Electrolytes

Hypercalcemia

Trevor Stevens, Madison Bandler

Evaluation

  • Total serum calcium >10.5 (normal 8.5-10.5g/dl)
  • Most (99%) Ca2+ is anhydrous and stored in bone.
  • The remaining 1% is 60% bound (mostly to albumin) and 40% ionized and able to exert a physiologic effect
  • There is an inverse relationship between pH and free Ca2+. As pH declines, serum Ca increases due to H+ binding to albumin and releasing Ca2+
  • Don’t forget to correct calcium level if hypoalbuminemia (or check ionized calcium level)
    • Corrected Ca2+ = ((Normal albumin – Patient’s albumin) x 0.8)) + Patient’s Ca2+
  • It is not unusual to have pseudohypercalcemia in the setting of dehydration due to an increased concentration of albumin, in which case ionized calcium would remain normal
  • Hypercalcemia of malignancy may occur through multiple mechanisms:
    • Osteolytic lesions (as in multiple myeloma or bony metastatic disease)
    • Activation of vitamin D (as in lymphoma)
    • PTHrP mediated (most commonly squamous cell carcinoma of lung, head and neck/renal and bladder cancer/breast and ovarian cancer)

Presentation

  • Ca2+ > 12 can cause shortened QT interval, 2nd and 3rd degree heart block, ventricular arrhythmias, and ST elevations mimicking MI
  • Severe manifestations uncommon at Ca2+ < 14
  • “Stones, bones, thrones, belly groans, and psychiatric overtones”
    • Bone pain, Polydipsia/polyuria: due to nephrogenic DI, Nausea/constipation, Depressed mood/cognitive impairment, Decreased level of consciousness

Physical Exam

  • Examine mucous membrane dryness
  • Eye exam for band keratopathy or corenal degeneration from calcium deposits if chronic
  • Skin exam for calcinosis cutis
  • GI exam for abdominal tenderness
  • MSK exam for bone pain, especially along spine
  • GU exam for CVA tenderness suggestive of kidney stones

Labs & Imaging

  • PTH level can help distinguish between PTH-dependent and PTH-independent causes of hypercalcemia
    • Normal or ↑ PTH
      • Primary hyperparathyroidism: ↑ Ca+2 and ↓ PO4-3
      • Tertiary hyperparathyroidism (autologous secretion of PTH in CKD/ESRD)
      • Familial hypercalciuric hypercalcemia (often asymptomatic, no treatment required)
      • Li toxicity
    • ↓ PTH
      • Humoral hypercalcemia of malignancy (PTHrP)
      • Malignancy (boney metastases)
      • Excess vitamin D intake
      • Granulomatous disease: 1,25-dihydroxy vitamin D, 25-hydroxyvitamin D, or ACE level
      • Milk-alkali syndrome
      • Medications (classically HCTZ)
      • Thyrotoxicosis
      • Adrenal insufficiency
  • Serum phosphate, creatinine, and alkaline phosphatase levels to assess renal function and bone turnover
    • Remember- phosphorus should be lower end of normal if hypercalcemia is PTH dependent
  • Serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels can help identify vitamin D-related causes of hypercalcemia, such as vitamin D intoxication or granulomatous diseases
  • 24-hour urinary calcium excretion helps differentiate primary hyperparathyroidism (PHPT) from FHH. In PHPT, urinary calcium excretion is typically normal or elevated, whereas it is low in FHH
  • Imaging studies, such as neck ultrasound or Tc-sestamibi scan may be indicated to localize parathyroid adenomas in cases of primary hyperparathyroidism
  • Bone density measurement, particularly at the distal third of the radius, and renal ultrasound to detect nephrolithiasis or nephrocalcinosis

