test 3 Flashcards
What are the methods for determining maintenance fluid needs
Holliday Segar Method
4-2-1 (still holliday segar)
BSA
what weight requirement for determining maintenance fluid needs using the BSA method
> =10kg
formula for maintenance fluid needs BSA
normal vs critical
1600ml/m2/day
if critically ill
1200mL/m2/day
why would critical ill children need 1200mL/m2/day instead of 1600
increased ADH (SIADH) secretion due to stress response
AKI risk - don’t want to fluid overload them if kidneys are not functioning at full capacity
Ventilators, headers and humidification cut the need by 20-50%
why would we not fluid restrict to 1200mL/m2/day in critically ill?`
insensible fluid losses
-Febrile or Tachypnea or GI (diarrhea, ileostomy, NG with suction)
so maybe febrile patients
persistently febrile or spiking high
increase fluid needs by 12% for every degree above 37C
Basic insensible fluid loses estimation
400ml/m2/day
Dehydration classifications is categorized how based on what?
mild, moderate or severe
based on serum sodium levels
Hypernatremic, Hyponatremic and isotonic dehydration
Name that dehydration
A dehydrated pt who has lost salt over a period of time. lost water and salt.
maybe seen in diarrhea. especially if replacing with water without electrolytes
Hyponatremic dehydration
hypernatremia would be diarrhea but here you are replacing water without electrolytes
name that dehydration
rate of water loss is greater than the solute. (salt did not follow)
Hypernatremic dehydration
most common type of dehydration
isotonic
type of dehydration where water and salt loss is equal (acute process)
isotonic dehydration
what type of osmolality is
1/2 NS
Hypotonic
what type of osmolality is
1/4 NS
Hypotonic
what type of osmolality is
3% NS
Hypertonic
what type of osmolality is
Albumin 5%
Colloid
what type of osmolality is NS
Isotonic
what type of osmolality is LR
Isotonic
what does LR contain that NS does not
K
HCO3
normal Na
135-145
Sodium is key to what mentioned functions
skeletal muscle function
nerve and myocardial action potentials
Hypervolemia
Hypovolemia
Normovolemic
Congestive Heart failure puts you at risk for what?
Hypervolemia
Hypervolemia
Hypovolemia
Normovolemic
renal failure puts you at risk for what?
Hypervolemia
Hypervolemia
Hypovolemia
Normovolemic
Nephrotic syndrome puts you at risk for what?
Hypervolemia
Hypervolemia
Hypovolemia
Normovolemic
Water Intoxication puts you at risk for what?
Hypervolemia
Hypervolemia
Hypovolemia
Normovolemic
Diarrhea puts you at risk for what?
Hypovolemia
Hypervolemia
Hypovolemia
Normovolemic
Renal Losses puts you at risk for what?
Hypovolemia
Hypervolemia
Hypovolemia
Normovolemic
diuretics puts you at risk for what?
Hypovolemia
Hypervolemia
Hypovolemia
Normovolemic
cerebral salt wasting may put you in what fluid status?
Normovolemic
low sodium levels
Hypervolemia
Hypovolemia
Normovolemic
Meningitis may put you in what fluid status?
Normovolemic
low sodium levels
Hypervolemia
Hypovolemia
Normovolemic
Burns puts you at risk for what?
Hypovolemic
Acute Hyponatremia symptoms
Nausea
lethargy
seizures
coma
can lead to neurological consequences
In acute hyponatremia the symptoms are _______
more severe
how to diagnose hyponatremia
check serum Na and osmols
urine studies if unsure of cause
How to treat Hyponatremia
Replace deficit slowly
-Goal rise of Na 2-4 mEq/L every 4 hours (10-20 in 24 hours)
If they are seizing
- Replace to 125 quickly with HTS (3%) - bolus using formula for amount
formula
- 0.6x(weight in kg) x (target Na-measured Na)
after bolus to achieve 125 you calculate out what you need to get to 135 and this should be given over 24 hours.
formula for Na treatment
0.6x(weight in kg) x (target Na - measured current Na) = ____mEq of Na needed
3% hypertonic has how much Na per L
513mEq Na per L
Causes mentioned of Hypernatremia
Breastfeeding failure (baby not getting enough)
Severe Diarrhea
Diabetes Insipidus
presentation of hypernatremia
weakness
lethargy
decreased DTRs (deep tendon reflexes)
irritability
muscle cramps
renal failure
AMS
Seizures
how to diagnose hypernatremia
serum Na levels
osmols
treatment for hypernatremia
Avoid decreasing more than 12-15 mEq/L in 24 hours
At risk for cerebral edema if drops too fast
If hypovolemic - calculate free water deficit
0.6xkg x (current Na/desired Na) - (0.6 x wt kg) = gives you how much water they need in 24 hours - if they can drink it, they can PO
you can use D5 water for IV
Check electrolytes q 2-4 hours to make sure you aren’t dropping too fast
These patients will be on regular maintenance plus D5W or 1/2NS or 1/4NS to help bring it down slower
Balancing game with constant monitoring
Potassium is needed for ____ gradients and important for
transmembrane voltage gradients
important for muscle and nerve cells
important with acid base balance
primary route of excretion for potassium is
kidneys
normal potassium
3.5-5.2
EKG changes with hyperkalemia
increasing in severity from top to bottom
Peaked T waves
Wide PR interval
Wide QRS duration
Peaked T waves
(precursor to V.Fib)
Loss of P waves
Sinusoidal wave
acidosis causes K to
rise
alkalosis causes k to
drop
DKA patients come in acidotic….when do you add k
your first bags usually don’t have K but then you add it in later
causes of Hyperkalemia
Acute or chronic renal failure
Tissue injuries ( crush injuries)
hemolysis
Acidosis
Medications (Spironolactone, Bactrim, ACE inhibitors)
what medications cause hyperkalemia
spironolactone
Bactrim
ACE inhibitors
Treatment for Hyperkalemia
Calcium Chloride - to stabilize that cardiac membrane
Sodium Bicarb - shifts the potassium to cell
D25/50% with insulin - Insulin causes potassium to shift intracellularly
Albuterol - helps shift k to intracellular
Kayexalate - removes potassium for exchanging for sodium in the GI tract and excretes through stool
Hypokalemia symptoms
can by asymptomatic
Diastolic dysfunction
ECG changes
Cramping
Fatigue
ileus
ECG changes seen in Hypokalemia
flat or absent T waves
long QT
Prolonged QRS
Presence of U-waves
diagnosis for hypokalemia
BMP with magnesium - magnesium and potassium work together
Urine osmolality
Treatment for hypokalemia
identify cause
replace K
-KCL 0.5-1meq/kg/dose
you can also give this other ways
remember minimum is over an hour……has to be given very slow
think central line or peripheral…….ect
where is magnesium mostly found
less than 1% of Mg is extracellular, much is stored in our bones
what is Mg used for
ATP generation, DNA transcription, Membrane stabilization, regulation of K excretion
what electrolyte works together with K
Magnesium
normal Mg levels
1.7-2.2 mg/dL
causes of hypomagnesemia
GI losses: diarrhea, vomiting, refeeding syndrome, pancreatitis
IBD, Celiac disease, CF
Renal: hypercalcemia, diuretic use, RTA
Endocrine: DM, DKA, Hyperaldosteronism
Presentation of hypomagnesemia
Anorexia, nausea, vomiting
Seizures, ataxia, hyperreflexia
EKG changes: Torsades de pointes, long QT
Diagnostic eval for hypomagnesemia
Mg level
iCal
EKG
Management of hypomagnesemia
Repletion with Magnesium sulfate or chloride
Consider K repletion (mag and K are buddies and go together)
Hypermagnesemia causes
excessive intake
-mg containing laxatives, antacids
Chronic renal failure
tumor lysis
presentation for hypermagnesemia
hypotonia
decreased reflexes
hypotension
flushing
diagnosing hypermagnesemia
Mg level
Management for hypermagnesemia
Stop any mag intake
fluid for volume expansion
inotropes for BP management
Ventilatory assistance for muscle weakness
For rapid removal, dialysis can be used or exchange transfusion
chloride has a direct relationship with
sodium
chloride has an inverse relationship with
bicarb
what can lead to hypochloremia
CF
Bulimia
Diuretics
high chloride and ph
acidosis
presentation of hypochloremia
rarely occurs by itself
arrhythmias
decreased resp effort
seizures
tachycardia
Treatment for hypochloremia
find cause
replace with potassium, sodium or ammonium chloride or arginine chloride
hyperchloremia causes
diarrhea
chloride administration
metabolic acidosis
presentation of hyperchloremia
often no symptoms but have symptoms r/t acidosis such as:
kussmaul respirations
lethargy
headache
confusion
treatment for hyperchloremia
find underlying cause
treat acidosis: can use sodium bicarb
when can you see hypophosphatemia
refeeding syndrome
DKA
severe resp alkalosis
Vit D deficiency
Burns
symptoms of hypophosphatemia
impaired energy utilization
diaphragmatic/resp muscle weakness
tissue hypoxia
treatment for hypophosphatemia
IV phos
Hyperphosphatemia causes
renal failure
phosphate containing enemas
tumor lysis syndrome
Treatment for hyperphosphatemia
phosphate binders
mannitol
diuresis
Calcium is present in how many different forms?
3 forms
- Bound to albumin (plasma protein)
- Diffusible (CaCitrate or CaPhoshate)
- Unbound ion
what type of calcium is most important for body functions
ionized Ca
normal Ca
8.8-10.8
at risk for hypocalcemia
Post PRBC infusion - because of the preservatives….citrate —calcium binds with citrate
so your CRRT patients and ECMO as well
-CRRT uses citrate to keep them from clotting but can drop their calcium
Hypoparathyroidism
Sepsis
tumor lysis
DiGeorge syndrome
symptoms of hypocalcemia
neuromuscular irritability confusion muscle cramps numbness tingling
cardiac: prolonged QT, AV blocks, sinus tachy
diagnosing hypocalcemia
Ca level (total and iCal)
CMP
PTH
EKG
Treatment for hypocalcemia
Calcium chloride (10-20mg/kg/dose)
Calcium gluconate (100mg/kg/dose)
risk for hypercalcemia
Williams syndrome
excessive intake
immobility
malignancy - cancer attacks the bones - the breakdown causes a calcium spike
presentation of hypercalcemia
nausea anorexia constipation lethargy headaches seizures arrhythmias
Diagnostic for Hypercalcemia
Total calcium iCal PTH pH EKG
Treatment for Hypercalcemia
Hydration
loop diuretics for diuresis
Calcitonin for rapid correction
what electrolyte imbalance is Williams syndrome at risk for?
Hypercalcemia
what electrolyte imbalance is DiGeorge syndrome at risk for?
Hypocalcemia
what electrolyte imbalances can cause seizures
Hypercalcemia
Hypochloremia
Hypomagnesemia
Hyponatremia
Hypernatremia
What electrolyte imbalances are you at risk for with DKA
Hypophosphatemia
Hyperchloremia
Hypomagnesemia
What electrolyte imbalances can cause EKG changes
Hypocalcemia
Hypomagnesemia
Hypokalemia
Hyperkalemia
what electrolyte imbalances can cause arrhythmias
Hypochloremia
Hypercalcemia
what electrolyte imbalances are associated with tumor lysis syndrome or cancer
Tumor lysis syndrome
- hypocalcemia
- hyperphosphatemia
- hypermagnesemia
Cancer when it attacks the bone
- bone breaks down and releases Ca+
- Hypercalcemia
what electrolyte imbalances are you at risk for in renal impairment/failure
hyperphosphatemia
hypermagnesemia
hyperkalemia
hypernatremia
What electrolyte imbalances associated with acidosis
hyperchloremia
hyperphosphatemia
hyperkalemia
what electrolyte imbalance is associated with loop diuretics
hypercalcemia
what electrolyte imbalance associated with diuretics
hypochloremia
hypomagnesemia
what electrolyte imbalance associated with sepsis
hypocalcemia
What electrolyte imbalances associated with constipation
Hypercalcemia
what electrolyte imbalance associated with anorexia and nausea
hypercalcemia
hypomagnesemia
Nausea only
-Hyponatremia
what electrolyte imbalance associated with acute diarrhea
hypernatremia
what electrolyte imbalance are you at risk for with PRBCs
hypocalcemia
what electrolyte imbalance associated with Ataxia
hypomagnesemia
what electrolyte imbalance associated with confusion, AMS
hypocalcemia
hypernatremia
what electrolyte imbalance associated with muscle cramps
hypokalemia
hypernatremia
hypocalcemia
what electrolyte imbalance associated with hyporeflexia
hypermagnesemia
what electrolyte imbalance associated with hyperreflexia
hypomagnesemia
what electrolyte imbalance associated with resp weakness or decreased resp effort
hypophosphatemia
Hypochloremia
the lower the pH the ____ the H ion concentration
Higher
the higher the pH the ___ the H ion concentration
Lower
normal pH range
7.35-7.45
normal PCO2 (partial pressure)
35-45
normal Bicarb
22-26
carbonic anhydrase helps with what formula important in acid base balance
CO2 + H20 H2Co3
If your hyperventilating or your vent settings are too high, you could become
alkalotic
If your hypo-ventilating you could become
acidotic
pH < 7.35
CO2 >45
Respiratory acidosis
Asthma can cause what type of acid base imbalance
Resp acidosis
How can kidneys compensate if your building up CO2 becoming acidotic
makes more bicarb which will pair with Hydrogen ions and excreted in urine.
