Electrolytes

# Chronic Kidney Disease
— Diagnosis confirmedd: sustained eGFR <60 with markers of renal disfunction for at least the past three months
— Evaluation of present renal function
– Latest eGFR on DATE was GFRPASTE trend
– Latest sCR on DATE was CRPASTE, trend
– Latest urine protein/albumin was ALBPASTE, trend
– No urinalysis with protein/albumin ordered
— Evaluating patient’s related markers: (1) BP: poorly/well controlled HTN with SBP baseline on record SBPPASTE (since at least DATE ); (2) Volume: no clinical evidence of edema today, records do NOT demonstrate recent wt gain, (3) Electrolytes: latest ( DATE ) appearing WNL, (4) Hgb appropriate // consistent with anemia, reviewed iron studies; (5) mineral-bone: no phos or PTH noted on prior labs, patient with NO reported hx recurretn fractures
— Renal imaging on records reviewed
PLAN
— Labs:
– CMP (sCr, eGFR, K, HCO3), CBC, iron studies, ferritin
– Spot urine ACR or 24-hr urine protein for albuminuria assessment
– PTH, phos, sCa
— Renal US ordered
— EKG (hyperkalemia >5.5)
— Optimization of BP:
– counseled patient on dietary optimization, including the DASH dietary
– medication management:
continue
starting new medication, will follow-up 1-2wks on sCr/K
– Losartan 25 mg daily
– Losartan 50 mg daily
– Losartan 100 mg daily
– Lisinopril 2.5 mg daily
– Lisinopril 5 mg daily
– Lisinopril 10 mg daily
– Lisinopril 20 mg daily
– Lisinopril 30 mg daily
– Lisinopril 40 mg daily
— Volume management
– Restrict Na to <2 g/day
– Diuretic therapy if hypervolemia: furosemide 20-80 mg PO/IV QD; titrate PRN
— Electrolyte Correction
– Hyperkalemia: low-K diet, Na polystyrene sulfonate (15-30 g PO PRN), or patiromer
– Metabolic acidosis: NaHCO3 tabs 650 mg PO BID-TID to maintain serum HCO3 >22
5. Anemia management
– Iron supplementation if TSAT <30% or ferritin <500: oral (ferrous sulfate 325 mg PO TID) or IV iron
– Consider ESA (e.g., darbepoetin alfa 0.45 mcg/kg QW or Q2W) if Hb <10 g/dL
— Mineral-bone evaluation
– Phosphate binder (e.g., sevelamer 800 mg PO TID with meals if hyperphosphatemic)
– Adjust dietary phosphorus; aim for serum PTH levels per KDIGO stage-specific targets
— Follow-up
– Labs Q4-6 wks initially for therapy titration
– Adjust frequency based on progression of CKD

 

 

