Case Reports

Spontaneous
Intracerebral
Hematomas
in Juvenile
Diabetic Ketoacidosis
V i j a y a L. A t l u r u , M D

Ketoacidosis is one o f the c o m m o n complications o f
Type I i n s u l i n - d e p e n d e n t diabetes mellitus. Several
neurologic (cerebral) deficiencies have b e e n associated
with diabetic ketoacidosis, i n c l u d i n g cerebral e d e m a
with increased intracranial pressure resulting i n coma;
partial a n d generalized seizures; a n d cerebmvascular
occlusive disease resulting in m o t o r a n d / o r sensory
dysfunction. Intracerebral h e m a t o m a s have n o t b e e n
reported. A child is described who h a d i n s u l i n d e p e n d e n t diabetes mellitus with hyperglycemic
ketoacidosis who developed m u l t i p l e s p o n t a n e o u s
intracerebral hematomas. Possible mechanisms are
discussed.
A t l u r u VL. Spontaneous intracerebral h e m a t o m a s in
juvenile diabetic ketoacidosis. Pediatr Neurol 1986;
2:167-9.

Introduction
Spontaneous intracerebral h e m a t o m a s in children are
u n c o m m o n . These h e m a t o m a s are most likely caused
by r u p t u r e d arteriovenous malformations or aneurysms,
bleeding diatheses, and rarely by m a l i g n a n t hypertension and hemorrhages into neoplasms [1]. Metabolic
disturbances, such as diabetic ketoacidosis, have n o t
been associated with intracerebral hematomas. The
patient reported here presented with behavioral
disturbances, lethargy, and generalized seizures. The
patient was investigated further when her m e n t a l status
failed to improve after adequate treatment for diabetic
ketoacidosis a n d seizures. Multiple intracerebral
hematomas were identified initially by u n e n h a n c e d
c o m p u t e d tomography (CT). The p a t i e n t was m a n a g e d
conservatively a n d the h e m a t o m a s resolved after several
weeks.

From the Departments of Pediatrics and Neurology; State University
of New York at Stony Brook; Divisionof Pediatric Neurology;Nassau
County MedicalCenter; East Meadow, New York.

Figure 1. Unenhanced CT scan documents bzlateral posterior
temporal bematomas. Right-sided lesion has surrounding edema.

Case Report
An l 1-year-old white girl was admitted with behavioral disturbances and lethargy. Insulin-dependent diabetes mellitus had been
diagnosed at 5 yearsof age. She was in good health until the morning
of admissionwhen she complained of malaise. Urinalysisrevealed a
5% glucosecontent and 4 + acetone. She received her usual morning
dose of insulin (6 units regular, 10 units NPH). She vomited after
breakfast and lunch. She was incoherent, abusive, and belligerent,
and later was observed to have tachypnea and increased lethargy.
When seen in the emergencyroom, she was unresponsiveand had a
temperature of 37.3 °C, pulse rate 140, respiratory rate 48, and blood
pressure 120/70 mm Hg. Blood glucose content determined by
Dextrostix® was very low and she was given glucose intravenously
(250 cc of 50% glucose). She had a generalized tonic-clonicseizure
which was treated with diazepam (7.5 rag) and phenobarbital (150
rag). The child was admitted to the pediatric intensivecare unit.
She was the product of a term gestation and a normal vaginal
delivery, followed by normal developmental milestones. She had
experienced several episodes of diabetic ketoacidosis. A single seizure
unrelated to diabetes occurred a year prior to admission;she had been
receiving phenobarbital (90 mg/day). Cranial CT was normal. The
mother and paternal aunt had seizures during adolescence, and 2
siblingshad speech problems.
The child's physical examination on admission revealed Kussmal
type respirations at 48/rain, pulse rate of 152/min, temperature of
37.3 "C, and blood pressure of 94/66. Auscultation of the chest was
normal and the liverwas palpable 3 cm below the right costal margin.
The child was unresponsive to noxious stimuli. Her neck was
supple. The optic fundi were normal. Extraocular movements were
full on oculocephalicmaneuver. Pupils were dilated and nonreactive
bilaterally; the corneal reflex was present. Motor examination
revealed generalizedhypotonia and areflexia.
On admission the blood glucose content was 1,890 mg/dl, sodium
135 meq/L, potassium 5 meq/L, chloride 105 meq/L, bicarbonate
1 meq/L, blood urea nitrogen 18 mg/dl, white blood cell count
22,900/mm 3 with normal differential count, platelet count
414,000/mm 3, and reticulocyte count 1.9%. Hemoglobin and
hematocrit were normal. Liverfunction tests documented: SGOT 166
IU/L (normal= 0-45), SGPT 195 IU/L (normal=0-45), LDH 409

