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http://yahweh.com/NUKEBABY/author.htm Yisrayl Hawkins is not a Doctor. Many of of our members are getting sick, and dying because Yisrayl Hawkins is telling everyone to take the cleanses, which include peroxide baths, essential oils, colloidal silver, other herbs and cleanses sold in their health food store, and salting every single thing they eat. http://www.mayoclinic.com/health/lead-poisoning/FL00068/DSECTION=3 Salt Poisoning http://www.bmj.com/cgi/content/full/326/7381/157 BMJ 2003;326:157-160 ( 18 January ) Education and debateDistinguishing between salt poisoning and hypernatraemic dehydration in children
Malcolm G Coulthard a Department of Paediatric Nephrology, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, b Guy's, King's, and St Thomas's School of Medicine, London SE1 9RT Correspondence to: M G Coulthard malcolm.coulthard@nuth.northy.nhs.uk Hypernatraemia caused by salt poisoning or dehydration must be distinguished correctly, as the two situations need different legal and medical approaches. Two nephrologists discuss the physiology of hypernatraemia and explain how to differentiate between cases caused by salt poisoning and dehydration The criteria most widely used to diagnose salt poisoning in children were formulated by Meadow.1 These criteria focus on hypernatraemia with high urinary concentrations of sodium and chloride, but this combination may also be found in children with dehydration caused by diarrhoea. The medical and legal management of the two conditions fundamentally are different, so reliable ways to distinguish them are needed.
We consider the physiology of salt overload
and hypernatraemic dehydration.2
We explain how to differentiate the two situations on the
basis of history; examination; and biochemical analysis
of serial, paired, blood, and "spot" urine samples. We illustrate
the method with two cases that have been tested in court.
Salt poisoning
Hypernatraemic dehydration The boy was taken into foster care after he was admitted at age 8 months, because doctors believed his biochemistry results confirmed salt poisoning and because his siblings' medical histories were considered suspicious. Three siblings had become hypernatraemic under similar circumstances: one died after remaining at home (on the general practitioner's advice) with pyrexia, explosive diarrhoea, and weight loss but without haemorrhagic encephalopathy.3 In addition, one sister, who was eunatraemic, died suddenly and unexpectedly. The odds of a second innocent death were suggested (incorrectly) to be 73 million to one.4 A court found that the mother was not guilty of manslaughter.
Exclusion of other medical causes Essential hypernatraemia is a rare disorder of children and adults in which hypertonicity causes neither thirst nor the release of antidiuretic hormone but the release of antidiuretic hormone mediated by baroreceptors is normal. 5 6 The mechanism behind the condition is almost certainly selective destruction of the anterior hypothalamic osmoreceptor. Plasma concentrations of sodium >170 mmol/l are not unusual in this condition. In practice, children who can maintain completely normal plasma concentrations of creatinine and electrolytes when they are well, eating a normal diet, and drinking a normal amount of fluids are extremely unlikely to have significant, persistent, underlying medical causes for hypernatraemia.
Clinical history
Salt overload The notion that severe hypernatraemia cannot be caused by water depletion alone is also incorrect, because it is seen in babies who are inadequately breast fed 7 8 or who had undiagnosed oesophageal atresia.8 In healthy people, hypernatraemia causes vomiting and intense thirst, which may be recognised even in babies,3 and neurological signs, such as irritability, drowsiness or coma, and fits.
Hypernatraemic dehydration
In patients with infective diarrhoea,
undigested proteins and carbohydrates reach the colon, where
bacteria metabolise them to small, osmotically active
molecules that draw water but not sodium from the plasma
into the colon; this makes the plasma hypernatraemic.11
The continued administration of glucose polymers in the
presence of diarrhoea greatly increases this risk12
Dehydration associated with hypernatraemia undoubtedly is under-recognised. Even babies who lose up to 27% of their weight may not be diagnosed correctly outside hospital.8 Only half of such babies' paediatricians seem to notice this hypernatraemia.8
Clinical observations: acute changes in
body weight
Salt poisoning
Dehydration
Biochemistry
Measurements of plasma concentrations
The paediatrician in case 2 considered the boy's values to be unremarkable, although they indicated that his glomerular filtration rate was only two thirds of the normal value.15 The rate recovered after the boy was rehydrated. The plasma concentration of urea is influenced by too many factors other than hydration to be a reliable indicator of renal function.1 Nevertheless, the differences in plasma concentrations of urea in cases 1 and 2 at presentation and after treatment are striking, and they certainly support the diagnosis of volume repletion and expansion in case 1 and volume contraction in case 2.
