Fluid and electrolyte management Practice Questions

Q: A 58-year-old cirrhotic man with ascites undergoes large volume paracentesis (6 liters removed). Four hours later, he becomes hypotensive (BP 80/50 mmHg) and tachycardic (HR 115/min). Labs show: Cr 2.1 mg/dL (baseline 1.0), Na+ 128 mEq/L, Hct 38%. What is the most appropriate immediate management?

5% albumin 6-8 grams per liter of ascites removed. ***5% albumin 6-8 grams per liter of ascites removed*** - This patient is experiencing **post-paracentesis circulatory dysfunction (PPCD)**, characterized by hypotension and **acute kidney injury** (doubled creatinine) following a large volume paracentesis (>5L). - Administration of **intravenous albumin** is the gold standard treatement to expand the **effective arterial blood volume** and prevent further deterioration into hepatorenal syndrome. *Normal saline bolus 2 liters* - In cirrhotic patients, **crystalloids** are less effective as they rapidly redistribute into the **interstitial space** (third-spacing) and can worsen ascites/edema. - Saline does not provide the **oncotic pressure** required to counteract the splanchnic vasodilation typical of PPCD. *Octreotide and midodrine for hepatorenal syndrome* - While these agents are used for **Hepatorenal Syndrome (HRS)**, the immediate priority in post-procedure hypotension is **volume expansion** to correct the circulatory dysfunction. - These medications are typically reserved for patients who do not respond to **volume expansion with albumin** or meet specific criteria for type 1 HRS. *Vasopressors to maintain blood pressure* - Vasopressors like **norepinephrine** are generally considered after fluid resuscitation with **albumin** has failed to restore hemodynamic stability. - Using pressors alone ignores the underlying **intravascular volume deficit** caused by the fluid shift after paracentesis. *Re-infusion of filtered ascitic fluid* - This is not a standard or recommended clinical practice due to risks of **infection**, **coagulopathy**, and lack of evidence for efficacy. - The specific requirement in this pathology is **concentrated albumin** to maintain oncotic pressure, which ascitic fluid does not provide efficiently.

Q: A 42-year-old woman with prolonged vomiting from gastroparesis is admitted with weakness. Labs show: K+ 2.1 mEq/L, pH 7.51, HCO3- 42 mEq/L, Mg2+ 1.4 mg/dL. She receives 80 mEq of IV potassium chloride over 24 hours, but repeat K+ is 2.3 mEq/L. What explains the refractory hypokalemia?

Hypomagnesemia preventing potassium retention. ***Hypomagnesemia preventing potassium retention*** - Low **intracellular magnesium** inhibits **ROMK channels** in the renal collecting duct; without magnesium inhibition, these channels allow excessive **potassium secretion** into the urine. - **Magnesium** is also a necessary cofactor for the **Na+/K+-ATPase pump**, which is required to transport potassium into the cells and maintain serum levels. *Secondary hyperaldosteronism from volume depletion* - While **volume depletion** triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**, leading to potassium loss, it does not typically cause absolute refraction to supplementation in the presence of adequate IV fluids. - Addressing the **volume status** alone will not fix the hypokalemia if the **magnesium deficiency** is still driving renal wasting. *Insufficient potassium replacement dose* - A dose of **80 mEq** over 24 hours is a significant amount of supplement for a patient who is hospitalized and being monitored. - Failure to increase serum potassium by more than 0.2 mEq/L despite high-dose IV replacement suggests an **active wasting mechanism** rather than just an under-correction. *Ongoing losses from continued vomiting* - Although vomiting causes loss of **hydrochloric acid** and induces **metabolic alkalosis**, the gastric fluid itself contains relatively low concentrations of potassium. - The primary cause of hypokalemia in vomiting is **renal loss** (due to alkalosis and RAAS) rather than direct loss of potassium from the stomach. *Metabolic alkalosis promoting intracellular potassium shift* - **Alkalosis** causes an intracellular shift of potassium as **hydrogen ions** exit cells to help buffer the serum pH. - While this contributes to the initial low lab value, it does not explain why **exogenous IV potassium** fails to raise the serum concentration over a 24-hour period.

