Hypovolemic hyponatremia – sodium loss (renal, non-renal)
Presentation:
Acute can cause coma, brainstem herniation, seizures
Death not seen in chronic hyponatremia
Chronic hyponatremia can cause motor and gate problems, which puts them at increased risk of falls
Correcting chronic low sodium can lead to osmotic demyelination syndrome
Simultaneous low K+, sodium<105
Treatment:
Asymptomatic: free water restriction
Moderate hyponatremia: IV normal saline, Loop diuretics may be added
Severe hyponatremia: acute treatment=50 mL bolus of 3% saline
Serum Na should be corrected slowly—by ≤ 10 mEq/L over 24 h to avoid osmotic demyelination syndrome
Picmonic
Hyponatremia is a low serum sodium level less than 135 mEq/L. This causes a shift of fluid volume from the extracellular fluid to the intracellular fluid resulting in cellular swelling and reduced excitable depolarization of cells. Many things cause may precipitate hyponatremia including actual sodium deficits or relative sodium deficits. Some relative causes include water intoxication (water excess) which results in a hypoosmolar imbalance. An additional assessment is done to determine if the patient has hyponatremia related to fluid overload or a fluid deficit, as these conditions manifest slightly differently.
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hypovolemic hypernatremia
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Question 1
A 70 year-old man is brought to the emergency department by his daughter due to lethargy and change in mental status. His daughter states he was recently diagnosed with Alzheimer's disease and had to move in with her family to help with his activities of daily living. The patient has not had any fevers, chills, coughing, or changes in urination or stool. He has no other medical problems and takes no medications. Vital signs include Temp 36.9 C, BP 104/68 mmHg, HR 100/min, and RR 16/min. After standing for 10 minutes, his blood pressure is 82/58 mmHg. On physical exam, he is a frail, elderly man with dry oral mucosa. He is oriented to person only. His skin examination is shown here. Cardiac and pulmonary auscultation are within normal limits.
Laboratory results are as follows:
sodium 165 mEq/L
potassium 4.8 mEq/L
bicarbonate 30 mEq/L
chloride 124 mEq/L
The patient is started on IV 0.9% normal saline. Twenty-four hours later, his blood pressure is 120/74 mmHg sitting and 118/72 mm Hg after standing for 10 minutes. He is still rather lethargic but is now oriented to person and place. He now has moist mucous membranes and normal skin turgor.
His post-resuscitation labs are as follows:
sodium 156 mEq/L
potassium 4.2 mEq/L
bicarbonate 24 mEq/L
chloride 112 mEq/L
What is the best next step in the management of this patient?
A
Continue IV 0.9% saline
Hint:
Continuing IV 0.9% saline is no longer necessary, as the patient's physical exam indicates that his volume status is now restored. Administering IV 0.45% saline will allow for faster repletion of free water and correction of the sodium concentration.
B
Switch to IV 0.45% saline
C
Switch to oral free water
Hint:
Oral free water is a reasonable choice for well-functioning patients with free water depletion. However, this patient has dementia and may benefit from sodium correction with IV fluids.
D
Switch to IV free water
Hint:
IV free water carries the risk of RBC lysis in patients with hypernatremia.
E
Discharge the patient
Hint:
The patient should be discharged following normalization of his mental status and serum sodium level.
Question 1 Explanation:
This patient is suffering from hypovolemic hypernatremia, which should be initially treated with IV 0.9% normal saline, followed by IV 0.45% (half-normal) saline once the volume deficit has been eliminated.
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Decrease circulating volume = decrease of flow to kidneys means more bound urea in the blood, which means ↑ BUN
Treatment: intravenous (IV) 5% dextrose in water (D5W)
Rapid overcorrection causes cerebral edema and pontine herniation
Diabetes insipidus - Low urine sodium (but high serum sodium) and polyuria usually indicate diabetes insipidus
Neurogenic (central) is caused by deficient secretion of vasopressin (ADH - anti-piss-hormone) from the posterior pituitary
Nephrogenic DI is caused by kidneys that are unresponsive to normal vasopressin levels - usually inherited X-linked or from lithium or renal disease
Urine osmolality of less than 250, despite hypernatremia, indicated Diabetes Insipidus
Picmonic
Hypernatremia is characterized by a serum sodium level above the normal range of 145 mEq/L. Hypernatremia is an increase in osmolarity of the extracellular fluid volume (ECF). This may be attributed to an actual sodium excess in the ECF like hyperaldosteronism or a relative sodium excess which is caused by a decrease of free water in the ECF like dehydration. High serum sodium levels causes a fluid shift from the intracellular fluid volume (ICF) to the ECF. This causes cellular shrinking. Hypernatremia should be assessed along with fluid balance as it often is associated with a fluid excess or deficit.
