Complete Nursing Diagnosis

hyponatremia in the critically ill child,by dr. andrea moscatelli. my name is andrea moscatelli. i'm the directorof the neonatal and pediatric intensive care unit at the gaslini children's hospital ingenova, italy. in the next few minutes, we'll talk about the treatment and prevention ofhyponatremia in the critically ill child. we will start with the definition and pathophysiologyof hyponatremia, then we will go through some case presentation, and we'll focus on thetreatment and prevention of hyponatremia. pathophysiology of hyponatremia. you have hyponatremia when there is a relativeexcess of free water with an underlying condition that impairs the kidney's ability to excretefree water. this might happen in the case

of excessive intake of water, if there isa marked reduction in the glomerular filtration rate, or if there is a renal hypoperfusion,either if there is an adh excess. types of hyponatremia. we will address the issue of hypotonic hyponatremia,and we will skip to other conditions, which are hypertonic hyponatremia and pseudohyponatremia.hypertonic hyponatremia is a condition that you see in the case of hyperglycemia or incase of mannitol infusion, while pseudohyponatremia is a condition that is related to the cellularmeasurement in plasma when you have high levels

of proteins or lipids. so if you have a kid with hypotonic hyponatremia,the first thing to do is to assess the volume status. if the patient is hypovolemic, thenext step is to measure urniary sodium. if the urinary sodium is above 20 mmol/l, youshould suspect renal losses, while if the renal sodium is below 20 mmol/l you shouldsuspect extrarenal losses. if the patient is euvolemic, and the urinary sodium is about20 mmol/l, the most probable diagnosis is an inappropriate secretion of adh. while ifthe patient is hypervolemic and the urinary sodium is above 20 mmol/l, the most probablediagnosis would be an acute or chronic renal failure. while if sodium is below 20 mmol/l,you should suspect a secondary hyperaldosteronism,

like nephrotic syndrome, or cirrhosis, orheart failure. we will now briefly talk about hospital-acquiredhypernatremia. consider that hospital-acquired hyponatremia is leading more than 600 kidsto death in the united states each year in the postoperative period. so it is extremelyimportant to prevent hyponatremia in hospitalized children. and the way to do that is to limithypotonic fluids to patients which have a serum sodium of above 145 meq/l or a urinaryfree water loss, and to use normal saline or d5 normal saline as maintenance fluidsin patients at risk of adh excess like in the conditions that are listed below. correcting severe hyponatremia.

the approach to treatment of hyponatremiadepends on the underlying etiology, degree of symptoms, and whether the hyponatremiastate is acute or chronic. sometimes hyponatremia is associated withhypovolemia, so the first thing to address is shock, and corrective the volume status,and this can be done with normal saline. and after that, you should focus on the correctionof hyponatremia. you can predict the changes in serum sodiumwith 1 liter of infusate with this formula. here you have the sodium in the infusate plusthe potassium in the infusate minus the serum sodium in the patient divided by the totalbody water plus the 1 liter that you give. so if you have a 30 kilogram kid with a serumsodium of 130, who is administered with 1

liter of normal saline, what would happenis a change of 0.7 meq/l in serum sodium. so normal saline is not effective in changingthe serum sodium. and if you want to correct the serum sodium, it's better to use 3% hypertonicsaline. point of clarification. hypertonic salineis often indicated for correction of severe hyponatremia in a patient who is acutely symptomaticwith neurological symptoms, such as encephalopathy or seizures. once the neurological symptomshave improved in the context of a rising serum sodium level, treatment with hypertonic salinecan be stopped and ongoing serum sodium correction with normal saline can be initiated. so the usual approach is to start with 2 ml/kgof 3% hypertonic saline given in 10 minutes,

with a maximum of about 100 ml in one bolus.the bolus can be repeated 1-2 times until symptoms of acute encephalopathy are reversed. so the goal is to have an increase of 5-6meq/l in serum sodium in the first one to two hours. and it is wise to recheck serumsodium every two hours. the therapy should be stopped when the patient is symptom freeor if there is a rise in serum sodium of more than 10 meq/l in the first five hours. thecorrection in the first 48 hours should not exceed 15 and 20 meq/l. and you do not haveto target normal or hyponatremia. if the brain is exposed to an hypoosmolarenvironment, there is a movement of water from the extracellular compartment to theintracellular compartment, leading to brain