The plasma concentration of bicarbonate usually is normal in salt poisoning (as in case 1), but tissue underperfusion from dehydration induces metabolic acidosis and reduces the plasma concentration of bicarbonate (as in case 2). Concentrations of potassium in plasma are unhelpful, as they remain normal in salt poisoning and vary in dehydration, when release of aldosterone makes potassium concentrations fall and reduced glomerular filtration rate makes them rise.
Calculations of fractional excretions of
salt and water
Fractional excretions of sodium and water,
which are calculated from the sodium and creatinine concentrations
of paired plasma and "spot" urine samples, can
distinguish the two situations (see box A on bmj.com).
The values should be
Estimates of salt and water balance
On admission, the child in case 1 had an
estimated urine output in the normal range, but his sodium excretion
was about 15 mmol/kg/day
Reliance on urinary concentrations of sodium to diagnose salt
poisoning in hypernatraemic children is unsafe because dehydrated
infants may be diagnosed falsely as poisoned. The child's
clinical history and acute changes in their weight
provide important evidence that, combined with fractional
excretions of sodium and water calculated from serial
paired "spot" blood and urine samples and estimates of
net sodium and water balances, allow the correct
diagnosis to be made.
Contributors: MGC and GBH were involved equally in conceiving the idea for the paper and in developing and writing it. MGC is the guarantor of the paper.
Funding: None.
Competing interests: None declared.
(Accepted
4 October 2002) © 2003 BMJ Publishing Group Ltd Related Article
This article has been cited by other articles:(Search Google Scholar for Other Citing Articles)
Rapid Responses:Read all Rapid Responses
http://www.hawaii.edu/medicine/pediatrics/pemxray/v3c14.html
Severe Hypernatremia - Salt Poisoning
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 appearance. 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 management. 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.
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http://members.tripod.com/~Prof_Anil_Aggrawal/POISO014.HTML MY FORENSIC
ARTICLES IN SCIENCE REPORTER
-Dr. Anil
Aggrawal
"Good morning
doctor. Oh, my God, what are you doing today? You have the dead body of a very
young female infant today. What happened to her? Please tell me."
"Good morning Tarun. The name of this 6 month old tiny girl is Babli. When she was born, her mother died due to some obstetric complication. Her father Ramdev soon remarried a nubile young girl Rekha. Before marriage she had promised that she would look after Babli well, but after marriage she often showed frank animosity towards this girl. She would not look after her well and would often not even feed her properly.." "Oh, so she probably starved her to death?" "Don't jump to conclusions Tarun. Look at her body. She doesn't look starved. An infant who dies of starvation looks just like a bag of bones. There is no fat in his or her body. But this girl is looking fairly well fed. What I was going to tell you is that Babli's grandmother Shanti Devi, i.e. Ramdev's mother, is still alive. She was not in favor of Ramdev getting married to Rekha in the first place. She probably knew that Rekha was not of good nature. Rekha was undoubtedly not feeding her well, but Shanti would always make up for her, giving her feeds in time. In fact that is why starvation was never a problem for Babli." "Then how did Babli die?" "Babli died of some respiratory disorder. At least that is what her physician told me just now. I will tell you what happened yesterday. Till yesterday morning, Babli was fine. Ramdev left for work in the morning at 8. As usual Rekha started seeing TV just after that, completely ignoring Babli. Seeing that it was her feeding time, Shanti prepared her feed, and filled her milk bottle with that. Just then a neighbor came to meet her, and she went to the drawing room to attend her, leaving the bottle in the kitchen. For half an hour they discussed about some religious programme they were going to attend that evening. After the guest left, Shanti went back to the kitchen, picked up the bottle and gave the feed to Babli. About half an hour later, Babli, who had consumed only about half the bottle by that time, started showing some strange symptoms. She started crying. It appeared as if she was irritable. She vomited twice. Shanti tells me that she had convulsions and muscular twitchings, fluttering of eyelids and of facial muscles. She displayed avid thirst. Shanti knows this because when she gave her water, she would feel a little relaxed, but after some time she would start crying again. But what was most prominent was that she was not breathing well. She had extreme difficulty in respiration. Shanti called Rekha for help, but she kept on seeing TV. Then Shanti phoned her son Ramdev, who immediately got in touch with their family doctor on phone. Dr. Saxena, the family doctor, arrived within 15 minutes, and found that the child was in real bad shape. Ramdev also reached home soon after. Dr. Saxena injected some medicines for respiratory distress, but although the injections