Management

  • If Ca+2 < 12 and asymptomatic
    • Encourage PO hydration
    • Normal saline if hypovolemic
      • NS provides a higher sodium load that LR
      • Sodium delivery to the distal tubule enhances calcium clearance by the kidneys
    • Evaluate for underlying cause
  • If Ca+2 > 12 with symptoms or Ca > 14
    • Trend Ca q8 hrs, EKG, monitor on telemetry; strict I/Os ± foley catheter
    • Volume expansion with NS bolus followed by continuous infusion at ~ 200cc/hr
      • Goal UOP 100-150cc/hr
    • Add loop diuretic (Lasix) once patient is volume expanded
    • Bisphosphonates
      • Zoledronic acid 4mg IV (EGFR >60) given over 15 minutes normalized calcium in 80-90% of patients over 48-72 hours, with a median treatment duration of 30-40 days.
      • Pamidronate 90mg IV (EGFR 15-60) given over 2 hours normalizes calcium in 60-70% of patients over 48-72 hours, with a median treatment duration of 11-14 days
  • If Ca+2 >14 or neurologic symptoms, consider subq (not intranasal) calcitonin
    • VUMC: requires approval from an oncology or endocrine attending
    • Tachyphylaxis after ~48H
  • If etiology of hyperparathyroidism is due to primary hyperparathyroidism, indications for parathyroidectomy include:
    • Age <50
    • Calcium level >1mg/dL above ULN
    • Renal dysfunction
    • Kidney stones or high risk of kidney stones
    • Fragility fractures or osteoporosis
  • Additional Information
    • CHF: consider early addition of a loop diuretic, especially if volume overloaded
    • ESRD with hypercalcemia (rare), oliguric AKI not responsive to IVF, or severely elevated Ca 16-18: consult Endocrine and Nephrology early
    • Sarcoidosis or lymphoma: consider glucocorticoids

Hypocalcemia

Trey Richardson

Background

  • Can be divided into low PTH and high PTH states
    • Low PTH
      • Magnesium deficiency
      • Post-operative for parathyroidectomy
      • DiGeorge syndrome
      • Medications: bisphosphonates, denosumab, aminoglycosides, gadolinium
      • Infiltrative disease: sarcoid, hemochromatosis, malignancies
      • Autoimmune hypoparathyroidism
      • CRRT (if using regional citrate anticoagulation)
    • High PTH
      • Late-stage CKD
      • Hyperphosphatemia
      • Vitamin D deficiency
      • Alkalemia (Serum Ca is inversely proportional to pH)
      • Pseudohypoparathyroidism/Parathyroid resistance
      • Consumption/deposition: pancreatitis, rhabdomyolysis, some osteoblastic metastases
      • Sepsis or critical illness

Presentation

  • Chvostek (facial muscle twitching), Trousseau’s sign (carpopedal spasm) , laryngospasm, seizures, widened QRS and arrhythmias
  • Hemodynamic instability

Evaluation

  • Check PTH, albumin, iCal, VBG, Vitamin D
  • Review medications for possible offenders

Management

  • Under most circumstances there is no need to replace calcium. Instead, focus on correcting the underlying perturbation (e.g. acidemia, hypomagnesemia, treating pancreatitis, etc. )
  • If hemodynamic instability, cardiac electrical instability, or seizures, then aggressive intravenous replacement is warranted.
    • Also consider preemptive repletion for patients requiring high-volume of blood transfusions (citrate in blood products can cause hypocalcemia)
    • 1 g of CaCl is equivalent to 3 grams of Ca Gluconate
  • Avoid treatment in hyperphosphatemia, advanced CKD/ESRD, and rhabdomyolysis

Hypernatremia

Lauren Chan

Overview of dysnatremias

  • Fluctuations in serum Na reflect fluctuations in plasma free water
  • Sodium is the major driver of tonicity. The clinical signs and symptoms of serum Na fluctuations are related to changes in tonicity with most profound effects on cerebral tissue
  • Two major mechanisms maintain plasma osmolarity between 275 and 290: Thirst and secretion of ADH. When these mechanisms malfunction, dysnatremias occur

