Pediatric and Adult Fluid Delivery & Electrolyte Therapy
© 2005-2017 Dwight D. Collman, M.D., DABEM, DABFM
reprinted from article published by request for the Journal of the Board of Certification in Emergency Medicine also known as the AAPS (American Association of Physician Specialists)
Fusion Thoughts are for Board Exam. Prep and live practice. Always consult standard references i.e., your pharmacist, poison control center and appropriate consultant(s) when you have a question about medical care and best practices. The most important concept to remember when you have a question in clinical arena is to obtain consultation. I like to say it this way only because it is this simple: if you have a heart question call a heart physician (cardiologist). It seems silly for me to mention this possibly but you would be amazed at the hundreds of video tapings I have of physicians with a doubt, a question about care and they either do not call a consultant or they don’t call the best consultant for the sick organ system(s). This protects your patient and maintains the highest quality of the healthcare delivery.
Pediatric Maintenance Intravenous Fluid and Electrolyte Therapy [Tx]; Resucitative boluses and Dehydration fluid Tx. Special case simulations-required knowledge.
The primary goal of maintenance fluid and electrolyte therapy in children is to provide the body with appropriate amounts of water, sodium, potassium, chloride, and bicarbonate under the given clinical circumstances in order to maintain homeostasis. In addition, sufficient calories (as glucose) are needed to prevent ketosis and minimize initial activation of protein catabolism. Normal maintenance requirements provide water and electrolytes to replace those lost through urine, stool, and insensible routes. Urine fluid losses account for 50% of the maintenance fluid daily need, while insensible water losses via the respiratory tract and the skin account for the other half. Stool water losses are usually negligible.
Of course with illness, such as diarrhea this is no longer the case and mild, moderate or severe dehydration can rapidly develop in pediatric patients. Your first goal is to establish the fluid deficit so you can determine how you will replace it. Thus you are no longer simply giving maintenance needs. We will get back to this later in this discussion.
THESE ARE THE CLINICAL EXAM-BASED ESTIMATES FOR TOTAL FLUID DEFICITS IN PURE DEHYDRATION W/O COMPLICATING FACTORS: e.g., any case of diarrhea or vomiting (or both):
DEHYDRATION 2 YO OR YOUNGER: 5% (50 ML/KG DEFICIT)/MODERATE: 10% ( 100 ML/KG DEFICIT)/SEVERE: 150 ML/KG DEFICIT
DEHYDRATION 3 YO OR OLDER: 3% (30 ML/KG DEFICIT)/MODERATE: 6% ( 60 ML/KG DEFICIT)/SEVERE: 90 ML/KG DEFICIT
ESTABLISHING MAINTENANCE FLUID/ELECTROLYTES
[BASED ON BODY WEIGHT (KG)]
FLUID AND ELECTOLYTE NEEDS FOR BASIC MAINTENANCE
(This comes after resuscitation, i.e., resuscitative boluses of 10-20 mL/Kg up to three boluses then blood as boluses of 10 mL/Kg in pediatric trauma (class III/IV hemorrhages as described in the ATLS manual ed 9))
The following estimations and calculations provide a useful approach to fluid needs for pediatric patients requiring a maintenance intravenous line. However, I will initially discuss that resuscitative fluids are always administered first when indicated and I present several important cases below.
This approach for maintenance fluids will allow the clinician to both rapidly and accurately calculate a maintenance IV fluid rate and fluid type. Remember that maintenance fluids are not to manage a resuscitation, burns, or prior dehydration. They simply keep the patient hydrated while in bed with little physical activity. Other calculations and fluid needs are provided tor the above-mentioned problems prior to supplying the child with maintenance fluids. All adult and pediatric patients require maintenance fluids which may be administered even orally but should not be forgotten especially for patients who are in the department for more than an hour.
The needs for maintenance fluids cannot be over-stated because dehydration is so common. IV resuscitative boluses are always administered until signs of shock are reversed (delayed capillary refill, anuria or <1mL/Kg/hr of U/O in a child or infant, altered mental status, decreased skin turgor with tenting and diminished or absent tears: just remember the “T’s”: absent “Tears”, skin “Tenting”, decreased “Turgor”, increased capillary refill “Time” more than 2 sec, altered “Thinking” (altered mentation) are all signs of a need for fluid therapy that should be corrected immediately. A resuscitation is done in the first 10 minutes not hours. The blood pressure (BP) may fool you as it actually may be elevated in hypovolemic shock even severe elevations of the systolic bp may be seen (adrenergic surge release of adrenalin) as well as diastolic hypertension (a narrowed pulse pressure)-the latter is more commonly cited but the former (systolic hypertension) is an indication for an IV fluid resuscitation which can rapidly be proven with ultrasound examination of the the heart and inferior vena cava (this exam requires only seconds to perform).
