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Rogers (1990) Neurologic Collapse During Treatment
Rogers (1990) Neurologic Collapse During Treatment
Brian Rogers, MD, Irene Sills, MD, Michael Cohen, MD, F. Glen Seidel, MD
Diabetic Ketoacidosis (DKA) remains the leading cause of death in children with type I diabetes
mellitus. Complications occurring during DKA treatment include cerebral edema and neurologic
collapse. Developmental outcomes following neurologic deterioration during DKA have varied from
no sequelae to severe developmental disabilities.
A total of three children developed neurologic deterioration during treatment of DKA at Buffalo
Children’s Hospital between 1984 and 1987. The authors treated aggressively for cerebral edema.
Characteristic findings on the computed tomography (CT) scans and magnetic resonance imaging
(MRI) of the brain included hemorrhagic infarctions of the thalami, basal ganglia and lentiform nuclei.
The authors conducted developmental follow-up examinations between 1-1/2 - 3 years following
recovery from DKA coma. Although they noted significant recoveries over time, developmental
disabilities persisted.
The clinical courses and neuroradiographic findings of these patients are compatible with sequelae
of central brain stem herniation and cytotoxic brain injury. Continued efforts are needed in the
prevention and early detection of clinically significant cerebral edema during treatment of DKA.
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DIABETIC
common cause
KETOACIDOSIS (DKA) is the most
of death in children with type I diabetes
had a right-sided tonic seizure and was started on intrave-
nous phenobarbital. She required a tracheostomy 10 days
mellitus.’I Most of the deaths associated with DKA are after admission. Computed tomography (CT) performed
secondary to central nervous system (CNS) pathology, 12 days after admission, demonstrated what appeared to
primarily cerebral edema.’ Neurologic deterioration dur- be a hemorrhage into the right basal ganglia. A follow-up
ing treatment of DKA is often associated with severe CT scan taken 21 days after admission confirmed a hem-
cerebral edema and signs of brain stem herniation.2.3 The orrhagic infarction of the right caudate nucleus and the
development of brain stem herniation has been linked with anterior limb of the internal capsule. Nonhemorrhagic and
high mortality and morbidity.’-’ edema of the thalami were also present (Fig. 1). Approxi-
We report the short- and long-term neurodevelopmental mately five weeks after admission, she had a severe
morbidity and neuroradiographic abnormalities in three communication disorder and asymmetric spastic
children who developed neurologic collapse during treat- quadraparesis. She was dependent on nasogastric feedings
ment of DKA at Buffalo Children’s Hospital (CHOB) and was subsequently transferred to a community hospital
between 1984 and 1987. Potential etiologies of these for chronic care.
unfortunate complications will be reviewed. Three years later, she was referred for an evaluation of
her behavior. She had frequent stereotypical behaviors,
Case Reports pica, wild mood swings and an attention deficit disorder
with hyperactivity. A left hemiparesis was noted. She
Patient 1 ambulated independently, but was clumsy. The WISC-R
Intelligence Test revealed a full-scale IQ score of 53, a
Patient 1 was a nine-year-old girl who was diagnosed as verbal score of 60, and a performance score of 54. Addi-
having diabetes mellitus at 20 months of age and treated tional diagnoses included mild mental retardation and an
with daily subcutaneous insulin. She was attending regu- uneven cognitive profile. She required a personal aide in
lar third grade, achieving A and B grades and by no report a special education classroom.
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Patient 2
*
Duration of diagnosis
t Calcula~ion of corrected Na+: 1.6 mEq of Na+ to be added for every 100 mg/100 ml of glucose over 100 mg/100 ml.
