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Pneumomediastinum in Diabetic Ketoacidosis: Comments on Mechanism, Incidence, and Management
Donald E. Girard, Victor Carlson, Ethan A. Natelson and Herbert L. Fred Chest 1971;60;455-459 DOI 10.1378/chest.60.5.455 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/60/5/455
CHEST is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright 1971 by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692
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Pneumomediastinum
in Diabetic
Ketoacidosis:
Comments on Mechanism,
Incidence, and Management*
Donald E. Girard, itI.D.;#{176}#V{1ic7t6o}r Carl$on, M.D.;t Etlian A. Natelson, Z'I.D.;t and Herbert L. Fred, M.D., F.C.C.P.
We describe
three cases of pneumomediastinum
associated
with diabetic
ketoacidosis
and give reasons why these disorders may coexist more frequentiy
than heretofore
realized.
The pathogenesis
of pneumomediastinum
in such
patients remains obscure. Previous authors have considered
the pneumomediasti-
num to be a consequence
of vomiting or hyperpnea
accompanying
diabetic
ketoacidosis,
but we point out that it sometimes
precedes the onset of the
metabolic disturbance.
We also acknowledge
that the appearance
of these entities
in the same patient could be coincidental.
In each of the I I documented
cases so
far, primary therapeutic
attention
to the diabetic ketoacidosis
has resulted in an
uneventful
course and rapid recovery.
This experience
calls for conservative
management
of the pneumomediastinum.
M ore than 30 years ago
patient in whom pneumomediastinum
1 described
a
and dia-
betic ketoacidosis
coexisted,
but only recently has
anyone directed
attention
to such an association.
We comment
here on the pathogenesis,
incidence,
and treatment
of pneumomediastinum
accompany-
ing diabetic ketoacidosis
and present three illustra-
tive cases.
CASE REPORTS
CASE 1
A previously healthy 16-year-old boy entered the hospital
in August 1970 complaining
of diffuse abdominal discomfort,
occasional
voniiting,
and pleuritic,
precorelial
chest pain, all
of one day's duration.
He had experienced
polydipsia
and
p()lyuria during the preceding t\V() weeks.
On examination
he was hyperpneic,
lethargic,
and dehy-
drated. His 1)lood pressure was 120/60 mmmi Hg; pimise, 120
1)eats per minute; respirations,
40 per minute; and oral
temperature,
100.2#{176F}. Sumhcutaneoums
cre'pitius
was l)reseflt
in
tile right smmpraclavicular
area. A popping,
extracardiac
sound
( Haniman's
sign ) was ammdible along tile left stc'rnal border in
the fourth interspace.
No other physical
abnormalities
were
evident.
#{176}From tile Departments
of Internal
Medicine
and Radiol-
ogy, St. Joseph Hospital, Hotmston.
#{176}#{176}Resideinnt Internal Medicine.
tStaff Radiologist.
Researci
Associate,
Hematology
Department,
Wilford Hall,
USAF Hospital,
Lackland
Air Force Base, San Antonio.
Director
of \Ieclical
Education.
Initial lal)oratory studies gave the following results: he-
umiatocrit
reading,
48 ix'rc'ent;
total leukoc'yte
coemmit.
17,5OO/mm,3; hlocl sugar
urine sugar and acetone lest'1, 406 mug percent;
concentratioms, blood urea
4+ nitroge'n
concentration,
15 mg percent;
serum C02-combining
power,
less than 5 mEq/liter;
and Plasmila ketone value, `4+", at a
dilution
of 1 :8. The electrocardiogram,
(.lemonstrated
simumus
tachycarclia.
Roentge'nogrammus
of th e..'he'st (iisc'lose(i air immtile
mediastintmni
and in the rigi,t smmpraclavictmlar
and infraciav-
icular spaces ( Fig 1).
Therapy
consisted of insulin and fimmids. The ketoacidosis.
chest pain, abdoumminal discomm,fort,
and Haummnmamm's sigmm dil-
appeared within 24 hours. Four days after admission the
subcutaneous
crepitus had resolved and chest roemmtge'ne)gram 11
was normal.
CASE 2
A 13-year-old girl, previously in good health, ente're'cl the
hospital in Decemmmber 1970 complaining
e)f re'troste'rnal
1)lt'um-
ritic pain of five clays' duration
t\V() days duration.
Tile ch('st
and nausea
paiml
and vomiting
of
i)egun graelimallv,
could nOt be related
II) a precipitating
event, and was not
associate.'d
with feve'r, cough, or spmutunm prodmmction.