If there is collapsing of the IVC this is a clear indication to begin a fluid resuscitation prior to maintenance fluids and is a sign of substantial intravascular volume loss. It is also nonspecific and could indicate acute blood loss. The presentation commonly establishes if this is a concern.
It is important to realize that no one sign of hydration is a reliable indicator AND CAN EVEN BE MISLEADING. A classic and important case is the child with sickle cell anemia and isosthenuria (an inability to concentrate the urine). Thus, even when dehydrated they do not have an elevated urine specific gravity (SG). The maximal reported urine SG in severe dehydration is 1.035 but anyone with an SG > 1.025 is in need of resuscitative fluids. The patient with isosthenuria will have a urine specific gravity that never exceeds 1.015 falsely indicating mild dehydration (if any) by itself. Thus, relying on just this one piece of clinical data for decision-making or relying on any one of the signs of dehydration (when absent) is risky and even dangerous. Assume all children with sickle cell anemia have isosthenuria until proven otherwise.
Another very important comment is also that because diabetic ketoacidosis (DKA) is a scenario requiring rapid fluid resuscitation, it is important to remember that in pediatric patients can rapidly develop brain edema and even a brain herniation syndrome may occur and can cause sudden death during a fluid resuscitation i.e., not just maintenance fluid replacement. Thus, any child who complains of a headache or has a worsening of mentation during a fluid resuscitation should have it stopped and the patient re-evaluated. Treatment for any brain edema should be managed with head elevation, ensuring venous outflow from the head, (thus ensuring no tight straps around the neck), loop and even osmotic diuretics (mannitol 0.25 mg/kg as a 10% solution is administered intravenously over 20 minutes; recall the % means number of G in 100 mL, e.g., 10% means 10 G in 100 mL) and a pediatric neurosurgeon should be consulted immediately. Head CT will show lack of a normal sulcus appearance globally this tissue space is filling with fluid during brain edema.
There are multiple herniation syndromes and so not all patients display dilated pupils bilaterally. But the pupil and eye exam is important when considering a headache due to impending herniation. Subfalcine herniation can also produce a contralateral pupil that is dilated (a false-localizing pupil) in cases of edema or hemorrhage that are focal and intially causing one cortex to swell and pass under the falx cerebrii to the opposite side and the latter then herniates inferiorly…however, this situation is more common in hemorrhagic causes of increased intracranialal pressure such as in a subdural hematoma and not global brain edema. The “sunset sign”: both eyes are directed inferiorly is a sign of increased intracranial pressure with now advanced edema and pressure on the upper brainstem. This is an ominous sign of uncorrected and advancing CNS edema. Ataxic breathing may follow with pressure on the medulla just prior to death if edema is left untreated. This scenario is unique to the and occurring most commonly in the younger pediatric patients (≤2 years of age); it may be related to the lack of a completed blood brain barrier.
The infusion of room temperature fluids has been reported as a cause of death during a resuscitation and thus warmed fluids (104°F) should be used. Any patient who is shivering during a fluid resuscitation has an iatrogenically-induced problem and thus a sign that they need warming and warmed fluids!
Maintenance fluid needs should be based on a child’s ideal body weight.
Although formulas and tables are available to estimate pediatric weights,
all children should be weighed in the emergency department whenever
possible. The only real contraindication to obtaining a weight is if the
child is in imminent danger of immediate cardiopulmonary arrest.
Additionally, a Broselow TapeTM can be used to estimate the child’s weight.
Table of Estimated Pediatric Weights
If an actual weight is not available, these estimates are used.
Newborn:……….3.5 kg (birth weight)
6 mos old:……….7.0 kg (double birth weight)
1 year old:………..10.0 kg (triple birth weight)
2 year old:………..12.0 kg
(Remember there is a “2” in the number two and a “2” in the number twelve)
3 year old:………..15.0 kg
(“3” is 1/2-way between a 1-year-old [10 kg] and a 5-year-old [20 kg] = 15kg)
1 + 2= | 3 | + 2 = 5
10 kg 1 y-o + 5 kg = 15 kg 3 y-o + 5 Kg = 20 kg 5 y-o
4 year old = 17.0 kg (= 1/4 of the adult weight of 70 kg)
Between 4 and 10 years add by
3 kg for each year of life
5 year old: 20 kg
6 year old: 23 kg
7 year old: 26 kg
8 year old: 29 kg
9 year old: 32 kg
10 year old:: 35 kg (1/2 an adult weight of 70 kg)
Maintenance fluid requirements depend on a child’s rate of metabolism
and caloric requirements. Daily caloric and fluid requirements are
summarized below. These estimates include basal metabolic
expenditure plus an allowance for minimal activity in bed: The 4-2-1 hourly rule is derived from the standard daily maintenance rates published for pediatric patients. These values are the same as those for caloric requirements at basal metabolic rates, i.e., the body needs 1 mL of water for every 1 kilocalorie expended. Thus, 100 mL [kcal] /kg/day for the first 10 kg of body weight, 50 mL [kcal]/kg/day for the second 10 kg of body
weight, and 20 mL [kcal] /kg/day for each kg of body weight over 20 kg.)
