DWI Lesions Following Oral Rehydration for Diarrheal Disease in

Infants Presenting with HypernatremiaAbstract No:

1439

D Shaw1, T Ahmed2, M Islam2, G Ishak1 1Seattle Children's Hospital, University of

Washington; Seattle, WA 2Dhaka Hospital of ICDDR,B; Dhaka,

Bangladesh

Purpose3- 5% of infants hospitalized in Dhaka with

diarrhea and dehydration present with hypernatremia (serum sodium > 150).

Clinical concern had been raised as to neurocognitive impairment in a subset of infants surviving dehydration treated with oral rehydration who presented with hypernatremia.

This observation prompted a pilot study including MR imaging in this subset of infants treated with this oral rehydration protocol.

Materials and Methods1.5T MRI was performed immediately post

hospital discharge following oral rehydration for an episode of diarrheal induced dehydration associated with hypernatremia at the primary pediatric hospital in Dhaka, Bagladesh.

Clinic data was collected and scans (T1, T2, DWI and GE) retrospectively reviewed by two pediatric neuroradiologists. The study was approved by the local IRB.

Results4 children studied (ages 6-14 months) Admitted with serum sodium between 165 and 208

meq/l; All treated with oral rehydration (ORS) over 46-70 hours

(no IV fluids); (see following clinical data table).All were reported clinically normal at discharge. Brain MR were abnormal in 3 of 4 children; mostly

symmetric extrapontine foci of diffusion restriction were seen in central gray and internal capsule. In one infant, additional patchy areas of diffusion restriction were seen in the central white matter.

No evidence of venous thrombosis or hemorrhage was detected.

W/A=weight for age (minus score indicates under-nutrition), W/L=weight for length (minus score indicates wasting); GORS=glucose based ORS

Patient Clinical Data:

Patient G4

P-0537617G3

P-0540842G1

P0541887G2

P-0543952

Age 6 months 8 months 3 months 27 days 1 yr 2 months

Nutrition status No Oedema Non pitting oedema No oedema No oedema

Initial Na(meq/l) 208.2 189.7 183.01 164.88

Correction withGORS

1320ml over70 hours

1008ml over46 hours

888ml over48 hours

1247ml over48 hours

Final Na(meq/l) 145.8 143.4 142.18 145.1

Outcome Discharge: full recovery Discharge: full recovery Discharge: full recovery Discharge: full recovery

Final Na(meq/l) 145.8 143.4 142.18 145.1

OutcomeDischarged with full

recoveryDischarged with full

recoveryDischarged with full

recoveryDischarged with full

recovery

EEG findingsFocal slowing restricted to left posterior temporal

and occipital regionNormal

Ac excess of slow waves noted over the right

posterior temporal and right occipital regions

Normal

Case 4: 6 month old. DWI trace: bilateral diffusion restriction in thalami, internal capsules and hippocampi

Case 3: 8 month old: DWI trace: symmetric diffusion restriction in anterior limbs of internal capsule, medial putamen, asymmetric patchy restriction in cerebral white matter.

Case 2; 14 months old: DWI trace: mild symmetric diffusion restriction in Globus pallidus and medial putamen.

DiscussionDiffusion restriction seen in 3 of 4 cases.Largely symmetric involvement.Central gray and white matter tracts,

internal capsule.Only 4 cases, but the most extensive

findings were seen in the case with the highest sodium level.

DiscussionConsidering the clinical setting, osmotic

myelinolysis was thought the likely etiology

Whether secondary to or preceding electrolytic correction is unresolved (imaging was done outside the treating institution and only available after discharge).

No evidence of venous thrombosis or hemorrhage was seen.

Osmotic demyelination syndrome: (ODS)Overly rapid correction hypo, and

hypernatremia. Other electrolytic derangements and

clinical scenarios have also been implicated (hypophosphatemia and hypokalemia; acute hepatitis; renal failure; hemodialysis; emesis gravidarum; anorexia nervosa; diabetes mellitus; Wilson disease; leukemia; lymphoma; AIDS; various autoimmune diseases)

Osmotic demyelination syndromeMalnutrition has been a potential factor since

the original reports in alcoholic liver disease/anorexia being present apparently in some cases without rapid correction.

Initial cases of Central Pontine Myelinolysis (CPM) with overly aggressive/rapid correction of hyponatremia in alcoholic liver disease were fatal, diagnosed at autopsy; with modern imaging there has been increasingly recognized to be a broader phenotype, non-fatal CPM and extrapontine myelinolysis.

Prior Literature in Pediatrics: Ranger et al 2012: Central Pontine and Extrapontine Myelinolysis in Children: A Review of 76 PatientsRanger A M et al. J Child Neurol 2012;27:1027-1037

76 pediatric cases from 5 decadesOsmotic demyelination syndrome attributed to

either very high or very low serum sodium.Vast majority (62 of 65, 95%) of patients presented

with at least moderate neurologic deficit ranging from ataxia, altered gait, dysarthria to generalized seizures, quadraplegia, coma, locked-in syndrome.

Increasing number of reported cases, decrease mortality: 94% of cases prior to 1990; 7% of cases after 1989

DiscussionBrain cells adjust to changes in extra

cellular osmolarity by changing levels of osmolytes: inositol, betaine, glutamine.

Rapid changes in Na+ can exceed the ability for cells to adjust intra cellular osmolytes; seen usually with IV hydration.

Malnutrition may compromise the cellular response to changes in osmolarity.

SummaryMRI of infants treated with oral

rehydration for dehydration presenting with hypernatremia revealed patterns of diffusion restriction suggesting osmotic demyelination, without perceived overly rapid correction or use of IV fluids.

Osmotic demyelination syndrome has been usually associated with rapid correction of severe osmolyte derangement.

ConclusionThough the originally reports of ODS cases

involved the pons and were uniformly fatal, modern imaging has recognized less severe injuries and extrapontine myelinolysis.

The present cases may have been complicated by malnutrition resulting in abnormalities in metabolism or protein osmolytes.

Recognition of this injury should prompt evaluation of rehydration strategies in infants presenting with dehydration and hypernatremia in this population potentially complicated with compromised nutrition.