NORMOCALCEMIA
– [calcium 8.5-10mg/dL (serum corrected) | 1.12-1.31 mmol OR 1.15-1.32 (ionized)]
– 1/2 of serum calcium is bound to protein (inactive)
– serum pH affects calcium binding to albumin
HYPOCALCEMIA
– [calcium <8.5 | <1.15]
PREVALENCE
– Steen et al (I) pts w/ albumin <30 g/L, 75% normocalcemic using the Payne formula in fact had hypocalcemia based on ionized calcium levels.
– Another study (II) found that adjusted calcium values derived by applying the Payne formula agreed with ionized calcium levels in only 55-65% of patients.
– In contrast, unadjusted total calcium correctly categorized 70-80% of patients.
– The poor performance of the calcium correction has also been observed in the hypoalbuminemic geriatric population (7)
SYMPTOMS
RESOUCE
I. Steen O, Clase C, Don-Wauchope A. Corrected calcium formula in routine clinical use does not accurately reflect ionized calcium in hospital patients. Canad J Gen Int Med. 2016;11(3):14-21. DOI: 10.22374/cjgim.v11i3.150.
II. Smith JD, Wilson S, Schneider HG. Misclassification of calcium status based on albumin-adjusted calcium studies in a tertiary hospital setting. Clin Chem. 2018;64(12):1713-1722. DOI: 10.1373/clinchem.2018.291377.
III. Sorva A. ‘Correction’ of serum calcium values for albumin biased in geriatric patients. Arch Geron Geri. 1992;15(1):59-69. DOI: 10.1016/0167-4943(92)90040-B.
TEMPLATES
======================================================
NORMOCALCEMIA
– [calcium 8.5-10mg/dL (serum corrected) | 1.12-1.32 mmol (ionized)]
# Hypocalcemia, mild-moderate
– mild by serum (8-8.4)
– moderate by serum (7-7.9)
– mild-moderate by ionized 1.0-1.12 (or 1.15)
– asymptomatic on assessment
– mild neuromuscular symptoms reported by pt including paresthesias and cramping
PLAN [goal 1.5-2g of elemental calcium daily total]/2-3 doses
– calcium carbonate (PO)
– contraindicated for patient on PPI
– calcium citrate (PO)
– vitamin D supplementation
– for ionized calcium 1-1.1 —> calcium gluconate 1g IV over 1hr
– check Mg, phos, PTH, vitamin D
– serum lipase if suspected pancreatitis
# Hypocalcemia of renal disease
PLAN
– ergocalciferol (D2) 50K U weekly for 8-12wks
– cholecalciferol (D3) 1K-5K U QD
– informed pt of risk – nephrolithiasis, should incr water consumption
# Hypocalcemia, severe (<1 and/or symptomatic)
[calcium <7.0 (serum) | <0.9-1 (ionized)]
– paresthesia/cramping non-specific but described by patient
– tetany, Chvosteks (CN 7), Trousseau’s sign, and QT prolongation on EKG
– severe symptoms including seizures, QT prolongation, torsades, and laryngospasm
PLAN
– EKG
– Torsades —> Mg IV
– for ionized calcium 0.85-0.99 —> calcium gluconate 2g IV over 1hr
– for ionized calcium <0.85 —> calcium gluconate 2g IV over 1hr, notify attending
For All Severities:
– Lab orders: serum calcium, ionized calcium, PTH, magnesium, phosphate, vitamin D levels, EKG
Mild Hypocalcemia:
– Oral calcium supplementation:
  – Calcium carbonate 500-1000 mg PO TID w/ meals
  – Vitamin D supplementation: Calcitriol 0.25-0.5 mcg PO daily
– Monitor serum calcium and adjust treatment as necessary
Moderate Hypocalcemia:
– Oral supplementation with closer monitoring:
  – Increase calcium carbonate dosage as needed
  – Ensure adequate vitamin D levels and supplement as necessary
– If symptoms persist or worsen, consider IV calcium gluconate as below
Severe Hypocalcemia:
– (1) IV calcium gluconate:
       – 10% solution, 1-2 g (90-180 mg of elemental calcium) diluted in 50-100 mL of D5W over 10-30 min
       – Monitor for bradycardia during infusion
– (2) Magnesium repletion (if low):
       – MgSO4 1-2 g IV over 1-2 hrs
       – Goal serum magnesium > 2 mg/dL
– (3) Once stabilized, transition to oral calcium and vitamin D as for mild to moderate hypocalcemia
– (4) Monitor serum calcium Q4H initially, then daily once stabilized
– (5) EKG monitoring for QT interval changes

 

 