Background

  • Definition: Na+ >145
  • Hypernatremia = decreased free water
  • Almost always due to inadequate free water intake (ICU patients, dementia, limited mobility, tube feeding/TPN, impaired thirst/adipsia from hypothalamic stroke). Hospital acquired hypernatremia is iatrogenic and correlates with poor outcomes
  • Can also occur from: Na+ overload (salt poisoning, iatrogenic from NS infusion, over correction), osmotic diuresis (hyperglycemia, SGLT-2 inhibitors, urea, mannitol), diabetes insipidus

Presentation

  • Lethargy, irritability, confusion
  • Seizures, coma, hemorrhagic stroke, or subarachnoid hemorrhage (from the effects of hypertonic serum on cerebral vasculature)

Evaluation

  • Step 1: Treat underlying cause (vomiting, hyperglycemia, medications)
  • Step 2: Determine volume status. If severely hypovolemic, the patient will need IV crystalloid to restore volume in addition to free water
  • Step 3: Estimate and replace free water deficit (FWD):
    • FWD = TBW x [(serum Na/140) - 1]
  • Step 4: Account for ongoing insensible losses and electrolyte free water clearance
    • Rule of thumb for accounting for electrolyte free water clearance. This is in addition to replacing free water deficit
    • 0-1 Liter of urine output: ignore, no need to replace
    • 1-3 Liters of urine output: replace half of the losses
    • >3 liters of urine output: replace all urine losses
  • No evidence that overcorrecting hypernatremia is harmful. In fact, there is increased mortality with overly cautious correction or under correction
  • If able, replace free water enterally. Otherwise, administer D5W intravenously 

Additional Information

  • Suspected DI: Consult Nephrology (may require desmopressin or may receive desmopressin once stabilized to differentiate between central and nephrogenic DI)
  • Hypokalemia: giving K decreases total amount of free water you are giving the patient

Hyponatremia

Lauren Chan

Background

  • Definition:
    • Mild: Na+ 130-134
    • Moderate: Na+ 125-129
    • Severe: Na+ <125
  • Hyponatremia occurs when free water reabsorption (i.e ADH is on) or intake exceeds free water excretion

Presentation

  • Mild to moderate symptoms: lethargy, N/V, dizziness, confusion, fatigue, cramping
  • Severe symptoms: obtundation, coma, respiratory arrest, seizure

Evaluation and Management

  • Step 1: Serum osm
    • >295: Hyper-osmolar, presence of other molecules that contribute to serum osmolarity
      • Glucose, mannitol, iodinated contrast
      • If hyperglycemic, corrected serum Na+ = measured Na+ + 1.6*[(glucose – 100)/100]
        • If corrected Na+ is normal, treat hyperglycemia; not a water balance problem
        • If corrected Na+ is low, there is hypotonic hyponatremia + coexisting hyperglycemia
      • Renal failure (urea) and ethanol: Ineffective osmoles that can freely diffuse across cells and do NOT lead to hyponatremia
    • 275-295: Iso-osmolar
      • Pseudohyponatremia due to hypertriglyceridemia, paraproteinemia, or lipoprotein X: Serum Na not actually low, due to how the lab is calculated
    • <275: Hypo-osmolar  step 2
  • Step 2: Urine osm
    • Surrogate for ADH activity
    • Uosm <100 or Uosm < Sosm correlates with low ADH (the body is appropriately trying to get rid of water so ADH is appropriately suppressed)
      • Primary polydipsia: free water intake>output
      • Tea and toast: lack solute to effectively concentrate urine
      • Beer drinkers’ potomania: mixture of the two above
    • Uosm >100 or Uosm > Sosm correlates with high ADH → Step 3 (the body is retaining water, so ADH is elevated)
  • Step 3: Urine Na
    • Is ADH on in the setting of decreased effective arterial blood volume (EABV) or decreased mean arterial pressure (i.e. appropriate ADH)?
    • UNa <20: Low EABV → RAAS upregulation with Na avidity → appropriate ADH release
      • If true volume depletion, then trial 500cc-1L NS bolus and monitor serum Na. IVF bolus → increase EABV → decrease ADH release →→ free water excretion
      • If edematous state (e.g. heart failure or cirrhosis), then decongestion with diuretics may improve serum Na
    • UNa >40: euvolemic with no stimulus for ADH → SIADH
      • SIADH from: n/v, malignancy, meds, surgery, pulmonary disease, hormones, pain, bladder distension: ↑ ADH out of proportion to stimulus
        • Treat with water restriction. Can add NaCl or urea tabs if fluid restriction is severe
        • Water restriction (L/day) = 600 / uosm (600 mEq Na in American diet/day)
        • Salt wasting: diuretics, cerebral salt wasting (aka hypovolemic SIADH), SSRIs
        • Get a Chest Xray – look for treatable pulmonary etiologies (effusions, pneumonia etc.)
        • Other: hypothyroidism, adrenal insufficiency
  • If still stumped, can check a FeNa and measure a serum uric acid
    • FeNa <0.5 % suggests appropriate ADH activity
    • High uric acid suggests some degree of volume depletion and appropriate ADH activity

