Sodium Flashcards
1
Q
Hypovolemic Hypotonic Hyponatremia
Treatment
A
- Correct the hypovolemia by minimizing losses and reversing it by giving 0.9% NaCl (normal saline) which will correct the hyponatremia “automatically”
- Hypertonic saline (like 3% NaCl) in CSWS and marathon runners
- Fludrocortisone in CSWS
2
Q
Hypertonic Hyponatremia
Treatment
A
Treat the hyperglycemia
3
Q
Euvolemic Hypotonic Hyponatremia
Work up
A
- Serum osmolality less than 280 mEq/L
- Iso or euvolemic on clinical assessment
- Measure ADH, thyroid function tests, cortisol levels
- Measure serum uric acid too because it is typically reduced in SIADH and salt wasting syndrome. After correction of hyponatremia, the hypouricemia corrects in SIADH but remains in salt wasting syndrome
4
Q
Hypovolemic Hypotonic Hyponatremia
Work up
A
- Serum osmolality less than 280 mEq/L
- Hypovolemia on clinical assessment
- Measure urine sodium concentration:
- < 10 mEq/L means non-renal causes
- > 20 mEq/L means renal causes
5
Q
Hypernatremia due to pure water deficits
Treatment
A
- Central DI: give vasopressin (DDAVP)
- Nephrogenic DI:
- Correct hyperclacemia and hypokalemia
- Stop the offending drug (if present)
- If no response to the above then give hydrochlorothiazide or NSAIDs
6
Q
Hypernatremia
Treatment guidelines
A
- Acute (< 24 hrs): correct it fast with an initial rate of 2-3 mEq/L/h (for 2-3 hrs) [maximum is 12 mEq/L/day]
- Chronic (>24 hrs): 0.5 mEq/L/h and a total of 8-10 mEq/L/day
- If there is a volume deficit too, restore the intravascular volume with Isotonic NaCl prior to free water administration
7
Q
Hypertonic Hyponatremia
Causes
A
Normal sodium level and total body water but there is a dilutional drop in measured serum sodium due to presence of osmotically active molecules in the serum:
- Glucose (every 100 above 100 mg/dL will decrease Na+ by 1.6 mEq/L, but if serum glucose is greater than 400 mg/dL each 100 above 100 mg/dL will decrease Na+ by 2.4 mEq/L)
- Mannitol
- Maltose (used with IV Ig administration)
8
Q
Hypernatremia due to pure water deficits
Causes
A
- Usually due to impaired intake that is combined with increased loss through kidneys or insensible water loss
- Impaired intake:
- Lack of access to water (incarceration, restraints, intubation, immobilization)
- Altered mental status (medications or diseases)
- Neurologic disease (dementia or impaired motor functions)
- Abnormal thirst (geriatric hypodipsia, osmoreceptor dysfunction [reset of threshold], injury to the hypothalamic thirst centers [metastasis, granulomatous disease, vascular abnormalities, trauma], autoantibodies to sodium-level sensor in brain
- Increased water loss:
- Diabetes insipidus
- Loss of water through respiratory tract
9
Q
Hypervolemic Hypotonic Hyponatremia
Causes
A
Increase in both sodium level and total body water with greater increase in water due to:
- CHF
- Liver cirrhosis
- Nephrotic syndrome
- Severe hypoproteinemia (albumin < 2 g/dL)
- Acute renal injury
- Chronic renal disease
10
Q
Hypernatremia due to Hypotonic fluid deficits
Work up and Diagnosis
A
- The patient is Hypovolemic
- Renal fluid loss:
- Isotonic or hypotonic urine (300 mOsm/kg or less)
- Urine sodium is higher than 20 mEq/L
- Extra-renal fluid loss:
- Hypertonic urine (greater than 600 mOsm/kg)
- Urine sodium is less than 20 mEq/L
11
Q
Hyponatremia
Classification
A
- Isotonic
- Hypertonic
- Hypotonic:
- Hypovolemic
- Hypervolemic
- Euvolemic
12
Q
Isotonic Hyponatremia
Work up
A
- Serum osmolality 280-295 mEq/L
- Measure glucose, lipids and proteins
13
Q
Hypovolemic Hypotonic Hyponatremia
Causes
A
Decrease in both sodium level and total body water with more decrease in sodium due to:
- Decreased IV volume:
- Severe hemorrhage
- Severe volume depletion secondary to GI or renal loss
- Diuretic use (especially Thiazides)
- Cerebral Salt Wasting syndrome (CSW) due to intracranial disorders (subarachnoid hemorrhage, carcinomatous or infectious meningitis, metastatic carcinoma, and neurologic procedures) which will disrupt the sympathetic neural input to kidneys and release of 1 or more natriuretic peptides
- Salt-wasting nephropathy may develop rarely in any renal disorder with low salt intake
- Ultra endurance athletes and marathon runners (single strongest predictor is weight gain during the race, the others being longer race time and BMI extremes)
14
Q
Nephrogenic Diabetes Insipidus
Causes except drugs
A
- Genetic: V2-receptor defects, aquaporin defects; 90% by AVPR2 mutations (X-linked recessive), AQP2 gene mutation
- Structural: urinary tract obstruction, papillary necrosis and sickle cell nephropathy
- Tubulointerstitial disease: medullary cystic disease, polycystic kidney disease, nephrocalcinosis, Sjogren’s syndrome, lupus, analgesic-abuse nephropathy, sarcoidosis, M-protein disease, cystinosis, and nephronophthisis
- Any prolonged state of severe polyuria (due to washing out the renal medullary-intramedullary concentration gradient needed for urine concentration and down regulation of AQP2 water channels (partial DI)
- Electrolytes disorders: hypercalcemia and hypokalemia
- Others: distal renal tubular acidosis, Bartter syndrome, and apparent mineralocorticoid excess
15
Q
Hypernatremia
Work up
A
- Serum electrolytes (Na+, K+, Ca++)
- Glucose level
- BUN and creatinine
- Urine electrolytes (Na+, K+)
- Urine and plasma osmolality
- 24-hour urine volume
- Plasma arginine vasopressin (AVP) level (if indicated)