Presentation: Peaked T waves prolonged QRS, muscle fatigue
Treatment: Insulin, sodium bicarbonate, and glucose. (drive potassium back into the cell). Calcium gluconate
(antagonize the effect of potassium on the heart)
Pearls: hyperkalemia with EKG changes must be treated immediately. The next progression is sine waves, V-tach, and V-Fib
Picmonic
Hyperkalemia is a condition in which a person's serum potassium level is higher than normal. It can result from a number of causes, such as severe tissue trauma, untreated Addison's disease, acute acidosis, misuse of potassium-sparing diuretics, or overdose with IV potassium.
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HYPERKALEMIA
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Question 1
An 84-year-old man is brought to the emergency room from his nursing residence with symptoms of nausea, diarrhea, and poor oral intake for the last three days. He has also appeared weak and fatigued. His past medical history is significant for hypertension and Alzheimer's disease. His medications include enalapril, metoprolol, amlodipine and donepezil. His temperature is 99.1 F, blood pressure 128/70 mm Hg, heart rate 96/min, and respiratory rate 17/min. On physical exam, he appears fatigued but in no acute distress, with normal skin turgor but dry mucous membranes. Cardiac, pulmonary, and abdominal exams are within normal limits. His electrocardiogram (ECG) is shown here. In addition to initial laboratory evaluation, which of the following is the best next step in the management of this patient?
A
Administer calcium gluconate
B
Administer kayexalate
Hint:
Kayexalate is used in the treatment of hyperkalemia but is not the best initial therapy when there are ECG changes.
C
Administer magnesium
Hint:
Magnesium is used in the treatment of hypokalemia.
D
Cardioversion
Hint:
The patient is not hemodynamically unstable and therefore would not require cardioversion.
Question 1 Explanation:
The patient most likely has hyperkalemia, as evidenced by his symptoms and ECG findings. The most appropriate next step in his management would be the administration of calcium gluconate to stabilize cardiac cell membranes.
Question 2
A 69-year-old male with a history of diabetes, hypertension, and chronic kidney disease presents to the ED with fatigue, muscle weakness, and palpitations. He states that it seemed to start yesterday and has progressed since that time. The emergency room PA obtains an EKG which demonstrates peaked T waves. The patient comments that a few days ago his blood pressure medications were changed. Which of the following medications was most likely added during that visit?
A
Lisinopril
B
Furosemide
Hint:
Furosemide is a loop diuretic and may contribute to hypokalemia.
C
Hydrochlorothiazide
Hint:
Hydrochlorothiazide is a thiazide diuretic and may contribute to hypokalemia
D
Nifedipine
Hint:
Nifedipine is a calcium channel blocker and is not known to affect potassium levels.
Question 2 Explanation:
This patient presents with hyperkalemia, most likely induced by the recent addition of lisinopril, an ACE inhibitor which is known to cause hyperkalemia.
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Hypokalemia
Definition: serum potassium of < 3.5 mEq/L
Causes:
Overuse of diuretics
Cushing’s syndrome
Presentation: Muscle cramps, constipation, flattened/inverted T waves, U waves
Treatment
Potassium repletion
remember to NOT use dextrose-containing fluids as this will stimulate insulin release and shift potassium within the cell, which worsens the hypokalemia
Replace magnesium in magnesium deficiency
Picmonic
Hypokalemia is defined as low serum potassium levels with the most common cause being from loop or thiazide diuretic use. Other causes include insufficient potassium intake, alkalosis, excessive insulin, increased renal excretion of potassium, and potassium loss from vomiting, diarrhea, and abuse of laxatives.
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HYPOKALEMIA
HYPOKALEMIA
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HYPOKALEMIA.
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Question 1
A 48-year-old male with a history of chronic alcoholism presents to the emergency department with complaints of fatigue, muscle cramps and weakness, and constipation. He reports that these symptoms have developed over the past several weeks, and he admits to currently drinking 750 ml of whiskey daily. Physical examination is significant for 1+ reflexes at the bilateral patellar tendons and absent reflexes distally at the bilateral Achilles tendons. A complete blood count, complete metabolic panel, and EKG are ordered. The patient's EKG is seen here. The results of the complete blood count and metabolic panel are pending. Which of the following is the best management for the most likely cause of this patient's condition?
A
IV potassium replacement alone
Hint:
Potassium replacement alone without correcting likely coexisting hypomagnesemia will make effective potassium replacement difficult.