Pediatric Maintenance Fluid calculations
based on the 4-2-1 hourly rule
1st 10 kg (10 kg = 1-yr-old)
100 mL/kg/day converts to….
4 mL/kg/hr = 40 mL/hr for the 1st 10 kg
2nd 10 kg (20 kg = 5-yr-old):
50 mL/kg/day converts to……
2 mL/kg/hr = 20 mL/hr for the 2nd 10 kg
For each kg > 20 kg: 20 mL/kg/d converts to…
1 mL/kg/hr = 1 mL/hr for each kg greater than 20 kg
Calculation example #1:
12 kg, 20 month-old maintenance IV fluid calculation:
4 mL/kg/hr x 10 kg = 40 mL/hr
2 mL/kg/hr x 2 kg = 4 mL/hr
Total maintenance rate = 40 + 4 = 44 mL/hr
Fluid choice: D5W 0.2NS or, D5W 0.25NS
See discussion below for more information about fluid choice
Calculation example #2:
23 kg, 6 yr-old maintenance IV fluid calculation:
4 mL/kg/hr x 10 kg = 40 mL/hr
2 mL/kg/hr x 10 kg = 20 mL/hr
1 mL/kg/hr x 3 kg = 3 mL/hr
Total maintenance rate = 40 + 20 + 3 mL/h = 63 mL/h
[Fluid choice: D50.2NS or, D50.25NS
see discussion below for more information about fluid choice]
Daily maintenance requirements of sodium and potassium are
2 to 3 mEq/kg per 24 hours. Anions are generally given as chloride.
Since the normal kidney produces the maintenance bicarbonate
requirement, additional bicarbonate does not usually need to be given.
Five grams of glucose per 100 kcal expended (or per 100 mL of maintenance
fluid, i.e., a solution of 5% glucose—D5W) provides approximately 20%
of the total daily caloric expenditure and will usually prevent ketosis.
However, with this caloric intake, a daily weight loss of 1 – 2% of
body weight can occur. Newborn infants, especially premature babies,
may require 10 grams of glucose per 100 kcal expended (or per 100 mL
of maintenance fluid, i.e., a solution of 10% glucose—D10W) due to their
higher basal metabolic rate.
Maintenance requirements can be provided by an intravenous [IV] solution
that contains 25 mEq/L of sodium, 25 mEq/L of potassium, 50 mEq/L of
chloride, and 50 g/L of dextrose. Standard intravenous solutions that
meet these requirements are D50.2NS or D5 0.25NS with 20 mEq/L of
potassium chloride added. It should be noted that potassium should
be witheld from IV therapy if there is reason to suspect renal or
primary adrenal insufficiency and until adequate urine output
has been established. Often the bladder is drained and that urine can be sent for analysis but the urine SG of that initial urine will likely be high in moderately and severely dehydrated patients. Many conditions can influence or alter a child’s metabolic rate, including increased environmental temperature, artificial
ventilation, fever, or intense activity. Maintenance fluid and electrolyte requirements may then need to be adjusted accordingly.
If you spend 15 minutes a day practicing pediatric weights bolus calculations (using 10-20 mL/kg/bolus up to three boluses = initial maximum of 60 mL/kg over three boluses) and practicing pediatric maintenance fluids you will know this and never forget it…it is one of the most important functions of an emergency provider. We are all fluid resuscitating “machines” and is it absurd not to know this information; this is one of your daily key functions so it is worthy of memorization for all ages and weight and is simple if you look at the math and recreate the list of numbers presented above.
Glucose is as we all know is just “sugar water” yet most physicians do not rehearse this math enough and it is simple: Neonates get D10W, 4 year-olds D25W and 8 years and older get D50W to correct hypoglycemia which may often be present with dehydration or altered mental state. Note that 2-4 mL per kg of D25 corresponds to the 0.5 to 1 G/Kg of glucose administered in an ideal body weight 4-year-old.