seemed to help initially, they weren't of any lasting help. The doctor couldn't really understand what had happened to her. He thought that probably it was an attack of asthma. But what was most confusing was that Babli never displayed this symptom before. They were preparing to shift her to some big hospital for diagnosis and treatment, but before arrangements could be made, Babli died." "Oh, I see. So Babli's body has been brought to you to let them know how she really died?" "Yes, that's right. Actually Dr. Saxena was quite prepared to give the cause of death as asthma, but Shanti Devi immediately raised doubts. She has alleged that while her guest came to meet her, Rekha went to kitchen and mixed some poison in her feed. That is why Babli started having those strange symptoms immediately after having that feed. Rekha, of course, vehemently denied this, and Ramdev too refused to believe her mother, but she wouldn't listen to anyone. She phoned police immediately and called them to their house. The police ransacked the whole house and even searched all Rekha's belongings, but they couldn't find any poison anywhere in the house. That is what is lending weight to Dr. Saxena's theory that Babli indeed died of asthma. Every one including the police is thinking that Shanti Devi is making all this fuss, because she didn't like Rekha in the first place." "Yeah, that looks likely to me as well. So what are you going to do now?" "Tarun, since the matter has reached the police, Dr. Saxena preferred not to give cause of death and leave that to me. The body has been brought to me for post-mortem so that I could comment upon the cause of death." "How do you think Babli died?" "Tarun, the symptoms that Babli displayed surely point towards some respiratory trouble. But the symptoms also point towards a very unusual poison, a poison no one can ever think of. And that is why I have to be extra careful. You have got to remember, that I have a reputation as a poison sleuth, and so I can not afford to leave out even a remote possibility as far as administration of poison is concerned. "Come on doctor. No poison was ever found in the possession of Rekha. Not even that, there was no poison in the whole house. How could anyone administer any poison to Babli?" "Yeah, that sounds very convincing to the police, and that's why they think Shanti Devi is a nut. But I don't think so. I know of a poison which produces exactly the same symptoms as displayed by Babli..." "Please don't talk in riddles doctor. Explain everything to me in clear terms." "Yeah sure. To test my theory, I took some of the stomach contents of Babli and subjected them to chemical analysis. Not to my great surprise, they have shown very high concentrations of salt. Then I took Babli's blood and examined it chemically too. And again it showed very high levels of sodium. I am inclined to think that Babli has been killed with ...." "With what?" "With common salt!" "Common salt? You must be joking doctor. How can anyone be killed with common salt. This is what all of us take daily in our food. Well my father is so fond of common salt he always puts an extra teaspoonful of common salt in his dal." "Yeah, this is what is not known to most people. Common salt is a deadly poison. The only difference between this and other commonly known poisons is that one has to administer rather large quantities to kill with it. One or two teaspoonfuls of salt would not kill an adult but can easily kill a 6 month old baby. Come to think of it, even an adult can be killed with common salt. Only he would have to be fed larger quantities. About 40 teaspoons of common salt would kill an adult human being too." "Well the information is getting interesting. Why don't we begin from the beginning doctor?" "Tarun, before you start visualizing it as a villain, I must hasten to add that there is no doubt that common salt or sodium chloride (NaCl) is indeed essential to all life. It is the basic milieu of mammals. It occurs as colorless cubic crystals or as white crystalline powder. When salt is administered in larger quantities than required, it can cause death too. One teaspoonful of salt weighs about 5 gms. Normal uptake by adults is about 5 to 15 g daily or about 1-3 teaspoonfuls. Children consume less. Salt is even necessary for normal growth in children. The sodium needed for growth is 0.5 mEq/kg from birth to 3 months of age, which decreases to 0.1 mEq/kg at 6 months. The average content of sodium in human milk is 7 mEq/L and that in cow milk is 21 mEq/L ..." "Doctor, you started your answer telling me weights in grams, but suddely you have switched to milliEquivalents. I don't really understand the concept of milliEquivalent so well. And why should we talk in milliEquivalents, when we can talk equally well in grams?" "Tarun, in ordinary day-to-day life, it is useful and convenient to talk in grams and kilograms, but chemists and biochemists often find it easier to talk in terms of equivalent weights because of several reasons. You would surely agree that chemists are mainly interested in chemical combinations, and Equivalent weights are actually measures of the characteristic proportions in which given elements combine. For this reason, this