Scenario 2 – Part 2:

Brain imaging revealed small chronic lacunar infarctions. EEG did not show significant changes. Surface EMG showed dysfunction of lower limb muscles. All other body imaging was unremarkable. Serum magnesium was found to be 6.6 mmol/L and uric acid 7.8 mg/dL.

C. What is the most likely cause of the patient’s neurological symptoms?

D. What is your next management step?

E. Appraise the rationale for diuretics use  and various dialysis modalities in this case.

31 Comments

  • Radwa Ellisy


    The most likely cause is hypermagnesemia

    the next step is antagonizing the effect of hypermagnesemia by giving the patients by calcium gluconate, then diuretics by higher doses then last step dialysis therapy

  • Marwa Alm


    . Neurological symptoms most likely caused by hypermagnesemia
    . Next step:

    • Stop Mg supplements
    • IV calcium gluconate (reverse Mg effect)
    • Diuresis if good UOP, mentaining euvolemic state with iv fluids
    • Dialysis if oliguric, hemodialysis is faster and more effective in removing Mg, CRRT or peritoneal dialysis if hemodynamically unstable.
  • Muhammad Soobadar


    C increased mg levels
    D Stop laxatives
    E iv fluids , iv diuretic consider HD if no improvement
    HD will work faster than PD

  • Areij Alotaibi


    1-hyperMG
    2-stop mg oxide , hydration and loop diuretics
    3-Hemodialysis faster than peritoneal dialysis in lowering magnesium levels

    loop diuretic exerts its effect through Inhibiting sodium chloride reabsorption also inhibits the back leak of potassium and the generation of the lumen-positive potential, thereby decreasing the electrical gradient for magnesium reabsorption and increasing urinary magnesium excretion.
    Thiazide diuretic acts by blocking Na-Cl cotransporter so reduces renal expression levels of TRPM6 which is responsible for magnesium reabsorption 

  • Asma Aljaberi


    C. What is the most likely cause of the patient’s neurological symptoms? 
    Hyeprmagnesemia causing muscle weakness, especially speech muscles leading to dysarthria and lower limb muscle weakness

    D. What is your next management step?
    Stop Mg supplement, good hydration, IV Ca gluconate, beta agonist nebs, IV glucose, also IV diuretics.

    E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    Both diuretics and dialysis can effectively remove excess magnesium and uric acid from the blood.The choice of dialysis modality will depend on several factors, including the patient’s age, overall health, and personal preference.

    Hemodialysis and peritoneal dialysis have their advantages and disadvantages. Hemodialysis is generally faster and more efficient at removing excess magnesium from the blood, while peritoneal dialysis may be less effective at removing excess magnesium and may require more frequent treatments.

  • Mohammed Farag


    Hypermagnesemia
    the effects of magnesium can be temporarily antagonized by the administration of intravenous calcium salts (5 to 10 mL of 10% calcium chloride). Renal magnesium excretion can be enhanced by administering furosemide (20 to 40 mg every 4 hours) together with a saline infusion (0.9% NaCl at 150 mL/ hour, titrated to replace urinary losses). In patients with advanced renal insufficiency, the most effective method of magnesium removal is hemodialysis.

  • Mahmoud Sobh


    Model Answer Approved By The Board:
    What is the most likely cause of the patient’s neurological symptoms? 
    Hypermagnesemia causes neuromuscular symptoms including diminished deep tendon reflexes, somnolence and muscle paralysis. the patient is CKD stage and received big dose of magnesium (5).

    What is your next management step?

    Intravenous calcium gluconate (15 mg/kg) should be given over a 4-h period. Ca+antagonizes the neuromuscular and cardiovascular effects of hypermagnesemia for patients with normal kidney function, intravenous fluid plus loop diuretics are effective.

    Patients with moderate CKD (eGFR 15-45 ml/min/1.37m2) and mild AKI initial treatment with saline and loop diuretics (consider higher doses required in these cases). If these measures fail, dialysis should be considered.

    Dialysis is often required in patients with severe or symptomatic hypermagnesemia who have advanced CKD or moderate to severe AKI, hemodialysis is the treatment of choice (1).

