Severe Hypernatremia - Salt Poisoning
Radiology Cases in Pediatric Emergency Medicine
Volume 3, Case 14
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
     Paramedics are called to the home of a 3-year old 
male child because the child is noted to be poorly 
responsive.  Upon arrival 11 minutes after the 911 
called was received, the child is being carried by an 
adult outside the home toward the ambulance.  
Paramedics note the child to have agonal respirations.  
His EKG rhythm shows a bradycardia with multifocal 
PVC's.  He is mask ventilated, then intubated at the 
scene.  His rhythm improves to a sinus tachycardia.  He 
is noted to have fixed and dilated pupils at the scene 
with a Glascow coma score of 3.  He is transported to a 
rural emergency department.
     Exam in the ED:  VS T36.4 (axillary), P120, R 45 
(bag ventilation), BP 80/60.  Weight 10 kg.  He shows 
no significant neurological response.  His pupils are 
fixed and dilated.  He is small for age and emaciated in 
     Initial laboratory studies:
ABG pH 7.02, pCO2 51, pO2 80
Na 193, K 3.3, Cl 146, Bicarb 13
Glucose 300, BUN 28, Creat 0.7
Drug screen negative
CBC WBC 14.2, 61%  segs, 11% bands, 26% lymphs,
     3 monos, Hgb 10.8, Hct 34.2, platelets 330,000.

     He is given IV fluids and furosemide.  He is then 
transferred to a children's hospital for further 

     Upon arrival, his management is assumed by a new 
set of physicians.  His pupils are still fixed and dilated.  
No neurological response is noted.  Retinal 
hemorrhages are noted on fundoscopy.
     His laboratory tests are repeated:
Na 179, K 3.3, Cl 148, Bicarb 16
Glucose 169, Bun 23, Creat 0.9
     A CT scan of the brain is performed.

View CT scan.

     The image on the left is taken through the orbits.  
This cut is significant for hemorrhages noted over the 
surface of the retina.  The image on the right is taken 
through the brain and the lateral ventricles.  Although IV 
contrast has NOT been administered, the falx appears 
to be prominent.  This white enhancement represents 
hemorrhage in the interhemispheric space.  It is most 
prominent posteriorly.  This represents a posterior 
interhemispheric subdural hematoma.  There is 
evidence of cerebral edema and a slight midline shift.
     This CT scan is pathognomonic of a shaken child 
injury (see Case 1 in Volume 1, Toxic Infant with a Full 
Fontanelle).  The retinal hemorrhages are also highly 
indicative of child abuse.
     Retinal hemorrhages are usually identified on 
fundoscopic examination.  For medical legal reasons it 
may be best to have these substantiated by an 
ophthalmologist.  In subtle cases, the retinal 
hemorrhages may not be seen on direct 
ophthalmoscopy, thus, an ophthalmologist is usually 
needed to perform indirect ophthalmoscopy.  Most 
retinal hemorrhages are not visible on CT scan.  Thus, 
CT scan is not useful to rule out the presence of retinal 
     The finding of a prominent posterior falx on an 
unenhanced CT scan (no contrast) is indicative of a 
posterior interhemispheric subdural hematoma.  In an 
infant, this classically is seen in the shaken infant 
syndrome.  Blood also enters the subarachnoid space.  
Thus, if an LP is performed, it will most likely be grossly 