swelling and increase of intracranial pressure.there are several factors that can be considered risk factors for the development of brainswelling and intracranial hypertension, which are young age, because in young children there'sa high brain-to-skull volume ratio, but also an underlying central nervous system disease,like meningitis or brain tumor or hypoxia. the thing that you have to be aware of isthat early signs off hyponatremic encephalopathy can progress very rapidly into advanced signsand symptoms of hyponatremic encephalopathy. and they indicate the rapid progression throughthe development of intracranial hypertension, leading to possible brain herniation. the brain tries to compensate to this statuswith a rate of adaption that is due to the

extrusion of sodium, potassium, and waterfrom the brain cells. and this rapid adaption follows a slow adaption which is due to theextrusion of hydrogenic osmolytes, like glutamate and glycine. this is a slow adaption and ifin this moment, we correct too rapidly, sodium, this would lead to a brain shrinkage, whichcan cause osmotic demyelination. the osmotic demyelination is a severe damageof the myelin in the brain and usually occurs after a slow adaption, which takes about 48hours to occur. risk factors for osmotic demyelination are chronic hyponatremia lasting more than48 hours, an increase in serum sodium of more than 25 meq/l/4 hours, hypoxia, liver diseases,and malnutrition. here you see how osmotic demyelination canpresent on an mri. on the left side, there

is a typical presentation with the pons lesions,but also other areas of the brain, like the basal ganglia can be effected. what happens after the correction of sodiumis that you have initial clinical improvement associated with the correction of sodium,which is followed by a neurological deterioration in 1-7 days with mutism, dysarthria, spasticquadriplegia, pseudobulbar palsy, ataxia, locked-in syndrome. 1/3 of the patients recover,1/3 remain disabled, but are able to conduct an independent life, and 1/3 third are severelydisabled. cases. we will go now through several casepresentations which are illustrative of the concepts that we have talked about previously.

case 1. so case 1-- we have a previously healthy kid,13 years old, 38 kilograms, on post-operative day 2 after appendectomy, presenting withgeneralized seizures. he has been treated with diazepam and phenytoin, intubated, andon mechanical ventilation. he has been given about 2.7 liters of d5 ofnormal saline on day 1, drunk an unknown amount of water, and is euvolemic, responding topain. serum sodium is 112. serum potassium is 4.4. serum osmolarity is 228. urinary osmolarityis 500, with a urinary sodium and potassium of 100. given that the patient is euvolemic, whatis your diagnosis? please click the new comment

button to leave your answer. so in this case, we have an hypotonic hyponatremia,with a urinary sodium which is well above 20. this picture shows how the intracellularand the extracellular compartments behave in this case. and the diagnosis is an acutecondition called inappropriate increation of adh. so you can have high levels of adh-- vasopressin--in patients with hyponatremia that can be due to readily reversible causes, like a loweffective circulating volume. but also it can be due to anxiety, stress,pain, or nausea, or to the administration of drugs that are causing nausea, like chemotherapeuticagents, or morphine.

there are also not easily reversible causes,like vasopressin producing tumors, central nervous system diseases, or lung lesions,and granulomas. case 2. case 2. we have a 10 kilogram, one-year-oldchild, surgical removal of an astrocytoma. the post-operative fluids were d5 normal salineat 40 mls/h. after 25 hours from surgery, the baby develops a decreased level of consciousnessand seizures. the fluid balance is -400 mls. and there is a weight loss of 0.5 kilograms.the baby is tachycardic. serum sodium is 120. serum potassium is 4.0meq/l. and serum osmolarity is 238 mosm/kg, with a urinary osmolarity of above 600 mosm/kg,and the urinary sodium and potassium of 260

meq/l. what is the patient's volume status? pleaseclick the new comment button to leave your answer. now that you have assessed the patient'svolume status, what is your diagnosis? so this case is similar to the previous one.you have a hypotonic hyponatremia with a level of potassium and sodium in the urine whichis very high. but as you can see, the patient is tachycardic. so he is in a low volume status. here again, we can see how the extracellularand intracellular compartments behave in this case. and the diagnosis is a cerebral saltwasting syndrome, which is another acute condition. and it is quite difficult to make a differentialdiagnosis between these two conditions.

the most important issue is the assessmentof the volume status because while in the case of inappropriate increation of idh, youdidn't have hypovolemia. you have hypovolemia in case of cerebral salt-wasting syndrome.and it is extremely important to put together several different parameters in order to makethe right diagnosis, having in mind that the most important issue is the assessment ofthe volume status. case 3. case 3. we have three kilogram five-month-oldbaby with bronchopulmonary dysplasia who was admitted for incarcerated hernia. he had poorfeedings in the last three days and presents with loss of consciousness and seizures.