    Appraise the rationale for diuretics use and various dialysis modalities in this case.
    Hemodialysis, with its higher flow rates, works more rapidly than peritoneal dialysis, lowering magnesium levels to a nontoxic range within two to four hours.
    loop diuretic exerts its effect through Inhibiting sodium chloride reabsorption also inhibits the back leak of potassium and the generation of the lumen-positive potential, thereby decreasing the electrical gradient for magnesium reabsorption and increasing urinary magnesium excretion.
    Thiazide diuretic acts by blocking Na-Cl cotransporter so reduces renal expression levels of TRPM6 which is responsible for magnesium reabsorption (6). 

  • Khaldon Rashed Ahmed Moqbil


    C- ⬆️ mg
    D-High fluid volume,Calcium gluconte ,diuretics.
    +/- hemodialysis.
    E- if not response for H.D

  • HASSAN ALYAMMAHI


    C
    sever hypermagnesemia

    D
    Stop MgO, rehydrate if dehydrated, Ca gluconate, may need dialysis

    E
    loop diuretics reduce lumen positivity, so reducing paracellular reabsorption and increasing urinary loss
    Dialysis is a last option

  • Rania Mahmoud


    C. What is the most likely cause of the patient’s neurological symptoms?
    severe symptomatic hypermagnesemia
    D. What is your next management step?

    Patients with normal renal function (GFR over 60 ml/min) and mild asymptomatic hypermagnesemia require no treatment except the removal of all sources of exogenous magnesiumIntravenous calcium gluconate or chloride [Dosage: 1 g in 2 to 5 min (repeatable over 5 minutes)].Intravenous normal saline (e.g., at 150 ml/hour)E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    Severe clinical conditions require increasing renal magnesium excretion through:Intravenous loop diuretics (e.g., furosemide 1 mg/kg), orHemodialysis, when kidney function is impaired, or the patient is symptomatic from severe hypermagnesemia. This approach usually removes magnesium efficiently (up to 50% reduction after a 3- to 4-hour treatment). Dialysis can, however, increase the excretion of calcium by developing hypocalcemia, thus possibly worsening the symptoms and signs of hypermagnesaemia.The use of diuretics must be associated with infusions of saline solutions to avoid further electrolyte disturbances (e.g., hypokalemia) and metabolic alkalosis. The clinician must perform serial measurements of calcium and magnesium. In association with electrolytic correction, it is often necessary to support cardiorespiratory activity. As a consequence, the treatment of this electrolyte disorder can frequently require intensive care unit (ICU) admissionParticular clinical conditions require a specific approach. For instance, during the management of eclampsia, the magnesium infusion is stopped if urine output drops to less than 80 mL (in 4 hours), deep tendon reflexes are absent, or the respiratory rate is below 12 breaths/minute. A 10% calcium gluconate or chloride solution (10 mL intravenously repeatable over 5 minutes) can serve as an antidote.

  • Asmaa Salih KHUDHUR


    Case of severe symptomatic hypermagnesemia
    need :
    IVF
    diurtics
    calcium to protect the heart
    if no response go for dialysis.

  • Alaa Abdel Nasser


    What is the most likely cause of the patient’s neurological symptoms?
    Hypermagnesemia

    What is your next management step?
    Initial treatment consists of cessation of magnesium-containing medications and therapy with intravenous isotonic fluids plus a loop diuretic .
    If these measures fail to improve the serum magnesium concentration, dialysis may be required, especially if there are severe neurologic manifestations (eg, paralysis, somnolence, coma)
    patients with symptomatic hypermagnesemia should be given intravenous calcium as a magnesium antagonist to reverse the neuromuscular and cardiac effects of hypermagnesemia. The usual dose is 100 to 200 mg of elemental calcium over 5 to 10 minutes. 

  • Mahmud ISLAM


    Elevated magnesium levels may block acetylcholine release from the neuromuscular endplate, leading to neurologic symptoms.
    The next step is iv hydration and furosemide. Ca+ can be needed to stabilize heart rhythm. In resistant or unresponsive cases, dialysis can be performed.

