Severe Hyponatremia and Non-Reactive Pupils in a 3-Year Old
Radiology Cases in Pediatric Emergency Medicine
Volume 3, Case 15
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
     To most effectively appreciate the findings in this 
case, it is recommended that you review the previous 
case (Case 14 in Volume 3, Severe Hypernatremia - 
Salt Poisoning) prior to reviewing this case.
    A 3-year old male who is a recent immigrant from 
Asia is seen in a physician's office following a 4-minute 
seizure.  He appears to be lethargic.  Without much of 
an evaluation, his parents are told to drive him to the 
hospital for admission.  He is seen on the pediatric ward 
by a first year resident who obtains the following 
     He has been in the U.S. for one month and has not 
seen a physician in the U.S. until today.  He has been 
having fevers up to 40 degrees for the past two days.  
Today, he did not feel hot, but his parents describe a 
4-minute generalized seizure.  Over the past two days 
his condition has worsened.  He is weak and can no 
longer get up or walk around.  He has a mild cough, 
occasional loose stools, and about three episodes of 
emesis per day for the past two days.  He has not been 
eating well.  His only fluid intake has been three cups of 
rice soup per day.  A friend told the family to spoon feed 
him a small amount at a time and they have tried to do 
     His past history is significant for "being a little slow".  
Further questioning reveals that he can only say two 
words (mother and father) in his native Asian language.  
His birthweight was 3.5 kg.  He was bottle fed, but to 
date, he cannot feed himself.  He must be fed by his 
parents (even before this illness).  He is fed soft table 
foods.  He underwent a language test in his birth 
country which he did very poorly on.  He underwent a 
hearing test of some type which was reportedly normal.  
His vision is also in question since at an earlier age, he 
would bump into walls frequently.  However, in the past 
9 months, he has been doing this less often.  One of his 
physicians in his birth country felt that he was autistic.
     Exam:  VS T37.4 (rectal), P120, R25, BP 88/64.  
Weight 15.5 kg (50th percentile), height 90th percentile.  
He is lethargic and moaning.  His body is well 
developed and nourished.  He has no dysmorphic 
features.  He is not toxic or irritable.  There is no 
respiratory distress evident.  His visible perfusion and 
color are good.  Head normocephalic without external 
signs of head trauma.  Pupils 7mm and not reactive to 
light.  His eyes are roughly conjugate, but he does not 
follow objects.  His eyes do not blink with sudden 
confrontation.  Fundi show sharp disc margins.  
However, the discs are extremely pale, practically 
resembling a large pit.  There is no cup within the disc.  
The retina is very pale with a sparse paucity of blood 
vessels.  Those blood vessels that are present are very 
thin.  The normal vessels coming through the optic disc 
are extremely thin.  His fundi are easy to view since his 
pupils are dilated and do not constrict.
     His neck, heart, lungs, and abdomen are normal.  
His facial function is good.  He is generally hyporeflexic 
and hypotonic.  Babinski signs are positive bilaterally.
     A CBC, chemistry panel, and a CT scan of the head 
are ordered.  A complex patient is currently on the CT 
scanner and a delay of at least 2 hours is anticipated 
before our patient can be scanned (this case actually 
takes place in the early 1980's).  The following lab 
results return before the CT scan is performed:

Na 97, K 1.6, Cl  54, Bicarb 28
BUN 3.0, creat 0.6, glucose 110
Ammonia 7.0, SGOT 94
CBC WBC 9.1, 53% segs, 44% lymphs, Hgb 10.9,
     Hct 33.9, platelets 300,000.

     The first year resident contacts the senior resident 
and informs the senior resident that this patient has a 
sodium of 97 with non-reactive pupils.  The first year 
resident is told that these findings are not compatible 
with life.  The senior resident arrives and concurs that 
the pupils are dilated and non-reactive.  He draws 
another blood sample via a radial artery puncture:

ABG in room air:  pH 7.57, pCO2 30, pO2 80, BE +6
Na 97 with the other electrolytes essentially the same.

     In evaluating a patient with hyponatremia, a urine 
sodium measurement is very useful in narrowing the 
differential diagnosis.  However, the urine sodium must 
be obtained while the patient is hyponatremic for it to be 
useful.  Once the patient is normonatremic, the urine 
sodium value can be anything.  In hyponatremic 
patients, their urine sodium should be low (less than 10 
mEq/liter).  A high value indicates that the kidneys are 
inappropriately wasting sodium.  Examples of such 
conditions include SIADH (syndrome of inappropriate 
antidiuretic hormone), mineralocorticoid deficiency (eg., 
Addisonian crisis), diuretics (eg., furosemide, thiazides, 
etc.), and a salt losing nephropathy (in a patient with 
renal disease).  In the rush to correct our patient's 
hyponatremia, a urine sodium was ordered, however, it 
was not actually collected until the patient was already 
receiving sodium supplements.