Unless a bedside test for the glucose is measured we are forgetting one of the most common tests we perform everyday and it is again so common you must know this. You will be tested on any item I emphasize such as this because these are common problems and you would be surprised how long it can take some clinicians to order a simple fingerstick glucose yet they have leaped to a head CT scan without correcting a most common [MC] cause of altered mentation, i.e., hypoglycemia! Diabetics come into EDs in droves everyday and it is not only the absolute glucose level but the rate of change of the glucose that is important to determine their alterations in mental state. Rememember also that glucose metabolism is largely balanced by the liver and kidneys via glycolysis and gluconeogenesis and any patient with altered hepatic or renal function is likely to have an abnormal glucose value. Hyperglycemia does not produce alterations in mental status by itself until it has increased the serum osmolarity to 350 mOsm/L and thus the glucose has to be over 800-1000 mg/dL to explain any altered mentation.
Recall that in the formula for s-omolarity the s-Sosm = 2x NA + glucose/18 + BUN/2.0 and any ethanol (must be accounted for as it will add to the serum osmolality initially when the alcohol is first absorbed but not yet metabolized. Once metabolized all of the toxic alcohols no longer have a substantial influence on serum osmolarity and thus you cannot use the absolute alcohol level when the patient arrives late into an intoxication to say anything about serum osmolarity without measuring it. A calculated value may be entirely inaccurate.
A diabetic (often obese) may decide to diet and yet even continue to use their insulin. This is a serious presentation and can be lethal. You will only know this in a confused patient because you can give boluses of glucose and you must keep measuring the glucose frequently and see that it goes up for a short time and then falls within a few minutes. The patient needs a constant glucose infusion and admission.
The most serious missed diagnosis is when there is morning hypoglycemia and the patient presents in coma. This is a classic presentation for insulinoma and can be a cause of morning deaths. Everyone’s longest fast is typically from dinner to morning breakfast. Always repeat the glucose when there are sudden reversals of correction of both glucose and mentation in diabetics.
The longest acting sufonylurea, (diabenese) can cause prolonged hypoglycemia that last days because this drug has a very long half life. Some get prolonged hypoglycemia even with normal doses but an overdose is an automatic admission for up to five days due to it’s long half life and requires a constant infusion of glucose.
Always call a poison control center in any overdose even if you know the management because you are also to report all poisonings so we can gather data to create poisoning statistics. This is part of your responsibility.
Repetition and rehearsal is the key to learning the fluid therapy I am discussing! These seemingly specialized case simulations are key to know so that when they present you don’t manage them in a delayed fashion by waiting for a glucose from the lab.
Simply do calculations based on age and body weight until you can do them for all ages. Recall that the 4-2-1 rule maintenance even works for adults and there is a basis for why it is simplified to 3 L of saline per day…one nurse, one 8-hour shift, 1L to keep track of! All you need to know is how many Kg the patient weighs (ideal) above 20kg (the 5 year old who gets 60 mL/hour for maintenance) and you add one ml/kg per hour for each kg greater than 20 kg in adults. I push this into this presentation because then you know all adult maintenance rates and you can even work the math based on the exact ideal body weight of the adult patient without a calculator. You just need to keep reminding yourself that beyond 4 years of age the patient weights 3 additional Kg for each year of life. It is that simple..so 5-year-old 20 kg = 60 mL/hour (40 mL per hour for the 1st 10kg and then 2 mL/kg for each additional 10 kg up to 20 kg i.e., a 5-year-old, 6-year-old 23 kg = 63 mL/hour, 7 year old 66 mL/H, 8 year old 69 ml/h, 9 year old 62 ml/h, 10 year old (half an adult) gets 65 ml/hour and a 70 kg adult gets 60 mL + the additional 50 ml above 20kg so 115 mL/hour…this is very close to the standard 8 hour IV bag rate of 125 mL/h. Again this was simplified long ago because it means one nurse manages one liter of iv fluid per 8 hour shift…and this “magic” number of 125 mL per hour was born out of a need to simplify. So you should be able to do this in your head if you practice. Just add the number of kg >20 to the number 60 and you have the answer in mL/hour for maintenance for all patients greater than 4 years of age. Also simple: mathematically, 3 is exactly ½ way between 1 and 5
and that is 10kg for a 1-year-old and 20 kg for a 5 year-old. Hence a 3-year-old weighs 15 kg…also recall both 3 and 15 are odd numbers. Likewise there is a “2 in the number 12 and a 2 in the number 2 and a 2-year-old weighs 12 kg. These reminders should make the math simple now.
