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
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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