     There was some question as to whether this child 
was chronically water intoxicated as a result of child 
abuse.  His non-reactive pupils and developmental 
delays could possibly represent a severe CNS injury 
sustained any time in the past.
     Water intoxication has been described as a 
syndrome of child abuse if water is forcibly administered 
to a child, usually as punishment.  Once water is forced 
in the mouth, if the child is too young to spit it out, it 
must be swallowed.  Case reports of forced water 
intoxication describe children who were forced to drink 
many glasses of water.  Another case described the 
parents forcing a water hose in the child's mouth.  
Another case described a child with severe 
hyponatremia due to water administration and water 
enemas.  The water is often used as a punishment for 
bed wetting.  These cases are often associated with 
other signs of child abuse such as fractures, bruises, 
burns, or failure to thrive.  However, in the cases 
described in the literature, these children had sodium 
values in the 108 to 122 mEq/liter range.  
     After reviewing the previous case, Case 15 (Severe 
Hypernatremia - Salt Poisoning), the factors 
surrounding forcible salt poisoning and forcible water 
intoxication are very similar with respect to child abuse, 
however, the opposite extremes of sodium result.
     Causes of hyponatremia not associated with 
deliberate child abuse include infant swimming lessons 
(infants swallow a lot of water while "swimming"), 
excessive dilution of infant formula, and drinking large 
amounts of cold water to help with a toothache.  
Teenagers and adults have been known to drink large 
amounts of water prior to urine drug testing to dilute 
their urine as much as possible to minimize the chance 
of drug detection.

     Further history from our patient's family did not 
suggest child abuse.  In addition to the child's mother, 
four siblings of the child were present.  None of them 
noted that the child was fed an excessive amount of 

     Can you explain his clinical findings ?
In summary, his findings consist of fever, a seizure, 
hyponatremia, hypokalemia, non-reactive pupils, 
blindness, optic atrophy, and developmental delays.  
However, he was able to walk around prior to his 
current illness.

The CT scan is completed.
View CT scan.

     This CT scan shows a 2.5cm cystic partially calcified 
suprasellar mass which undergoes peripheral 
enhancement with contrast.  This is most likely a 
craniopharyngioma.  Other structures such as the 
tentorium are also enhancing.
     His non-reactive pupils are due to erosion of the 
optic nerves.  His fundoscopic findings are due to 
severe optic atrophy.  It is difficult to believe that the 
child's family could not tell that he was blind.  His motor 
and developmental delays are now well explained.  It is 
amazing that this child could walk around.  It is not 
surprising that he would bump into the walls since he 
could not see.
     His severe hyponatremia is probably longstanding.  
Only a child with chronic hyponatremia would be able to 
tolerate such a low sodium value of 97 mEq/liter.  
Although this patient probably had long standing 
panhypopituitarism it is unclear why both his growth 
and his glucose homeostasis were satisfactory.  
One would expect that he should have growth hormone 
deficiency and insufficient adrenal stimulation.  
Diabetes insipidus would not account for his 
hyponatremia since diabetes insipidus should result in 
hypernatremia.  Hypoaldosteronism coupled with 
SIADH could explain this, but this degree of 
hyponatremia is so severe that a concomitant element 
of water intoxication cannot be ruled out.
     It is usually taught that hypernatremia should be 
corrected slowly, while, if symptomatic (seizures, 
lethargy, etc.), hyponatremia can be corrected 
quickly.  However, if the history suggests that the 
hyponatremia may be long standing, it may be prudent 
to correct the hyponatremia slowly (if the patient is not 
severely symptomatic) to prevent rapid fluid shifts 
between the intracellular and extracellular 
compartments that have been accustomed to a low 
sodium environment.  This would be difficult to prove 
since such severe long standing hyponatremia is very 

     Bays J.  Child Abuse by Poisoning.  In:  Reece RM.  
Child Abuse:  Medical Diagnosis and Management.  
Philadelphia, Lea & Febinger, 1994, pp. 88-89.
     Morimer JG.  Acute Water Intoxication as Another 
Unusual Manifestation of Child Abuse.  Arch Dis Child 
     Keating JP, Schears GJ, Dodge PR.  Oral Water 
Intoxication in Infants - An American Epidemic.  Am J 
Dis Child 1991;145:985-990.

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Web Page Author:
Loren Yamamoto, MD, MPH
Associate Professor of Pediatrics
University of Hawaii John A. Burns School of Medicine