  • Mahmoud Elsheikh


    Sever symptomatic hypermagnesemia.
    Management:
    

    • High fluid volume.
    • Calcium preparation.
    • Combined diuretics.
    • +/- hemodialysis.
  • Hagar Ali


    c)hypermagnesemia
    D)stop intake, diuretics if his fluid status allow us ,ca gluconate IV
    Dialysis if no improvement
    E)diuretics if his renal function intact
    hemodialysis will offer a good option for clearing s.mg in renally impaired patients

  • Riaan Flooks


    C: Hypermagnesemia

    D: Admit to an ICU or High-Care for observation
    Stop the offending drugs, and if his fluid status allows, administer IV-fluids
    Diuretic therapy (Loop diuretic) since the patient is having impaired renal function
    Calcium gluconate to antagonize the neuromiscular and cardiovascular effects

    E: Hemodialysis with a Mg-free dialysate would be treatment of choice, since it provides an efficient way of lowering the s-Mg level

  • Rihab Elidrisi


    This is hypermagnesemia which causes abnormality in EMG
    I will start by stopping the offending cause
    good rehydration
    diuretics
    Iv Ca gluconate
    We may need to have dialysis if not responding to medical managment

  • Emad mohamed mokbel Salem


    C-mostly due to hypermagnesemia

    E- ABCD approach
    1-stop mg containing medications
    2-hydration according to volume status
    3- diuretics
    4- iv calcium gluconate
    5- hemodialysis if not responding to other treatments

    E-
    Diuretics promote Mg excretion in patient with normal GFR
    Dialysis for patient symptomatic with renal insufficiency

  • Rabab ALaa Eldin keshk Rabab


    C. Most likely causing symptoms was hypermagnisimia.
    D. Next step for management stop mg oxide medication give pt good hydration
    Loop diuretics if all measure diaylisis with low mg diaylisate.
    E.the use of diuretic is essential dueto increase mg excration provided good hydration of patient.
    Diaylisis not needed of patient untill sever renal dysfunction or failure if diuretics

  • Amna Kununa


    C. What is the most likely cause of the patient’s neurological symptoms?

    • severe hypermagnesemia in the setting of constipation and Magnesium oxide.
    • hypermagnesemia is primarily seen in three settings:

    *Renal impaired.
    *A large magnesium load is given (iv, orally, or as an enema).
    *Increased absorption from the GI due to constipation, colitis, gastritis, or gastric ulcer disease.

    Hypermagnesemia itself increases the neuromuscular blocking actions of Mg, further increasing gastrointestinal Mg absorption and resultant hypermagnesemia.

    D. What is your next management step?

    • Cessation of magnesium-containing medications
    • Intravenous isotonic fluids (NS 0.9%) plus a loop diuretic, higher diuretic doses may be required in this patient since he has advanced CKD.

    E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    • If the above measures fail to improve the s.Mg concentration, dialysis may be required, especially if there are severe neurologic manifestations or cardiovascular manifestations.
    • Hemodialysis, with its higher flow rates, works more rapidly than peritoneal dialysis, lowering magnesium levels to a nontoxic range within two to four hours.
    • Consider iv calcium as a magnesium antagonist to reverse the neuromuscular effect of hyperMg, as the bridge till dialysis is organized.
  • KAMAL ELGORASHI


    The most likely cause
    Sever symptomatic hypermagnesemia.
    Management

    • High fluid volume.
    • Calcium preparation.
    • Combined diuretics.
    • +/- hemodialysis.

    Diuretics;

    • Loop diuretics act on the thick ascending limb of the loop of Henle, it helps renal excretion of Mg.
    • Thiazide diuretic excrete Mg via inhibition of transcellular reabsorption of Mg..

    Diuretic vs hemodialysis;

    • Diuretic with high-volume IV fluid is usually sufficient for the treatment of hypermagnesemia, especially in patients with normal kidney function.
    • In severe symptomatic hypermagnesemia in advanced CKD or ESKD, the hemodialysis option is vital, especially if the response to treatment is delayed with life-threatening hypermagnesemia.
  • Nour Al Natout


    C. Hypermagnesimia
    D. Hydratation i.v. + loop diuretics i.v
    Intravenous .calcium gluconate to antagonise magnesium
    If not approved consider HD.
    E. Loop diuretics inhibit reabsorption of Mg inTALH and prox tubule
    Dialysis is the fastest and last choice.

  • Mark Nagy Zaki Amin Mark


    C- hypermagnesemia
    D- stop mg oxide , loop diuretics with good hydration

  • Israa Hammoodi


    C. Symptoms due to hypermagnesemia
    D. Stop source of Mg
    IV fluid, IV Calcium ampoule
    , give diuretic, if no response dialysis
    E. Diuretic use increase the Mg excretion in urine
    Hemodialysis used if no response
    If peritoneal dialysis used with low Mg level

  • Ahmed Altalawy


    C. What is the most likely cause of the patient’s neurological symptoms?
    Severe symptomatic Hypermagnesemia .
    D. What is your next management step?

