Clinical Approach to Hyponatremia/Hypernatremia and Hypokalemia/Hyperkalemia (Selby) Flashcards
What is hyponatremia defined as and what is the difference between mild, moderate, and severe forms?
Who is it commonly seen in?
Hyponatremia - serum sodium < 135 mEq/L
Mild - 130-134 mEq/L
Moderate - 120-129 mEq/L
Severe - < 120 mEq/L
- more commonly seen in hospitalized pts, especially in the ICU, and less common in outpatients
What is the normal serum osmolarity in the body and what are the two systems that help regulate it?
What are the osmotic and non-osmotic stimuli that regulate ADH release?
Normal osmolarity = 280-290 mOsm/L
- serum osmolarity regulated by ADH and thirst mechanisms
ADH release due to:
- Osmotic Stimuli - inc. osmolarity detected by OSMORECEPTORS in anterior hypothalamus
- Non-osmotic Stimuli - dec. in BP or blood volume detected by arterial BARORECEPTORS
What are 4 additional Non-Osmotic Stimuli for ADH release (N/H/P/M)?
What are two medications that cause ADH release?
- Nausea (vomiting = hypovolemia), Hypoxia, Pain (post-op pt.), and medications
Medications: opiates and antidepressants (SSRIs)
What is the primary cause of hyponatremia and what are two examples of it?
- results primarily from increases in TOTAL BODY WATER (less from changes in total body sodium)
Increases in TBW occur due to:
- excessive water intake (oral/IV)
- dec. renal water excretion (can’t suppress ADH)
What is the time difference between Acute and Chronic Hyponatremia?
Acute = < 48 hours Chronic = > 48 hours
same time-frame for pts with HYPERnatremia
What is the stepwise approach to diagnosis of Hyponatermia?
When should labs be taken?
- Measure serum osmolarity
- determine if hypotonic, isotonic, hypertonic hyponatremia
- if pt. has hypotonic hyponatremia, assess volume status
- measure random urine sodium lvl
- measure urine osmolarity
all labs need to be drawn at the SAME TIME - get plasma sodium, urine sodium, and urine osmolarity
What lab should be obtained if you suspect a patient has hyponatremia due to SIADH?
How is SIADH diagnosed and what are two main etiologies that must be ruled out?
- get SERUM URIC ACID levels (will be LOW in SIADH)
- inc. uric acid excretion in the urine
- SIADH diagnosis is a diagnosis of EXCLUSION (should rule out other causes, like cortisol deficiency and hypothyroidism)
What is the stepwise process if a patient with hyponatremia is determined to be HYPOVOLEMIC?
- check urine osm > 300 mOsm/L
- check urine sodium lvls
- if > 20 mEq/L –> Renal Fluid Loss
- diuretics, RTA, adrenal insufficiency, etc
- if < 20 mEq/L –> Extrarenal Fluid Loss
- vomiting, diarrhea, 3rd spacing, blood loss, etc
What is the stepwise process if a patient with hyponatremia is determined to be EUVOLEMIC?
- check urine Osm lvls
- if urine osm < 100 mOsm/L = Primary Polydipsia
- pt. drinking too much water –> STOP IT
- if urine osm > 300 mOsm/L –> check urine sodium
- if urine sodium > 20 mEq/L
- SIADH, hypothyroidism, adrenal insufficiency, thiazide
What is the stepwise process if a patient with hyponatremia is determined to be HYPERVOLEMIC?
- check urine osm > 300 mOsm/L
- check urine sodium lvls
- if urine sodium < 20 mEq/L
- nephrotic syndrome, heart failure, cirrhosis
- if urine sodium > 20 mEq/L
- acute or chronic kidney failure (low GFR)
What are two common causes of SIADH?
- Small Cell Lung Carcinoma
- most common malignancy associated with ectopic ADH production
- Postoperative state
many things can cause the development of SIADH
What are 6 drugs commonly associated with SIADH development?
- antidepressants, anticonvulsants, antipsychotics, cyclophosphamide (ANTICANCER)
- also opiates and MDMA (ecstasy)
What is the general rule of thumb for the treatment of Hyponatremia?