Your goal: by the time a patient arrives and you see the chart you have calculated in your head their resuscitative bolus and maintenance rate before you walk in the room. If the patient is ranked as a 3-5 (5 being the most ill) you are never wrong to start the fluids and then you have really an algorithm that starts with just this: when I walk in the room what do I notice:
IN THE MIDDLE CASE (THE QUESTION MARKS MEAN….YOU HAVE NOT DECIDED SO YOU NEED MORE ASSESSMENT AND QUESTIONS AND THIS TAKES SECONDS)…..THEN
YOU DO 3 THINGS: OXYGEN TO KEEP THE SAT AT 95%, a cardiac and saturation monitor and fluid therapy…it may be with an iv or orally…but I always offer well patients a quart of po water while I talk to them…because most, if not all are dehydrated and not taking enough fluid and that is a universal. You are not going to harm the patient and it is good for interpersonal skills and health outcome scoring which I will talk about later because this is how your board ranks and scores you during board certification. You may argue that a patient with peripheral edema has total body fluid overload; however if they present in shock, they need intravascular repletion and you can prove this with assessment of the IVC with US in seconds.
In pediatrics the World Health Organization (WHO) and Unicef has an online updated a oral formula for how to mix an oral replacement electrolyte solution and you can find this if you type “ORAL REHYDRATION SALTS production the new ORS (oral rehydration solution) on your search engine. This is used worldwide for all dehydrated children of any age and you should know this resource is available as a pdf downloadable file.
In the file they have some simple key definitions and they indicate that the new ORS provides better outcomes.
WHO/UNICEF Key definitions:
- Dehydration: “Loss of water and dissolved salts from the body, occurring, for instance, as a result of diarrhea.
- Rehydration: “The correction of dehydration.”
- ORT (oral rehydration therapy: “The administration of fluid by mouth to prevent or correct the dehydration that is a consequence of the diarrhea.”
- ORS: “Specifically, the complete, new WHO/Unicef formula.” [since 2003]
Oral rehydration is commonly done worldwide and the formula is prepackaged.
“The new ORS formula composition has been proven to be effective in exhaustive evaluations and stability tests.” The article notes that “glucose facilitates the absorption of sodium (and hence water) on a 1:1 molar basis in the small intestine. Sodium and potassium are needed to replace the body losses of these essential ions during diarrhea (and vomiting)” trisodium citrate corrects the acidosis that occurs was a result of diarrhea and dehydration. Dissolution in drinking water yields specific concentrations which are cited in table one in the article. You should read this article and reread it once a year. The advantage of using citrate over bicarbonate is due to the stability of citrate in tropical climates and the ORS has a shelf life of at least 2-3 years without particular storage precautions. Even the packaging is not as critical as the prior bicarbonate formulation and it can be stored in permeable polyethylene bags. The addition of other ingredients has not been shown to be of any further advantage specifically zinc and vitamins are mentioned. The final product is available as tablets, liquid, or powder.
Some key caveats about the ORS formula when used: Preparation of solution for oral use: Dissolve the entire content of packet in one liter of drinking water.
Infants: on liter over 24 hours.
Children one liter over 8-24 hours according to age.
Adults: advised to drink liberally as required and all patients are advised to continue to rehydrate until the diarrhea stops.
There is a warning to discard all remaining solution 24 hours after mixing it with water.
World-wide the need for oral rehydration is a huge undertaking and millions of packets are needed annually. There is a lot of information in the article on chemistry and preparation you don’t need but near the conclusion the author is cite that children under 5 years of age in developing countries experience at least 2 episodes of diarrheaa per year. This fact is used in estimating the needs of the ORS in specific countries.
Recall that simple diarrhea typically produces a nonanion gap metabolic acidosis. THE Anion GAP is calculated as AG = Na – (CL + HCO3). When the body is wasting bicarbonate in diarrhea, the kidneys increase chloride reabsorption in the distal renal tubules. Thus the AG does not typically change.
All texts will provide you with a list of the causes of AG and nonAG metabolic acidosis. Likewise, excess loading of NaCL during large fluid resuscitations will produce an increased chloride load to the kidneys producing a compensatory decreased regeneration of bicarbonate. This is what I recall as the “ying-yang relationship” of chloride and bicarbonate. Statistically, the most common cause [MCC] of metabolic acidosis in acutely volume depleted patients who have been or are being resuscitated is the high chloride load which shuts down renal bicarbonate regeneration. It is an iatrogenic problem. Several ICU studies have shown a recommendation for use of LR in lieu of isotonic saline during such resuscitations because of improved outcomes but the emergency medicine literature has not changed its recommendations.
For those taking exams it is important to note that any such issue that is still largely under study is not a true test item but could be a field test item [FTI]. About ⅓ of the questions on the certification examination are FTIs. That is why you should not worry about this examination as you proceed. You will always “feel bad” when taking this test and this is universally reported to me by candidates in private conversation.
Parents should be advised this is a slow and constant process which they will likely continue at home when you discharge the child/infant.