Communicationsshould be addressed to:
Dr. Atluru; Divisionof Pediatric Neurology;Nassau County Medical
Center; East Meadow, NY 11554.
ReceivedJanuary 6, 1986; accepted March 5, 1986.
Atluru: IntracerebralHematomas in Ketoacidosis

167

A

B

Figure 2 (A) Unenhanced scan demonstrates resolving hematomas in the posterior temporal regions bilaterally. (B) Contrast injection reveals
ring-enhanced lesions.
IU/L (normal=60-200), creatinine 2.2 mg/dl (normal= 0.7-1.4),
prothrombin time 10.2/10.8 sec, partial thromboplastin time
26.7/32.0 sec, and cholesterol 266 mg/dl (normal = 120-205 mg/dl).
Phenobarbital was not detectable in the serum. Urinalysis revealed
pH 5, specific gravity 1.021, glucose 4 +, and ketone 3 + .
Hemoglobin Alc was 9.7%. Arterial blood gases were pH 6.69,
bicarbonate 2 meq/L, Paco2 17 mm Hg, PaO2 105 mm Hg. The
calculated serum osmolality was 320 mOsm/kg. Chest x-ray
documented a fight pulmonary infiltrate.
The patient was treated with insulin, sodium bicarbonate, and
intravenous fluids. The patient's pupils became 3 mm in size and
reacted briskly to light. Withdrawal response to noxious stimuli was
present in all extremities. On the following day the patient remained
unresponsive and developed a temperature of 40.5 °C. Lumbar
puncture revealed xanthochromic fluid; analysis revealed glucose 325
mg/dl, protein 175 mg/dl, 5,904 crenated red blood cells/mm~, and
no white blood cells. The fluid was sterile. Cranial CT performed on
the fourth hospital day indicated multiple intracerebral hematomas
(Fig 1). Radioisotope nuclear brain scan showed normal blood brain
flow and no evidence of sagittal sinus or cerebral venous thrombosis.
Cerebral angiography was not performed. The patient was managed
with fluid restriction. She recovered gradually, eventually attaining a
normal neurologic examination.
The child also had acute renal insufficiency from which she
recovered completely. CT of the abdomen showed a slightly enlarged
liver with no other abnormalities. Liver function tests were normal on
subsequent examination. A repeat scan performed on the sixteenth
day documented resolving intracerebral hematomas (Fig 2A).
Following contrast injection, ring enhancement was seen around the
lesions bilaterally (Fig 2B).
She was discharged from the hospital on insulin (10 units NPH)
and phenobarbital (90 mg/day). Follow-up unenhanced CT four
months later demonstrated a low density lesion in the right temporal
region (Fig 3).

also have been reported [2]. Diabetic ketoacidosis has
been known to be associated with encephalopathy,
focal neurologic dysfunction, and seizures, but intracerebral hemorrhage has not been reported in
children.
A variety of possible causes of the spontaneous
hemorrhages in this patient can be postulated.
Malignant hypertension can lead to intracerebral
hemorrhage. Dolger [3] found that vascular disease was
present in varying degrees of severity in every diabetes
mellitus case of some years duration regardless of the
age of the onset, severity of the diabetes, or type of
treatment. Hyperaldosteronism has been reported with
ketoacidosis, resulting in hypertension [4]. This
patient, however, was normotensive 2 years prior to the
ictus.
It is unlikely that a pre-existing vascular malfor-

Discussion

Neurologic complications of juvenile insulin-dependent diabetes mellitus are uncommon; they include
peripheral neuropathy, myelopathy, encephalopathy,
autonomic dysfunction, and central nervous system
changes associated with hyperosmolality. Cerebrovascular disease and acute hemiplegic syndromes
168