B
IV magnesium and potassium replacement
C
Calcium gluconate followed by sodium bicarbonate, albuterol, insulin, and glucose
Hint:
These medications and treatment options are indicated in patients suffering from hyperkalemia, not hypokalemia. Treatment of hyperkalemia includes calcium gluconate for cardiac membrane stabilization, sodium bicarbonate, ß2 adrenergic agonists, insulin/glucose, kayexalate, loop diuretics, and hemodialysis (for severe/intractable hypokalemia or in patients with renal failure).
D
Kayexalate and furosemide
Hint:
These medications and treatment options are indicated in patients suffering from hyperkalemia, not hypokalemia. Treatment of hyperkalemia includes calcium gluconate for cardiac membrane stabilization, sodium bicarbonate, ß2 adrenergic agonists, insulin/glucose, kayexalate, loop diuretics, and hemodialysis (for severe/intractable hypokalemia or in patients with renal failure).
E
Hemodialysis
Hint:
These medications and treatment options are indicated in patients suffering from hyperkalemia, not hypokalemia. Treatment of hyperkalemia includes calcium gluconate for cardiac membrane stabilization, sodium bicarbonate, ß2 adrenergic agonists, insulin/glucose, kayexalate, loop diuretics, and hemodialysis (for severe/intractable hypokalemia or in patients with renal failure).
Question 1 Explanation:
A chronic alcoholic presenting with hypokalemia is likely also hypomagnesemic. In order to achieve effective correction of potassium levels, both potassium and magnesium must be replaced.
Question 2
Which of these is most accurate regarding hyperkalemia?
A
Excessive potassium intake alone is more commonly responsible for hyperkalemia than decreased renal potassium excretion
Hint:
Decreased potassium excretion is the most common cause of hyperkalemia. Excessive potassium intake and a shift of potassium from the intracellular to the extracellular space are also potential pathophysiologic mechanisms.
B
Drugs responsible for hyperkalemia include angiotensin-receptor blockers (ARBs) and nonsteroidal anti-inflammatory drugs (NSAIDs)
C
Transtubular potassium gradient (TTKG) measurement is required in all patients with suspected hyperkalemia
Hint:
Measurement of the TTKG remains widely used to assess whether decreased renal excretion of potassium is contributing to hyperkalemia. Despite its initial promise, some research has called its accuracy into question. Some experts recommend that TTKG measurement be abandoned.
D
Hemodialysis is required, even in mild cases of hyperkalemia without ECG abnormalities
Hint:
Definitive therapy is hemodialysis in patients with renal failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis; pharmacologic therapy alone is not likely to bring about adequate reduction of potassium levels in a timely fashion.
Question 2 Explanation:
ACE inhibitors lower the levels of aldosterone, thereby promoting potassium retention in the kidneys and bloodstream. People with diabetes and kidney disease are at increased risk of hyperkalemia so ACE inhibitors must be used with caution in these patients. The hypothesized mechanism for hyperkalemia associated with NSAIDs is related to the inhibition of prostacyclin. In contrast to COX-1, COX-2 mediates prostacyclin synthesis, which increases potassium secretion at the distal tubule.
Medications that impair renal potassium excretion, as follows:
Potassium-sparing diuretics, which are especially used in the treatment of cirrhosis and chronic heart failure
NSAIDs
ACE inhibitors
The combination of spironolactone and ACE inhibitors
Treatment: IV calcium gluconate or calcium chloride
Pearls:
If suspicious of phosphorus or calcium imbalance, always order a PTH level
Always remember it is the effect on the EKG that counts the most, not the serum levels
Picmonic
Hypocalcemia is defined as serum calcium < 8.5 mg/dL. Parathyroid hormone (PTH), albumin, vitamin D, magnesium, and phosphate are all involved in calcium homeostasis, and derangements in their levels can cause changes in total and active calcium levels. Acid-base changes due to medications or critical illness alter calcium-binding. Critical illness such as sepsis or severe burns also causes hypocalcemia through actions on calcium homeostasis and end-organ effects. Many medications, including calcium chelators, bisphosphonates, and chemotherapeutic agents can cause hypocalcemia through effects on calcium binding and homeostasis. Acute treatment begins with IV calcium gluconate, which is cardioprotective. Chronic hypocalcemia treatment includes calcium carbonate, calcium citrate, and oral vitamin D supplements. Finally, patients who are hypomagnesemia should have this electrolyte addressed. This is because hypomagnesemia can lead to decreased PTH secretion, leading to decreased availability of calcium.