Never forget to look for sources of blood loss and septic shock as a cause of hypotension and all of the positive signs of dehydration. Never forget that the IVC exam on ultrasound and a small rapidly beating heart are both confirmation of hypovolemia. You will also see aggressive contractions of the heart muscle when there is no cardiac pathology.
There are multiple types of shock described but in hypovolemia shock the pulse is always elevated, the cardiac output reduced and the systemic vascular resistance is elevated (i.e., the patient is vasoconstricted). The most common site of sepsis is the genitourinary tract for all patients, the second most common is any form of pneumonia. The third most common site is listed as an unknown site and requires a more vigorous search. Meningitis must also be considered especially in young patients who may not have yet been fully immunized. Meningitis can occur at any age as can encephalitis and Summer and Fall show increases due to increases in vector populations such as mosquitoes in cases of viral etiologies.
Remember that when resuscitative boluses are administered in a burn victims there is no subtraction for the addition of maintenance fluids. Meaning the boluses are given to correct shock and then the burn fluids are given for the fluid loss for the burn (it must be at least a 20% 2nd degree burn to require intravenous burn fluid therapy. Wt (kg) x % TBSA burn/4 is a rapid method to determine the burn fluid needs from the time of the burn for the first 8 hours. The remaining fluid calculation is to give have that rate for the next 16 hours to treat a burn. Example calculation: a patient who is 5 and has a 40% second degree burn would get resuscitative boluses until signs of shock are corrected such as a return of urine output to 1 ml/kg/h and then for the burn would get
20 kg x 40/4 = 20 x 10 = 200 mL/hour for the first 8h from the time of the burn. Then 100 mL/hour for the next 16 hours and again, this is to treat the burn fluid loss. Patients often develop hypokalemia from such large fluid resuscitations 1-2 days post treatment in the ED and acutely hyperkalemia is possible from the burn but typically takes up to 8 hours to develop.
Finally recall that the kidney regenerate bicarbonate based on the chloride load (inversely to that load) that is filtered through the glomerulus. This will be a high chloride load during a fluid resuscitation with isotonic normal saline. Thus the kidneys will regenerate less bicarbonate than they do when the patient is not burned (in the normal state) and this will promote metabolic acidosis. Thus, large boluses of normal saline can cause a non anion gap metabolic acidosis. This is the basis for the use of Lactated Ringer’s solution. Half of the lactate, the L-Isomer is converted to bicarbonate in the liver and thus metabolic acidosis is avoided. Large volumes of LR could in theory produce a metabolic alkalosis in a patient that was administered such a resuscitation in error but this is not a common problem except in one scenario: if a patient on constant NG suctioning is receiving LR and not NS the patient now has two mechanisms to promote alkalosis: The LR and the suctioning of acid from the stomach). All patients who have prolonged (24 hours of NG suctioning have it replaced with D5 ½ NS with potassium because there is loss of potassium, water, sodium, chloride and a lack of substrate intake (glucose lack) during prolonged NG suctioning. It is possible that if the patient is allowed to develop a substantial metabolic alkalosis they will present with hypoventilation as a way for the body to correct the alkalosis. SO you must associate the use of an NG tube with the possibility of the induction of metabolic alkalosis. Thus all patients who are not adequately ventilating have a “standard” cause for their hypoventilation…the NG tube is the clue! This is why most EPs do not write admission orders because they would fail to order the NG aspirate replacement fluid every time. I know this only from testing 12,000 physicians. Not one ever answered this issue and I will discuss it in the acid base lectures. It may not seem important to you but a patient may be discharged only to return with an iatrogenic problem. This is not uncommon and fluid and electrolyte disturbances are the low hanging everyday working fruit of our existence. You MUST know this information!
In Dehydration cases you establish the degree of dehydration and note age because for patients less than 2 years of age mild dehydration is 50 mL/Kg, moderate is 100 mL/kg and severe is 150 mL/Kg as a fluid deficit. For patients ≥3 years mild dehydration is 30 mL/Kg, moderate is 60 mL/kg and severe is 90 mL/kg as a fluid deficit. In pure dehydration as a cause for a patient’s presentation of shock the resuscitative boluses ARE subtracted from the total fluid deficit calculation of mild, moderate or severe based on multiple criteria including BP, P, T, urine SG, reduced or absent tears, diastolic hypertension and the T’s above. As we age we are less water so we require less in the calculation.
Most cases are isonatremic dehydration (normal sodium of 135-145 mEq/L); but it may also be low (hyponatremic (<130 mEq/L and may or may not present with seizures usually when the sodium is <120 mEq/L and often closer to 110 mEq/L). Finally the least common form is hypertonic dehydration with an elevated sodium using in the range of 170 mEq/L or higher.