This takes days
pH > 7.45
CO2 <35
Respiratory alkalosis
what type of acid base balance
Pt who is hyperventilating
On a ventilator and settings are too high
salicylate intoxication
Hyperthyroidism
Resp alkalosis
How can kidneys compensate if your in resp alkalosis
getting rid of bicarb
pH < 7.35
HCO3 < 22
Metabolic acidosis
Diarrhea
and hyperchloremia
can cause what type of acid base imbalance
Metabolic acidosis
Diarrhea you are loosing bicarb through your GI tract
normal anion gap
4-12
pH <7.35
HCO3 <22
anion gap >12
Anion Gap Metabolic Acidosis
Calculate anion GAP
Na
K
Chloride
HCO3
Take your positives
Na+ and subtract potassium, chloride and Bicarb to get your gap.
Kussmaul breathing happens because you are trying to get rid of
CO2
Vomiting or Ng Suctioning can lead to what acid base imbalance
Metabolic Alkalosis
pH >7.35
HCO3 >26
Metabolic Alkalosis
when you loose your chloride your body starts to make more
bicarb
diuretics can lead to what type of acid base imbalance
Metabolic alkalosis bc your dumping Na, K, Ca, Cl and your bicarb starts to come up bc of this
How does your lungs compensate in Metabolic acidosis
because you have a higher bicarb your lungs compensate by increasing CO2 that you have
If I told you a pt had chronic renal failure, what would you think about in regard to acid base balance
kidneys may not be able to keep up with excreting Hydrogen ions
metabolic acidosis
If I told you a pt had vomiting the last few days, what would you think about in regard to acid base balance
Metabolic alkalosis
If I told you a pt had drug ingestions, what would you think about in regard to acid base balance
Respiratory alkalosis - depressed resp
Metabolic alkalosis
If I told you a pt taking Lasix, what would you think about in regard to acid base balance
Metabolic alkalosis (you can see a bump in bicarb)
If I told you a pt had cyanosis, what would you think about in regard to acid base balance
Respiratory acidosis
If I told you a pt had Kussmaul breathing, what would you think about in regard to acid base balance
Metabolic acidosis - your trying to hyperventilate to breathe off CO2
If I told you a pt had AMS from seizures, what would you think about in regard to acid base balance
Respiratory acidosis - if you aren’t breathing well, cant blow off CO2
pH 7.15
bicarb 6
PCO2 18
His serum levels reveal Na 135 chloride 114 potassium 4.5 bicarb 11
what does the pH tell you?
what kind of acid base disorder is this?
what is the anion gap?
Metabolic Acidosis
PCO2 is low bc of compensation
135-114 = 21 - 11= 10 (anion gap)
Non-anion gap hyperchloremic metabolic acidosis
poorly controlled asthma
pH 7.54 pO2 of 60 PCO2 29 Na 138 Chloride 103 bicarb 25
Resp alkalosis
3 month old
chronic lung disease
home meds include lasix
pH 7.37 pCO2 70 Na 136 Cl 88 Bicarb 37
compensated resp acidosis
what do ketones produce
B-Hydroxybutyrate »_space;»acetoacetate (6:1)
How is B-Hydroxybutyrate measured
blood
How is acetoacetate detected
Urine ketone strips
whats your renal threshold for glucose excretion? - point at which osmotic diuresis occurs
180 mg/dL
Osmotic diuresis ->dehydration ->electrolyte wasting ->further stimulates stress hormones
severe dehydration, poor tissue perfusion leads to lactic acidosis
what electrolytes are DKA pts depleted of
K+
May be high initially and should fall as the acidosis corrects pulling K back into the cells
Na+ - sodium level that you see is actually lower than what you see - calculate 1.6mEq to sodium levels for every 100 rise above 100 glucose level
if Na appears normal on arrival - reflects extreme free water loss
Phosphorous
Cl is normally ____ in DKA
high
DKA pt who during treatment, as b-hydroxy levels are decreasing but bicarb isnt correcting, what should you consider
Chloride is rising with fluids
May need to change fluids
What lab can be a predictor for cerebral edema in DKA pt
BUN - elevated - have to be more careful of DKA
when is cerebral edema more likely in DKA
first 3-12 hours after start of treatment
< __ yrs old has increased risk of cerebral edema
5 yrs
Serum test for DKA
K, Na, K, HCO3, Cl, glucose Bun/creatinine B-hydroxybutyrate Venous blood gas Ca, Mg, Phos
if fever - blood and urine cultures
- lactate if shock or sepsis
- CBC
- Hematacrit
ECG
labs to collect for new onset diabetes
Diabetes associated antibodies (glutamic acid decarboxylase antibodies, insulin auto-antibodies, islet cell antibodies, zinc transporter 8 antibodies)
HA1C
insulin
C-peptide
Celiac panel
Thyroglobulin antibodies
Anion Gap =
Na-(Cl+HCO3)
Normal anion gap
around 12
what Anion gap do you normally see in DKA
20-30
If you have a DKA with an anion gap >35, this suggests concomitant ___ ____
lactic acidosis
mild, moderate or severe DKA?
pH <7.30 or serum bicarb <15
mild
mild, moderate or severe DKA?
venous pH <7.2 or serum bicarb <10
moderate
mild, moderate or severe DKA?
venous pH <7.1
serum bicarb <5
Severe
These factors make the pt ICU status for DKA (at some facilities)
Severe DKA <7.1
Age < 5yrs
AMS
Received >40mL/kg of fluid
Sepsis/SIRS
Received sodium bicarb treatment
High BUN at presentation
intubation is encouraged or discouraged in DKA
discouraged if possible. At high risk for cardiac event due to level of acidosis
fluid resuscitation in DKA pt who is not in shock and has no evidence of cerebral edema
NS or LR bolus of 10-20ml/kg over 30-60 min
fluid resuscitation in DKA pt who is in shock
rapid fluid resuscitation with 20mL/kg and reassessment after each bolus
DKA fluid management calculation
replace remaining fluid deficit:
-use deficit estimate of 5-7% body weight for moderate DKA
-use deficit estimate 7-10% body weight for severe DKA
fluid deficit plus maintenance fluids volume over 24-48 hours
DKA fluid management - what fluid type should you consider using if there is a concern for hyperchloremic acidosis
LR instead of NS
when is insulin started in DKA management
after fluid replacement
Insulin in DKA management
insulin infusion at 0.05-0.1 units/kg/hr while receiving IV fluids
0.05 units/kg/hr is for children <5yrs of age
Why do you not want to bolus insulin in DKA
increased risk of cerebral edema
When do you add dextrose to fluids in DKA treatment
when plasma glucose falls to 250-300 mg/dL or if its correcting too quickly
In DKA treatment you do not want your glucose to come down more than ___ mg/dL/hr
100
Insulin management in mild DKA (7.2-7.3) or when insulin infusion is not feasible
may administer subcutaneous rapid-acting insulin every 1-2 hours or regular insulin every 4 hours
In DKA management when is Potassium chloride or Potassium phosphate added to fluids
K<5.5
Pt has voided
Severe hypophosphatemia in DKA should be treated. Don’t forget to monitor for
hypocalcemia
when your replacing phosphate can lead to hypocalcemia
Bicarb in DKA treatment
Do not give - no benefit in DKA and associated with worse outcomes and cerebral edema
Reserved for cases of life threatening hyperkalemia or severe acidosis with cardiac compromise
As your glucose comes down what should your sodium be doing
what happens if this does not occur
Serum Na should increase
Failure of Na+ to increase prompts intense neurologic monitoring due to risk associated with cerebral edema
2 bag system for DKA what are in the 2 bags
Bag A: NS or LR
Bag B: 10% dextrose added to NS or LR
Add KCL and Kphos according to serum K level (<5.5)
For DKA pt how do you calculate the IVF rate
2.5L/m2 - bolus given and then divide by 24 hours
example BSA = 1.6, received 400ml bolus
Total IVF rate = (2,500 ml * 1.6) - 400=3,600mL/24 hours = 150ml/hr
what resolves first in DKA
Hyperglycemia or metabolic acidosis
hyperglycemia
once hyperglycemia resolves, maintain glucose levels between
100-200mg/dL
In DKA management, where the glucose is falling too fast or the acidosis is not correcting what do you do?
Change to D12.5% or increase fluid rate
what labs are you monitoring every 2-4 hours in DKA
What else are you monitoring closely
hourly capillary blood glucose checks
labs
- electrolytes
- blood gas
- B-hydroxybutyrate
- BUN/Cr
- Serum glucose
- Ca, Mg, Phos every 4-6 hours
hourly neurologic exams
when do you transition them off the 2 bag system in DKA treatment
HCO3 >15 mEq/L
B-hydroxybutyrate <1.0-1.5
Abd pain and vomiting resolved, patient can tolerate oral intake
when do you transition to subcutaneous insulin in mgmt of DKA
- Before a meal
- carbohydrate consistent diet
- administer basal insulin along with a short acting insulin
- to prevent rebound hyperglycemia and ketoacidosis, administer subcutaneous insulin 30 min before discontinuing insulin infusion
in Pediatric DKA the incidence of cerebral edema is ____ and the mortality rate is ___
rare
high
risk factors for cerebral edema in DKA
severe acidosis on presentation
High initial serum BUN
Low initial pCO2
Failure of corrected serum Na+ to rise during treatment
Age <5 years
new onset diabetes
Received NaHCO3 treatment
Rapid administration of hypotonic fluid
signs/symptoms of cerebral edema in DKA
onset headache after treatment
progressively worsening headache
Altered sensorium
changes in neurologic status
inappropriate slowing of HR
increase in BP
decrease oxygen sats
Cushing’s triad (late signs) - rising BP, bradycardia and resp depression
cerebral injury clinical diagnosis (DKA)
Can be one diagnostic criteria
- abnormal motor or verbal response to pain
- decorticate or decerebrate posture
- cranial nerve palsy
- abnormal neurogenic resp pattern (grunting, tachypnea, cheyne-stokes, apneusis)
-or-
2 major criteria
-AMS, confusion, fluctuating level of consciousness
-Sustained HR deceleration (>20 beats/min) not attributable to improved intravascular volume
-Age inappropriate incontinence
or 1 major and 2 minor (>5 yrs old)
1 major and 1 minor (<5 yrs old)
minor vomiting headache lethargy or not easily arousable Diastolic BP >90 mmHg Age <5 yrs
-only count signs that occurred after treatment
treatment of cerebral edema (DKA)
initiate treatment as soon as cerebral edema is suspected. Do not delay for CT imaging
-Adjust fluid rate to maintain normal bp or avoiding excessive fluid administration
- Give mannitol or hypertonic (3%) saline
- mannitol 0.5-1g/kg IV over 10-15 min
- Hypertonic saline (3%) 2.5-5mL/kg over 10-15 min
- Head of bed elevated to 30 degrees keep the head in midline position
- intubation may be necessary - hyperventilation below pCO2 appropriate to pt degree of acidosis associated with poorer outcomes
- after treatment, consider CT
Mannitol dosing and time to give Mannitol for DKA related cerebral edema
mannitol 0.5-1g/kg IV over 10-15 min
Hypertonic Saline dosing and time to give for DKA related cerebral edema
2.5-5mL/kg over 10-15 min
The top zone on the adrenal cortex, Zona Glomerulosa makes ___ that turns into ___
Angiotensin II
Aldosterone
The second from top zone on the adrenal cortex, Zona fasciculata makes ___ that turns into ___
ACTH
Cortisol
The third zone on the adrenal cortex, Zona Reticularis makes ___ that turns into ___
ACTH
Androgens
The adrenal medulla makes ___
Catecholamines
The hypothalamic-pituitary adrenal axis
the main mechanism is
regulating cortisol production
ACTH is made in the
pituitary gland
congenital adrenal hyperplasia is affecting the ____and not the pituitary
gland
A group of autosomal recessive disorders characterized by impaired cortisol synthesis ->hypersecretion of CRH and ACTH that leads to hyperplasia of adrenal glands
Congenital Adrenal Hyperplasia
what enzyme deficiency is associated with Classical Congenital Adrenal hyperplasia
21-Hydroxylase Deficiency (for 90% of the cases)
Classical Congenital adrenal hyperplasia is more prevalent in what race
1: 15000 - Caucasians
1: 42,000 African Americans
what forms of congenital adrenal hyperplasia
Salt-wasting - 67%
Simple viralizing-33%
Classical Congenital adrenal hyperplasia is diagnosed by
elevated 17-hydroxyprogesterone level
21 Hydroxylase Deficiency in CAH
Hypotension
salt wasting
Cortisol deficiency
your progesterone and 17-OH progesterone go up which leads to hyper-androgenism
salt wasting =
mineralocorticoid deficiency
what organs are involved in blood pressure regulation
liver
lungs
kidneys
adrenal cortex
When you don’t make aldosterone….what happens
Hyponatremia
hyperkalemia
acidosis
hypotension