How should acute and chronic hyponatremia be treated?
What should SYMPTOMATIC patients receive?
Rule of Thumb: serum sodium should be corrected over the SAME TIME PERIOD it took to become low
Acute: rapid correction has little risk of osmotic demyelination syndrome (ODS)
Chronic: pt. at HIGH risk of developing ODS
- raise serum by 8-10 mEq/day with no more than 18 within first 48 hrs
Symptomatic: give HYPERTONIC SALINE (3%) to quickly raise sodium
- raise it enough so no longer symptomatic
What are common treatment options for hyponatremia caused by:
- Hypovolemic hyponatremia (2)
- Primary Polydipsia (Euvolemic)
- SIADH (3)
- Hypothyroidism
- Cortisol Deficiency
- Thiazides
- Hypervolemic hyponatremia (2)
- isotonic saline (no symptoms) and hypertonic saline (symptoms)
- water restriction and hypertonic saline (symptoms)
- water restriction, furosemide, salt/urea tablets
- vaptans and demeclocycline
- thyroid replacement
- prednisone
- stop thiazides
- *hypertonic saline for above 4 if symptoms**
- water restriction and furosemide
What are 4 common complications of Hyponatremia (S/C/D/ODS)?
- seizures, coma, death, Osmotic Demyelination Syndrome (ODS - occurs with rapid Na correction)
Osmotic Demyelination Syndrome
When do symptoms manifest, what neurons are affected (2), and what is required for diagnosis?
- symptoms occur 2-6 days after rapid Na correction (occurs in PONTINE and EXTRAPONTINE neurons)
- symptoms are often irreversible or partially reversible (some pts. get “Locked-in” Syndrome where they are awake but cannot move)
Dx: head MRI (may take 4 wks to see changes)
too quick of correction causes brain cells to SHRINK, causing axonal shear damage as water enters extracellular space
What is Hypernatremia and what two pt. populations are commonly affected?
What are 5 common risk factors for development and what is the most common cause of development?
- defined as serum sodium > 145 mEq/L, typically seen in infants and the elderly (impaired thirst mechanism)
RF: trauma, burns, ICU pts, dementia, and uncontrolled diabetes
- typically caused by unreplaced water loss (DEHYDRATION) and less commonly by Na overload
- GI water loss (vomit/diarrhea), renal water loss, sweating, impaired thirst mechanism
What does Hypernatremia result in and what clinical manifestations does it present with?
Which clinical manifestation is commonly seen in pediatric and neonate pts?
- results in cellular shrinkage since there is an osmotic gradient for water to move out of cells into ECF
- clinically manifests as NEUROLOGICAL symptoms (lethargy, seizures, irritability, altered mental status)
- INTRACEREBRAL HEMORRHAGE more common in pediatric and neonate pts
What is the 2 step approach to treating pts. with Hypernatremia?
How should Acute and Chronic Hypernatremia be treated?
- Replace the water deficit
- 5% dextrose in water (D5W), hypotonic solutions
- correct underlying cause leading to water loss
Acute: can rapidly correct with little risk of cerebral edema
Chronic: pts. at inc. risk of cerebral edema
- goal: lower sodium by 10-12 mEq/L
What is the primary regulator of serum potassium in the body?
What two cell types are responsible for secretion and reabsorption of potassium in this regulator?
THE KIDNEY (distal nephrons = urinary K secretion)
- Principle Cells = K secretion
- a-intercalated Cells = K reabsorption
Immediate Response: transcellular shift
Long-Term Response: renal excretion
What is Hyperkalemia defined by?
What are 3 major clinical manifestations of Hyperkalemia?
- Hyperkalemia = serum potassium > 5-5.5 mEq/L
C: cardiac arrhythmia (bradycardia), skeletal muscle weakness (diaphragm weakness), metabolic ACIDOSIS (dec. ammoniagenesis = dec. ammonium chloride excretion in kidneys)
How do Hyperkalemia and Hypokalemia affect the resting membrane potential of skeletal muscle?