     The hypernatremia in this case is extreme and is 
what makes this case particularly interesting.  One 
should be highly suspicious that this degree of 
hypernatremia may be long standing.  Thus, a rapid 
correction of this hypernatremia may be clinically 
detrimental.  It may be best to correct this slowly.  
Clinical hydration and neurological parameters should 
be followed closely to maintain a fluid balance most 
appropriate for the clinical situation.  Rapid fluid and 
electrolyte shifts may result in cerebral edema.  Fluid 
boluses may be required to correct hypovolemia and 
diuretics agents may be necessary to reverse cerebral 
edema; however, all such agents should be 
administered with extreme caution.
     According to the child's father, they were at the 
beach four hours before calling the ambulance.  The 
father states that the child was sitting in the water and 
began drinking salt water.  The father told him to stop 
and he did so.  The family went home and the child was 
playing and watching television.  Three hours after this 
episode, while at home, he complained of some 
abdominal pain and vomited once.  He then developed 
respiratory difficulty and rapidly worsened, prompting 
the 911 call.
     This degree of hypernatremia is not possible from 
drinking sea water for a short period of time.  Salt water 
near-drowning victims do not have this degree of 
hypernatremia.  Whenever the history of events as 
described by the caretaker is not consistent with the 
clinical findings, child abuse should be suspected.  In 
this case, the description of the child drinking some sea 
water at the beach in the afternoon, playing happily 
later that afternoon, then being found in a pre-arrest 
state a few minutes later by paramedics with extreme 
hypernatremia, retinal hemorrhages, and the posterior 
interhemispheric subdural hematoma noted on arrival at 
the hospital are an impossible sequence of events.
     Deliberate poisoning of children by their caretakers 
is a recognized syndrome of child abuse.  Sometimes, 
this is part of Munchausen Syndrome by proxy, but in 
most instances, it is just another form of inflicted harm 
on a child.  Non-accidental salt poisoning is a common 
type of chronic poisoning administered to children by 
caretakers.  Although many practitioners have not 
heard of this, it probably occurs more commonly than 
most believe.  It may only present to medical attention if 
the poisoning results in severe hypernatremia.
     Substantiated cases of salt poisoning are associated 
with severe hypernatremia, usually above 160 
mEq/liter.  It is sometimes in excess of 200 and is often 
in the 170 to 190 range.  This finding is often found in 
association with other signs of physical abuse such as 
fractures, retinal hemorrhages, burns, failure to thrive, 
and emotional deprivation.  In many of these instances, 
salt administration is used as a form of punishment.  
The following case examples of children with extreme 
hypernatremia are most illustrative.  In each instance, 
their parents' explanation for the hypernatremia was 
inconsistent with clinical findings.
     a) Parents of one child said they had used salty 
foods to treat the child's sudden onset of voracious 
appetite and thirst.  These behaviors were not observed 
while the child was hospitalized.
     b) A 5-year old child was given spoonfuls of salt by 
his mother for enuresis.  He was also noted to have 
burns on his feet and ankles.
     c) A 6-year old child died of hyperkalemia and 
hypernatremia after eating food his stepfather had 
heavily seasoned with "light salt" (a salt substitute 
consisting of KCl and NaCl) as punishment to break the 
child's habit of adding too much salt to his food.
     d) A 3-year old child was found with a cup of salt 
beside her crib.
     These instances are not as benign as they sound.   
For the serum sodium to elevate this high, the child 
must be deprived of water and/or salt must be forcibly 
administered.  In an attempt to re-create a serum 
sodium of 170 by mere salt administration as explained 
by the child's mother, investigators were able to 
administer only 20 grams of salt with great difficulty to 
the child which resulted in a maximum serum sodium of 
only 147.  This implies that salt must be forcibly 
     Some mothers were noted to put excessive amounts 
of salt in their infant's formula.  Although two teaspoons 
of salt may not sound like much, this amount is capable 
of elevating one's sodium to 200 although one's kidneys 
would generally excrete as much sodium as possible to 
prevent this from happening.  Two teaspoons of salt 
have a very strong taste and when added to formula, 
infants will reject it.  Thus, only when conventional fluids 
and formula are withheld, would an infant be desperate 
enough to drink such salt-laden formula.
     It is important to rule out organic causes of 
hypernatremia.  Renal function should be ascertained, 
and normalization of the serum sodium under hospital 
or foster care with normal feedings should be 
documented.  A urine sodium obtained while the child is 
hypernatremic should be obtained.  Hyperaldosteronism 
and diabetes insipidus are associated with low urine 
sodiums suggesting inappropriate sodium retention, 
while salt poisoning is associated with highly elevated 
urine sodiums (the kidneys are attempting to correct the 
hypernatremia by excreting sodium).  Hypernatremic 
dehydration secondary to gastroenteritis may mimic 
many of these findings, however, gastroenteritis and 
dehydration are usually associated with an elevated 
BUN, while salt poisoning does not result in as much 
azotemia.  While hypernatremic dehydration generally 
results in only modest sodium elevations, salt poisoning 
is associated with extremely high degrees of sodium 
      The absence of polyuria by history makes diabetes 
insipidus less likely.  However, the presence of 
polydypsia is often seen in salt poisoning in an attempt 
to compensate for the hypernatremia and/or fluid 
deprivation.  Such children have been observed to lick 
water off windows and to drink from puddles, toilets, 
and fish tanks.
     Although accidentally (or out of ignorance) 
administering undiluted formula concentrate to infants 
usually results in hypernatremia, this type of 
unintentional hypernatremia is usually not as extreme, 
and the other associated findings such as failure to 
thrive or inflicted injuries are not present.
     Although initial interviews with parents guilty of salt 
poisoning their children did not reveal a willful attempt 
to harm the child, in repeated interviews months later, 
some parents confessed to wanting to kill their child.  In 
a few instances when salt poisoned children were 
returned to their parents, the salt poisoning behavior 
recurred despite the parents' knowledge that this was 
harmful.  This suggests that such perpetrators are 
severely disturbed, and these children should be placed 
in protected environments away from the perpetrator(s).
     Although speculative, it is likely that there are lesser 
degrees of salt poisoning that result in only modest or 
transient hypernatremia, or hypernatremia that is 
difficult to distinguish from hypernatremic dehydration 
due to gastroenteritis.  This may not be very harmful 
unless it leads to more severe salt poisoning.  It is 
probably prudent to routinely question the caretakers of 
any child with even mild hypernatremia for the 
possibility of salt administration.  If this inquiry is 
suspicious, or the child has any other high risk factors 
(failure to thrive, fractures, burns, inappropriate social 
behavior, developmental delays, etc.), frequent clinical 
and laboratory follow-up monitoring for signs of salt 
poisoning or other forms of child abuse and neglect 
would be in the child's best interest.  Reporting a case 
to the local child protective service authorities would 
enable one to determine if any other suspicious events 
have ever been reported about the child.

     In the case of our patient, one could speculate that 
this child was chronically salt poisoned.  Because of 
extreme thirst, he began drinking sea water when he 
went to the beach that day.  He also endured an acute 
or possibly chronic shaking episode(s) resulting in 
cerebral and retinal hemorrhaging.  This type of injury 
results in axonal shearing and cerebral edema.  If this 
was acute and severe enough, it may account for his 
vomiting and rapid demise.  Rapid changes in serum 
osmolarity may have also contributed to the cerebral 
edema.  The father's history of events could not 
possibly account for the child's clinical findings.  This 
child was small for age.  Failing to thrive at a mere 10 
kg at age 3 years, he was not brought in for routine 
medical care.  This family was previously known to the 
local child protective services, who had received reports 
in the past of suspected child abuse and neglect.

     Meadow R.  Non-accidental salt poisoning.  Arch Dis 
Child 1993;68:448-452.
     Bays J.  Child Abuse by Poisoning.  In:  Reece RM.  
Child Abuse:  Medical Diagnosis and Management.  
Philadelphia, Lea & Febinger, 1994, pp. 87-88. 

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