medication for CAH to replace cortisol
dosing to start
hydrocortisone 20mg/m2/day divided TID
medication for CAH to replace mineralocorticoid (aldosterone)
Fludrocortisone 0.1mg BID and
salt solution since they salt waste
what does the newborn screen test for in regards to CAH
focuses on 21-hydroxylase deficiency by testing for 17-hydroxyprogesterone
if you get an abnormal newborn screen back for CAH, what needs to be ordered
clinical eval lytes confirmatory 17OHP High dose ACTH stim test Preterm-> different normative values Referral
treatment for acute/new diagnosis for CAH
Hydrocortisone 100mg/m2 Iv/IM
(HC at high doses has mineralocorticoid activity so you dont have to give fludrocortisone)
+/- IVF with dextrose - hypoglycemia is common with adrenal insufficiency due to low cortisol
Fludrocortisone (mineralocorticoid) - after hydrocortisone is at maintenance dosing
ECG frequent neuro checks NS bolus 20ml/kg D5 or D10LR or NS approx 1800ml/m2/day Hydrocortisone 25 mg/m2 per dose every IV 6 hours after the initial dosing or PO q8
lytes q 2-4 hours till stable
signs/symptoms of adrenal crisis
hyponatremia
hyperkalemia
hypotension
hypoglycemia
daily treatment for adrenal insuf s/t CAH
what does this do
Hydrocortisone 10-20mg/m2/day (infants are 20)
- suppresses ACTH and adrenal androgens
- maintains normal growth and weight
-tablets, not suspension (does not stay in suspension and will not be even dosing
stress doses when sick is usually 3 xs usual dose
if salt waster
Fludrocortisone 0.1mg
Salt 17-34 mEq/day in infancy
at start of illness for a CAH pt
stress dose steroids IV med (solucortef) if not tolerating PO early/aggressive rehydration
long term complications in CAH
growth can be accelerated then later stunted if undertreated
virilization continues to occur in girls who are undertreated
BP
Excessive glucocorticoids -> Cushings
- HTN
- obesity
- short stature
- metabolic syndrome
elevated renin in CAH
need more mineralocorticoid
we dont want to normalize 17-OHP in CAH because we can cause
Cushing’s by overtreating
inadequate treatment of CAH can lead to
virilization
early puberty
Reduced adult final height
Advancement of bone age -> leads to early epiphyseal closure
Infertility ->
males: testicular adrenal rests (can cause testicular function)
Females: PCOS/anovulation
autosomal recessive in CAH means that every ___ in ____ will have CAH
1 in 4
a life-threatening condition that causes salt wasting and adrenal insufficiency in most cases
Classical Congenital Adrenal Hyperplasia
A girl with clitoromegaly
what should you suspect
Classical Congenital Adrenal Hyperplasia
A boy with microphallus or bilat undescended testes
What should you suspect
Classical Congenital Adrenal Hyperplasia
non-classical forms may present with premature adrenarche or as polycystic ovary syndrome
Classical Congenital Adrenal Hyperplasia
does not require stress dose steroids
2 things to draw in the EC when you suspect CAH
17 Hydroxyprogesterone
Cortisol levels
which type of CAH needs the Fludrocortisone
Salt wasters
the non classical or the virilizers do not
which type 1 DM is auto immune mediated
Type 1A
Type 2B is not
Name 5 rare forms of Diabetes
MODY (maturity onset diabetes of young)
Neonatal Diabetes (<6mos age)
Gestational Diabetes (2nd or 3rd trimester)
Steroid induced diabetes
- usually post organ transplant
- Cystic Fibrosis related Diabetes (CFRD)
- 2/2 disease of exocrine pancreas
Mitrochondrial forms of diabetes
- MELAS
- look for neuro, other abnormal exam findings)
risks based screening for Diabetes (Type 2 or pre-diabetes
obesity/overweight: BMI >= 85th percentile PLUS
maternal history of DM or gestational DM
Metabolic syndrome: Acanthosis nigricans (sign of insulin resistance), HTN, Dyslipidemia, PCOS, SGA or LGA
Family history of T2 DM
Race/ethnicity (native American, Hispanic, AA, Latino, Asian American, pacific islander)
normal A1C
<5.7
Prediabetes A1C
5.7-6.4
Diabetic A1C
> 6.4
Normal fasting blood glucose
<100
prediabetic fasting blood glucose
100-125
Diabetic fasting blood glucose
> 125
Oral glucose tolerance test normal glucose
<144
oral glucose tolerance test prediabetic
144-199
oral glucose tolerance test diabetic
> 199
ADA diagnostic criteria for diabetes
FBG >=126
or
2 hour pG>=200 during OGTT
or
HA1C >=6.5
or
pt with classic symptoms of hyperglycemia, hyperglycemic crisis, a random plasma glucose >200
classic symptoms of diabetes
polyuria (include nocturia) Polydipsia Polyphagia Weight loss fatigue/lack of energy DKA
other concurrent illness?
- frequent infections (vaginal yeast infections, abscess, UTI)
- Flu like symptoms
- strep throat
- gastroenteritis
pathophysiology of T2DM
Genetic (molecular defect identified- insulin secretion)
Environmental factors
- Diet
- Sedentary lifestyle (BMI >=85%)
Dysregulation - insulin secretion and sensitivity
Heterogenous disorder
Insulin resistance (lack of same biological effect) - Obesity, Puberty
treatment guideline for new onset DM in overweight youth with HA1C <8.5% without acidosis or ketosis
Metformin PO BID
titrate up to 2,000mg per day as tolerated (start with 500mg once daily)
draw pancreatic antibodies
negative -> continue metformin
if unable to manage with metformin, start insulin
positive -> insulin as indicated for type 1 DM
treatment guideline for new onset DM in overweight youth with HA1C >=8.5% no acidosis, with or without ketosis
start basal insulin at 0.5/units/kg/day - titrate up every 2-3 days as indicated by glucometer reading
Metformin
-Titrate up to 2,000mg/day as tolerated
(start with 500mg once daily)
draw pancreatic antibodies
negative -> continue metformin (wean insulin)
if unable to manage with metformin, start insulin
positive -> insulin as indicated for type 1 DM
treatment guideline for Acidosis under DKA and/or HHNK
manage DKA/HHNK
IV insulin until acidosis resolves. then subq insulin until pancreatic antibodies are known
lifestyle modifications for someone in pre-diabetes. Research shows metformin does not prevent diabetes full blown progression at this time
Healthy diet
- portion control
- complex carbohydrates
- caloric reduction: (500kcal/day => 1lb/wk weight loss)
Daily exercise
-moderate to vigorous activity for at least 60min/day
How does metformin work
A biguanide that
- insulin sensitizer
- inhibits gluconeogenesis
- helps with weight loss
Metformin is used as monotherapy in Type 2DM when A1C is less than
8.5%
Black box warning for Rosiglitazone
Congestive heart failure and bladder cancer in diabetics
when you start someone on metformin, what is your initial dose and how often do you titrate up based on glucose readings
500mg once a day with the goal of 2000mg daily or 1000mg BID
- increasing by 500mg weekly
what baseline labs do you need prior to starting metformin
LFTs
Renal function
If AST/ALT 2.5 times the norm, consult liver team to see what they say…..if 3-4 x we dont start
The concern is fatty liver
pt education for metformin
Avoid alcohol - Black box warning - lactic acidosis
can cause pernicious anemia
glucose targets 90-130 fasting and post prandial glucose concentration <180
(check BID BG) specifically fasting
side effects metformin
nausea
vomiting
diarrhea
can try extended release
Contraindications for metformin
Hepatitis impaired renal function cirrhosis alcoholism cardiopulmonary insufficiency
If Type 2DM failing therapy with Metformin and insulin, you can add a 3rd agent as adjunct therapy ….which agent are you thinking
Victoza (Liraglutide)
Refer to endocrinology
this is a once a day shot
How does Victoza (Liraglutide) work
Glucagon-like-peptide (GLP-1) receptor agonist
Incretin hormone
- Increases glucose dependent insulin secretion
- Increases B cell growth/replication
- slows gastric emptying and PO intake
what is C-peptide lab
marker of the B cell function
If I am looking to see if the body is naturally making any insulin we look at this lab
HHS and ketosis
HHS does not present with ketosis
what are the antibodies test for type 1 DM
Islet cell antibodies (Alpha, Beta, Delta)
GAD 65 (targets enzyme glutamic acid decarboxylase)
Insulin AutoAB
Zinc Transporter
if any are positive - definitive diagnosis for type 1 DM
B - Hydroxybutyrate are essentially
blood ketones
what are some labs that you should be drawing on DKA -new onset
POC glucose C-peptide HgA1C Beta-hydroxybutrate chem10 VBG celiac panel GAD autoantibody ICA 512AutoAB Insulin AutoAB IgA Thyroglobulin AB Thyroid panel tissue Transglut IGA
leading cause of death in T1DM
DKA
ISPAD guidelines for diagnosis of DKA
uncontrolled hyperglycemia (>200) metabolic acidosis (pH <7.3) Ketonemia
risk factors for DKA
sepsis and infections
Inadequate insulin intake including pump malfunction
Pancreatitis (7-20% r/t hypertriglyceridemia) Age <2 yrs delayed diagnosis recurrent DKA underlying mental health issues
s/s DKA
n/v/abd pain (rule out pancreatitis)
Tachypnea/kaussmal resp
tachycardia
fruity odor
lethargy/obtunded (concern for cerebral edema)
3 Ps
how can you explain insulin to pt
Your body needs insulin to open up all of the cells so that glucose can enter the cells and make energy (generate ATP).
When the body cant get the glucose, the body looks at other sources like fat cells, muscle cells. from that you get fatty acids and glycerol and your body will convert to ketones. and thats where you get B hydroxybutyrate.
type 1 DM age of onset
6 mos - adulthood, peaks at age 12
Type 2 DM age of onset
> =10 yrs
Acanthosis Nigricans is common in what DM
type 2
which type DM has diabetic ketoacidosis at onset
> 50% for type 1
<50% type 2
C-peptide high or normal seen in what type DM
Type 2 DM
In type 1 its low or undetectable
Pancreatic antibodies are likely to be positive in what type of DM
DM type 1
what does positive pancreatic antibodies mean
it just means there has been B cell loss
type 1a DM patho
autoimmune B cell destruction leading to absolute insulin deficiency
does not happen overnight
genetic predisposition…..with a precipitating event
When you have one autoimmune, your at risk for more. What other autoimmune diseases are they at risk for with type 1 DM?
Hashimoto’s thyroiditis (most common)
Celiac disease
Adrenal insufficiency
other
- Multiple sclerosis
- Lupus
- Gastritis
- Autoimmune arthritis
- Vitiligo
what labs are obtained at diagnosis for Type 1 DM and every year (after 5 years into Diabetes)
Thyroid Antibodies plus TFTs
Celiac Disease Antibodies
Screening for Addison’s disease and others based on symptoms
insulin is a ____ hormone produced by ___ ____
peptide hormone
beta cells
how does insulin work
regulated and secreted in oscillations (typically every 3-6 min) as a response to increased blood glucose
Newest ultra long acting insulin
what is it
how long does it last
Insulin Degludec (Tresiba) up to 42 hours
Rapid acting insulins
Aspart (Fiasp) - ultra rapid acting
Lispro (Humulog)
Apidra
Short acting insulin
Regular
Intermediate acting insulin
NPH
long acting insulin
glargine (Lantus, Toujeo)
detemir (Levemir)
Ultra rapid acting insulin
Fiasp
Lyumjev
what does basal insulin cover
glucose released by liver
what does bolus insulin cover
carbohydrates and correct high blood glucose levels
dosage of insulin in type 1 DM depends on what factors
Age of presentation (DKA?)
Honeymoon period/partial remission (10-15% pancreas is functioning for a short period - longest milli has seen is 2 years)
Family preference
Insulin starting dose guide formula
TDD = 0.x unit/kg/day (x= age in years)
if in DKA
1unit/kg/day (max)
Basal dosing for insulin should be ___ -___% of TDD
50-60%
Bolus dosing for insulin should be ___-____ of TDD
40-50%
Target BG for Type 1 DM normally
80-120mg/dl
Target BG for Type 1 DM if toddler, developmental delays or CF
150 mg/dl
How often should a type 1 DM be injecting insulin
3-4 times/day
How is insulin given when using a pump
continuous basal rate
Food bolus
correction bolus
Insulin side effects
hypoglycemia
- rule out alcohol intake
Lantus/Basaglar can burn: may use Tresiba
weight gain
Lipoatrophy or Lipohypertrophy: Rotate sites
when a pt is on insulin having frequent hypoglycemia, what needs to be ruled out
alcohol intake
If a DM pt is using Lantus/Basaglar and its burning. What can you switch to?
Tresiba
For insulin dependent pt. How do you prevent Lipoatrophy or Lipohypertrophy?
Rotate sites
In diabetic pt low glucose is considered low
70mg/dl
Adrenergic: Palpitations, tremors anxiety
Cholinergic: Sweating, hunger, paresthesias
In diabetic pt low glucose is considered severely low
<55
Headache, irritability, difficulty concentrating, confusion, seizures, coma
what can you give a diabetic pt for severe hypoglycemia
Glucagon (peptide hormone, alpha cells)
how many times per day should a diabetic check blood sugars
at least 4xs
MODY
maturity onset diabetes of Youth
monogenic disorder
misdiagnosed as type 1 or type 2
High genetic predisposition (50% chance if parent has it)
14 genes identified for mutation causing MODY
Pathogenesis - insulinopenia - subtle onset - insulin often not required
occurs before age 25 yrs
islet autoimmunity is absent
treatment depends on type of MODY
Signs of MODY
Mild fasting hyperglycemia = about 140
insulin requirement <= 0.5 units/kg/day
(some endogenous insulin beyond 3-5 yrs after onset of diabetes)
Negative autoantibody testing
Measurable C-peptide
Lack of significant obesity
Strong family history
lack of insulin resistance
treatment for MODY
Sulfonylureas
-Glyburide
Refer to endocrinology for initiation of therapy
Acute complications for DM
hypoglycemia
DKA (Diabetic Ketoacidosis)
HHS (hyperglycemic hyperosmolar state)
Chronic complications for DM
Microvascular
- Retinopathy
- Nephropathy
Neuropathy
Macrovascular: Cardiovascular
Delayed puberty
Growth disturbance (short stature)
psychosocial/Psychiatric
what screening should be done for a type 2 DM at diagnosis, then yearly
Retinopathy: dilated eye exam
Nephropathy: spot urine albumin to creatinine ratio
Neuropathy: foot exam
HTN should be evaluated at diagnosis and every visit
Dyslipidemia should be evaluated at diagnosis. If abnormal - reevaluate yearly. If normal, every 3-5 years
what screenings should be done in patients 10 yrs old and older in Type 1DM who has been a diabetic for 5 years. These should be done yearly after the initial
Retinopathy: dilated eye exam
Nephropathy: spot urine albumin to creatinine ratio
Neuropathy: foot exam
Dyslipidemia should be evaluated at diagnosis. If abnormal - reevaluate yearly. If normal, every 3-5 years
what screenings should be done in Type 1DM shortly after diagnosis; if normal - repeat every 1-2 yrs
autoimmune thyroid disease: TSH
what screenings should be done in Type 1DM shortly after diagnosis or with symptoms
Celiac
IgA
TTG
IgA
if your HA1C is 7.0 your average blood glucose over the past 90 days
170
If your HA1C is 5.0, your average blood glucose over the past 90 days
100
If your HA1C is 8.0, your average blood glucose over the past 90 days
204
why do we recommend keeping the HA1C 7%
reduces the risk of long term complications significantly
Retinopathy - 76%
Nephropathy - 54%
Neuropathic - 60%
what is the depression screening called
PHQ-9 Depression screening
number of solute particles in 1 kg of solvent
osmolality
this is the term used in medicine
number of solute particles in 1 L of solvent
Osmolarity
formula for serum osmolality
(2x {Na}) + {glucose} + (Bun)
effective osmolality or the measure of the osmotic pressure gradient that reflects the concentration of solutes that don’t cross cell membrane easily and affect distribution of water
Serum tonicity
transfer of soluble components (not protein) from blood into glomerulus
filtration
water and solutes move from renal tubule back into circulation
reabsorption
transfer of solutes and waste from plasma into the renal tubule for excretion (urine)
secretion
content of urine, end result of above processes
Excretion
content of urine, end result of filtration, reabsorption, secretion
Excretion
what does Antidiuretic hormone (ADH) aka Vasopressin do
recruits renal water channels in collecting duct -> water reabsorption in renal tubules -> concentrates urine (decreases urine volume)
“Adds
Da
H2O”
drinking water increases or decreases your plasma osmolality
decreases
at what plasma osmolality does thirst begin to autoregulate osmolality
280 mosmol/kg
at what plasma osmolality does plasma ADA start to risk to autoregulate osmolality
285 mosmol/kg
when there are problems with ADH and water homeostasis regulation what can it affect
thirst
urine output
Intravascular volume status
Serum osmolality
Serum Sodium (Na) level
Urine osmolality
Urine Na level
decreased production of ADH
central diabetes insipidus
decreased renal response to ADH
nephrogenic Diabetes insipidus
decreased ability to reabsorb water in the renal tubules ->cannot concentrate urine ->excess loss of water in urine
(inappropriately dilute urine and serum hyperosmolality)
Diabetes Insipidus
what causes central DI - Hypothalamus doesn’t produce ADH
Cancer (craniopharyngioma, germinoma) trauma meningitis hypoxic brain injury infiltrative disorders (histiocytosis, leukemia) surgery, radiation holoprosencephaly, congenital hypopituitarism Anorexia nervosa idiopathic
what causes nephrogenic DI - collecting ducts don’t respond to ADH
kidney disease (polycystic kidney disease, sickle cell)
Medications - lithium, foscarnet, amphoteracin)
pregnancy
Bartter syndrome
Bardet Biedl syndrome
Hypercalcemia
Hypokalemia
Hereditary (Aquaporin-2 gene mutation)
what medications can cause nephrogenic DI
lithium, foscarnet, amphotericin
what syndromes can cause nephrogenic DI
Bartter syndrome
Bardet Biedl syndrome
what gene mutation is associated with nephrogenic DI
Aquaporin-2 gene mutation
DI symptoms
symptoms of dehydration and hypernatremia
- Tachycardia, hypotension
- irritability, restlessness
- weakness
- seizures
- AMS, Coma
- FTT or obesity
- Fever (infants)
- Polyuria
- Nocturia
- Absence of primary polydipsia
- Absence of excess solute excretion or osmotic diuresis (hyperglycemia, high protein diet)
- Patients not taking diuretics
In DI what is their volume status
Hypovolemic
In DI what should their urine output be
increased
In DI what should their serum sodium be
High >150 mEq/L
In DI what should their serum osmolality be
High >300 mOsm/L
In DI what should your urine specific gravity be
Low (<1.010)
In DI what should your urine sodium be
Low (<20 mEq/L)
In DI what should your urine osmolality be
low (<100-300 mosm/L)
when does water deprivation test start
after breakfast and after 1st void of the day and you don’t get any fluids
when you give DDADP (vasopressin) and your urine osmols do not rise this is
nephrogenic DI
when you give DDADP (vasopressin) and your urine osmols do rise this is
central DI
DI: Acute management - hypernatremia
Severe dehydration - NS bolus 20mL/kg
Free water replacement over 24-48 hours
- Goal is to correct Na 0.5mEq/L per hr (12mEq/L/day)
- Risk cerebral edema - plasma osm drops to quickly
Monitor Na level frequently
remember that NS is hypotonic in this situation….may need 0.45% NaCl
or use NS for bolus then go with D5W
Free water deficit formula (DI)
Free water deficit (liters) = measured Na - Goal Na all divided by goal Na then multiply by 0.6L/kg x weight (kg)
what is key to regulate plasma osmolality in a pt with DI
someone that has an intact thirst mechanism
monitoring in DI
intake/output
Na levels
adjustments to daily fluid requirement based in I/O, Na levels, change in insensible losses, growth
medication used for acute management for DI
Vasopressin
what med is most commonly prescribed for DI management
Desmopressin (DDAVP)
- longer half life
- no pressor effect
- every 12-24 hr dosing for IV/nasal; q 8-12 hr dosing for oral
monitor for breakthrough mild polyuria-occurs when dose is due (good sign that the dose is right)
Nephrogenic DI management
if drug induced - stop if able
Low salt, low protein diet
NSAIDS - indomethacin is more effective than ibuprofen
Diuretics - hydrochlorothiazide, amiloride
Partial nephrogenic DI - higher doses of DDAVP may work
inability to suppress ADH
impaired water excretion
inappropriately concentrated urine + serum hypo-osmolality
SIADH - syndrome of inappropriate ADH
list pulmonary causes of SIADH
mechanical ventilation
pneumonia
bronchiolitis
asthma
cystic fibrosis
list neurologic causes of SIADH
tumor
surgery
trauma
hemorrhage
meningitis
Encephalitis
severe nausea
list oncology causes of SIADH
Medulloblastoma
lymphoma
list medications that causes of SIADH
Oxcarbazepine
Valproate
chemotherapies
narcotics
nsaids
list other causes of SIADH
Anesthesia
idiopathic
post-op
s/s of SIADH
symptoms of hyponatremia
- n/v
- anorexia
- headache
- cramps or tremors
- irritability
- confusion
- malaise
- seizure
- stupor or coma
normal cardiac, renal, liver, adrenal, thyroid function
patient not taking diuretics
Absence of renal salt wasting
no evidence of hypovolemia
BUN usually low
uric acid low
volume status in SIADH
Euvolemic to hypervolemic
urine output in SIADH
Decreased (<1mL/kg/hr)
serum sodium in SIADH
low (<135 mEqu/L)
serum osmolaltiy in SIADH
low (<280 mOsm/L)
Urine specific gravity in SIADH
High (>1.020)
Urine Sodium in SIADH
High (>20-40 mEq/L)
treatment for SIADH
severe symptoms - treat immediately with 3% saline
gradual correction of hyponatremia - 1st line therapy is fluid restriction
Acute hyponatremia
duration
severity?
goal Na correction?
develops within 48 hours
severe symptoms more likely
at risk for complications
more tolerant of sodium correction
goal Na Correction is 6-8mEq/L per 24 hours
Chronic hyponatremia
duration
severity?
goal Na correction?
Duration >48 hours
cerebral volume adaption
less likely to be symptomatic
at risk for osmotic demyelination if corrected too quickly
requires more gradual correction
goal Na correction 4-6 mEq/L per 24 hours
treatment for severe symptomatic hyponatremia (seizure, obtunded, coma)
(SIADH)
3% saline 3-5mL/kg (max 100mL) raises by 2.5-4 mEq/L
SIADH management
fluid restriction is first line
- restrict to 1/2 to 3/4 daily maintenance fluid requirement
- Monitor sodium levels
- Goal rate of Na correcting 4-8mEq/L per 24 hours depending on acuity
Alternative therapy for chronic SIADH
- low diuretic (+/- sodium supplementation)
- Urea supplementation - increases water excretion
- Vasopressin receptor antagonist (Vaptans, rarely used in pediatrics)
hyponatremia + hypovolemia due to inappropriate sodium wasting in urine
Cerebral salt wasting (CSW)
What is cerebral salt wasting seen in
CNS insult: subarachnoid hemorrhage, post-surgery, trauma, meningitis, encephalitis, tumors, status epilepticus
Volume status in Cerebral salt wasting
Hypovolemic
urine output in Cerebral salt wasting
increased
Serum sodium in Cerebral salt wasting
Low (<135 mEq/L)
Serum osmolality in Cerebral salt wasting
low
urine specific gravity in Cerebral salt wasting
High (>1.050)
urine sodium in Cerebral salt wasting
High (>40 mEq/L)
Urine osmolaltiy in Cerebral salt wasting
High (>100-300 mOsm/L)
Managing Cerebral salt wasting
Treat underlying cause
Volume repletion and treat hyponatremia
- isotonic saline - provide fluid and restore sodium stores
- Moderate-severe hyponatremia
- Provide additional sodium as 3% saline or salt tabs
- limit free water (not volume)
Monitor sodium levels
-avoid quick correction of hyponatremia - risk osmotic demyelination syndrome
-correct Na no more than 8-10 mEq/L per day
Fludrocortisone may be useful
what lab represents the unbound, biologically active T4
Free T4
If free T4 is high …most likely
Hyperthyroidism
If free T4 is low …most likely
Hypothyroidism
If free TSH is high …most likely
Hypothyroidism
If free TSH is low …most likely
Hyperthyroidism
3 types of hypothyroidsm
congenital
acquired
Transient
what are the types of congenital hypothyroidism
dysgenesis - did not form correctly
dyshormonogenesis - it formed, but doesnt function properly
If not caught and treated early, what can happen
developmental delay
T3, T4 and TSH and placenta
do not cross the placenta - when your testing the baby at day of life 1 - those are the babies numbers
Thyroid meds that mom takes can cause
Transient hypothyroidism - can last 3-4 weeks (this can be over or underproduction)
what are the causes of transient hypothyroidism
maternal antithyroid drugs
Maternal TSH receptor blocking antibodies
what are the causes of acquired hypothyroidism
hashimoto thyroiditis
Iodine deficiency
causes of secondary hypothyroidism
Hypothalamus or pituitary
-Free T4 and TSH low or normal
Malformation
-Holoprosencephaly - midline defects (cleft lip/palate)
what does hypothyroidism look like in baby
low hr low energy so dont feel well Acrocyanosis abd distension umbilical hernia mottled skin thick lips large fontanel weakness hypotonia constipation prolonged jaundice cold intolerance
Congenital Hypothyroidism and goiter
RARE 1:30k live births - most often r/t dsyhormonogenesis or transient
Newborn screen and congenital hypothyroidism
We do screen for this in all 50 states
Acquired Hypothyroid/hashimoto Thyroiditis
Setup and symptoms
Subtle
decline in growth velocity without weight loss
25-33% have family history
Common in Turner & Trisomy 21
iodine deficiency (table salt (not sea salt), milk products, eggs, fish) - Cretinism (when cause is iodine deficiency)
Acquired Hypothyroid/hashimoto Thyroiditis
Evaluation
Goiter
Antithyroid peroxidase & antithyroglobulin antibodies
Elevated TSH, low FREE T4
Elevated TSH and normal T4 may be prelude to failure
Treatment Acquired Hypothyroid/hashimoto Thyroiditis
Congenital or Acquired
- Levothyroxine
- Infants 15mcg/kg and children 3mg/kg
Hyperthyroidism is most commonly cause by ____ in children
Graves Disease
Graves Disease Setup and Symptoms
Adolescent girls
emotional lability, personality changes, school performance
Tremor, anxiety, inability to concentrate
Weight loss
Graves Disease Evaluation
Free T4, T3 high
TSH low
Hyperthyroid symptoms
increase sensitivity to heat
sudden weight loss
frequent bowel movements
sweating
Thyroid storm
Rapid pounding heartbeat
nervousness
irritability
tremor
difficulty sleeping
change in menstrual patterns
Treatment Graves disease
Methimazole x 1-2 yrs (watch for agranulocytosis(aplastic anemia) - can switch to PTU - 2nd option (risk for liver failure) (the idea is to get you to a euthyroid state)
Surgery (needs to be a skilled surgeon) (goal is to get you to a euthyroid state)
Iodine (in a hyperthyroid state, iodine is suppressive) - temp till surgery
Radioiodine - this one you will need thyroid hormone replacement after
Beta blocker =- symptom control
Thyroid storm setup and symptoms
Medical emergency
rare complication of hyperthyroidism
Tachycardia
disorientation
elevated BP
Hyperthermia
Evaluation of Thyroid storm
Free T4 and T3 - high
TSH low
Treatment for thyroid storm
cooling blanket beta blocker iodine hydrocortisone support if they have adrenal insufficiency associated with the thyroid storm heart failure therapy - if needed
Neonatal Hyperthyroid/neonatal graves disease setup and symptoms
Hyperthyroid mom - transplacental passage of maternal thyroid stimulating immunoglobulins (TSI)
may be masked for few days - due to maternal antithyroid treatment
Hallmark: Irritability, tachycardia, heart failure, polycythemia, craniosynostosis, advanced bone age, poor feeding, FTT
Evaluation for Neonatal Hyperthyroid/neonatal graves disease
Free T4 high
TSH low
treatment for
Neonatal Hyperthyroid/neonatal graves disease
none if symptoms are minimal
methimazole
B Blocker
spontaneous resolution 2-3 mos based on half life of TSIs
obesity muscle wasting muscle weakness decreased glucose tolerance hyperglycemia buffalo hump
Cushing Syndrome symptoms
what 3 types of hormones do the adrenal glands produce
Glucocorticoid (cortisol, corticosterone)
mineralocorticoid (Aldosterone, dehydroepiandrosterone)
sex hormones (androgens, progestins and estrogens)
acute adrenal insufficiency
adrenal crisis
chronic adrenal insufficiency
Addison disease
the most common causes of acute adrenal insufficiency are
Waterhouse-Friderichsen syndrome - sudden withdrawal of long term corticosteroid therapy
in primary adrenal insufficiency what hormones are not produced in sufficient amounts?
which one in particular
Glucocorticoid
mineralocorticoid
cortisol
what is the most commonly identified cause of primary adrenal insufficiency in children
Congenital adrenal hyperplasia (CAH)
Congenital adrenal hyperplasia (CAH) is an _____ _____ disorder
autosomal recessive disorder
Congenital adrenal hyperplasia (CAH) is due to a defect in what enzyme
largely due to 21-hydroxylase deficiency required in the synthesis of cortisol to cholesterol
what gender has a higher incidence of Congenital adrenal hyperplasia (CAH) at birth
females
when do males usually present with Congenital adrenal hyperplasia (CAH)
with a life-threatening salt-wasting crisis in the first month of life
between 1-4 weeks of life -Vomiting -dehydration -cardiac arrhythmias -hyponatremia -hyperkalemia -salt-losing crisis All results in circulatory collapse
Congenital adrenal hyperplasia (CAH)
fatigue loss of weight hyperpigmentation of the creases of the skin nausea vomiting
Adrenal insufficiency
vomiting
abd pain
hypovolemic shock
adrenal crisis
Morning 17-OHP levels may be _____ in a partial enzyme deficiency
elevated
Congenital adrenal hyperplasia (CAH)
testosterone in females
elevated
Congenital adrenal hyperplasia (CAH)
Androstenedione is seen in
males and females
Congenital adrenal hyperplasia (CAH)
karyotyping is important for
ambiguous genitalia
CAH dosing of hydrocortisone
10-20 mg/m2/day daily
Adrenal insufficiency dosing for hydrocortisone
6-9mg/m2/day daily
Stress dosing of hydrocortisone
25-50mg/m2/day IV/IM
severe illness or surgical procedures, stress dosing of hydrocortisone
50-123 mg/m2/day IV
dosing for mineralocorticoid maintenance therapy in adrenal insufficiency
0.1-0.2mg oral fludrocortisone acetate daily
sodium supplementation for infants in adrenal insufficiency
17-34 mEq of sodium supplementation daily
when does cerebral salt wasting occur
following an acute CNS injury
Results in volume depletion and hyponatremia typically occurring within the first few days of an inciting intracranial injury, surgery or disease process
Cerebral salt wasting
symptoms of cerebral salt wasting
headache n/v depressed/AMS lethargy dehydration agitation seizures hypotension coma
the rate of renal sodium loss, degree of hyponatremia and overall fluid status impact the severity of the presenting symptoms
serum sodium <135 serum osmolarity <280 urine sodium >80 urine osmolarity >200 Urine specific gravity >1.010
cerebral salt wasting
urine output in cerebral salt wasting is - ml/kg/hr
2-3ml/kg/hr
what other studies should be done in cerebral salt wasting
CT/MRI - looking for structural abnormalities, tumors, AV malformation, hemorrhage
Lumbar puncture
-infection
In cerebral salt wasting serum sodium level should rise no more than __-__ mEq/day
10-12 - to reduce risk of central pontine demyelination of white matter in brain
unless having severe neuro symptoms
genetics of DI
typically x linked recessive
What syndrome is linked to DI
Wolfram syndrome
congenital DI typically X linked recessive involving what mutations
VR2 or AQP2
What conditions lead to the inability of the kidneys to respond to ADH in DI
Chronic renal failure Renal tubulointerstitial diseases Potassium depletion sickle cell disease medication induced from drugs alcohol lithium diuretics amphotericin B Demeclocycline
what dietary abnormalities can lead to DI
Primary polydipsia
decreased sodium chloride intake
severe protein restriction or depletion
is DI reversible?
Nephrogenic DI that results from a metabolic condition may be reversed if the medication is stopped or the metabolic condition is corrected
Polyuria Dilute urine Polydipsia inappropriately low urine sodium and osmolality urine specific gravity <1.005 Hypernatremia Serum Hypo-osmolality Dehydration
DI
the primary causes of polyuria and polydipsia are
Diabetes Mellitus
Central DI
other causes:
UTI
relief of renal obstruction
psychogenic polydipsia (excessive water intake)
Serum sodium >150 Osmolality >295 Urine sodium <30 Urine osmolality <200 specific gravity <1.005
DI
water deprivation test results:
concentrated urine output following ADH administration
Central DI
water deprivation test results:
excessive, dilute urine despite hypernatremia and hyperosmolality
nephrogenic DI
fluids are restricted until as much as 5 % of body weight has been lost to evaluate urinary response when the serum osmolality exceeds 295
water deprivation test
management of DI
restore hemodynamics
replace water deficit and correct electrolyte disturbances
decrease Urine output to within normal range (Vasopressin, desmopressin)
Treat underlying
Volume replacement:
-Maintenance IV fluids, plus mL per ML urine output replacement (usually allow 1-2 ml/kg/hr urine output and replace the remainder)
monitor serum sodium closely
central DI needs ADH replacement to control polyuria
critical care setting treat for DI
Vasopressin continuous IV
-short half life (10-20 min)
initiated at dose of 0.5milli-units/kg/hr and titrated until urine output is decreased
-urine output goal <4mL/kg/hr
other than critical care setting treat for DI
Desmopressin
Oral and intranasal
chronic therapy: dose range is 5-30ug/day with peak effect 1-5 hrs
what type of DI is resistant to vasopressin
Nephrogenic DI
diagnosis of DKA
blood glucose >200 presence of serum ketones urine ketones blood pH <7.3 serum bicarbonate <15
hyperglycemia leads to
osmotic diuresis electrolyte loss Dehydration Decreased glomerular filtration Hyperosmolarity
physical exam findings in DKA
Tachycardia decreased pulses poor perfusion dry mucous membranes enophthalmos poor skin turgor hypotension deep or labored breathing
what systems need to be monitored in DKA
Cardiac monitoring
-watch for T wave alterations seen in hyperkalemia or hypokalemia
Neuro monitoring
-cerebral edema
corrected sodium formula
={Na+} + {1.6 x (plasma concentration mg/dL-100}/100
In DKA treatment …as hyperglycemia improves, serum sodium should ___. If it ____ or does not _____, there is concern for what?
improve
if sodium does level increases or does not begin to fall, there is concern for the development of cerebral edema
Potassium in DKA treatment
serum K can start low, normal or high…you lose k as an effect of water moving out of the cells due to increase in serum osmolarity ….
add K to fluid when K level <6 and pt has voided
correction of hyperglycemia and giving insulin will shift potassium back into the cells
Phosphorous in DKA
cells are depleted as a result of acidosis, osmotic diuresis and insulin administration
risk of giving bicarbonate to DKA
CNS acidosis
Hypokalemia
cerebral edema
timing of blood glucose monitoring DKA
prior to meals and 2 hours after meal ends
a potentially fatal complication of diabetes, usually type 2 due to insulin deficiency and an increase in counterregulatory hormones
Hyperglycemic Hyperosmolar state (HHS)
enough endogenous insulin to suppress ketosis, although insufficient amount of insulin to prevent hyperglycemia
Hyperglycemic Hyperosmolar state (HHS)
Accumulation of ketoacids that cause cap metabolic acidosis
DKA
severe dehydration polyuria polydipsia weight loss AMS hyperglycemia increased serum osmolality no ketosis or mild
Plasma glucose >600 pH >7.3 serum bicarb >15 small ketonuria serum osmolality >320
Hyperglycemic Hyperosmolar state (HHS)
Mgmt Hyperglycemic Hyperosmolar state (HHS)
ABCs
restore circulatory volume and correct fluid deficit
correct hyperglycemia, hyperosmolality, and electrolyte imbalances
-fluid mgmt and insulin
frequent lab eval
-hourly serum glucose in acute phase, electrolytes and other lab studies
treat underlying (infection is most common precipitating factor)
Monitor signs of cerebral edema
-correcting fluids over a longer period (48 hrs) may reduce r/o cerebral edema
An increase in serum levels of T3 and T4 will result in what in regards to TSH
Lower levels of TSH
An decrease in serum levels of T3 and T4 will do what to TSH
higher levels of TSH
abnormal fetal thyroid development or a disturbance in production of thyroid hormone
Congenital hypothyroidism
autoimmune or iatrogenic hypothyroidism
acquired hypothyroidism
immune system response results in damage and altered function of thyroid
Autoimmune hypothyroidism
Chronic lymphocytic thyroiditis (Hashimoto) affects what gender more often
females
Common comorbidities of Chronic lymphocytic thyroiditis (Hashimoto) include
Type 1 DM
Juvenile RA
Trisomy 21
can be caused by head or neck radiation therapy, surgery or induced by drugs that increase thyroxine metabolism
iatrogenic hypothyroidism
occurs in infants of mothers with Graves disease, causing a transplacental transfer of the thyroid stimulating immunoglobulin (TSI) from mother to infant
Congenital or neonatal hyperthyroidism
Autoimmune and iatrogenic causes of hyperthyroid
Acquired hyperthyroidism
most common cause of acquired hyperthyroidism resulting in an overproduction of the thyroid hormone
Graves disease
Autoimmune disorder resulting in hyperthyroid state often associated with other disorders such as type 1 DM or celiac disease - usually followed by hypothyroid after initial surge of thyroid hormone
Hashimoto thyroiditis
congenital hypothyroidism symptoms typically develop within first - weeks of life
2-6 weeks
in congenital hypothyroidism what is critical due to the risk of irreversible neurocognitive deficits if untreated
Early diagnosis
lethargy hoarse cry bradycardia large size for gestational age large fontanels constipation hypothermia jaundice dry skin elevated Free T4 elevated TSH
Congenital hypothyroidism
linear growth deceleration weight gain fatigue dry skin brittle hair muscle cramps cold intolerance delayed tooth eruption
lab studies - elevated TSH
low T4 and low free T4 levels
Acquired hypothyroidism
thyroid peroxidase antibodies
thyroglobulin antibody titers
Hashimoto Thyroiditis
congenital hyperthyroidism findings usually develop when
initial days after birth
small fontanels fever irritability tachycardia vomiting diarrhea poor weight gain despite increased feeding
birth history might be positive for IUGR or premature birth
elevated free T3 and T4
decreased TSH
Antithyroid peroxisomal antibodies may be present
congenital hyperthyroidism
diffuse enlargement of the thyroid anxiety sweating weight loss tachycardia eyelid lag or retraction, periorbital edema, exophthalmus
elevated T3 and T4
Decreased TSH
+/- antithyroid peroxisomal antibodies present
Acquired Hyperthyroidism
what imaging used to look at thyroid for initial eval of acquired hyperthyroidism
US - soft tissue of thyroid
Scintigraphy - evaluates the function of thyroid gland
radiographic testing not commonly used in screening
evaluates the function of the thyroid gland
Scintigraphy
treatment of congenital hypothyroidism
L Thyroxine Administration
life long monitoring
normalization of T4
Treatment of congenital hyperthyroidism
Methimazole or Propylthiouracil (blocks thyroid hormone stimulation
Iodine - blocks the release of thyroid hormone already synthesized
treatment of acquired hypothyroidsim
L-Thyroxine - thyroid replacement
treatment Acquired hyperthyroidism
Propylthiouracil or methimazole
radioactive iodine
surgery (some cases)
primary function of the parathyroid gland and parathyroid hormone (PTH) is to
regulate the amount of calcium present in blood and bones
in Hyperparathyroidism, excessive secretion of PTH, leads to
hypocalcemia
hypocalciuria
hypophosphatemia
hyperphosphaturia
secretion of PTH is triggered by a reduction in the serum ____ level
calcium
When released, PTH targets musculoskeletal, renal and gI systems to regulate
serum calcium levels
PTH triggers ______ bone resorption - resulting in
increased
serum calcium and serum phosphate
in the kidney, PTH stimulates the reuptake of
calcium and magnesium and increases phosphorous excretion
In the intestine, PTH activates the enzyme responsible for
Vit D Absorption -> which controls the absorption of intestinal calcium
most common congenital cause of hypoparathyroidism
DiGeorge syndrome (22q11 deletion)
autoimmune hypoparathyroidism is usually associated with ____ disease or other endocrine diseases such as adrenal insufficiency with polyglandular autoimmune syndrome type 1
Addison
ingestion of anticonvulsants causing hypocalcemia can lead to
Acquired hypoparathyroidism
primary hyperparathyroidism is associated with
multiple endocrine neoplasia syndromes or adenomas
secondary hyperparathyroidism is largely due to
hypocalcemic states associated with chronic renal failure, vit D deficiency, rickets
PTH level decreased
serum and urinary calcium decreased
Hyperphosphatemia
EKG - shortened or prolonged QTc interval
hypoparathyroidism
Hypercalcemia abd pain vomiting constipation bone pain and paresthesias renal stones HTN
elevated PTH
Hypercalcemia
Hypophosphatemia
Alkaline phosphatase normal or elevated
Primary hyperparathyroidism
Hypercalcemia abd pain vomiting constipation bone pain and paresthesias renal stones HTN
serum calcium low or normal
EKG with prolonged QTc interval
nephrolithiasis
parathyroid adenoma
secondary hyperparathyroidism
management of hypoparathyroidism
calcium and vit d supplementation
ECG monitoring
long term monitoring of dietary calcium intake
labs every 3-6 months to check: serum calcium serum phosphorous serum magnesium alkaline phosphate levels 25-(OH)D3 1.25-(OH)2D3
urine calcium to creatinine level monitoring
Management of hyperparathyroidism
aggressive hydration and diuretics
restriction of calcium and vit D intake
Hydrocortisone
calcitonin
surgical removal of parathyroid glands
Neuroendocrine tumor arising from the adrenal medulla (chromaffin cells)
can be benign or malignant
often bilat
Pheochromocytomas
associated with von Hippel-Lindau disease, multiple endocrine neoplasia type 2, familial paraganglioma syndrome or neurofibromatosis type 1
Pheochromocytomas
Sustained HTN (due to tumor associated catecholamine release)
triad (headache, diaphoresis, palpitations)
tachycardia
abnormal skin sensation
anxiety
Hyperglycemia
Pheochromocytomas
diagnosis of Pheochromocytomas
metanephrine or catecholamine levels; plasma or urine
- 24 hr urine collection
- urinary vanillylmandelic acid
- eval for causes
- CT scan: head, neck, chest, abdomen - used to localize tumor
- Scintigraphy or positron emission tomography may also be used to localize tumor
mgmt of Pheochromocytomas
HTN control
-A or B blockers may be used presurgically
-surgical resection
metastatic Pheochromocytomas requires antineoplastic therapy
a common cause of hyponatremia
SIADH
excessive release of ADH from pituitary gland
SIADH
Hyponatremia
decreased serum osmolarity and increased urine osmolarity
decreased urine output with increased urine concentration
cerebral edema may ensue in severe cases of hyponatremia
SIADH
serum sodium <135
serum osmolarity <280
urine osmolarity >200
BUN < 10
Urine sp gravity >1.020
urine sodium >25
SIADH
managing SIADH
identify and treat underlying
fluid restriction to <75% daily maintenance fluid requirement
Avoid hypotonic IV fluids
correct hyponatremia slowly by 0.5 - 1mEq/hr
for severe hyponatremia, correct to 125 with 3% Hypertonic saline
Na+ deficit = (body wt in kg) x (0.6% in extracellular fluid: ECF) x (Desired serum sodium level {125}) - Actual serum sodium level = mEq
labs for initial eval for child newly diagnosed with diabetes
CBC with diff
BMP
HA1C - >=6.5 supports diagnosis for type 2 DM
insulin level
Insulin antibodies
-islet cell antibodies
-GAD-65
C peptide
12 lead EKG
Celiac disease
thyroiditis
measures adrenal gland response to administration of ACTH
ACTH stimulation testing
how to perform ACTH stim test
obtain baseline cortisol level
30-60 min following injection, a second cortisol level is obtained
results: Cortisol levels
- <16ug/d: suggests failing or insufficient response
-18-20ug/dL is minimal response
> 30 ug/dL is a normal response
As much as ___ % of lean body mass in infants is water
70%
Children, in general, have approx ___% of lean body mass as water and an overall higher concentration of extracellular fluid than adults
60%
daily maintenance fluids for healthy children include fluid for
physiologic needs
daily output
insensible losses
dehydration is a concern for morbidity and mortality in children
< 5yrs of age
___ is generated in the process of metabolism
H2O
heat regulation requires H2O
solute excretion requires H2O
Metabolic rate (kcals/day) approximates _______
fluid requirements (mL/day)
Holliday segar method for calculating maintenance fluid requirements for 24 hr period in children
2-10kg: 100ml/kg
11-20kg: 1,000mL + 50ml/kg for each kg between 11 and 20kg
21-70kg: 1,500mL + 20ml/kg for each kg between 21 and 70 kg
calculate the total volume for 24 hrs and then divide by 24
4-2-1 method
first 10 kg: 4 mL of fluid per kg (ie) 4 kg pt = 4kg x 4 mL = 16ml/Hr)
for second 10kg- 2mL/kg
each kg over 20kg, 1 mL/hr given
BSA maintenance fluids calculation
Square root of kgxcm/3600
maintenance fluids calculation using BSA = 1,500-2000 mL/m2/day
the proper balance between water and electrolytes
hydration
conditions that alter maintenance fluid requirements
fever
tachypnea
hyperpnea
postop state
increased physical activity
diarrheal illness
altered kidney function (anuria, polyuria)
very low birth weigh infants: decreased skin integrity - surface area to weight ratio_
burns
trauma
excessive sweating
Endocrine disorders (SIADH, DI, Hyperthyroidism)
___ and ____ are involved in the dehydration and rehydration process
fluid and electrolytes
in dehydration what can usually explain changing lab values in many cases
shifts from intracellular to extracellular
_____ is released in response to the renin-angiotensin-aldosterone release in cases of extracellular volume depletion
Aldosterone
______ is released in response to volume depletion, which results in decreased urine output and increased absorption of water by kidneys
Antidiuretic hormone (ADH)
hydration status more common in young children and has classic components on physical exam
- mental status
- HR
- presence of tears
- skin condition
- cap refill
- blood pressure
- UOP
Hydration can be classified based on serum sodium levels
dehydration
Serum Sodium 130-150
isotonic dehydration
serum sodium <130
Hypotonic/hyponatremic dehydration
serum sodium >150
Hypertonic/hypernatremic dehydration
time frame to restore intracellular and extracellular water and electrolyte deficits in hyponatremic and isonatremic dehydration
24 hours
time frame to restore intracellular and extracellular water and electrolyte deficits in hypernatremic dehydration
48 hours
infants can develop _____ from incorrect mixing of formula with too much water
hyponatremia
formula to calculate volume of fluid to replace
current weight x 1,000 x %dehydration = volume of fluid to replace
the most precise method of determining fluid deficit is
weight loss, however not typical to have recent pre-illness weight results
Fluid deficit calculation
fluid deficit = pre-illness weight - illness weight
% dehydration = (pre-illness weight-illness weight) all divided by illness weight and x 100%
once fluid deficit is calculated, subtract boluses and then calculate hourly
oral rehydration fluids should have goal of replacing deficit volume over
4-6 hours, then to replace ongoing losses
IV fluid replacement in isotonic and hyponatremic dehydration
replace half of the deficit plus 1/3 of the maintenance over 8 hours
then the remaining half of the deficit and 2/3 of the maintenance over the next 16 hours
or replace the whole deficit over 8 hours then the whole day’s maintenance over 16 hours
IV fluid replacement in hypernatremic dehydration
combine the total volume deficit plus the maintenance volume for 48 hours; administer this total volume divided over 48 hours.
Prevents osmotic fluid shifts resulting in cerebral edema and seizures. Ensure serum sodium level is not corrected by ?10meq/l/d
calculation of insensible loss
300mL x BSA = approx insensible loss for 24 hours. Divide by 24 to get the hrly rate of insensible loss
daily electrolyte replacement
Sodium: 2-3 mEq/100mL fluid
Potassium: 2mEq/100mL fluid
chloride: 5-6 mEq/100mL fluid
calculation for sodium deficit
Na deficit = (135-measured Na) x 100/L
It is difficult to assess ____ electrolyte deficit as its mainly intracellular and shifts based on catabolism, cell-injury and acid base balance
Potassium
estimated that 1meq/L = 10-30% total body potassium loss
component of multisystem body functions -neuronal activity muscular contraction myocardial contraction hemocoagulation bone formation
Calcium
Calcium is present in 3 forms in plasma
bound to albumin (plasma protein)
diffusible (calcium citrate or phosphate)
unbound ion
____ calcium is the form most important for body functions
ionized
calcium concentrations is regulated by what systems
renal
skeletal
GI
serum calcium <9
ionized Calcium <1.1
hypocalcemia
serum calcium >10
hypercalcemia
ethylene glycol ingestion can lead to
hypocalcemia
PRBC transfusion can lead to
hypocalcemia _ binding of ionized calcium to citrate after transfusion
malabsorption and hypoparathyroidism can lead to
hypocalcemia
renal failure can lead to
hypocalcemia
rhabdomyolysis sepsis tumor lysis syndrome pancreatitis can lead to,,,
hypocalcemia
what medication can lead to hypocalcemia
furosemide
What syndrome is connected to hypercalcemia
Williams syndreome
what electrolyte disorder is associated with malignancy, sarcoidosis
Hypercalcemia
what medication can lead to hypercalcemia
excessive Vitamins A and D
Thiazide diuretics
what electrolyte abnormalities associated with hyperphosphatemia and hypomagnesemia
hypocalcemia
risk of hypocalcemia in neonates
increased due to decreased calcium intake
increased fetal calcium levels leading to transient parathyroid suppression
PTH resistance
Can include neuromuscular irritability, Chvostek sign, confusion, irritability, laryngospasm, muscle cramps, numbness and tingling, parasthesias and weakness, seizures, tetany, and Trousseau sign.
ECG changes include sinus tachycardia, long QT interval, and AV blocks. • Evidence of myocardial irritability with severe hypocalcemia can include hypotension and bradycardia.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 716). Wolters Kluwer Health. Kindle Edition.
Hypocalcemia
can be asymptomatic
severe ->nausea, anorexia, constipation, neurologic signs such as anxiety, depression, headache, lethargy, hypotonia, seizures, and coma. Cardiac arrhythmias include shortened QT interval, sinus bradycardia, first-degree heart block, and ventricular tachycardia.
can lead to polyuria, renal calculi and renal tubular dysfunction
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 716-717). Wolters Kluwer Health. Kindle Edition.
hypercalcemia
hypocalcemia workup
total serum calcium
ionized calcium
CMP
PTH
pH
25-hydroxy vit D
1, 25-dihydroxy vitamin D
urine calcium, phosphate, creatinine
xray of ankle and wrist for bone density
Chest x ray -looking for thymus
ECG
Hypercalcemia workup
total serum calcium
ionized calcium
CMP
PTH
pH
25-hydroxy vit D
1, 25-dihydroxy vitamin D
urine electrolytes
PTH related protein level if suspected malignancy
ECG
Abd radiographs - KUB or renal US to look for calculi
treatment for hypocalcemia
10-20mg/kg/dose calcium chloride (only give through central venous catheter)
Calcium gluconate (100mg/kg/dose) given through either peripheral or CVC
treatment for chronic hypocalcemia
enteral supplements such as calcium carbonate, citrate, calcium gluconate, glubionate, lactate, along with vit d supplements and 1, 25 dihydroxy vitamin D fo rpt unable to convert vit d
Hypercalcemia treamtent
hydrate with NS (2-3 xs maintenance rate)
-Hypercalcemia may cause increased UOP results in dehydration
-Loop diuretics - helps excrete calcium
(no thiazides - preserves calcium)
Glucocorticoids - reduce effects and level vit D
only calcitonin for rapid correction of calcium or if hypercalcemia is refractory to hydration and diuresis
Bisphosphonates for rapid treatment of severe hyperphsophatemia
if severe or refractory- hemodialysis may be needed
Hypomagnesemia may lead to
hypocalcemia
If hypocalcemia is refractory, replace
magnesium
Correct severe hyperphosphatemia prior to correction of related ______ to avoid soft tissue calcification
hypocalcemia
the major role of ______ is to maintain electrical neutrality by balancing cations (usually sodium) in the blood
chloride
regulates acid base balance in body due to inverse relationship with bicarbonate
Chloride
serum chloride normal
97-108
serum chloride <97
hypochloremia
serum chloride >108
hyperchloremia
metabolic alkalosis contributes to ____chloremia
hypochloremia
electrolyte imbalance associated with Bartter syndrome
Hypochloremia
electrolyte imbalance associated with Cystic fibrosis bulimia nervosa diuretic usage Removal of gastric secretions by ng tube permissive hypercapnia
hypochloremia
electrolyte imbalance associated with diarrhea excessive chloride administration metabolic acidosis Renal tubular acidosis urinary diversion into colon or ileum
hyperchloremia
passively follows renal sodium reabsorption and passively follows sodium absorption in GI tract
Chloride
When associated with metabolic alkalosis, may exhibit arrhythmias, decreased respiratory effort, seizures in severe states. •
When associated with volume depletion or dehydration, may exhibit thirst, lethargy, tachycardia, tachypnea, and delayed capillary refill.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 719-720). Wolters Kluwer Health. Kindle Edition.
Hypochloremia.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 719). Wolters Kluwer Health. Kindle Edition.
Often does not result in any symptoms. • May exhibit Kussmaul respirations (especially in diabetes ketoacidosis); possible neurologic symptoms include lethargy, headache, and confusion. • Altered cardiac function and response to inotropes. • Associated with hypernatremia and hyperkalemia.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.
Hyperchloremia.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.
diagnostics for hypochloremia
• Serum electrolyte evaluation and serum pH. •
Urine chloride and sodium.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.
treatment of hypochloremia
First address known causes, including fluid resuscitation, and add potassium-sparing diuretics or acetazolamide to reduce reabsorption of bicarbonate. •Chloride repletion: can be replaced with sodium, potassium, and ammonium chloride compositions. Arginine chloride or hydrochloric acid can be used for severe hypochloremia-related seizures, arrhythmias, or respiratory depression.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.
treatment for hyperchloremia
Address underlying cause and treat associated acidosis. • Consider sodium bicarbonate IV if severe metabolic acidosis.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.
chloride has a direct relationship with
sodium
chloride has a inverse relationship with
bicarbonate
about 50% of magnesium stores are contained
in bone
magnesium is primarily excreted and regulated in the
kidney
normal mag levels
1.7-2.2
GI causes of hypomagnesemia
GI losses with diarrhea, vomiting, steatorrhea, refeeding syndrome, pancreatitis.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 721). Wolters Kluwer Health. Kindle Edition.
diseases and syndromes associated with hypomagnesemia
Celiac disease, cystic fibrosis, inflammatory bowel disease, and short gut syndrome.
Bartter and Gitelman syndromes, autosomal dominant hypoparathyroidism, and mitochondrial hypomagnesemia.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 721). Wolters Kluwer Health. Kindle Edition.
renal causes of hypomagnesemia
hypercalcemia, chemotherapy, chronic adrenergic stimulants, diuretic use, hypercalciuria, nephrocalcinosis, and RTA.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 721). Wolters Kluwer Health. Kindle Edition.
Medication causes of hypomagnesemia
amphotericin, cisplatin, loop and osmotic diuretics.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 721-722). Wolters Kluwer Health. Kindle Edition.
endocrine causes of hypomagnesemia
diabetes mellitus, diabetic ketoacidosis (DKA), excessive bone uptake after parathyroidectomy, hyperaldosteronism, and PTH disorders.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.
causes of hypermagnesemia
Excessive intake, including magnesium-containing laxatives or antacids, total parenteral nutrition, maternal magnesium therapy in neonates. • Altered renal function, renal failure, tumor lysis syndrome, milk alkali syndrome, and lithium ingestion.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.
neonates may experience transient hypomagnesemia or develop idiopathic hypomagnesemia associated with
maternal magnesium depletion
GI symptoms of hypomagnesemia
anorexia
nausea
vomiting
Neuro symptoms of hypomagnesemia
depression, malaise, nonspecific psychiatric symptoms, hyperreflexia, seizures, paresthesias, ataxia, tetany, decreased deep tendon reflexes, weakness, paralysis, muscle weakness, delirium, carpopedal spasm, and clonus.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.
Cardiac symptoms of hypomagnesemia
ECG changes - atrial or ventricular ectopy, torsades de pointes and long QT interval
endocrine symptoms of hypomagnesemia
Hyperglycemia can occur if hypomagnesemia is related to insulin resistance.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.
Neuro s/s of hypermagnesemia
impairment of the neuromuscular junction; hypotonia, decreased deep tendon reflexes, weakness, paralysis, CNS depression, lethargy, and confusion.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
cardiac s/s hypermagnesemia
altered vascular tone, hypotension, flushing, possible ECG changes (prolonged PR, QRS, or QT intervals), heart block.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
GI s/s hypermagnesemia
abdominal cramping, nausea, and vomiting.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
resp symptoms hypermag
resp failure
hypo mag workup
serum laboratory studies; basic metabolic panel with magnesium and ionized calcium; ECG and arrhythmia monitoring.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
hyper mag workup
serum laboratory studies; basic metabolic panel with magnesium and ionized calcium; ECG and arrhythmia monitoring.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
management of hypomagnesemia
• Severe, acute management. • Magnesium sulfate or magnesium chloride. •
Consider potassium repletion, particularly if refractory. •
Mild, subacute management. • Magnesium gluconate, oxide, or sulfate.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
management of hypermagnesemia
Cessation of magnesium intake. • Monitoring of renal function and support of cardiovascular and respiratory function. • Parenteral calcium supplements (calcium chloride or calcium gluconate) for heart block. •Removal of magnesium with volume expansion, forced diuresis, loop diuretics, dialysis if life-threatening or exchange transfusion if life-threatening and unable to perform dialysis.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.
hypomagnesemia may result in refractory
hypokalemia
A rapid increase in serum mag r/t rapid bolus may cause
increased mag excretion -> give it slow
if torsades de pointes on ECG, give
magnesium
phosphorous absorbed through
jejunum
phosphorous excreted through
kidneys
normal phosphorous
2.5-4.1
what vit def can cause hypophosphatemia
Vit D def and Vitamin D-resistant rickets
causes of hypophosphatemia
Malnutrition or starvation situations such as protein energy malnutrition or malabsorption, respiratory or metabolic alkalosis. • DKA treatment without adequate repletion. • Corticosteroid use. • Renal tubular defects or diuretic use. • Vitamin D deficiency and vitamin D-resistant rickets. • Reduced intake/supplementation in very low-birth-weight infants. • Chronic use of aluminum-containing antacids. • Tumor-induced osteomalacia resulting in renal phosphorus wasting. • Extensive burns. • Hyperparathyroidism.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 724-725). Wolters Kluwer Health. Kindle Edition.
causes of hyperphosphatemia
Excessive administration or intake. • Tumor lysis syndrome. • Hypoparathyroidism. • Rhabdomyolysis. • Renal failure when decreased glomerular filtration rate <25% or smaller glomerular filtration rate reductions in neonates. Pathophysiology
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 725). Wolters Kluwer Health. Kindle Edition.
A sudden increase in serum phosphorus may result in precipitation of
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 725). Wolters Kluwer Health. Kindle Edition.
calcium, thus resulting in symptoms of hypocalcemia such as tetany.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 725). Wolters Kluwer Health. Kindle Edition.
s/s hypophosphatemia
Neurologic signs of confusion, irritability, coma, muscle weakness, paresthesias, seizures, and apnea in very low-birth-weight infants. • Hemolytic anemia. • Hypoxia. • Impaired granulocyte activity. • Thrombocytopenia. • Rhabdomyolysis. • Myocardial depression. • Rickets.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 725-726). Wolters Kluwer Health. Kindle Edition.
s/s hyperphosphatemia
Altered mental status, seizures. • Tetany, weakness, paresthesias. • Fatigue. • Cramping. • Laryngospasm. • Neuromuscular irritability. • Cardiac arrhythmias. • Chronic hyperphosphatemia may result in calcium deposits in soft tissue.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.
diagnostic hypophosphatemia
Serum: basic metabolic panel, phosphorous, magnesium and ionized calcium, vitamin D levels, and PTH. • Urine: calcium, phosphorous, creatinine, pH.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.
diagnostic hyperphosphatemia
• Serum: basic metabolic panel, ionized calcium, phosphorous and magnesium, PTH, vitamin D, complete blood count, and arterial blood gas. • Urine: calcium, phosphorous, creatinine.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.
treatment for hypophosphatemia
Acute. • Parenteral repletion is indicated with potassium or sodium phosphate. • Subacute or gradual onset of symptoms. • Replace with potassium or sodium phosphate enteral supplements.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.
treatment for hyperphosphatemia
restrict dietary intake of phosphorus (protein restriction). • Phosphate binders which include sevelamer hydrochloride, lanthanum carbonate, calcium carbonate, or aluminum hydroxide. • If cell lysis with normal renal function, forced diuresis with NS and osmotic diuretic such as mannitol. • Consider dialysis if severe and underlying poor renal function; dialysis may be of limited effectiveness.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 726-727). Wolters Kluwer Health. Kindle Edition.
risk of calcium-phosphorous precipitation particularly with
tumor lysis syndrome or renal failure
______ is important in potassium regulation by the kidney
aldosterone
Serum potassium normal
3.7-5.2
medications that can cause hypokalemia
amphotericin B, decongestants, diuretics, dopamine, dobutamine, and bronchodilators.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 728). Wolters Kluwer Health. Kindle Edition.
causes of hypokalemia
Medications: amphotericin B, decongestants, diuretics, dopamine, dobutamine, and bronchodilators. • Anorexia nervosa. • Bartter and Cushing syndromes. • Fanconi, Liddle, and Gitelman syndromes. • Hematologic: leukemia. • GI: diarrhea, use of laxatives and enemas, and vomiting. • Endocrine causes: DKA, hyperaldosteronism, increased insulin levels, and excess mineralocorticoid. • Renal: increased renin levels, renovascular disease, metabolic alkalosis, and type I RTA. • Magnesium depletion and malnutrition.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 728). Wolters Kluwer Health. Kindle Edition.
causes of hyperkalemia
Acidosis, acute increase in serum osmolarity. • Addison disease, aldosterone insensitivity, hypoaldosteronism, pseudohypoaldosteronism, and associated aldosterone resistance. • Medications: angiotensin II receptor blockers, ACE inhibitors, theophylline, and nonsteroidal anti-inflammatory drugs. • Congenital adrenal hyperplasia. • Trauma: crush injury. • Excess supplementation. • Rhabdomyolysis. • Tumor lysis syndrome. • Renal impairment or RTA. • Spitzer–Weinstein syndrome. •Technical problems in obtaining a blood sample can result in hyperkalemia if the blood is hemolyzed, if there is existing thrombocytosis, or leukocytosis at the time of serum sample, or if the child has received blood that has been stored for a long time.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 728-729). Wolters Kluwer Health. Kindle Edition.
s/s hypokalemia
Often, no symptoms. • Diastolic dysfunction, hypertension, or ventricular arrhythmias in patients with heart disease, heart failure, or left ventricular hypertrophy. •ECG changes can include delayed depolarization, flat or absent T waves, long QT, prolonged QRS, ST changes, and the presence of U waves. • Cramping. • Decreased perfusion. • Fatigue. • Ileus. • Impaired insulin release. • Impaired muscle contraction, paralysis. • Polyuria.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 729). Wolters Kluwer Health. Kindle Edition.
s/s hyperkalemia
ECG changes: most commonly peaked T waves, low-voltage P waves, prolonged PR and QRS interval, ST changes, AV block, ventricular tachycardia and fibrillation, loss of PR interval, merging of QRS, and T waves to produce a sine wave pattern, asystole. • Neurologic: muscle weakness, paresthesias, and tetany with severe hyperkalemia (≥9 mEq/L).
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 729-730). Wolters Kluwer Health. Kindle Edition.
diagnostics hypokalemia
• Serum: basic metabolic panel with magnesium, creatine kinase, renin, pH, and cortisol levels. • Urine studies: urinalysis, electrolytes, osmolality, and urine 17-ketosteroids. • ECG.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 730). Wolters Kluwer Health. Kindle Edition.
diagnostics hyperkalemia
Serum: basic metabolic panel with magnesium, creatine kinase, renin, pH, and cortisol levels. • Urine studies: urinalysis, electrolytes, osmolality, and urine 17-ketosteroids. • ECG.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 730). Wolters Kluwer Health. Kindle Edition.
treatment of hypokalemia
• Identification of cause. • Potassium repletion. • Acute, risk for arrhythmia. • Calculate electrolyte deficiency to minimize risk of hyperkalemia with treatment. • Potassium chloride 0.5 to 1 mEq/kg/dose IV; maximum 20 mEq/dose; central administration is preferred and cardiac monitoring required. • Subacute, chronic repletion. • Potassium chloride, phosphate, or bicarbonate enteral supplement, based on etiology.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 730). Wolters Kluwer Health. Kindle Edition.
treatment for hyperkalemia
• Evaluate for accuracy of the laboratory sample (may be falsely elevated with hemolysis, thrombocytosis, or leukocytosis). • Remove all exogenous potassium sources. • Hyperkalemia with ECG changes. • Administer calcium chloride or calcium gluconate IV for membrane stabilization. • Administer IV insulin and glucose (e.g., D25 or D50), IV sodium bicarbonate, inhaled β-agonists (e.g., albuterol); all temporarily shifts potassium intracellularly. • Diuretics, if normal renal function (results in potassium removal). • Cation exchange resin, such as sodium polystyrene sulfonate (exchanges potassium for sodium in the GI tract, resulting in potassium removal).
dialysis
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 730-731). Wolters Kluwer Health. Kindle Edition.
Potassium should be interpreted in relation to the serum pH. Why
bc it shifts intracellularly with alkalosis and extracellularly with acidosis
Severe ___kalemia is a medical emergency
hyperkalemia >7
normal Na
135-145
hypervolemic hyponatremia is caused by
• Congestive heart failure. • Renal failure. • Nephrotic syndrome. • Water intoxication. • Cirrhosis.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 732). Wolters Kluwer Health. Kindle Edition.
hypovolemic hyponatremia is caused by
Renal losses through osmotic diuresis or RTA. • Extrarenal losses through diarrhea, vomiting, burns, or pancreatitis.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 732). Wolters Kluwer Health. Kindle Edition.
normovolemic hyponatremia is caused by
SIADH, adrenal insufficiency. • CNS diseases: cerebral salt wasting, meningitis, intracranial tumors. • Pulmonary disease: cystic fibrosis. • Diuretic use.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 732). Wolters Kluwer Health. Kindle Edition.
• Rapid decrease in serum sodium level is associated with more severe symptoms. • Irritability, poor feeding, nausea, lethargy, seizures, coma, seizures. • Can lead to cerebral edema.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 734). Wolters Kluwer Health. Kindle Edition.
Acute hyponatremia
Weakness, lethargy, decreased deep tendon reflexes, fever, high-pitched cry, irritability, muscle cramps, rhabdomyolysis, renal failure, respiratory failure, altered mental status, seizures.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 734). Wolters Kluwer Health. Kindle Edition.
acute hypernatremia
workup for hypo/hypernatremia
Serum: sodium and osmolality. • Urine: sodium, specific gravity, and osmolality.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 734). Wolters Kluwer Health. Kindle Edition.
treatment for hyponatremia
Identify and treat cause of hyponatremia. • Restore normal intravascular volume. • Replete sodium deficit. • Serum sodium correction must be done in a slow, controlled manner to avoid central pontine myelinolysis. • Goal rate of sodium rise is 2 to 4 mEq/L every 4 hours or 10 to 20 mEq/L in 24 hours. • If seizures are present, goal is to raise serum sodium acutely to 125 mEq/L for seizure cessation. • Hypertonic saline solution; NS bolus 20 mL/kg may be administered if hypertonic saline is not available. • Hypertonic saline is calculated based on this formula: mEq sodium to raise sodium to desired level. • 0.6 × (Weight in kg) × (target sodium − measured sodium).
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 734-735). Wolters Kluwer Health. Kindle Edition.
Treatment for hypernatremia
•Avoid decreasing serum sodium more than 15 mEq/L in 24 hours to minimize risk for cerebral edema or no faster than 0.5 to 1.0 mEq/L/hour. • Therapy is guided by a combination of sodium level and serum osmolarity, and intravascular volume status. • Hypernatremic, hypovolemic dehydration. • Calculation of free-water deficit, solute fluid deficit, solute sodium deficit, solute potassium deficit, maintenance fluid requirements, and ongoing losses determines composition of IV fluids and rate of administration. • Hypernatremic, hypervolemic dehydration. • May require natriuretic agent for increased weight.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 735). Wolters Kluwer Health. Kindle Edition.
reported sodium concentrations may be low in association with
hyperlipidemia
hyperproteinemia
hyperglycemia
who is at a increased risk for hypernatremia and associated hypovolemic dehydration
infants small children developmental delay hx AMS critical illness rendering them unable to respond to thirst mechanism
a serum level of
<125
hyperkalemia - what on ECG
peaked T waves
ventricular arrhythmias, prominent u waves, ST segment depression
hypokalemia
electrolyte imbalances that can cause seizures
Hyponatremia Hypernatremia Hypophosphatemia Hypochloremia Hypocalcemia Hypercalcemia
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 736). Wolters Kluwer Health. Kindle Edition.
Ventricular ectopy, torsades de pointes
hypomagnesemia
Hypotension
AV block
hypermagnesemia
Long QT interval
AV block
hypocalcemia
electrolyte abnormality associated with eating disorders
chloride responsive metabolic alkalosis and significant hypophosphatemia
eating disorders carry risk for cardiac arrhythmias due to electrolyte abnomalities
abnormalities: depletion of total body potassium, hypomagnesemia, serum hypophosphatemia, and altered acid–base balance.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 737). Wolters Kluwer Health. Kindle Edition.
evaluating degree of malnutrition in eating disorders
serum complete metabolic panel, carotene levels, zinc, copper, prealbumin, amylase and lipase, cholesterol, and liver function tests.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 738). Wolters Kluwer Health. Kindle Edition.
analysis for fluid and electrolyte evaluation
BMP or CMP
indicate dehydration but not predictive alone
BUN
serum bicarb levels of ____, along with clinical findings of moderate to severe dehydration
<17
serum bicarb levels of ____, associated with high risk of failing oral rehydration therapy
<13
normal chloride levels
98-108
normal k
3.5-4.5
what does CMP include
electrolytes - sodium, potassium, chloride, carbon dioxide, BUN, creatinine, magnesium, phosphorous, LFTs (AST or SGOT and SLT or SGPT), bilirubin level, serum total protein and alkaline phosphatase
pH of < ____ with normal PCO2 and normal or low bicarbonate may indicate dehydration
7.35
Urinalysis: dark color, high specific gravity and presence of ketones can indicate
dehydration
urine electrolytes: if Na+ is low, kidneys may
be conserving sodium due to dehydration
fractional excretion of sodium assists in differentiating
between dehydration and poor kidney function
What would a CBC show in dehydreation
elevated RBC, WBC or both
most metabolic disorders are inherited as
autosomal recessive traits
a group of disorders that result in abnormalities in the synthesis or catabolism of proteins, carbohydrates, or fats.
Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 753). Wolters Kluwer Health. Kindle Edition.
Genetic metabolic disorders
Acute finding vs chronic findings of inborn errors of metabolism
Seizures/lethargy/coma
Hypotonia
Acute finding vs chronic findings of inborn errors of metabolism
Poor feeding/vomiting
FTT
Acute finding vs chronic findings of inborn errors of metabolism
Hypoglycemia
Recurrent unexplained illnesses
Acute finding vs chronic findings of inborn errors of metabolism
Signs of sepsis
Developmental delay/loss of milestones
Acute finding vs chronic findings of inborn errors of metabolism
Hyperammonemia
Cardiomegaly
Acute finding vs chronic findings of inborn errors of metabolism
ketosis
macro/microcephaly
Acute finding vs chronic findings of inborn errors of metabolism
Metabolic/lactic acidosis
Eyes/hair/skin abnormalities
Acute finding vs chronic findings of inborn errors of metabolism
abnormal urine odor
“course” appearance”
Urine odors associated with IEM
Maple Syrup
Maple syrup urine disease
Urine odors associated with IEM
Musty
Phenylketonuria
Urine odors associated with IEM
sweaty feet
Isovaleric/Glutaric acidemia
Urine odors associated with IEM
Boiled cabbage
Tyrosinemia
Urine odors associated with IEM
Fishy
Trimethylaminuria
Metabolic labs
what do you grab first when you have a suspicion
if anything is positive then what do you snag
CBC Blood gas Serum glucose (looking for hypoglycemia) Serum electrolyte panel (look at anion gap) Liver function tests Ammonia (look for hyperammonemia)
Urinalysis Urine pH urine color and specific gravity odor urine ketones
then
Plasma amino acids
Acylcarnitine profile
lactate
urine amino acids
urine organic acids
urine reducing substances
what tests can be done for glucocorticoid excess
24 hr urinary free cortisol
midnight salivary or plasma cortisol
overnight low dose dexamethasone suppression test
tests for adrenal insufficiency
8AM plasma cortisol and ACTH concentration
Low dose ACTH stim test
High dose stim test
Metyrapone test
Serum renin level
Aldosterone level
Test for congenital Adrenal hyperplasia
High dose ACTH stim test
17-hydroxyprogestrone
Cyp21 analysis
tests for calcium homeostasis
Total calcium
ionized calcium
parathyroid hormone
PTH-related protein
Urine Calcium: Creatinine ratio
Test for Vit D status
25-OH
1-25 (OH) 2D
Markers of bone turnover
Osteocalcin
bone specific alkaline phosphatase
N-telopeptides
tests for water homeostasis
serum and urine osmolality
urine sp. gravity
water deprivation test
vasopressin challenge
serum vasopressin levels
tests for autoimmune thyroid disease
TSH
Thyroid receptor antibody (TRAb)
Antithyroglobulin (ATG)
Thyroid peroxidase antibodies (TPO)
from 2 years of age until puberty approx __ -___cm linear growth/year is considered normal
4-5
mid-parental height calculation: Target height
male: {paternal height +maternal height}/2 +5cm
females same just minus 5 cm
if I want to look at ambiguous genitalia what radiographic study?
US
if I want to look at thyroid nodules what radiographic study?
US
if I want to look at pituitary tumors what radiographic study?
CT or MRI
if I want to look at osteoporosis or osteomalacia what radiographic study?
Plain film or DEXA scan
tanner staging male
early adolescence (10.5-14 yrs)
no pubic hair
preadolescent penis
prepubescent testes
Tanner 1
tanner staging male
early adolescence (10.5-14 yrs)
scanty pubic hair
penis - slightly increased in size
enlarging testes
Tanner 2
tanner staging male
middle adolescence (12.5-15 yrs)
pubic hair - darker with curls
longer penis
larger testes
Tanner 3
tanner staging male
middle adolescence (12.5-15 yrs)
pubic hair - course and curly
larger penis
scrotum darkens
Tanner 4
tanner staging male
late adolescence (14-16 yrs)
pubic hair - adult
adult penis
scrotum adult
Tanner 5
tanner staging female
early adolescence (10-13 yrs) preadolescent pubic hair preadolescent breasts
Tanner 1
tanner staging female
early adolescence (10-13 yrs)
sparse, straight pubic hair
small mound breasts
Tanner 2
tanner staging female
middle adolescence (12-14 yrs)
dark curls pubic hair
breasts - larger with no overt contour separation
tanner 3
tanner staging female
middle adolescence (12-14 yrs)
course and curly pubic hair
breasts - secondary mound of areola
tanner 4
tanner staging female
late adolescence (14-17 yrs)
pubic hair adult triangle shape appearance
breasts - Nipple projects, areola becomes a part of the breast
tanner 5
what type of AI is a result of a destroyed or inactive adrenal gland or hormone production failure
Primary AI
in infancy, what is the most common cause of primary AI
CAH
what type of AI is associated with a deficiency of ACTH
Secondary AI
hypothalamic decrease in CRH secretion or production is what type of AI
Secondary AI
hypopituitarism secondary to primary pituitary disease, congenital pituitary lesions and developmental anomalies (ancephaly, holoprosencephaly, and craniopharyngiomas are the causes of ACTH deficiency).
what are the most common reason for ACTH deficiency in childhood
Craniopharyngiomas
Secondary AI
hypothalamic decrease in CRH secretion or production falls under what type of AI
most often from suppression of the HPA axis from prolonged use of glucocorticoids
Tertiary AI
drugs that associated with tertiary AI
Glucocorticoids
spironolactone
etomidate
ketoconazole
HPA axis may not return to normal for up to how long after long term steroid treatment
more than 1 month
what type of AI is experienced to some degree by every critically ill pt
relative AI
If a child is responsive to fluids in shock, what is their AI status
absent
explain neonatal adrenal insufficiency
infant HPA axis is immature
further limit infants ability to increase cortisol production in response to stress
cortisol level that suggests AI
<16 ug/dl or <440 nmol/L