# Hypotonic Hyponatremia
– Hypotonic hyponatremia: In ER, patient presenting w/ serum sodium (sNa) <135 mEq/L. Clinical features include headache, nausea, vomiting, muscle cramps, lethargy, and in severe cases, seizures or coma.
– Risk factors: SIADH, hypothyroidism, adrenal insufficiency, diuretic use, kidney or liver disease, congestive heart failure (CHF), and excessive water intake.
– Differential diagnosis (Ddx): SIADH, hypovolemia, adrenal insufficiency, hypothyroidism, renal failure, congestive heart failure (CHF), cirrhosis, nephrotic syndrome.
– Diagnostic criteria: Serum osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg, and urine sodium >40 mEq/L in the setting of euvolemia.
Complications:
– Central pontine myelinolysis (CPM) if correction is too rapid
– Cerebral edema and increased intracranial pressure (ICP) in acute cases
– Cardiac arrhythmias
– Osteoporosis and fractures in chronic cases
PLAN
– Initial lab orders: CMP, CBC, urine osmolality, urine sodium, TSH, cortisol levels, ACTH stimulation test if adrenal insufficiency suspected
– Additional lab orders to consider: Brain MRI, chest X-ray (CXR), EKG, ABG/VBG
– (1) Fluid restriction:
– Limit to 800-1000 mL/day (adjust based on patient’s total fluid balance and output)
– (2) Sodium correction:
– For acute symptomatic hyponatremia: 3% saline IV at 0.5-2 mL/kg/hr, aim for increase of 4-6 mEq/L in the first 24 hours
– For chronic asymptomatic hyponatremia: oral salt tablets or fludrocortisone in SIADH cases
– (3) Monitor electrolyte levels:
– Recheck sNa Q4H initially, then daily once stable
– Aim for correction rate not to exceed 8-10 mEq/L in 24 hours to avoid risk of CPM
– (4) Treat underlying cause:
– Address contributing factors like medication use, hormonal imbalances
– Specific treatment for conditions like CHF, liver cirrhosis, or renal failure
– (5) Frequent clinical monitoring:
– Neurological assessment Q4H
– Fluid status and input-output charting

# SIADH (E22.2, E87.1, R60.9)
– SIADH: In ER, patient presents w/ euvolemic hyponatremia, serum sodium (sNa) <135 mEq/L, urine osmolality >100 mOsm/kg, and urine sodium >40 mEq/L. Symptoms include nausea, headache, confusion, and in severe cases, seizures.
– Risk factors include CNS disorders, malignancies, pulmonary diseases, and medications (e.g., SSRIs, antiepileptics).
– Ddx: adrenal insufficiency, hypothyroidism, renal disease, diuretic use, psychogenic polydipsia.
Complications:
– Severe hyponatremia can lead to cerebral edema, seizures, and coma.
– Overcorrection of hyponatremia risks central pontine myelinolysis.
– Ongoing hyponatremia can contribute to osteoporosis and fractures.
PLAN
– Initial lab orders: CMP, CBC, urine electrolytes, urine osmolality, TSH, cortisol, chest X-ray (CXR) if respiratory pathology suspected.
– Additional lab orders to consider: brain MRI if CNS pathology suspected, adrenal function tests.
– (1) Fluid restriction:
– Limit fluid intake to 800-1000 mL/day.
– (2) Pharmacological management:
– Consider vasopressin receptor antagonists (e.g., tolvaptan) for severe or symptomatic cases.
– Monitor sodium levels closely
– target correction rate <8 mEq/L in the first 24 hours.
– (2) Monitoring and adjusting treatment:
– Serial sNa and serum osmolality checks Q4H initially, then Q6-12hrs-QD when stbale
– Aim for a gradual correction of sNa (not to exceed 8-10 mEq/L in the first 24 hours).
– Monitor for signs of fluid overload, especially in CHF or CKD patients.
– (4) Treat underlying cause:
– Address underlying malignancy, CNS, or pulmonary disorders.
– Review and adjust medication regimen that may contribute to SIADH.

