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
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
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.
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.
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).
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.
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.
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.
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
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
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
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
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
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.
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.
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.
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
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.
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
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
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 .
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
. Neurological symptoms most likely caused by hypermagnesemia
. Next step:
C increased mg levels
D Stop laxatives
E iv fluids , iv diuretic consider HD if no improvement
HD will work faster than PD
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
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.
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.
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).
C- ⬆️ mg
D-High fluid volume,Calcium gluconte ,diuretics.
+/- hemodialysis.
E- if not response for H.D
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
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.
Case of severe symptomatic hypermagnesemia
need :
IVF
diurtics
calcium to protect the heart
if no response go for dialysis.
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.
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.
Sever symptomatic hypermagnesemia.
Management:
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
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
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
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
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
C. What is the most likely cause of the patient’s neurological symptoms?
*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?
E. Appraise the rationale for diuretics use and various dialysis modalities in this case.
The most likely cause
Sever symptomatic hypermagnesemia.
Management
Diuretics;
Diuretic vs hemodialysis;
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.
C- hypermagnesemia
D- stop mg oxide , loop diuretics with good hydration
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
C. What is the most likely cause of the patient’s neurological symptoms?
Severe symptomatic Hypermagnesemia .
D. What is your next management step?
E. Appraise the rationale for diuretics use and various dialysis modalities in this case.
C. What is the most likely cause of the patient’s neurological symptoms?
Severe symptomatic Hypermagnesemia
D. What is your next management step?
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.
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
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.
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
C. What is the most likely cause of the patient’s neurological symptoms?
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.
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.