term is also often known as Combining weight. Equivalent weights can be used for elements as well as for compounds. In plain and simple words, they are the measure of the combining capacity of a substance with other chemical substances. Well, even if after this, you are feeling inconvenient with equivalent weights, let me add that 1 mEq of sodium equals 23 mg and that of salt equals 58.5 mg. I would also like to tell you that 1 milliequivalent would be equal to 1/1000 Equivalent weight. Now when I say that the sodium needed for growth is 0.5 mEq/kg from birth to 3 months of age, I simply mean that for every kg of baby's weight, 0.5 mEq of sodium is needed. Thus if the infant weighed, say, 4 kg, he would need 4x0.5 or about 2 mEq of sodium. Since 1 mEq of sodium is 23 mg, it would mean that the infant would need about 46 mg of sodium daily. This much sodium would be available from about 117 mg of salt. Thus in effect, a baby from birth to 3 months needs about 117 mg of salt. Similarly you can convert other values which I told you earlier in grams. I told you the sodium contents of human milk, because this is the only food available to young babies." "Oh, I see. Doctor, you were saying that 40 teaspoons of salt would kill even an adult?" "Yes Tarun. The toxic oral dose of salt is 0.5 to 1.0 gm/kg. For a 70 kg man this amounts to about 35-70 gm. That means that if an adult consumes about 70 g of salt (or about 14 teaspoons), he would be severely poisoned. The estimated fatal amount, i.e. one that would kill is about 1 to 3 gm/kg. This amounts to about 70-210 gm (or about 40 teaspoonfuls) of salt for a 70 kg man." "Oh, that is interesting. Has salt been used to kill people before?" "Tarun, interestingly the Chinese used saturated salt solution for suicide. Salt intoxication and death have occurred when it is used to induce vomiting." "Why would one want to vomit anyway?" "When somebody has consumed some poison, it is imperative to remove as much poison from his stomach as possible. One of the best ways to do this is to make the person vomit. It has been known from ancient times, that a strong solution of common salt induces vomiting, and that is why for centuries, it was a favorite method of doctors to induce vomiting in poisoned patients. But it is known now that saturated solution of salt itself can cause salt poisoning, so it is rarely used these days." "Oh, I see. So you are suggesting that Rekha mixed salt in Babli's feed when Shanti was talking to her neighbor in the drawing room." "Babli's stomach contents, and her blood analysis definitely tells me that salt has been administered to her. I have examined her brain tissue under the microscope too, and I have found that the capillaries of her brain are damaged. They are full of blood, and there are innumerable bleeding points - technically known as hemorrhages- in her brain. There is bleeding underneath one of the coverings of the brain. We call it subarachnoid bleeding, because it occurs underneath the covering known as arachnoid mater. Many venous channels of her brain - technically known as dural sinuses- are blocked. All these findings are strongly in favor of salt poisoning. I have no doubt that someone had indeed mixed salt in her feed. To tell you the truth now, I surreptitiously picked up the milk bottle from Ramdev's house and have analyzed it for salt. It showed as much as 11 g of salt and it was only half full. It means that the full bottle must have contained about 22 g of salt. In other words, Rekha must have put about 4 teaspoonfuls of salt in Babli's bottle when Shanti was talking to her neighbor. There was no other person in the house at that time, and no one except Rekha could have done that." "Rekha indeed is a wicked woman. It is surprising she knew that salt can kill." "I have enquired about Rekha's background. She studied biochemistry in college, although she dropped out of college later. Surely when she was studying biochemistry she must have learnt that salt is a poison and can be used to kill infants. It is indeed a rather safe poison, because you don't need to buy anything. It is available right at everyone's home. And the police won't suspect you either, because they won't find any poison....any traditional poison, I mean. Come let us tell the police that Babli didn't die of asthma. It is Rekha who has added salt to Babli's feed to kill her." "Oh, how very clever of you doctor. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- iodine" *** (To protect the identity of the individuals, their names, as well as the various dates of occurrence have been changed) *** dr_anil@hotmail.com