Rate of correction

  • Acute (<48 hrs)
    • If symptomatic, give 150 cc bolus 3% NaCl up to two times.
    • Monitor Na+ q1-2 hr o Goal is an initial rapid 4-6 mEq/L correction and then hold
    • May require Hypertonic Saline infusion with DDAVP clamp if at risk of over-correcting
  • Chronic (>48 hrs or unknown, higher risk for osmotic demyelination if corrected too quickly):
    • Goal Na+ correction rate 4-6 mEq/L over 24 hrs (Max 8mEq/L)

When to call Nephrology

  • If you are worried about rapid over-correction
    • High risk patients are those with rapidly reversible causes
      • Low solute states (Beer drinker’s potomania, psychogenic polydipsia, tea-toast) as soon as they decrease their excess free water intake, they will rapidly clear free water
      • Volume depletion: As volume is replaced and the stimulus for ADH release is switched off, then patients will rapidly clear the excess free water if they have normal underlying kidney function
    • High risk for ODS includes chronic liver disease, Na <105 meq/dL, alcoholism, and malnutrition
  • Consideration of DDAVP clamp

Hyperkalemia

Mengyao Tang, Amanda Morrison

Background

  • Causes:
    • Cellular shifts: acidemia, rhabdomyolysis, TLS, beta blockade
    • Aldosterone deficient states: T4 RTA, primary adrenal insufficiency
    • Decreased distal tubular delivery: volume depletion
    • Decreased clearance: AKI, CKD, ESRD
    • Excessive intake
    • Medication-related: ACEi, ARB, MRA, NSAIDs, TMP/SMX, digoxin, heparin
  • Pseudo-Hyperkalemia: hemolysis, severe leukocytosis
  • Symptoms are rare, but usually manifest as cardiac dysrhythmias

Evaluation

  • Confirm hyperkalemia with repeat BMP
  • Check EKG for hyperkalemic changes (sensitivity for EKG findings in hyper K is poor)
    • K+ 5.5-6.5: peaked T waves, prolonged PR interval
    • K+ 6.5-8: prolonged QRS, loss of P wave, ST elevation, ectopic beats
    • K+ >8: sine wave pattern, asystole, PEA, VF

