Sodium + Water Flashcards
What are the features of hyponatramia in the setting of vomiting?
Metabolic alkalosis, hypovolaemia and hypochloraemia.
Give fluids - Losses related to vomiting typically lead to a discordance between urine sodium and urine chloride. A low urine chloride level is consistent with a chloride-responsive metabolic alkalosis.
45 yo woman with alcohol related cirrhosis comes in with weakness
Diuretics.
Drinking 4-6 beers per day
Na: 124
K: 2.8
Osmo: 258
Urinary Na: 30
Urinary Osmo: 320
What is the appropriate treatment of her hypernatraemia?
Oral potassium chloride.
- Plasma osmolality is affected by the exchangeable potassium pool
Plasma osmolality is proportional to 2(exchangeable Na pool) plus 2(exchangeable K pool) divided by the total body water.
In hypokalaemia, intracellular potassium stores shift to the serum and sodium move into the cells to maintain the elctroneutrality.
The administration of potassium chloride in this setting will directly increase the plasma osmolality. In addition, potassium will shift into cells in exchange for intracellular sodium. By entering the cells, potassium and chloride will increase the intracellular osmolality and cause water to move into cells from the extracellular compartment. Both of these mechanisms will result in an increase in the plasma osmolality and sodium concentration.
High Solute Intake can lead to polyuria.
How do you calculate daily urinary solute?
Measured urine osmo x Urine volume
For example
267 mOsm/kg x 6L/d = 1602mOsm/d
Typical daily solute is roughly 600- 900 mOsm/d so this patients intake is 2-3 times normal.
A solute diuresis should be considered when urine osmo is >300 or urinary solute excretion is > 1000
For this question I looked at urine urea nitrogen 32g/24 hours. Divide this by 16 and multiple by 100 so she is consuming 200 g per day of protein
What is the differential for polyuria?
What is the first step in evaluating polyuria?
Central DI
Nephrogenic DI
Primary polydipsia
Solute diuresis
- Need to determine is there a water diuresis or a solute diuresis by calculating the daily excretion of osmoles
Urine osm x 24 hr urine volume = total daily osmoles
If daily solute generation is < 600mOsm polyuria represents a water diuresis
If >1000mOsm it is the result of a solute diuresis
- Next need to distinguish primary polydipsia from DI
Polyuria with dilute urine is an appropriate response to primary polydipsia. Patients with primary polydipsia have serum Na levels in the low end of normal range and may even develop hyponatraemia.
Regardless - best to do a water deprivation test.
Water deprivation test is performed to determine whether hyperosmolality can stimulate endogenous vasopressin to produce concentrated urine. i,.e vasopressin = ADH; will increase the amount of free water that is reabsorbed.
Baseline data, including body weight, serum sodium, serum osmolality, and urine osmolality, are obtained. Then urine volume and body weight are measured hourly, and serum sodium, serum osmolality, and urine osmolality are measured every 2 hours. This process is continued until the urine osmolality reaches a plateau or serum osmolality exceeds 300 mOsm/kg.
- Trial of desmopressin, only to distinguish between types of DI ( If DI were suggested by water deprivation test)
Increase of urine osmo after desmopressin to > 600 = central DI
400- 600 = Incomplete nephrogenic response
If urine osmolality does not increase to greater than 400 then it is a nephrogenic DI
What is copeptin
Copeptin, a component of the precursor protein from which AVP is derived, is emerging as a more reliable marker to distinguish partial central DI from partial nephrogenic DI or primary polydipsia.
v high if nephrogenic DI
high in primary polydipsia
<4.9 = central DI
76 yo NH resident - Drinks served with every meal. On lithium in the past Na: 153 Serum osmo: 315 Urine Na: 132 Urine osmo: 852
What test should you do?
- Vasopressin level
- Water deprivation test
- 24 hour urine urea
- Serum glucose level
- MRI of brain
Ans: MRI B
Patient has hypernatraemia + hyperosmolality with an appropriately high urine osmolality. The urine osmo is a functional assay for vasopressin and confirms that vasopressin is activated
Hypernatraemia is unusual in individuals who are mobile + able to access fluids because thirst is a powerful stimulus. The most likely explanation is hypodipsai - he should have brain imaging to look for a hypothalamic lesion.
77 yo woman smoker. Fell. On a thiazide. Now confused. Na is 108
Weight is 55, euvolaemic on exam
Osmo: 226
Urinary Na: 60
K: 82
Osmolality: 368
After stopping her thiazide what is the best next step?
3% saline at 50mL/hr for 6 hours…
3% saline at a low infusion rate is the most appropriate initial fluid management for this woman with severe, symptomatic hyponatremia.