# Hyponatremia due to Hypovolemia
– Hyponatremia due to hypovolemia: In ER, patient presents w/ serum sodium (sNa) <135 mEq/L, signs of volume depletion (e.g., dry mucous membranes, tachycardia, hypotension).
– Key features include history of fluid loss (e.g., vomiting, diarrhea, diuretic use), decreased intake, and concentration weakness.
– Risk factors: Elderly, diuretic use, GI losses, renal losses, adrenal insufficiency.
Complications:
– Neurological symptoms like confusion, seizures, or coma due to rapid shifts in osmolality.
[- complications/considerations: cerebral edema or osmotic demyelination.]
– Hypotensive shock and renal failure due to severe volume depletion
– Orthostatic hypotension increasing risk of falls and injuries
PLAN
– Initial lab orders: CMP, CBC, urine electrolytes, urine osmolality, TSH, morning cortisol, ADH levels.
– Additional lab orders to consider: adrenal function tests, stool studies if diarrhea is present
– (1) IV NS (0.9% NaCl) @ initial rate of 20-30 cc/kg/hr (titrate based on hemodynamic response and urine output), strict I/Os
– (2) Monitoring and adjusting treatment:
– Serial sNa and serum osmolality checks Q4H initially, then Q6-12hrs-QD
– Aim for a gradual correction of sNa (not to exceed 8-10 mEq/L in the first 24 hours).
– Monitor for signs of fluid overload, especially in CHF or CKD patients.
– (3) Address underlying:
– d/c or adjust diuresis
– Manage GI losses: antiemetics or antidiarrheals
– Assess for adrenal insufficiency and replace steroids if indicated.
– (4) Monitor for complications: Q2-Q6 neurochecks
– (5) Long-term management:
– Educate patient on maintaining adequate hydration and sodium intake.
– Review and adjust medications contributing to hypovolemia.

The management of hypovolemic hyponatremia involves careful fluid and sodium repletion, monitoring for overcorrection, addressing the underlying cause, and vigilance for complications. The treatment must be individualized, considering the severity of hyponatremia and the patient’s overall clinical condition. Regular monitoring and adjustments to the treatment plan are key to effective management.

# Hyponatremia (E87.1)
– Hyponatremia: In ER, patients often present w/ sNa <135 mEq/L. Symptoms range from headache, nausea, vomiting, muscle cramps, lethargy to confusion and, in severe cases, seizures or coma.
– Risk factors vary by etiology: SIADH, hypothyroidism, adrenal insufficiency, diuretic use, kidney or liver disease, CHF, excessive water intake for euvolemic; GI losses, CNS disorders, malignancies, pulmonary diseases, medications like SSRIs, antiepileptics for hypovolemic.
– Ddx includes SIADH, hypovolemia, adrenal insufficiency, hypothyroidism, renal failure, CHF, cirrhosis, nephrotic syndrome.
– Diagnostic criteria: Serum osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg, urine sodium >40 mEq/L in euvolemia; assess volume status for differentiation.
Complications:
– Rapid correction risks central pontine myelinolysis (CPM).
– Cerebral edema, increased ICP, seizures, coma in acute cases.
– Cardiac arrhythmias, hypotensive shock, renal failure.
– Orthostatic hypotension, osteoporosis, fractures.
PLAN
– Initial lab orders: CMP, CBC, urine electrolytes, urine osmolality, TSH, cortisol levels; consider brain MRI, CXR, EKG, ABG/VBG, adrenal function tests.
– Fluid Management:
– Hypovolemic hyponatremia: IV isotonic saline (0.9% NaCl) @ 20-30 cc/kg/hr, adjust based on response.
– Euvolemic (SIADH): Fluid restriction to 800-1000 mL/day, vasopressin receptor antagonists (e.g., tolvaptan) for severe cases.
– Sodium Correction:
– Acute symptomatic hyponatremia: 3% saline IV at 0.5-2 mL/kg/hr for increase of 4-6 mEq/L in first 24 hours.
– Chronic asymptomatic hyponatremia: Gradual correction, oral salt tablets or fludrocortisone for SIADH.
– Monitoring and Adjustment:
– Serial sNa and osmolality checks Q4H initially, then Q6-12H; correction rate <8-10 mEq/L in 24 hours.
– Address Underlying Cause:
– Adjust medications contributing to hyponatremia.
– Manage GI losses, adrenal insufficiency, hormonal imbalances.
– Treat CHF, liver cirrhosis, renal failure as needed.
– Monitoring for Complications:
– Neurological assessments, vital signs for hypotension, shock.
– Fluid status and input-output charting.
– Long-term Management and Education:
– Hydration and sodium intake guidance.
– Medication review and adjustments.
– Endocrinology or nephrology consultation for complex cases.
This approach to hyponatremia management emphasizes careful etiological assessment, controlled sodium correction, and monitoring for complications. Treatment strategies vary according to the underlying cause and severity of hyponatremia, with specific focus on preventing rapid shifts in serum sodium and addressing the primary cause.