Management

  • If EKG changes or signs of instability
    • Calcium gluconate 1g IV (effective within 3-5 min)
      • Stabilizes cardiac membrane for ~60mins
      • SHOULD BE REPEATED HOURLY while hyperkalemic
  • Shift K+ (temporizing measures)
    • D50 with regular insulin 10 units (can order using Adult Hyperkalemia order set in Epic)
      • Use 5 units if there is renal impairment
      • Lasts for 4-6hrs (can be longer in renal impairment)
    • Correct acidosis: consider using isotonic bicarb
    • Beta agonists (e.g. high-dose albuterol nebulizer); lasts 2-4 hrs
      • Note that typical albuterol nebulizer is 2.5mg, need 10-20mg to have an effect
  • Increase K+ excretion
    • Loop diuretic: if the kidneys work, use them
      • If there is AKI or a volume deficit can administer with IVF
    • Volume expansion with IVF: increases distal Na delivery and K excretion. NS and LR are likely equally effective.
    • GI cation exchangers
      • Kayexalate (Polystyrene sulfonate): only effective if having BMs. 60g PO q2h until bowel movement (If using oral, ensure patient is having bowel movements and is not obstructed, could cause bowel injury/ necrosis). PO can take up to 6hrs to work. Consider per rectal administration for faster action but DO NOT GIVE WITH SORBITOL per rectum
      • Lokelma (Sodium-zirconium-cyclosilicate) 10 g PO TID for 48 H. Actively exchanges K for Na within the small bowel and works within 2 hours. Remember to stop once the K is normal since can cause hypokalemia. Also keep in mind the high Na content of Lokelma (400mg/5g dose of lokelma). Valtessa (Patiromer) Is an alternative, though not on VUMC Inpatient formulary.
    • Hemodialysis: Consult Nephrology early if severe hyper K+

Hypokalemia

Peter Thorne, Patrick Steadman

Background

  • Potassium (K+) < 3.5 mEq/L
  • 98% of total body K+ is intracellular (majority in muscle cells)
  • Goal: prevent life threatening complication (e.g. arrhythmia), replace deficit, elucidate cause
  • Insulin and catecholamines (beta adrenoreceptors) are key drivers of transcellular shifts
  • H+ and K+ will trade places to maintain electroneutrality

Presentation

  • Malaise, weakness, myalgias, decreased gastrointestinal motility
  • EKG changes:
    • Mild: ST segment depression, decreased T wave amplitude
    • Severe: U-waves (most commonly seen in precordial leads V2 and V3)
  • Severe hypokalemia can lead to rhabdomyolysis

Evaluation

  • History: decreased K+ intake, increased entry into cells (e.g. elevated beta-adrenergic activity, hypothermia), GI losses, urinary losses (diuretics, hypomagnesemia, RTA, tubular defects, hyperaldosteronism)
  • If concomitant metabolic alkalosis: Normal/low BP suggests diuretic use, vomiting or Gitelman/Bartter syndromes
  • Hypertension suggests renovascular disease or primary mineralocorticoid excess
  • Labs: BMP, CBC, VBG, urine electrolytes, magnesium, POC glucose, CK. Possibly aldosterone, renin, cortisol pending clinical context
  • Imaging: Renal US, CT AP

Management

  • Check Mg, replete to 2. Give empirically while waiting for serum Mg
  • K+ preparation (route); replete to 4
  • Choice of agent: o KCl is used for repletion in the hospital
    • PO tablets for mild asymptomatic hypokalemia
    • IV can be given through peripheral (rate is 10mEq/hr, may have burning sensation) or central access
  • K+ bicarbonate can be dissolved and put through G tube
    • Useful in patients with hypokalemia and metabolic acidosis
  • Dose:
    • Normal renal function: 10 mEq K+ is expected to raise serum [K+] by 0.1 mEq/L
    • Significant CKD or AKI: at risk of overcorrection
      • Shortcut: multiply the mEq by the Cr = how much K+ expected to rise
      • Once K+ higher than 5.5, K+ increases much faster and rules above do not apply

