
driving.
He
then
discovered
that
he
had
a
visual
field
loss.
He-
sought
advice
and
on
two
occasions
his
peripheral
fields
were
checked
by
confrontation.
These
proved
to
be
full
and
he
was
reassured
that
he
did
not
have
glaucoma.
As
he
realised
that
the
defect
was
approaching
fixation,
he
sought
further
advice
which
led
to
the
diagnosis
of
glaucoma.
Case
2-A
62-year-old
man
found
that
part
of
the
traffic
lights
dis-
appeared.
Case
3-A
65-year-old
man
said
that
a
car
coming
out
of
a
side
turning
suddenly
disappeared
from
view
and
then
reappeared.
This
nearly
led
to
a
crash.
Case
4-A
58-year-old
man
had
so
many
near
misses
that
his
wife
refused
to
travel
with
him
until
he
had
his
eyes
tested.
On
examination
he
had
an
extensive
field
loss
in
one
eye
and
a
moderate
loss
in
the
other.
None
of
the
six
patients
above
had
any
ocular
pathology
apart
from
glaucoma.
Twenty
patients
had
given
up
driving
because
of
their
eye
condition;
of
these,
13
had
a
further
eye
disease
(mostly
cataract)
and
three
had
given
up
driving
after
accidents.
In
one
accident
a
person
was
killed.
The
driver,
in
this
instance,
was
a
59-year-old
man
who
had
no
other
eye
disease
apart
from
glaucoma.
He
had
an
arcuate
scotoma
which
had
broken
out
to
the
periphery
in
the
right
eye
and
a
field
of
less
than
10'
in
the
left
eye.
His
central
vision
was
6/6
(right
eye)
and
6/9
(left
eye).
Out
of
the
total
of
214
patients,
61
(28
5%)
were
still
driving.
All
had
the
legally
required
standard
of
central
vision.
Twenty
of
the
drivers
were
aged
70
years
or
older.
Five
drivers
said
that
they
were
aware
of
their
field
loss
and
that
they
had
made
allowances
for
it
by
turning
their
heads
(one
of
these
was
a
lorry
driver).
One
58-year-old
woman
had
had
two
near
accidents
and
has
had
to
leave
her
car
in
the
road
because
she
does
not
trust
herself
to
miss
the
gate
post.
She
has
extensive
field
loss
in
both
eyes
as
well
as
cataracts.
Another
patient,
a
72-year-old
man,
knew
that
he
