Pediatr Radiol (1997) 27: 785–787
 Springer-Verlag 1997

Fatal cerebral edema and
intracranial hemorrhage associated with
hypernatremic dehydration

Raman Mocharla
Steven M. Schexnayder
Charles M. Glasier

Received: 21 February 1997
Accepted: 25 April 1997

)

R. Mocharla ⋅ C. M. Glasier ( )
Department of Radiology, Slot 105,
Arkansas Children’s Hospital,
800 Marshall Street, Litte Rock,
AR 72202-3591, USA
S. M. Schexnayder ⋅ C. M. Glasier
Department of Pediatrics,
University of Arkansas for Medical
Sciences, Little Rock, Arkansas, USA
S. M. Schexnayder
Department of Critical Care Medicine,
University of Arkansas for Medical
Sciences and Arkansas Children’s Hospital,
Little Rock, Arkansas, USA

Abstract We report neuroimaging
findings of intracranial hemorrhage
and cerebral edema in an infant with
obtundation and seizures, initially
suspected to be secondary to nonaccidental trauma but finally attributed to hypernatremic dehydration.
Neuroimaging findings due to hypernatremic dehydration have not
been previously described in the radiologic literature. Hypernatremia
should be included in the differential diagnosis of intracranial hemorrhage in the infant without evidence
of nonaccidental trauma.

Introduction

Case report

Hypernatremia is a potentially serious electrolyte disturbance which occurs most commonly in infants and
the elderly, usually secondary to dehydration or sodium
intoxication [1–3]. Previous clinical reports [1–3] and
animal experiments [4] documented hemorrhagic cerebral injury in hypernatremic dehydration. However,
there is a paucity of radiologic literature describing neuroimaging findings in infants with severe hypernatremia
who may present with obtundation, seizures, and evidence of intracranial hemorrhage on cranial CT examination, mimicking the findings seen in pediatric nonaccidental trauma victims.

A 5-week-old boy presented at a community hospital emergency
department following a 24-h period of decreased appetite, lethargy, fever, diarrhea, and emesis. The child was born at 33 weeks, gestation (birth weight 1570 g) following premature rupture of
membranes. He had been discharged from the neonatal nursery
3 weeks prior to admission. He was discharged on premixed 24-calorie/oz formula (1 oz ≈ 30 ml) to a non-air-conditioned home, and
the family reported keeping the infant covered with a blanket
while sleeping. Daily maximum ambient temperatures were in the
90 °F (32 °C) range with heat index (a number representing effective heat determined by a combination of temperature and moisture using a complicated mathematical formula) greater than
100 °F (37.7 °C).
On clinical examination at an outside institution, the infant was
lethargic, febrile, and appeared dehydrated. The patient’s vital
signs were heart rate 172 bpm, respiratory rate 62/min, BP 99/
77 mmHg. His skin was cool and dry; the mucous membranes
were pink. There were no focal neurologic abnormalities. The infant was admitted and a septic workup performed. Lumbar puncture revealed 1360 red blood cells/high-power field, 3 white blood

786

Fig. 1 a–c Five-week-old infant
with obtundation and seizures.
Cranial CT on the day of admission demonstrates right tentorial subdural hemorrhage
(arrow, a), diffuse cerebral edema (a, b), and intraventricular
hemorrhage (arrows, b). Follow-up coronal cranial ultrasound (c) shows diffuse
increased echogenicity and loss
of the sulcal-gyral pattern compatible with cerebral edema

a

b

c

cells/high-power field, protein 160 mg/dl, and glucose 57 mg/dl.
Following admission, the infant was reported to be jittery and on
examination had rhythmic movements of all extremities. He rapidly developed apnea and bradycardia with a heart rate of 60 and he
was intubated. Laboratory studies at that time revealed serum sodium of 214 mEq/l, chloride 179 mEq/l, potassium 7 mEq/l, and
CO2 15 mEq/l, BUN 58 mg/dl, creatine 1.4 mg/dl, glucose 189 mg,
and calcium 7.5 mg/dl. The baby was rehydrated with age-appropriate fluids based on the above laboratory values. The hematocrit
was 21 % with normal platelet count. Prothrombin time was 21 s
(control 12 s) and activated partial thromboplastin time was normal. Urine sodium was 179 mEq/l. The baby was transported to
our institution. Upon admission, serum electrolytes were sodium
193 mEq/l, potassium 7.1 mEq/l, chloride 167 mEq/l, bicarbonate
15 mEq/l, BUN 47 mg/dl, and creatinine 1.1 mg/dl. The patient
was rehydrated at our institution based on these laboratory values.
The urine output following admission was 153 ml/15 h. Analysis of
both the premixed infant formula and intravenous fluids from the