Hyperphosphatemia

Peter Thorne, Amanda Morrison

Background

  • Phosphate (PO4-3) > 4.5mg/dL
  • Etiologies
    • Cellular shifts: cellular lysis (TLS, rhabdomyolysis), acidemia (lactic acidosis, DKA)
    • Increased intake/absorption or iatrogenic hyperphosphatemia (over repletion, vitamin D toxicity, use of Fleet’s enemas, etc.)
    • Decreased phosphate clearance (acute or chronic renal disease, hypoparathyroidism, pseudohypoparathyroidism)

Presentation

  • Symptoms are usually secondary to coexistent hypocalcemia (psychosis, seizure, perioral paresthesias, muscle weakness)
  • Can cause acute phosphate nephropathy with phosphate containing laxatives
  • Calciphylaxis if concurrent hypercalcemia (high Ca+2 x PO4-3product)

Evaluation

  • Labs: BMP (calcium, creatinine), VBG, Vit D, PTH, PTHrP, lactate

Management

  • Acute
    • If renal function normal, can often treat with IVF (promote PO4-3 excretion)
    • Consider need for calcium supplementation (see hypocalcemia section)
    • If renal function impaired and severe hypocalcemia present, consider hemodialysis
  • Chronic
    • Usually secondary to chronic renal failure, goal PO4-3 3.5-5.5 in CKD patients
    • Renal diet (low PO4-3)
    • PO4-3 binders: Ca+2 containing (calcium carbonate and calcium acetate) and non Ca+2 containing (sevelamer, lanthanum, and iron based such as ferric citrate)
      • Sevelamer is significantly more expensive than calcium containing binders
    • Given 3 times daily with meals, started at 800mg (Can be ↑ to 1,600mg TID)
    • Should not be given if patient is not eating
    • Calcium acetate: started at 1334mg TID with meals
      • Limit dose changes to chronic binders upon discharge
      • Need to avoid calcium containing binders in patients with calciphylaxis

Hypophosphatemia

Peter Thorne

Background

  • Required for metabolic pathways (ATP production)
  • Most renal reabsorption occurs in proximal tubule via sodium-phosphate cotransporter
  • Common causes
    • Internal redistribution, reduced intestinal absorption
    • Refeeding syndrome
    • Alkalemia
    • Phos binders on purpose or inadvertently (calcium, aluminum, magnesium antacids)
    • Excessive loss (diarrhea, CRRT, increased urinary excretion)
    • Proximal tubular dysfunction such as in Fanconi Syndrome
    • Hyperparathyroidism causes renal phos wasting
    • Post-parathyroidectomy leading to hungry bone syndrome
    • Vitamin D deficiency or resistance

Presentation

  • Mild hypophosphatemia (serum >2.0) rarely symptomatic

  • PO4-3< 2.0: muscle weakness

  • PO4-3< 1.0: heart failure, respiratory failure, rhabdomyolysis, seizures

  • Failure to wean from ventilator

Evaluation

  • Urine PO4-3 level if cause not readily apparent
  • Calculate Fe PO4-3 ([U PO4-3 x PCr x 100]/[P PO4-3x UCr])
    • Fe PO4-3 < 5% = normal renal response to hypophos: redistribution or ↓ absorption
    • Fe PO4-3 > 5% = renal phos wasting

Management

  • Caution replacing in patients with impaired renal function. Start with half suggested dose
  • If K+ > 4 and patient requires IV repletion, may need to use sodium PO4-3 in place of K+ PO4-3 IV; PO preferred unless severe or symptomatic, or patient cannot take PO
    • K-Phos neutral: oral, each 250mg tablet has 8 mmol of PO4-3 and 1.1mEq of K+
    • K+ PO4-3: IV, each mL has 3mmol PO4-3, 4.4 meq K+
    • Na+ PO4-3: IV, each mL has 3mmol PO4-3 - PO4-3>1.5: PO: 40 – 80 mmol K+Phos neutral (aim for 1 mmol/kg) divided into 3-4 doses/day
  • PO4-3 1.25 - 1.5: oral 100 mmol K+ PO4-3neutral in 3-4 divided doses if asymptomatic
    • IV: 30 mmol K+ PO4-3over 6 hours (aim for 0.4mmol/kg) if symptomatic
  • PO4-3<1.25: IV: 80mmol K+Phos over approximately 12 hours (aim for 0.5mmol/kg)
    • Check serum PO4-3 2-12 hrs after last dose of PO4-3 to determine if additional needs