he has been under hyrochlorothiazide for bpdand is fed with the amino acid formula. serum sodium is 105 meq/l. serum potassium is 2.2meq/l. serum osmolarity is 205 mosm/kg. and the urinary sodium and potassium is above20 meq/l. what is the patient's volume status? pleaseclick the new comment button to leave your answer. now that you assess the patient'svolume status, what is your diagnosis? so here again, we have an hypotonic hyponatremiawith low levels of potassium in plasma, but with urinary sodium and potassium, which areabove 20 meq/l. this condition is similar to the previous ones. the patient is witha low volume status, but the main difference is that this a chronic condition.

and the other thing is that, as you can see,potassium is a major concern. so you can start with correcting potassium instead of correctingsodium. consider that if you are infusing potassium, it's like infusing sodium. andso when you correct potassium, you correct sodium, because potassium is going insidethe cells, and there would be an opposite movement of sodium outside the cell with arise in the plasmatic sodium. in this picture, which is identical to theprevious one, we can see the behavior of the excess cellular and intracellular compartmentsin this condition, which is, as we said, a chronic condition due to the loss or freewater in sodium. it is extremely important to make a differential diagnosis between anacute and chronic condition, because this

will affect the way we treat hyponatremia. case 4. let's put everything together with the lastcase. we have an 18-month-old kid, 10 kilograms, two days of gastroenteritis, admitted forintussusception, resolved with the contrast enema, not evident hypovolemia, but the impressionis of mild dehydration. the patient is presenting with severe pain and nausea. after 20 hoursfrom admission, the patient presents with seizures. he has been given 200 ml of normal saline.the maintenance fluids have been 2/3 d5 in water and 1/3 normal saline at 40 ml/h plus200 ml of water as ice chips. serum sodium

is 134 meq/l. urinary osmolarity is 320 mosm/kg.urine output is 0.5 ml/kg/h. and the urinary sodium and potassium are about 200 meq/l. to understand what has happened to this patient,we have to go through it in a sort of balance. the usual total body water for this patientshould be 7 liters and this is given by this formula 0.7 times 10 kilograms. but becauseof the losses that he had, the actual volume status is 6.3 liters. now, if we make a balancebetween the ins and outs, ins are the infusions-- and outs is what the patient is losing withurine, and it is something that we can measure instead of diarrhea-- we can understand that in this case we havea positive balance of sodium and a positive

balance of free water. and we can calculatethe new sodium levels through this formula by multiplying 134 meq by 6.3 liters and addingthe positive balance of sodium. this divided by the new volume status, that would be 6.3plus the volume that we have been giving with the fluids. so this patient has a serum sodiumof 120 meq/l. in this patient, sodium is low because ofthe excessive administration of free water with fluids, but also because there was aretention of free water that was due to non-osmotic stimuli to the secretion of adh. rememberthat this patient was presenting with pain and nausea, and the urine was concentrated. the usual behavior of a patient after volumeexpansion is the suppresion of the secretion

of adh, leading to diluted urine. so thiscan cause an overcorrection of serum sodium. and if this happens, you have to be carefulto monitor the urine sodium and osmolarity, and eventually replace the urine output withhypotonic fluids. so the prevention of the overcorrection ofhyponatremia is a key issue, and you have to monitor carefully for water diuresis, andyou have to limit the administration of hypertonic saline to the correction of sodium or theuse of normal saline to the correction of the volume status. it is important to restrictsodium containing fluids when you have a water diuresis, and to replace diuresis with ivfluids which are isotonic to urine. be also careful about the correction of potassium,because this would increase the serum sodium.

summary. hyponatremia is defined as serum sodium ofless than 135 meq/l. hyponatremia may result from a variety of different insults or underlyingdisease states. clinical signs and symptoms of hyponatremia range from nausea and vomitingand headache to seizure and coma. determination of serum osmolarity, volume status, and urinarysodium are important for determining the etiology of hyponatremia. know how to differentiatebetween the syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wastingbased on volume status. to conclude, if you have a patient who ishyponatremic, but he is also hypovolemic, the first thing to do is to correct hypovolemia.

always consider the duration of hyponatremia,because if hyponatremia is lasting less than 48 hours, it is an acute condition, if itis lasting more than 48 hours, it is a chronic condition, and you can take more time to correctserum sodium. always assess the volume status, the plasmaosmolarity, and the urine osmolarity. use 3% hypertonic saline for serum sodium correctionbecause this would be more easy, and monitor the response of urine osmolarity to the correctionthat you do. thank you for listening to this lecture onopenpediatrics. please help us improve the content by providingus with some feedback.