The high urinary osmo implies ADH activity while the relatively high urinary Na conc implies activity of the thiazide diuretic.
Although hyponatremia represents a state of relative water excess compared with sodium, acute therapy is based on the addition of solute, usually as an infusion of sodium-containing solutions, rather than the removal of water, which occurs subsequently as the solute load is excreted in the urine.
One strategy to accomplish this correction safely uses the following formula:
Vol-inf = Δ[Na] × TBW/(inf Na + K)
- Vol-inf represents the infusate volume necessary to correct plasma sodium by the incremental goal or desired change in the sodium concentration.
- Δ[Na] represents the desired change in sodium concentration.
- TBW represents total body water (0.5 × body weight in kg for an older woman).
- Inf Na + K represents the sum of the sodium and potassium concentrations in the infusate.
In this case, the Δ[Na] is 6 mEq/L. Therefore, for 3% saline, Vol-inf = 6 × (0.5 × 55)/513 = 0.32 L.
Thus, an infusion of 3% saline at 50mL/h for 6 hours would accomplish the goal to increase the sodium concentration by 6 mEq/L. Because 3% saline has a [Na + K] of 513 mEq/L, which exceeds the urine [Na + K] of 182 mEq/L, there is no risk of worsening the hyponatremia with this fluid.
45 yo w hyponatraemia BPAD on lithium thiazide Euvolaemic Na: 121 Serum osmo 262 Urine osmo 90 Urine volume = 8L/24 h
What is causing hyponatraemia?
- Low solute diet
- Primary polydipsia
- Nephrogenic DI
- Thiazide induced hyponat
- SIADH
Primary polydipsia.
You are urinating appropriately dilute urine ( complete suppression of ADH). Body is trying to get rid of the water without losing electrolytes
How does lithium lead to nephrogenic DI?
Lithium entering the tubular lumen via glomerular filtration can re-enter principal cells in the cortical collecting duct via the epithelial sodium channel (ENaC). After gaining entry to the principal cells, lithium inhibits translocation of aquaporin-2 and impairs free water reabsorption. Patients with lithium-mediated nephrogenic DI who are still receiving lithium may benefit from amiloride, which blocks lithium reuptake into principal cells.
Causes of pseudohyponatraemia?
Be careful of this - supposedly low serum Na, and high - normal serum osmolality i.e. 296
Extreme elevation in plasma proteins ( plasma cell dyscrasias)
Triglycercides ( as well as lipemic serum)
Total cholesterol + lipoprotein X ( as with obstructive jaundice)
How do you calculate free water deficit?
0.6 x weight (kg) x ( (serum na/ 140)- 1)
How do you correct Na for hyperglycaemia
The correction factor for sodium concentration is 1.6 mmol/L for every 100mg/dL increase in glucose concentration above normal
Euvolaemic hypo- osmolar hyponatraemia in a patient with GPA
Urinary osmo is >500
SIADH from cyclophosphamide
54 year old eval. for postural dizziness on cisplatin for ovarian cancer. She has postural hypotension + tachycardia. Na: 128 Serum osmo: 268 Urinary Na: 94 Urinary osmo: 440 Whats the diagnosis?
Ans: Salt wasting nephropathy
NOT SIADH.
Key is features of bolume depletion.
Salt wasting after cisplatin exposure has been reported in up to 10% of patients treated with this agent.
SIADH: Euvolaemia or mild hypervolaemia High urinary Na High urinary Osmo Low urinary volume
Salt wasting nephropathy: Hypovolaemia High urinary Na High urinary osmo High urinary volume.
Pregnant patient
On lithium in the past
Queried recent injury in an RTA
has polydipsia, polyuria and dilute urine.
Urine osmolality does not improve with fluid restriction but does after receiving desmopressin.
What is the best explanation for this patient’s polyuria?
Ans: Gestational diabetes insipidus
Gestational DI is a rare form of DI that occurs when ADH is synthesized and released normally but is degraded by placental vasopressinase, preventing it from reaching its site of action at the collecting tubule. Vasopressinase metabolism is hepatic, so liver impairment due to pregnancy-related disorders such as preeclampsia and the hemolysis, elevated liver function tests, and low platelets (HELLP) syndrome or preexisting liver disease predispose to gestational DI, as does a multiple-gestation pregnancy. Presentation is during the third trimester and gradual resolution over several weeks postpartum is the usual course. Treatment with desmopressin, which is resistant to degradation by vasopressinase, is effective at controlling symptoms while awaiting resolution.
Central DI would improve with exogenous vasopressin and desmopressin. Whereas if they dont respond to vasopressin its gestational DI