PEDIATRIC NEUROLOGY

Vol. 2 No. 3

Figure 3. Uneubanc~d CT scan demonstrates a low density lesion in
the right posterior temporal region.

marion could have resulted in hemorrhage because of
the distribution of multiple, widely-spaced lesions and
the normal contrast-enhanced CT performed a year
prior to admission. There was no evidence suggestive of
coagulopathy or disseminated intravascular coagulation
that would explain the multiple hematomas.
The role of hyperosmolality should be considered in
various neurologic ~ complications of diabetic
ketoacidosis. The degree of mental obtundation
correlates fairly well with the degree of hyperosmolality
in diabetic ketoacidosis. Cerebral edema has been
documented in some cases of treated diabetic
ketoacidosis, as a consequence of the rapid lowering of
the extracellular osmolality [5,9]. In ketoacidosis the
circulation is impaired by the decreased blood volume
and by the elevated blood viscosity typical of
dehydration. With hyperosmolar coma, a similar
circulation difficulty is indicated usually by renal
function impairment, as was the case with this patient.
Rarely, the combination of hyperosmolality with
dehydration and diabetic vascular disease can lead to
thrombotic occlusion of the arteries and veins [6].
Reports of adult diabetics indicated sclerosis of the
cerebral arteries with areas of softening, as well as
intracerebral and intraventricular hemorrhages [7].
Cerebral infarction has also been reported secondary to
dural venous sinus thrombosis in diabetic ketoacidosis
[8]. The primary venous drainage of the brain depends
on the patency of the lateral venous sinuses and the
internal jugular veins. Cerebral infarction may occur if
the venous occlusion is extensive. The predisposing
factors to intracranial venous sinus thrombosis include
severe dehydration due to polyuria and vomiting,
profound hypotension, and infection; all commonly
occur in diabetes mellitus. In this patient, both the
normal isotopic brain scan and the discrete nature of
the hematomas argue against dural sinus thrombosis
resulting in hemorrhagic infarction.

Due to the striking symmetry of these lesions, an
undetected hypotensive episode resulting in watershed
infarcts with softening and secondary hemorrhage
should be considered. A combination of factors might
be responsible for the intracerebral hematomas in this
patient: hyperglycemic hyperosmolar state with dehydration, diabetic cerebrovascular disease, and regional
tissue hypoxia with resultant loss of autoregulation.
Intracerebral hemorrhage should be included as one of
the central nervous system complications of diabetic
ketoacidosis, and appropriate studies should be performed when a child fails to recover after adequate
diabetic ketoacidosis therapy.
The author thanks Dr. Leon G. Epstein for helpful comments and
Christine Kolsch for secretarial assistance.

Rcfel'cncc$
[1] Bickerstaff ER. Cerebrovascular disease in infancy and
childhood. In: Vinken PH, Bruyn GU, eds. Handbook of clinical
neurology. New York: American Elsevier, 1972; 12: 340-51.
[2] McDonald JT, Brown DR. Acute hemiparesis in juvenile
insulin dependent diabetes mellitus (JIDDM). Neurology
1979;29:893-6.
[3] Dolger H. Clinical evaluation of vascular damage in diabetes
mellitus. JAMA 1947,124:1289.
[4] Quigley C, Sullivan PA, Gonggrijp H., et al.
Hyperaldosteronism in ketoacidosis and in poorly controlled
nonketotic diabetes. IrJ Med Sci 1982;151,135-9.
[5] Gordon EE. Invited review: Hyperglycemic hyperosmolar
syndrome. AmJ Med Sci 1976;261:253-68.
[6] McMiUanDE. Pathophysiology of diabetic macro and micro
vascular disease. In: Ellenburg M, Fiflan H, eds. Diabetes mellitus,
3rd ed. New York: Medical Examination Publishing, 1983,343-60.
[7] DeJong RN. The nervous system complications of diabetes
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Ment Dis 1950;3:181-206.
[8] Ata M. Cerebral infarction due to intracranial sinus
thrombosis.J Clin Path 1965;18:636-40.
[9] Rosenblum AL, Riley WJ, Weber FT, Malone Jl, Donnelly
WH. Cerebral edema complicating diabetic ketoacidosis in
childhood.J Pediatr 1980,96:357-61.

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