SALT POISON CASE EXCLUSIVEhttp://www.mirror.co.uk/news/tm_objectid=16425374&method=full&siteid=94762&headline=salt-poison-case-exclusive-name_page.htmlBy John Sweeney Winner Of The Paul Foot Award For Campaigning Journalism 29/11/2005THE other day I tried to poison myself with four and a half teaspoons of salt. That, apparently, is what Ian and Angela Gay did to three-year-old Christian Blewitt, the little boy they had taken into their home and planned to adopt. He'd been behaving badly, so they force-fed him the salt to teach him a lesson. He went into a coma and, four days later, he died. That at least, is what the prosecution says ... The Gays were arrested, tried and convicted of poisoning him with salt. Lock them up and throw away the key, you might say - unless, of course, they didn't do it. Let's presume for a moment that Ian and Angela are what their friends and family say they are - a loving and lovely couple, gifted, rich, and kind - and the only thing they lacked in life was children. Angela's womb was removed when she was 16 because of fears of cancer. So let's test the science that underlies the deduction - because no one saw it happen - that blond-haired Christian must have been poisoned with salt by mouth. That's why I poured four and a half teaspoons of salt into a pint of water, took a hefty swig - and threw up. Because I was reporting the story for both BBC radio and TV, I had to do it again for the camera. I drank five times and I vomited five times, a wholly involuntary reflex. You just can't poison yourself with salt. Now I challenge the Attorney General, the head of the Crown Prosecution Service, the police officers, the lawyers and the experts who had a hand in the conviction of Ian and Angela Gay to knock back a pint of water with four and half teaspoons of salt in it. If they can't, then they might consider they could have helped commit a terrible wrong. The impossibility of force-feeding salt down anyone's throat without them throwing up is just the first of a series of grave questions which cast doubt on whether Ian and Angela poisoned Christian. To begin with, the desperately ill boy was raced to hospital in Ian's sports car. There, doctors realised that he had a terrifyingly high level of salt in his blood - but throughout the four days until his death, they couldn't get the salt level down. Quite simply, the moment Christian got to hospital his salt level should have gone down because the source - his "evil" adopting parents - could no longer poison him. So if it didn't go down, then the cause of the salt overload had to be something else. As it happens, poor little Christian was not a well boy. The post mortem showed that he had actually suffered a heart attack some time before he met the Gays. Why would a healthy boy have a heart attack unless he was suffering from something else? Had Christian died from arsenic or cobra venom, I'd shut up. But in fact he died because he had too much of a substance that occurs perfectly naturally in the body. The number one cause of too much salt in the body is salt diabetes or diabetes insipidus. Like classic sugar diabetes, if undetected, salt diabetes can kill. But one of the experts in the case proclaimed, at a pre-trial meeting: "He clearly doesn't have diabetes insipidus." So the jury heard nothing about salt diabetes. Judge Pictures summed up: "Very sophisticated testing was done to rule out all known existing disorders which might have caused that high level of salt." That's that, then. Or is it? The Gays were convicted on the basis of complex calculations - and those sums were based on the "seminal paper" on salt poisoning, which plays up child abuse in the context of Munchausen's Syndrome By Proxy. That's no surprise because it was written by Professor Sir Roy Meadow, the rogue child abuse expert who wrongly accused cot death mothers Sally Clark, Angela Cannings and Donna Anthony of killing their babies. Sir Roy has been struck off - though he is appealing that decision - but he is still an authority on salt poisoning. Or is he? Prof Ashley Grossman, a neuro-endocrinologist at St. Barts, fears that at least some of the 12 cases of salt poisoning in Meadow's paper could be, in fact, salt diabetes. Prof Jean Golding, an epidemiologist at Bristol University, says Meadow's paper lacks control groups, and is "unscientific and unreliable". What doomed Ian and Angela Gay was the exclusion of salt diabetes - the number one natural cause of too much salt in the body - from their defence. It can be caused by things going wrong in two different parts of the body - the kidney and the brain, especially the pituitary gland. The experts tested the kidney and the adrenal functions and they were normal. And the pituitary gland? No tests were done because it has gone missing. So have the medical records for a large part of Christian's short life - but we've seen medical notes diagnosing Christian as suffering from hydrocephalus - water on the brain. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
sometimes
as low as 50 mmol/kg. In all other children, urine
osmolality can exceed 700 mmol/kg
2%
or more in a child who has been salt poisoned and is
volume replete and 
1%
in a dehydrated child with viable renal tubules (table).
Frequent serial data provide a dynamic picture
Two boxes with worked examples are available on bmj.com 
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
hemorrhages.
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
bloody.
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
administered.
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
elevation.
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.
References
After nine years with no suggestion of harm to David there has to be
some force driving a mother to behave towards their own child as you
did to David