referring hospital demonstrated appropriate sodium concentrations.
Noncontrast cranial CT on the day of admission showed a right
tentorial subdural hematoma (Fig. 1 a), cerebral edema, and intraventricular hemorrhage (Fig. 1 b). A follow-up examination of the
infant in the neonatal intensive care unit by cranial ultrasound on
the day before death (Fig. 1 c) demonstrated diffuse increased
echogenicity and loss of the sulcal/gyral pattern compatible with
cerebral edema/infarction. A complete radiographic skeletal survey as well as a bone scan showed no evidence of skeletal injury.
Ophthalmological examination showed no retinal hemorrhages.
After arrival, the infant had persistent seizures for 12 h, after which
his neurological condition rapidly deteriorated and he became hemodynamically unstable. At the request of the family, life support
was withdrawn, and the baby died.

787

Discussion
Symptomatic hypernatremia occurs most frequently in
infants, elderly or debilitated patients from the inability
to drink or from lack of access to water [1, 3]. Gastroenteritis and fever in infants, and disability related to dementia and stroke in the elderly, are the leading causes
of hypernatremic dehydration [1, 3]. Inappropriate oral
intake such as concentrated formula, a fad diet, or tribal
practice are some of the additional causes of hypernatremic dehydration. Widespread use of boluses of
concentrated sodium bicarbonate in premature infants
with acidosis was discontinued after publication of studies showing an increased incidence of intracranial
hemorrhage associated with bolus bicarbonate administration in these patients [2, 3].
Studies in infants, adults, and animal models have
shown that acute hypernatremia may cause significant
morbidity and mortality, most frequently related to
CNS injury. Severe hypernatremia (serum sodium greater than 180 mEq/l) in children has for many years been
associated with a high mortality and severe neurologic
disability among survivors [2]. Chronic hypernatremia
is better tolerated. Early manifestations of hypernatremia are nonspecific and include nausea, vomiting, fever,
and altered mental status. Progressive symptoms and
signs include stupor, hyperreflexia, tremors, seizures,
and finally death. This case of severe hypernatremia is
believed to have been caused by increased water losses
due to a hot ambient environment and by ingestion of

concentrated infant formula, prescribed because of the
infant’s prematurity.
Hypernatremic CNS injury is believed to be caused
by cerebral cellular dehydration [1–4]. Resulting brain
shrinkage leads to rupture of bridging veins, causing
subdural, subarachnoid, or intraparenchymal hemorrhage. Intracranial hemorrhage may be complicated by
cerebral edema or by thrombosis of the small veins or
the dural sinuses [1, 2, 5–7].
Findings of acute neurological deterioration, seizures, CT evidence of subdural and intraventricular
hemorrhage, and cerebral edema in the present case
led to the initial suspicion of pediatric nonaccidental
trauma. However, the nonaccidental trauma workup
was negative. While clinicians are very well aware of intracranial hemorrhage and venous thrombosis as serious, life-threatening complications of hypernatremic
dehydration in children and elderly patients, there is a
paucity of radiologic literature describing neuroimaging
findings in such patients. Here we have described neuroimaging findings of complications associated with severe hypernatremia not previously reported in the
pediatric radiologic literature.
In conclusion, in addition to various coagulopathies,
hypernatremia should be included in the differential diagnosis of intracranial hemorrhage in the infant without
obvious history or evidence of external trauma.
Acknowledgement We sincerely thank Ms Jan McKee for her excellent help with the preparation of this manuscript.

References
1. Finberg L, Kravath RE, Hellestein S
(1983) Hypernatremic dehydration. In:
Finberg L (ed) Water and Electrolytes in
Pediatrics, 2nd edn. Saunders, Philadelphia, pp 124–134
2. Votey SR, Peters AL, Hoffman JR
(1989) Disorders of water metabolism:
Hyponatremia and hypernatremia. Endocr Metab Emerg 7: 749–769

3. Solomon LR, Lye M (1990) Hypernatremia in the elderly patient. Gerontology 36: 171–179
4. Finberg L, Luttrell C, Redd H (1959)
Pathogenesis of lesions in the nervous
system in hypernatremic states. II. Experimental studies of gross anatomic
changes and alterations of chemical
composition of the tissues. Pediatrics 23:
46–53
5. Macauley D, Watson M (1967) Hypernatremia as a cause of brain damage.
Arch Dis Child 42: 485–491

6. Luttrell CN and Finberg L (1959) Hemorrhagic encephalopathy induced by hypernatremia. I. Clinical, laboratory, and
pathological observations. AMA Arch
Neurol Psychiatry 81: 424–432
7. Luttrell CN, Finberg L, and Drawdy LP
(1959) Hemorrhagic encephalopathy induced by hypernatremia. II. Experimental observations on hyperosmolarity in
cats. AMA Arch Neurol 1: 153–160