 

# Hyperkalemia
– Serum K (## @ ), on repeat (@):
– On EKG: QRS prolongation, peaked T-wave
– Contributory: AKI, CKD, urinary retention
– Treatment criteria met: sK> 6.5 mEq/L w/o any symptoms
– Treatment criteria met: sK 5.5-6.5 mEq/L w/ muscle weakness or paralysis, or changes in electrocardiogram (ECG) or significant tissue injury
– Check at Q3, Q6hrs
PLAN
– Administer in order:
– 1. Calcium gluconate [myocardial stabilization]
– 2. D50 IV 100mL
– 3. Insulin 10U IV
– Lokelma
– Sodium bicarb [induced hyperkalemia][note 1 amp sodium]
– Low potassium diet
– Severe, persistent: referral to renal
– Severe, persistent: ICU

 

# Incidental adrenal mass
(ICD-10: D44.1 – Neoplasm of uncertain behavior of adrenal gland, E27.8 – Other specified disorders of adrenal gland, E27.0 – Other adrenocortical overactivity)

— Diagnostic criteria: Adrenal mass >1 cm identified on imaging, incidentally detected in the absence of related clinical symptoms, requires biochemical evaluation to assess for functionality (hormonal hypersecretion) and malignancy risk assessment based on imaging characteristics (e.g., size >4 cm, irregular borders, inhomogeneous texture, rapid growth)
— Complications: Risk of hormonal hypersecretion (e.g., hyperaldosteronism, Cushing’s syndrome, pheochromocytoma), mass effect if large, malignancy risk (e.g., adrenal cortical carcinoma, metastasis)
— Red-flag findings: Mass size >4 cm, irregular borders, inhomogeneous texture, rapid interval growth, unenhanced CT Hounsfield units >10
— Reassuring findings: Stable size on interval imaging, homogeneous appearance, well-defined borders, unenhanced CT Hounsfield units <10

PLAN
— Biochemical workup to assess hormonal activity:
— 24-hr urine metanephrines and catecholamines
— Plasma free metanephrines
— 1-mg dexamethasone suppression test
— Aldosterone-to-renin ratio (if hypertensive or hypokalemic)
— Electrolyte panel (BMP)

— Imaging for malignancy risk stratification:
— Initial imaging: Non-contrast CT abd/pelv
— Consider MRI if indeterminate findings on CT
— PET-CT if suspicion for malignancy or metastasis

— Surgical referral if:
— Mass >4 cm
— Suspicious imaging characteristics (irregular borders, necrosis, calcifications)
— Biochemical evidence of hormonal hypersecretion

— Monitoring:
— Repeat imaging (CT/MRI) at 6-12 mo for non-surgical cases
— Continued biochemical testing based on initial findings

— Endocrinology referral for:
— Biochemical abnormalities suggestive of functional adenoma
— Ambiguous imaging findings

— Consider genetic evaluation if:
— Bilateral adrenal masses
— FHx of hereditary syndromes (e.g., MEN1, MEN2, VHL, Li-Fraumeni syndrome)

— Electrolyte management:
— Monitor sNa, sK, sCr, and phos lvls QD if biochemical abnormalities are present

— Patient follow-up:
— Outpatient follow-up w/ endocrinology Q6-12mo