Q: A 50-year-old man is 5 days post-operative from a Whipple procedure. He has had high nasogastric output (1500 mL/day) and has been NPO. Labs show: Na+ 132 mEq/L, K+ 2.9 mEq/L, Cl- 88 mEq/L, HCO3- 38 mEq/L, pH 7.52. Urine chloride is 8 mEq/L. What is the appropriate management?

Normal saline with potassium chloride. ***Normal saline with potassium chloride*** - The patient has **hypochloremic, hypokalemic metabolic alkalosis** due to high-output gastric suctioning; a **urine chloride <10 mEq/L** confirms it is **chloride-responsive**. - Administering **Isotonic Saline (0.9% NaCl)** restores volume and provides the chloride needed to promote renal **bicarbonate excretion**, while **KCl** corrects the hypokalemia that maintains alkalosis. *Discontinue nasogastric suction only* - While suctioning is the source of acid loss, stopping it alone does not address the existing **volume depletion** or the severe **electrolyte imbalances** already present. - The kidneys require exogenous **chloride replacement** to effectively reverse the metabolic alkalosis and restore acid-base balance. *Acetazolamide to promote bicarbonate excretion* - This carbonic anhydrase inhibitor can lower bicarbonate but may worsen **hypokalemia** and contributes to further **volume depletion**. - It is generally reserved for patients with severe volume overload who cannot tolerate saline, which is not the case for this **hypovolemic** patient. *Half-normal saline with potassium supplementation* - **0.45% Saline** provides less sodium and chloride than required for rapid volume expansion and correction of **contraction alkalosis**. - **Isotonic 0.9% saline** is preferred to reliably expand the **extracellular fluid volume** and suppress the renin-angiotensin-aldosterone system. *Hydrochloric acid infusion* - This is an extreme measure reserved for life-threatening **metabolic alkalosis (pH >7.55-7.60)** that is refractory to standard saline and potassium replacement. - It requires **central venous access** due to its caustic nature and is not indicated as initial management for **chloride-responsive** states.

Q: A 28-year-old trauma patient received 8 units of packed RBCs, 6 units of FFP, and 2 units of platelets during damage control surgery. Two hours post-op, he develops: peaked T waves on EKG, K+ 6.8 mEq/L, Ca2+ 7.2 mg/dL, ionized calcium 0.9 mmol/L, pH 7.25. Which metabolic derangement is most responsible for his cardiac instability?

Combined hyperkalemia and hypocalcemia. ***Combined hyperkalemia and hypocalcemia*** - Massive transfusion protocols involve multiple blood products that synergistically cause **hyperkalemia** (due to potassium leakage from stored RBCs) and **hypocalcemia** (due to **citrate anticoagulants** binding ionized calcium). - These two derangements are most responsible for cardiac instability because **hypocalcemia** lowers the threshold for action potential while **hyperkalemia** increases membrane excitability, significantly increasing the risk of **fatal arrhythmias**. *Hypothermia-induced arrhythmia* - While massive transfusion can cause hypothermia if blood products aren't warmed, the primary markers here are **hyperkalemia** and **hypocalcemia**. - Hypothermia typically presents with **Osborn (J) waves** on EKG rather than the **peaked T waves** seen in this patient. *Hyperkalemia from massive transfusion* - Hyperkalemia alone explains the **peaked T waves** and elevated K+ of 6.8 mEq/L, but it ignores the significant **low ionized calcium (0.9 mmol/L)**. - Cardiac stabilization in this setting requires treating both electrolytes; addressing potassium without calcium is insufficient for **myocardial membrane stabilization**. *Hypocalcemia from citrate toxicity* - Citrate in FFP and PRBCs binds calcium, leading to the reported **ionized calcium** level, which can cause QT prolongation and reduced contractility. - This option is incomplete as it fails to account for the **life-threatening hyperkalemia** evidenced by the elevated serum potassium and EKG changes. *Metabolic acidosis alone* - The **pH of 7.25** indicates a metabolic acidosis which can shift K+ out of cells, but it is a contributing factor rather than the primary cause of instability in this 2-hour post-op window. - Acidosis primarily worsens the severity of **citrate toxicity** by decreasing the liver\'s ability to metabolize citrate, further exacerbating the hypocalcemia.