The diagnosis can be made rapidly at the bedside and again, i cannot overstate the utility of bedside ultrasound to guide you and confirm your suspicions. Isonatremic dehydration is managed with resuscitative boluses of isotonic saline until signs of shock are corrected and then the calculations for the degree of dehydration determine the amount of the total deficit of fluid and then the resuscitative boluses are subtracted from that total and the residual is given half in the first 8 hours and the next half in the subsequent 16 hours PLUS maintenance fluids.
In hyponatremic dehydration in most cases the management is to fluid restrict the patient after giving enough fluid (0.9%NS) to correct shock as resuscitative boluses and allowing the body to correct the sodium with fluid restriction. If there are seizures the next step is to use a benzodiazepine to control them and if this fails then hypertonic saline is used but in general in adults this will be no more than 5-50 ml of 3% NS TO GET THE S-Na to 120-125 mEq/L and no higher initially. The initial goal is to use the hypertonic saline only when benzodiazepines fail or with a severely low serum sodium. Rapid correction can induce central pontine myelinolysis (CPM) which is more common in alcoholic adults than in pediatric resuscitations. The patient will then appear comatose except when asked to look up they will have intact upward gaze. This is generally irreversible and a serious iatrogenic cause of permanent disability. The other problem is inducing pulmonary edema. The serum sodium, in any case should not be corrected in the first 24 hours more than 10-12 mEq/L to avoid the complications below.
Another rule is correct electrolyte and fluid problems at the same rate that they developed…so knowing the length of time of the illness is important.
There is a formula to give hypertonic saline published originally in the third edition of “Tintnallli” in 1986 and it is (125 meQ/L- measured sodium) x 0.6kg of the ideal body weight. In the formula, 125 meQ/L is the goal or desired sodium to correct to and the measured is the starting point of the correction. 0.6x body weight is used in the formula because it reflects correcting only the intravascular compartment sodium not total body sodium. Then you must convert the number of MEq of sodium deficit to mL of 3% hypertonic saline.
Most references do not correct with hypertonic saline unless the serum sodium is 115 mEq/L or lower and the goal is to correct at a rate of no more than 0.5 mEq/Na/L per hour. You must then convert the MEq sodium to ML and most find this cumbersome to memorize so they use a calculator. You can find the calculator online if you type the “GlobalRPHINC Hypertonic sodium calculator” in Google. In most we correct shock with a 0.9NS bolus(es) and then limit fluid intake and control seizures with a benzodiazepine. We are allowing the body to excrete the excess water relative to the sodium first.
In mild hyponatremic dehydration 0.9NS is preferred and administered to increase the serum sodium no more than 0.5 mEq/L per hour. (cases of a sodium of 125-134 mEq/L.
Common causes of hyponatremic dehydration in pediatric patients include any cause of vomiting and diarrhea (that list is “encyclopedic”), ketonuria and also excess-use of diuretics. Common causes in adults are combinations of alcohol abuse plus use of a loop diuretic: causing hypochloremic, hyponatremic dehydration. Here is a more complete list of drugs that cause hypnatremic dehydration:
Carbamazepine, ethanol, all diuretics, morphine and it’s relatives, solfonylureas, triamterine and vasopressin (also called arginine vasopressin (also called antidiuretic hormone, i.e., ADH).
Finally hypertonic dehydration is also corrected initially with 0.9%NS since it is hypotonic to the patient in the ED. Tintinalli also recommended using 0.25% NS to correct the serum sodium slowly generally over 2 days again at a rate that is similar to the rate at which the problem occurred. Altered mentation is seen in all 3 types of dehydration when it is severe. The most common medications that cause hypertonic dehydration include: anabolic steroids, contraceptive pills, clonidine, corticosteroids, some antibiotics, laxatives, lithium and NSAIDS. Lithium is of note in that it promotes sodium wasting in the proximal renal tubule and the lithium level does not correlate with the severity of the illness. Acute lithium overdose may be less toxic than chronic use so the serum electrolytes and fluid status must be assessed as well in all patients by our standard clinical assessment above.
IN THE END YOU ARE MOSTLY THREE THINGS: OXYGEN, MONITORS, IV…with some variation on how they are done…the iv may be oral…the rates will vary with the condition. You get a glucose value in all young and elderly patients without thinking…so this is such a large part of your practice because if they are elderly and even mildly abnormal per their spouse…they need a glucose…
AS THIS PROGRESSES YOU WILL SEE YOUR LIFE IN THE ED IS MOSTLY THESE ELEMENTS, A QUICK BEDSIDE US, AND A DISPOSITION DECISION FROM THAT POINT>>>it may be yes, off to the CT scanner but the basics need to be well
established in your mind. You are not thinking…you are doing.