Hypomagnesemia

Mike Tozier

Background

  • Definition: Mg+2 < 1.8 mg/dL, most patients asymptomatic until <1.2 mg/dL. Severe [Mg+2] < 1 mg/dL
  • Causes
    • GI losses: diarrhea, malabsorption, acute pancreatitis, EtOH use, TPN, vomiting, NG suction, GI fistulas, anorexia, short gut syndrome, small bowel bypass
    • Drugs: PPIs, loop diuretics, thiazides, digoxin, amphotericin, aminoglycosides, foscarnet, cisplatin, calcineurin inhibitors, laxatives, pentamidine
    • Kidney losses: post-ATN diuresis, Bartter syndrome and Gitelman syndrome
    • Cellular shifts: DKA treatment/recovery, refeeding, hungry bone syndrome, correction of metabolic acidosis, pancreatitis, EtOH withdrawal
    • Other: DM, hyper Ca, hyperthyroid, hyperaldosteronism, burns, lactation, Vit D deficiency, heat, prolonged exercise, mitral valve prolapse, pseudohypomagnesemia due to EDTA tube, lactation

Presentation

  • Refractory hypocalcemia or hypokalemia, arrhythmias, muscle weakness
  • Severe symptoms: seizures, drowsiness, confusion, coma, arrhythmias
  • Vertical nystagmus, tetany (Chvostek sign, Trousseau), tremors, fasciculations

Evaluation

  • EKG: Initially wide QRS, peaked Ts. Progresses to wide PR, diminished T, arrhythmias
  • Labs: Ca+2, K+, can use FEMg (order urine Mg+2 and Cr, serum Cr and Mg) or 24-hour urine for Mg to distinguish renal vs GI etiology (FEMg >2% renal, <2% GI)

Management

  • Correct underlying cause, replete based on severity (Dosing below for normal GFR)
  • Oral: asymptomatic patients, can cause GI symptoms, not well absorbed
    • Sustained release (Mg Chloride or Mg L-lactate) better tolerated and absorbed, though standard preparations (Mg oxide) are faster acting
    • Mg chloride: 3-4 tabs BID (total 30 to 56 meq [15 to 28 mmol]) for severe hypo Mg
    • 2-4 tabs daily (total 10 to 28 meq [5 to 14 mmol]) for mild hypo Mg
    • Mg oxide: 400-800 mg BID (20 to 40 mmol [40 to 80 meq]) for mod-severe hypo Mg
  • Intravenous: for symptomatic patients or if GI intolerance to oral
    • Mg <1 mg/dL: 4 to 8g of MgSO4 (32 to 64 meq [16 to 32 mmol]) over 12 to 24 hrs
    • Mg 1 to 1.5 mg/dL: 4 g MgSO4 (16 to 32 meq [8 to 16 mmol]) over 4 to 12 hrs
    • Mg 1.6 to 1.9 give 1 to 2 grams MgSO4 (8 to 16 meq [4 to 8 mmol]) 1-2 hrs
      • VUMC only has 4g bags of IV mag so would need to ask nurses to only infuse 1/2 bag
    • Infusion rate should not exceed 2 g/hr to minimize urinary excretion

Additional Information

  • Renal impairment: replete with caution, reduce dose by 50-75% and monitor closely
  • If persistent hypo Mg in patients requiring diuresis, try K-sparing diuretic (e.g. amiloride)
  • Treat concomitant hypokalemia, hypocalcemia or hypophosphatemia
  • In patients with concomitant hypophos and hypocalcemia, IV Mg alone may worsen hypophos
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