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sistent with edema and hemorrhagic infarctions of the Seventeen months following onset of DKA coma, blood
basal ganglia, upper brain stem, and the surrounding glucose levels showed wide variation, and there were
portions of the frontal, temporal, and occipital lobes (Fig. episodes of hypoglycemia that required treatment. She
2). An electroencephalogram (EEG) revealed generalized required gastrostomy feedings and her posture was that of
slowing and poor background development. quadriplegia in flexion with extension of the left leg. Her
hands were clenched and there were multiple joint
contractures. She had a right gaze preference.
Oculocephalic reflexes were absent. A central right facial
paresis, profound mental retardation and asymmetric mixed
quadriplegia were documented.
Patient 3
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ing disabled by her school system and she underwent aseries of six children with hyperosmolar diabetic coma.
speech, physical and occupational therapies. She was also All had significant metabolic acidosis and four out of six
described as emotionally labile, requiring adult supervi- had ketonuria. They all experienced significant neuro-
sion. General physical examination was normal, cranial logic deteriorations, and two survived. One survivor
nerves were intact and no visual field deficits were noted. remained in a coma for five days and made a complete
She engaged in conversation and her speech was clear. A recovery. The other survivor remained comatose for two
mild left hemiparesis was noted. months and developed optic atrophy and blindness. Other
investigators have reported normal outcomes following
varying periods of follow-up.’,’
In recent years, investigators have coupled clinical
observations with various neuroimaging techniques.
Lufkin and colleagues6 reported a 15-year-old survivor of
DKA coma who, on follow-up, developed
panhypopituitarism, optic atrophy and learning problems
in school. Approximately 1-1/2 weeks following admis-
sion, an EMI scan was normal. In a case series of three
children experiencing neurologic collapse during treat-
ment for DKA, Jos et al.1 reported two survivors. A 5 1//
2-year-old boy experienced neurologic collapse after re-
ceiving eight hours of treatment for DKA. A CT scan
perforrried three weeks after the episode revealed diffuse
cortical atrophy and necrosis of the basal ganglia. On
follow-up, the boy was described as bedridden, requiring
rehabilitation hospital. The other survivor was a seven-
year-old girl who, on follow-up, had a residual right
hommonous hemianopsia. A CT scan revealed a hypodense
area in the left occipital lobe. Another case report de-
scribed a 13-year-old male survivor who developed tran-
sient third-nerve paresis and amnesia for the first three
FIG. 3. Patient 3 (10 mm CT without contrast) four days after admission days of hospitalization. Follow-up confirmed a full clinical
demonstrates a well-defined area of low attenuation involving the left recovery and a normal cranial CT scan.’° More recently,
lentiform nucleus (arrow) as well as subtle areas within the thalami and
one survivor developed isolated growth hormone defi-
peduncles bilaterally (arrowheads).
ciency, hemiplegia and aphasia.55 A CT scan revealed
cerebral atrophy and infarction of the thalamus and hypo-
thalamus. Kanter et al.&dquo; reported two survivors who had
Discussion .
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rapidly, often within one hour. These findings are most There has been a wide spectrum of clinical outcomes in
compatible with central brain stem herniation,12 but the survivors of neurologic collapse during treatment for
typical rostral-caudal progression of signs in central brain DKA.5-ll Neurologic recovery can be significant, but can
stem herniation have been present only inconsistently.2-lo be followed by persistently abnormal neurologic exami-
In recent reports and in our own case series, common nations and functional handicaps in academic achieve-
neuroradiographic findings aredescribed.5, 11 During the ment and social skills. These areas of performance should
course of central or uncal brain stem herniation, there are be assessed in all survivors of neurologic collapse during
a number of vascular compromises that may occur at the treatment for DKA.
tentorial notch.’2 The posterior cerebral artery can be
compressed during brain stem herniation. This artery has Acknowledgments
important branches, including the interpeduncular, Special thanks to Michael Msall, MD, for his thoughtful
thalamoperforate, thalamogeniculate and the cortical review of the manuscript, and to Maureen Codd for her
branches. Compression and limited flow through these secretarial assistance.
branches can produce infarctions of the cerebral peduncles,
References
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