Pearls: hypercalcemia in the elderly is cancer until proven otherwise
Picmonic
Dysfunction of several pathways can lead to high levels of calcium circulating in the blood. Calcium homeostasis is regulated by calcium absorption in the intestines, bone turnover, and reabsorption and excretion of calcium in the kidneys. Bone resorption is stimulated by increased levels of vitamin D and parathyroid hormone (PTH). Calcium absorption in the intestines is stimulated by vitamin D and high calcium intake. Renal excretion of calcium is mediated by PTH and vitamin D, and can be affected by many disease states. Malignancy is another important cause of hypercalcemia due to direct osteolytic effects on bone as well as hormonal changes in calcium homeostasis. The treatment of hypercalcemia depends on the cause, severity, and comorbid conditions of the patient. It should be aimed at lowering the calcium level as well as correcting the underlying cause where possible. The level of plasma calcium and the rate of rise are both important in determining the severity of hypercalcemia and the need for treatment. Patients with asymptomatic mild hypercalcemia (<12 mg/dL) do not need immediate treatment. Adequate oral hydration is often sufficient for control and can be tried initially. A calcium level of 12-14 mg/dL warrants intervention if the elevation was acute or the patient is symptomatic. Patients with severe hypercalcemia of >14 mg/dL need emergent intervention to lower their plasma calcium. The initial treatment for severe hypercalcemia is a combination of volume expansion with normal saline, calcitonin, and a bisphosphonate. Definitive treatment often involves treating the underlying cause
Hypercalcemia Picmonic
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Hypercalcemia
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Question 1
A 64-year-old man presents for a routine physical. He states that he is not doing very well and, in fact, has not had a bowel movement in over a week. Upon further questioning, the patient notes that for about 4 months he has experienced significant back pain and finds that he is easily fatigued. His wife has remarked that he is unusually "pale." In addition to his lack of a bowel movement for the past week, the patient has also had a loss of appetite, has been urinating more than usual, and has had a depressed mood. Which of the following is the most likely cause of this patient's constipation?
A
Hyperkalemia
Hint:
Hyperkalemia classically causes peaked T waves on EKGs, symptoms associated with hyperkalemia include nausea, vomiting, and muscle weakness.
B
Hypermagnesemia
Hint:
Symptoms of hypermagnesemia include lethargy, weakness and paralysis, not constipation.
C
Hypophosphatemia
Hint:
Hypophosphatemia typically causes diffuse muscle weakness and flaccid paralysis, not constipation.
D
Hypercalcemia
E
Hypocalcemia
Hint:
Hypocalcemia can present with abdominal pain, and muscle cramps but doesn't typically present with constipation.
Question 1 Explanation:
This patient likely has multiple myeloma with resultant hypercalcemia, an electrolyte disturbance that can cause severe constipation.
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Hypomagnesemia
Definition: serum magnesium < 1.8 mg/dL
Presentation: Muscle weakness, hyperreflexia, prolonged QT, PR and wide QRS, ventricular tachycardia, torsades de pointes
Treatment: IV magnesium sulfate (acute) or oral magnesium oxide (chronic)
Picmonic
Hypomagnesemia occurs when serum magnesium levels are below 1.5 mEq/L. Causes of hypomagnesaemia include diarrhea, vomiting, chronic alcoholism, and malabsorption syndrome. Other causes include NG suction, poorly controlled diabetes mellitus, and hyperaldosterone. Magnesium is an intracellular cation used to activate enzymatic reactions and maintain normal calcium and potassium balance. Clinical manifestations of hypomagnesemia include confusion, increased deep tendon reflexes, insomnia, and tachycardia. The patient may exhibit neuromuscular irritability characterized by seizures, muscle cramps, and tremors. Treatment for hypomagnesemia includes administering IV magnesium sulfate and increasing dietary intake of foods high in magnesium.
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Hypermagnesemia
Definition: serum magnesium > 2.6 mg/dL
Presentation: Muscle weakness, prolonged QT, PR and wide QRS
Treatment: IV isotonic saline, loop diuretics can be considered
Picmonic
Hypermagnesemia occurs when the serum level of magnesium exceeds 2.5 mEq/L. This is caused by excess magnesium intake and renal insufficiency. Pregnant women receiving magnesium sulfate to manage symptoms of eclampsia are also at risk. Magnesium is an intracellular cation used to activate enzymatic reactions and maintain normal calcium and potassium balance. Symptoms of hypermagnesemia include flushing, lethargy, muscle weakness, and decreased deep tendon reflexes. The patient may also present with decreased respirations, bradycardia, and hypotension. Interventions to address hypermagnesemia include administering IV calcium gluconate and diuretics. Patients who are renally impaired may require dialysis. Medications containing magnesium, such as certain antacids and laxatives, should be avoided.
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