Hyperkalemia: makes membrane potential LESS negative
- initially MORE excitable
- long-term = Na channel inactivation = net dec. in membrane excitability (VENTRICULAR FIBRILLATION)
Hypokalemia: makes membrane potential MORE negative
- see U-WAVE on ECG and flat-inverted T-Waves
What are the two main reasons that Hyperkalemia develops?
What should ALWAYS be reviewed in pts with Hyperkalemia?
- Transcellular Shift
- pseudohyperkalemia, metabolic acidosis, meds, exercise, blood transfusion (K leaks out of RBCs), insulin deficiency (no Na/K ATPase stimulation), hyperglycemia/hyperosmolarity (water drags K out of cells)
- Decreased Renal Potassium Excretion
- low aldosterone secretion (meds/adrenal insuff)
- aldosterone resistance (K-sparing, Na Channel Block)
- AKI/CKD (low GFR)
ALWAYS REVIEW medications of pts. with Hyperkalemia
What is Pseudohyperkalemia and what are 3 things that can cause it? (R/S/L)
- results from an artificial inc. in serum K due to K release from cells
1. RBC hemolysis (mechanical trauma to cells)
- Serum Blood Samples (clotting = K out of platelets)
- obtain plasma K to rule out thrombocytosis
- Leukocytosis (fragile WBCs in leukemia pts)
How is Hyperkalemia diagnosed and what does Fractional Excretion of K (FEK) tell us?
What test should NOT be ordered for Hyperkalemic pts?
- Dx based on HISTORY and EXAM (lab tests guided by suspected cause per history)
- FEK: < 10% (Renal etiology) and > 10% (extrarenal etiology)
- do NOT order Transtubular Potassium Gradient (TTKG) = Invalid test
Hyperkalemia Treatment
What are 5 ways to treat patients?
- calcium gluconate if Peaked T-waves (stabilize cardiac membrane)
- Transcellular shift - insulin/dextrose, B2-agonists
- Potassium Removal - loop diuretic/thiazides, also exchange resins
- low potassium diet
- discontinue meds that increase potassium lvls
Hyperkalemia and Exchange Resins
How do these resins work and where:
- Sodium Polystyrene Sulfonate
- Zirconium Cycloslicate
- Patiromer
- exchanges Na for potassium in COLON
- exchanges Na/H for potassium throughout INTESTINES
- exchanges Ca for potassium in COLON
What is Hypokalemia and what are 3 risk factors for development?
What are 5 clinical manifestations of this condition? (CA/SM/R/MA/NDI)
- Hypokalemia = serum potassium < 3.5 mEq/L
RF: diarrhea, vomiting, medications (diuretics/insulin)
C: cardiac arrhythmias, skeletal muscle weakness, rhabdomyolysis, metabolic ALKALOSIS, nephrogenic diabetes insipidus
How are these causes of Hypokalemia caused:
- Transcellular Shift (inc. K uptake by cells) - 3
- Extrarenal Loss - 2
- Renal Loss - 3
- due to Insulin, B2-agonists, and metabolic ALKALOSIS
- MOST COMMON reasons for shift
- GI Loss
- Upper GI - vomiting, NG suction
- Lower GI - diarrhea
- cutaneous loss through SWEATING
- Diuretics (thiazide/loop), inc. mineralcorticoid activity (aldosterone inc. Na reabsorption), and Hypomagnesemia
How is Hypokalemia diagnosed?
What are 2 Urinary Potassium Excretion tests that can be performed?
- often clinically diagnosed through history and exam
- laboratory test guided by these two processes
- 24 hr Urine Potassium Screen
- BEST METHOD to assess renal K excretion
- values > 25-30 mEq/L = renal K wasting
- Urine K/Cr ratio
- Cr corrects for variation in urine volume
- values > 13 mEq/g = renal K wasting (typically < 13 mEq/g is NORMAL)
What are the 4 main treatments for Hypokalemia? (UC/RP/RM/RK)
- treat the underlying cause
- replace potassium deficit (Potassium Chloride)
- K inc. by 0.1 mEq/L for every 10 mEq of KCl given
- replace magnesium if low
- magnesium oxide or magnesium sulfate 1-2g IV
- repeat K to ensure it has normalized