Polyeii p-
sia and p()lyuria had been present for the tsvo weeks prece'd-
ing aclmiission.
Physical
examiiination
revealed
a stuporous,
dehydrated.
and hyperpneic
girl whose i)lood pressure
was 1 10/70 mmmmum
Hg; pulse, 130 beats per minute; respirations, 40 mimlmut(';
and rectal temiperatmmre,
98.2#{176}F. The' only other al)normrualitv
was a strikingly
loud, crunching
noise ( Hammmian's
sign
audible ove'r tle' rnidsterntmmmm auul synchronous
vitlm time' h'art
i)eat. Suhcutaneotms
crepitus was absent.
Resimlts of initial laboratory
sttmdies were as follows : lm'-
455
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456 GIRARD ET AL
FIGuRE 1,. Case 1. Chest roentge'mlograms
clavicular
anti infraclavicular
spaces.
denionstrating
air in the mediastinum
and right supra-
mimatocrit
reading,
43 percent;
total leukocyte
count,
:39,00()/m,,m,,l;
urine sugar and acetone concentrations,
"4+";
1)100(1 sumgar level, 708 mg percent;
blood urea nitrogen
concentration.
24 mug lx'rce'nt; serimmii creatinine
value, 4 mg
l)erd'('mlt; serum mm C02-comimbining
6 mmmE I/lite'r; andl 1)iaS-
mma ke'tone illtme', "4+", it a clihmtion of 1 :8. Arterial i)loOd gas
analysis during oxygen therapy revealed a pH of 6.91. a Po2
(If 158 mmummHmg, aml(l a Pc:o of 8.2 mnmmmHg. Electrocardliogranl
si,(l\vd'dl
sinus tac'hvcarclia.
Time admission
chest
roentgenogranls
( Fig 2 ) were re-
Vie'WedI
in(le'1)endle'fltly
by six staff radie)logists,
each aware
timilt pne(mmnomllediastinum
was suspected
clinically.
Five diag-
muOS(.'(I mmm'diastinal
emuphysenia,
and witiu sui)Seqtueflt
filnms for
coulparison,
the sixth agreed that pneumiiomediastinurn
had
i)een present initially.
Twenty-four
hours after institution
of fluid and insulin
therapy,
chest Pain. Hammmmnan's Sign, and ketoacidosis
dlisal)-
peared, bimt small, bilaterally
symimmetrical,
pletmral effusions
i)ecame
evidemit 0mm I)ortable
cimest x-ray film. These roent-
genographic
changes
were not associated
with detectable
clinical evidence
of carcliopumlmiionary
disease or fluid overload
and cleared rapidly without specific treatment.
On the third
hOsI)ital day, tile patient appeared
clinically
well and all of
her previously
mentioned
laboratory
tests gave normal re-
suits. Five days after adinlission,
chest films ( Fig 3 ) showed
no ai)normality.
I
I"i;ume: 2, Case 2. Chest roentgeno)zram)ls
on admission
revealing
mmiecliastinal
emmiphysemiia.
CHEST, VOL. 60, NO. 5, NOVEMBER
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1971
PN EU MOM EDIASTI N U M I N DIABETIC KETOACI DOSI S
457
FIcuRE 3, Case 2. Chest roentgene)grams
five days after admission
showing
no ai)normality.
CASE 3
In January
1971 a previously
he'althy 19-year-okl
diabetic
i)OV ente're'cI Bayshore
Hospitml, Pasack'mia, Texas, because of
nausea, vomiting,
and diffuse 1i)de)mIliflal pain of one clay's
dituration and progressively
severe retrosternal
piemiritic
pain
of three hotmrs' dtmration.
His diabetes
mellitims, present for
e'ight years, imas i)e'eml mmiamageel
`asiiy witim insulin
therapy.
On examination
he was hyperpmleic
and diehydratedi.
His
blood pressure
was 135/60
mm Hg; pulse, 136 beats per
miml(mtt'; resl)iratiomls, 970 j.' A scratchy
22 iwr m,lintute; and oral temip'ratu
re,
to-and-fr()
sound thought
to rcpresemmt a
1)ericardiai
friction
rtmi WdS audible
along the left sternal
border. No eIther ai)mlormualities s'ere m)ote(l.
Initial laboratory
stimclies gave the following
results:
he-
mmmatocrit reading,
54 Ix'rcent;
total letukocyte
coumnt,
24,4(X)/mnmll1;
turifle sugar and acetone conce'ntrations,
`4+
bloOdl smgar level, 710 mug Ix'rc('nt; 1)lood urea nitroge'n alua',
37 mug pe'rcent; and serumu C02-commbining
pe)we.'r, 12 mmiEq/
liter. Ele'ctrocardiogramim
demmionstrated
sinus tachycardia.
i'm(;uImm.: 4, Case' 3. Ch('st
claviceular
spades.
roe'ntgenogrammis
CHEST, VOL. 60, NO. 5, NOVEMBER 1971
(1e)icting
air in the m,mediastinnmn
an(1 1)0th Stupra-
Downloaded from chestjournal.chestpubs.org by guest on July 29, 2010 1971, by the American College of Chest Physicians
458 GIRARD ET AL
Roentgenograms
of the chest disclosed
air in the mediasti-
num and in the right and left stmpraclavicular
spaces ( Fig 4).
It then became apparent that the "pericardial
friction rub"
was, in fact, Hamman's
sign. Moreover,
reexamination
of the
patient revealed
subcutaneous
crepitus
above both clavicles.
Therapy
with insulin and fluids corrected
the ketoacidosis
within
12 hours.
By the next morning
the patient
was
asymptomatic
and Hamman's
sign no longer was detectable.
On the fifth hospital day subcutaneous
crepitus
disappeared.
One week after admission chest roentgenogram
showed no
ai)mlOm'mflality.
DIscussIoN
Pneumomediastinum
develops
experimentally
when a sudden unfavorable
pressure
gradient
be-
tween alveolar spaces and lung interstices
causes
rupture of alveoli with consequent
dissection
of air
along perivascular
sheaths toward the hilum. #{176T}his
usually
occurs
clinically
as a result of trauma,7
following
Valsalva's
maneuver
during
8
or with mechanical
obstruction
of the airways, as in
bronchial
hm9
The pathogenesis
of pneumomediastinum
in the
1 1 reported
patients with associated
diabetic keto-
acidosis
remains
obscure.
Previous
authors
have
suggested
that severe vomiting4
or "the expiratory
effort and grunting
associated
with the ketotic
2 play a causative
role in its pro-
duction. We question these hypotheses,
because in
Hamman's
patient,'
symptoms
of pneumomediasti-
num definitely
appeared
before hyperpnea
and
were not associated
with hyperemesis.
Moreover, in
our second patient, chest pain also occurred long in
advance
of vomiting
or hyperpnea.
Such observa-
tions imply that pneumomediastinum
sometimes
precedes
the onset of diabetic
ketoacidosis
and
perhaps
initiates
or hastens
progression
of the
metabolic abnormality.
Review of data in all of the cases under discus-
sion provides no clue to the mechanism ( s ) respon-
sible for the pneumomediastirium.
Seven of the
patients were males and four were females. The
youngest
was seven years of age2 and the oldest, 29
4 Duration
of diabetes
mellitus varied from
two weeks2***
to 12 years.4 Findings
typical of
pneumomediastinum
per se consisted of chest pain
in five patients,1''4't
Hamm.an's
sign in
eight, 1' 2.4. 5.*,**,t
and subcutaneous
crepitus
in
eight."2454t
Chest roentgenograms
uniformly
demonstrated
mediastinal
emphysema
and, with
one exception,**
also showed subcutaneous
emphy-
sema. The emphysema
resolved within 4* to 25
days. Pulmonary
parenchymal
changes appeared
in
two patients'4
and questionably
in a third.
0 Case 1 , this report.
#{176}#{176}=Ca2s,e this report.
t=Case
3, this report.
Esophagography
gave normal results in the five
patients who underwent
such examination.
` ` Ob-
servations
consistent
with those of diabetic keto-
acidosis
alone were hyperpnea
in all patients,
tachycardia
and tachypnea
in
1 . 2. 4. 5.*,**,t
and
vomiting
in nine.24
5,*,**,'
The true incidence
of pneumomediastinum
in
patients with diabetic ketoacidosis
may be greater
than the number
of articles
on the subject
would
indicate. Not only did we encounter
our three cases
within five months,
but Beigelman
and colleagues4
also observed their four patients during a two-year
span. In fact, reports on all but one of the 11 cases
have appeared
since 1968. The growing number of
documented
cases may reflect more than broaden-
ing interest in the subject and suggests to us that
the two disorders are causally related. We acknowl-
edge, however,
that because unexplained
pneumo-
mediastinum
is being recognized
with increasing
frequency
in apparently
healthy
young adults,' #{1761}`1
its appearance
in a patient with diabetic ketoacido-
sis could be coincidental.
Several factors could account for failure to recog-
nize pneumomediastinum
in patients with diabetic
ketoacidosis.
Unless both clinician and radiologist
are alert to the possibility
of free mediastinal
air,
the metabolic
disturbance
will preoccupy
their
attention.
To complicate
matters,
symptoms
and
signs of pneumomediastinum
such as chest pain,
subcutaneous
crepitus, and the mediastinal
crunch
of Hamman,
can be misinterpreted,
evanescent,
or
absent. Finally, if only posteroanterior
or anteropos-
tenor chest x-ray films are obtained-an
approach
usually deemed
adequate
in a severely
ill person-
pneumomediastinum
will escape notice in about
one-half the
1 2 Addition of lateral chest films
improves diagnostic
accuracy
considerably.
Yet, as
our second case illustrates,
evidence
of pneumo-
mediastinum,
even on the lateral view, may not be
convincing
to all experienced
radiologists,
including
those looking specifically
for it.
Prognosis
in patients
with pneumomediastinum
and diabetic
ketoacidosis
has been excellent.
In
each case primary
therapeutic
attention
to the
diabetic
ketoacidosis
resulted
in an uneventful
course and rapid recovery. This experience
to date
calls for conservative
management
of the pneumo-
mediastinum.
ADDENDUM
In April, 1971, after this paper was accepted for publica-
tion, we encountered
a fourth case of pneumomediastinum
coexisting
with diabetic
ously healthy 15-year-old
ketoacidosis. boy, entered
The patient,
a previ-
the hospital because of
polydipsia
and polyuria of two weeks'
disabling
epigastric
discomfort
of two
and vomiting
of 12 hours' duration,
diuration,
progressively
days' duration,
nausea
and severe retrosternal
CHEST, VOL. 60, NO. 5, NOVEMBER
1971
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PNEUMOMEDIASTINUM
IN DIABETIC
KETOACIDOSIS
459
pleuritic
pain of four hours' duration.
On examination
he
was stuporous and afebrile and had hyperpnea,
tachypnea,
tachycardia,
and Hamman's
sign. Subcutaneous
crepitus
was absent. mediastinum
Chest roentgenogram
demonstrated
free air in the
and in the right supraclavicular
and infra-
clavicular
spaces.
Blood chemical
studies
revealed
ketoaci-
dosis and hyperglycemia.
Thirty-six
hours
of fluid and insulin therapy, ketoacidosis
tient appeared clinically well, and Hamman's
was detectable.
after resolved,
sign
institution the pa-
no longer
ACKNOWLEDGMENTS nard J. Blumenthal
and 3, respectively.
: Doctors Harold Selzman and Berkindly permitted us to include cases 2
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Reprint Branch,
requests: Houston
Dr. Fred, 77002
St. Joseph
Hospital,
1919 La-
The Birth of Psychoanalysis
The third period of psychiatric historiography
was mi-
tiated with Freud's interpretation
of Dreams, published
in 1900, although the volume was actually ready in 1899.
These same years coincided with the flourishing of nat-
uralism of Dostoevski, Zola, Tame, of the individualism
of
Kierkegaard,
of Nietzsche. No matter how strong an in-
fluence these men and others exercised on young Freud,
it cannot be doubted
that the Interpretation
of Dreams
opened a new era in the history of psychiatry.
It was
fortunate that Freud deliberately
avoided studying the
historical
antecedents
of his concepts
because
he was
more free to develop his ideas in an original way. Further-
more, in considering that up to that time psychiatric his-
tories dealt almost exclusively with psychotic institution-
alized patients and that Freud himself, was not interested
in this type of patient as not amenable to psychoanalysis,
it is not surprising
that he disregarded
the tradition of
care and treatment
of mental patients.
Mora, C, in Mora C in Mora, JL:
Psychiatry
and History, Springfield.
C C Thomas, 1970
CHEST, VOL. 60, NO. 5, NOVEMBER
1971
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Pneumomediastinum in Diabetic Ketoacidosis: Comments on Mechanism, Incidence, and Management
Donald E. Girard, Victor Carlson, Ethan A. Natelson and Herbert L. Fred Chest 1971;60; 455-459
DOI 10.1378/chest.60.5.455
This information is current as of July 29, 2010
Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/60/5/455
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