    • stop oral magnesium and any magnesium containing laxatives.
    • adequate hydration.
    • IV calcium gluconate.
    • IV loop diuretics to increase renal magnesium excretion.
    • in severe cases, HD may be needed for control of hypermagnesemia.

    E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    • Loop diuretics increase magnesium excretion.
    • HD is the last resort for managing resistant hypermagnesemia.
  • Weam El Nazer


    C. What is the most likely cause of the patient’s neurological symptoms?

    Severe symptomatic Hypermagnesemia

    D. What is your next management step?

    • stop Mg Oxide.
    • Patients with symptomatic hypermagnesemia should be administered intravenous calcium as a magnesium antagonist to counteract the neuromuscular and cardiac effects. 100–200 mg of elemental calcium over 5–10 minutes is typical.
    • intravenous isotonic fluids (eg, normal saline) plus a loop diuretic (eg, furosemide). Higher diuretic doses may be required in these patients since they have a reduced glomerular filtration rate (GFR).
    • If the level is still high, consider hemodialysis. especially if there are severe neurologic manifestations (e.g., paralysis, somnolence, or coma) or cardiovascular manifestations.

    E. appraise the rationale for diuretics use and various dialysis modalities in this case.

    Patients with severe or symptomatic hypermagnesemia, advanced CKD, or moderate to severe AKI typically need dialysis. Hemodialysis lowers magnesium levels to harmless levels faster than peritoneal dialysis. 

    Intravenous fluids and loop diuretics should also be initiated, especially in severe or symptomatic cases, while preparing for dialysis.

  • Elsayed Ghorab


    HYPER MAGNISEMIA cause the neurological symptoms

    start iv fluid and diuretic as ( Loop or thazid )
    evaluate k level if need interference w hyperkalemic managment
    assessment diet >>>restrict Mg diet
    dialysis if not improved w conservative treatment

  • Ben Lomatayo


    C. What is the most likely cause of the patient’s neurological symptoms?

    • Severe hypermagnesaemia ( he had Mg of 6 and the normal range is between 0.7 to 1.1 mmol/l).
    • He had hyperuricemia as well but this doesn’t explain his current presentation

    D. What is your next management step?

    1. ICU admission & cardiac monitoring
    2. Stop all Mg preparations
    3. IV Ca gluconate slow boluses
    4. Forced Mg diuresis by IV furosemide 40 t0 80 mg & replacement of urine output by NaCl 0.45% on ml to ml bases
    5. Emergency harmodialysis

    E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    1. Diuretics: As mentioned above will decrease Mg absorption & hence increase urinary excretion
    2. Haemodialysis: Provide rapid & effective normalization of Mg. Expect normalization of K with in 4 hours
  • Abdulrahman Almutawakel


    THE MOST LIKLY CAUSE IS HYPERMAGNESEMIA ( SEVERE ) , NEEDS ADMISSION FOR VIGOROUS IV FLUIED IF POSSIBLE , IV DIURETICS ( INCREASED EXCRETION AND REDUCE ABSORPTION ) , IF THOSE MEASURES NOT HELPS , MAY NEEDS FOR DIALYSIS WITH LOW MAGNESIUM DIALYSATE

  • Ashraf Ahmed Mahmoud


    C. What is the most likely cause of the patient’s neurological symptoms?

    • hypermagnesemia.

    D. What is your next management step?
    removal of the cause ( oral Mg).
    volme expansion
    loop diuretic
    iv Ca gluconate( 15 mg /kg) to avoid neuromuscular and cardiovascular complication .

    E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    • Loop diuretics decrease magnesium reabsorption in TALH.
    • HD using a Mg free dialysate is treatment of choice .
  • Ibrahim Omar


    C. What is the most likely cause of the patient’s neurological symptoms?

    • hypermagnesemia.

    D. What is your next management step?

    • stop oral magnesium and any magnesium containing laxatives.
    • adequate hydration.
    • IV calcium gluconate.
    • IV loop diuretics to increase renal magnesium excretion.
    • in severe cases, HD may be needed for control of hypermagnesemia.

    E. Appraise the rationale for diuretics use and various dialysis modalities in this case.

    • Loop diuretics increase magnesium excretion.
    • HD is the last resort for managing resistant hypermagnesemia. all modalities are effective but HDF and CRRT give more clearance.

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