The more algorithms you learn the more this becomes just that…and you turn it on in your head and you do it. What follows in that algorithm is based on simple better worse or unchanged. The most important goal is to get to disposition. It is less about the diagnosis and in fact, the diagnosis is only a small fraction of your score on oral exams…it is mostly did you do the process and that is the algorithms. I have 52 case simulations. if you know them…you know the algorithms of emergency medicine. It takes 6 days to learn them once. If you keep relearning them, you will realize it is 99% of your management during your career.
A simple exercise you should try is to not eat or drink any fluid for one day. You will not succumb….but you will then know what most of your patients are complaining about. If they have primary low adrenal function it is the same scenario just dehydration and lack of sodium from lack of hormones. What you then realize is much of these presentations have in common is fluid and electrolyte disturbance with various causes.
You will see every variation on each simulation:
CHEST PAIN CASE:
A patent says he can’t swallow easily but is not losing weight. He occasionally jumps up and down to swallow when it feels that food is stuck at the level of the mid-body of his sternum. He is 35 years-old and a nonsmoker and nondrinker. He is basically well. He needs an endoscopy (here are the images) and until then just a liquid diet since he has no problems swallowing liquids. He came to the ED because he had a severe episode finally today after ten years of this and he is an attorney. He takes no medications and has no other significant medical history and a normal physical exam. An oral antacid receives some of his residual burning in his chest and he denies any reflux into his mouth or nose. What he needs is an endoscopy and a blood test for celiac disease. He has allergic eosinophilic esophagitis. He has mild anxiety and prior to his endoscopy it would be appropriate to have him take one dose of a sleeping aid. His followup tests are pending and you will never see them which is unfortunate unless you maintain contact with your patients. His exam was entirely normal including all of his vital signs and he could guzzle two cups of water for you. Does he need an EKG? Some will say yes and some no but most will do it. It is normal . He had no vomiiting but he rated his pain as a 5/10 on arrival and 2/10 after the po antacid He has no history of recent endoscopy or NG tube placement or swallowed FB ever. He did have drooling today with his episode the he ate a soft shell burrito and the pain was severe enough he went to the ED by car. He drove himself and did not call an ambulance. He was feeling better on arrival and rated his discomfort as a 9/10 after he swallowed some of the burrito and
it was clearly his worst episode. He is active, married and appears healthy
just concerned. So the oxygen is room air, the monitor is done while you take the history, the EKG is done and he reports he has no family Hx of CV disease and exercises regularly. His sis are only related to eating but occur with every
meal. There is no hx of wheezing, aspiration or vomiintg…he is fully ambulatory. He does have a diagnosis but he does not have an emergency any longer. He needs endoscopy and even his blood tests could be done by his GI
physician. So you will see thousands of people in your career who get a CT of the chest, a chest X-ray, a troponin, abc and electrolyte panel but he did not need all of that. Just a discussion about what to eat and a referral. He was placed on a steroid for his esophagitis which is in his mid esophagus and his stomach exam was normal. He has a chronic problem he has been living with and ignoring. Why? He has a pregnant wife, a 4 year old, a law practice and, in fact, he is staring medical school after he finishes his undergrad requirements
in a few months. This is a real scenario. A real case. His hx is so strong for
an esophageal problem it is clearly not cardiac. An EKG at age 40 would be mandatory. Some might want it no matter what. It would not harm the patient just add to the cost of his visit. It is reasonable also because he will have general anesthesia for his endoscopy because he expresses he wants it and
not just conscious sedation for his procedure because he has some anxiety
about tubes being put in his body ever since he had a foley catheter for
his acute appendicitis when he was 21. Just the thought of a tube makes him
feel ill and afraid. he does give some history that could be consistent with
globus hystericus but he clearly is having a problem with food getting stuck
in his esophagus. He has no acid reflux by history which excludes benign
esophageal stricture caused usually by GERD. So he has something wrong
with his esophagus. He did. It is the history and he is a great historian.
He should not have required anytime in the ED more than 20 minutes. It is
an important case because it is a case of a form of not typical transfer dysphagia and not typical stricture. He has no trouble initiating swallowing which does not fit with transfer dysphagia. Cancer or extrinsic compression
of his esophagus to tumor is unlikely because he is not losing weight and the
problem has been present for 10 years at least ever other day. He is always careful to chew his food and yet still has a problem that recurred more severely
today. He was never pre syncopal by history but he was hyperventilating and he described temporary period oral numbness and fingertip numbness bilaterally that went away. His initial diagnosis is eosinophilic esophagitis by endoscopy with tests for celiac disease pending. Ultimately he was much better
with the steroid and his blood work showed: