Hypernatremia Flashcards
How does ADH respond to volume hypertonicity?
ADH release is more sensitive to small changes in plasma tonicity than small decreases in EABV
however, it is exponentially stronger when changes in EABV are greater
symptoms of hypertonic hypernatremia
recognized as a SNa above 145 mEq/L, symptoms become obvious around 160 mEq/L
seizures
coma
somnolence
lethargy
thirstiness
What effect does hypertonicity have on cells?
produces cellular dehydration, unlike isotonic volume depletion
In the absence of ADH, how does volume depletion or decreased renal solute load affect H2O diuresis?
impairs H2O diuresis
What are the ways to develop hypertonic hypernatremia?
hypertonicity is almost always associated with some reduction in TBW
hypertonic salt infusion
persistent H2O losses not replaced by intake
What are the categories of hypertonic hypernatremia?
hypertonic Na gain
polyuric (increased CefH2O)
non-polyuric (decreased CefH2O)
What are the classifications of polyuric hypernatremia?
solute diuresis
pure H2O diuresis
What are the categories of pure H2O diuresis?
central diabetes insipidus
nephrogenic diabetes insipidus
What are the common causes of acute hypertonic Na gain?
drinking sea water
hypertonic feeding
hypertonic enemas
receiving 3% NaCl
receiving NaH2CO3
primary aldosteronism
What is the mechanism of acute hypertonic Na gain?
acute exposure to hypertonic Na solutions will result in a shift in TBW from ICF to ECF
results in brain shrinkage, cerebral blood vessel tears
limbic demyelination
elevation of EABV, and acute pulmonary edema
What are the common causes of non-polyuric hypertonic hypernatremia?
hypodipsia
fever
sweating
vomiting
diarrhea
cathartics
insensible daily losses
~500 mL/day/m2 or 800mL/day for a 70 kg person of which 60% is through the skin and 40% through respiration
fever and sweating produce greater hypotonic losses of about 1-1.5 L/day including ~20 mEq/L of Na and ~10 mEq/L of K
What are the mechanisms of non-polyuric hypertonic hypernatremia?
hypodipsia - lack of thirst or access to water
gastrointestinal losses - hypotonic losses
failure to replase H2O - leaves patient dehydrated, some oliguria due to high ADH
What urine output suggests polyuria? How is urine volume calculated?
greater than 3L/day
Urinve V = [solute excretion (mOsms)/day] / [average urine mOsms/L/day]
What is the conversion between calories/protein and renal solute load?
100 Calories = ~20 mOsm/day of renal solute
10 grams of protein/day = ~50 mOsm of urea/day
pure water diuresis
produces a urine osmolarity of ~200 mOsm/L
often in the range of 150-200 mOsm/L because as urine flow rate increases, there is less tubular time to remove solutes like NaCl
solute diuresis
produces a urine osmolarity of ~300-350 mOsm/L because as urine flow rate increases there is less tubular time to remove H2O
urine losses are relatively H2O rich leaving the residual TBW hypertonic
mechanisms of solute diuresis
excess H2O in the urine due to solute such as glucose
additional H2O reduces Na concentration and transport out of tubule
increased tubular flow rate increases and washes out intersitial gradient
relative electronegativity from Na uptake facilitates K+ loss
hypotonic loss of renal H2O raises the tonicity of the residual TBW, and thirst ensues
if access to H2O is restricted, hypernatremia worsens
What are the common causes of central diabetes insipidus?
alcohol
pituitary tumors
post-surgery
trauma
cysts
granulomatosis
pregnancy
meningoencephalitis
genetic mutations - ADH
What is the mechanism of central diabetes insipidus?
fewer ADH-producing neurons recues the the amount of ADH produces in response to increases in plasma osmolality
urine osmolality cannot be increased as a result
causes of nephrogenic diabetes insipidus
hypercalcemia
hypokalemia
renal disease - MCD, SCD
drugs - lithium, V2RA, methoxyflurane, amphotericine B
genetic mutations - X-linked V2R and AD AQP2
H2O deprivation test int he setting of polyuria
if SNa is > 145 mEq/L and the Uosm is less than the Posm, primary polydipsia can be excluded
start the test in the morning after 2-3 hours of fasting
measure UV, Uosm, and weight every hours, and SNa and Posm every 2 hours
continue test until either 1) the Uosm >600 mOsm/L, 2) the Uosm is stable on 2-3 hourly measurements despite a rising Posm, or 3) the Posm >295 or the SNa > 145 mEq/L
In the H2o deprivation test, how does central diabetes insipidous respond to desmopressin?
Uosm rises > 100%
In the H2o deprivation test, how does partial central diabetes insipidous respond to desmopressin?
Uosm rises 15-50% (>300 mOsm)
In the H2o deprivation test, how does nephrogenic diabetes insipidus respond to desmopressin?
no increse in Uosm
In the H2o deprivation test, how does partial nephrogenic diabetes insipidus respond to desmopressin?
small rise in Uosm (<300 mOsm)
Treatment for acute Na intoxication with neurologic symptoms
administration of H2O as D5W
if the exposure is within 24 hours then the goal is to correct SNa to 145 mEq/L to minimize risk of cerebral shrinkage and limbic demyelination
if the exposure is longer than 40 hours, the SNa should not fall faster than 10 mEq/L/day to avoid cerebral edema
if there is pulmonary edema, diuretics should be used
estimation of target water deficit
current TBW x [SNa/(140-1)]
TBW in men is 0.6 lean body weight, 0.5 in women, and 0.45 in elderly
What is the equation to correct SNa for a higher serum glucose?
Correction = SNa + {[(Glucose - 100)/100] x 2 mEq/L}
How do you treat hypernatremia that results from sweating, gastrointestinal losses, or solute diuresis?
0.45% saline with potassium
equation describing rate of fall in SNa from a 1L infusion
[(infused Na + infused K) - SNa]/(TBW + 1)
treatment of central diabetes insipidus
treat acutely with2 mcg desmopressin intravenously every 12 hours, and when the polyuria resolves and the patient is able, the patient can be switched to intranasal desmopressin
treatment of nephrogenic diabetse insipidus
can be partially treated with a combination of low Na/low protein diet, thiazide diuretics, and NSAIDs