Question 1

A 58-year-old cirrhotic man with ascites undergoes large volume paracentesis (6 liters removed). Four hours later, he becomes hypotensive (BP 80/50 mmHg) and tachycardic (HR 115/min). Labs show: Cr 2.1 mg/dL (baseline 1.0), Na+ 128 mEq/L, Hct 38%. What is the most appropriate immediate management?

Accepted Answer

5% albumin 6-8 grams per liter of ascites removed

Answer

Normal saline bolus 2 liters

Answer

Octreotide and midodrine for hepatorenal syndrome

Answer

Vasopressors to maintain blood pressure

Answer

Re-infusion of filtered ascitic fluid

Question 2

A 42-year-old woman with prolonged vomiting from gastroparesis is admitted with weakness. Labs show: K+ 2.1 mEq/L, pH 7.51, HCO3- 42 mEq/L, Mg2+ 1.4 mg/dL. She receives 80 mEq of IV potassium chloride over 24 hours, but repeat K+ is 2.3 mEq/L. What explains the refractory hypokalemia?

Accepted Answer

Hypomagnesemia preventing potassium retention

Answer

Secondary hyperaldosteronism from volume depletion

Answer

Insufficient potassium replacement dose

Answer

Ongoing losses from continued vomiting

Answer

Metabolic alkalosis promoting intracellular potassium shift

Question 3

A 65-year-old diabetic man with TURP syndrome presents with confusion, nausea, and seizures 2 hours post-operatively. Labs show: Na+ 115 mEq/L, serum osmolality 240 mOsm/kg. He weighs 70 kg. What is the target sodium correction rate and fluid management strategy?

Accepted Answer

3% saline to increase sodium by 4-6 mEq/L in first 2-4 hours, then slower correction

Answer

Conivaptan infusion for water diuresis

Answer

Normal saline infusion with fluid restriction

Answer

Rapid correction to 135 mEq/L with 3% hypertonic saline over 4 hours

Answer

Increase sodium by 6-8 mEq/L in first 24 hours with 3% saline boluses

Question 4

A 50-year-old man is 5 days post-operative from a Whipple procedure. He has had high nasogastric output (1500 mL/day) and has been NPO. Labs show: Na+ 132 mEq/L, K+ 2.9 mEq/L, Cl- 88 mEq/L, HCO3- 38 mEq/L, pH 7.52. Urine chloride is 8 mEq/L. What is the appropriate management?

Accepted Answer

Normal saline with potassium chloride

Answer

Discontinue nasogastric suction only

Answer

Acetazolamide to promote bicarbonate excretion

Answer

Half-normal saline with potassium supplementation

Answer

Hydrochloric acid infusion

Question 5

A 28-year-old trauma patient received 8 units of packed RBCs, 6 units of FFP, and 2 units of platelets during damage control surgery. Two hours post-op, he develops: peaked T waves on EKG, K+ 6.8 mEq/L, Ca2+ 7.2 mg/dL, ionized calcium 0.9 mmol/L, pH 7.25. Which metabolic derangement is most responsible for his cardiac instability?

Accepted Answer

Combined hyperkalemia and hypocalcemia

Answer

Hypothermia-induced arrhythmia

Answer

Hyperkalemia from massive transfusion

Answer

Hypocalcemia from citrate toxicity

Answer

Metabolic acidosis alone

Fluid and electrolyte management — MCQs

Fluid and electrolyte management — MCQs

On this page

Practice by Chapter

Want unlimited practice?