Replacement of ongoing losses US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Replacement of ongoing losses. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Replacement of ongoing losses US Medical PG Question 1: A 62-year-old man presents to the emergency department with confusion. The patient’s wife states that her husband has become more somnolent over the past several days and now is very confused. The patient has no complaints himself, but is answering questions inappropriately. The patient has a past medical history of diabetes and hypertension. His temperature is 98.3°F (36.8°C), blood pressure is 127/85 mmHg, pulse is 138/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam is notable for a confused man with dry mucous membranes. Initial laboratory studies are ordered as seen below.
Serum:
Na+: 135 mEq/L
Cl-: 100 mEq/L
K+: 3.0 mEq/L
HCO3-: 23 mEq/L
BUN: 30 mg/dL
Glucose: 1,299 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
Which of the following is the most appropriate initial treatment for this patient?
- A. Insulin, normal saline, and potassium (Correct Answer)
- B. Normal saline and potassium
- C. Insulin and potassium
- D. Insulin
- E. Insulin and normal saline
Replacement of ongoing losses Explanation: ***Insulin, normal saline, and potassium***
- This patient is presenting with **hyperosmolar hyperglycemic state (HHS)**, characterized by severe hyperglycemia (glucose 1299 mg/dL), dehydration (dry mucous membranes, high BUN and creatinine), and altered mental status. The initial treatment involves intravenous fluids to correct dehydration, insulin to lower blood glucose, and potassium supplementation due to potential shifts as insulin is administered.
- **Normal saline** addresses the severe dehydration, **insulin** corrects hyperglycemia, and **potassium supplementation** prevents hypokalemia, which is common during HHS treatment as glucose and potassium shift intracellularly.
*Normal saline and potassium*
- While **normal saline** and **potassium** are crucial for rehydration and electrolyte balance, omitting **insulin** would fail to address the core problem of severe hyperglycemia in HHS.
- Without insulin, blood glucose levels will remain dangerously high, leading to persistent osmotic diuresis and worsening dehydration.
*Insulin and potassium*
- Administering **insulin** without addressing the profound **dehydration** with intravenous fluids can lead to **hypovolemic shock** as insulin further drives glucose and water into cells.
- Rehydration is the priority in HHS management before or concurrent with insulin administration.
*Insulin*
- Giving only **insulin** would be detrimental, as the patient is severely dehydrated and hypokalemic (K+ 3.0 mEq/L, and will drop further with insulin).
- This approach would exacerbate dehydration and could cause life-threatening arrhythmias due to severe hypokalemia.
*Insulin and normal saline*
- While addressing hyperglycemia and dehydration, omitting **potassium supplementation** is dangerous because insulin drives potassium into cells, potentially causing severe **hypokalemia** and cardiac arrhythmias.
- The patient already has a low-normal potassium level, which will likely drop further with insulin treatment.
Replacement of ongoing losses US Medical PG Question 2: A 17-year-old male presents to your office complaining of polyuria, polydipsia, and unintentional weight loss of 12 pounds over the past 3 months. On physical examination, the patient is tachypneic with labored breathing. Which of the following electrolyte abnormalities would you most likely observe in this patient?
- A. Hypophosphatemia
- B. Hypermagnesemia
- C. Hyperkalemia
- D. Hyponatremia (Correct Answer)
- E. Hyperphosphatemia
Replacement of ongoing losses Explanation: ***Hyponatremia***
- This patient's symptoms of polyuria, polydipsia, and weight loss, along with **tachypnea and labored breathing**, are highly suggestive of **diabetic ketoacidosis (DKA)**.
- **Hyponatremia** is the **most consistently observed** electrolyte abnormality in DKA, present in nearly all cases at initial presentation.
- This is typically **pseudohyponatremia** caused by the osmotic effect of severe hyperglycemia—glucose pulls water into the extracellular space, diluting the measured sodium concentration.
- The **corrected sodium** can be calculated using: Corrected Na = Measured Na + 0.016 × (Glucose - 100), which typically reveals a more normal sodium level.
- True hyponatremia from sodium loss via **osmotic diuresis** can also occur but is usually masked by the dilutional effect.
*Hyperkalemia*
- While serum potassium may appear normal or even elevated initially due to **transcellular shifts** (acidosis causes potassium to move from intracellular to extracellular space in exchange for hydrogen ions), this is not the most consistently observed abnormality.
- **Total body potassium is always depleted** in DKA due to osmotic diuresis and vomiting.
- Many patients present with normal or even low potassium levels despite acidosis.
- Potassium levels require careful monitoring during treatment as insulin therapy drives potassium back into cells, potentially causing life-threatening hypokalemia.
*Hypophosphatemia*
- While **phosphate levels** can fluctuate in DKA due to osmotic diuresis, initial presentation often involves normal or even elevated phosphate levels due to cellular shifts.
- Significant **hypophosphatemia** is more typically observed during treatment as insulin drives phosphate back into the cells, similar to potassium.
*Hypermagnesemia*
- **Hypermagnesemia** is uncommon in DKA and is usually associated with impaired renal excretion or excessive magnesium intake.
- The symptoms described do not point towards magnesium imbalance.
*Hyperphosphatemia*
- Although cellular shifts can initially raise serum phosphate, sustained **hyperphosphatemia** is not a characteristic or common electrolyte abnormality seen in the acute presentation of DKA.
- More typically, total body phosphate is depleted due to **osmotic diuresis**.
Replacement of ongoing losses US Medical PG Question 3: A 28-year-old research assistant is brought to the emergency department for severe chemical burns 30 minutes after accidentally spilling hydrochloric acid on himself. The burns cover both hands and forearms. His temperature is 37°C (98.6°F), pulse is 112/min, respirations are 20/min, and blood pressure is 108/82 mm Hg. Initial stabilization and resuscitation is begun, including respiratory support, fluid resuscitation, and cardiovascular stabilization. The burned skin is irrigated with saline water to remove the chemical agent. Which of the following is the most appropriate method to verify adequate fluid infusion in this patient?
- A. The Parkland formula
- B. Blood pressure
- C. Pulmonary capillary wedge pressure
- D. Heart rate
- E. Urinary output (Correct Answer)
Replacement of ongoing losses Explanation: ***Urinary output***
- Maintaining a specific **urinary output** (e.g., adult with major burns: 0.5-1.0 mL/kg/hr or 30-50 mL/hr) is the most reliable clinical indicator of adequate fluid resuscitation in burn patients.
- This ensures sufficient end-organ perfusion and avoids both under-resuscitation (leading to shock and organ damage) and over-resuscitation (risk of compartment syndrome and pulmonary edema).
*The Parkland formula*
- The **Parkland formula** is used to *calculate* the initial fluid volume needed, but it does not *verify* the adequacy of the infusion once started.
- This formula provides a starting point for fluid administration, which then needs to be adjusted based on the patient's response.
*Blood pressure*
- **Blood pressure** can be misleading in burn patients; it may remain deceptively normal due to compensatory mechanisms even with significant fluid deficits.
- It is a late indicator of hypovolemic shock, and relying solely on it can lead to under-resuscitation.
*Pulmonary capillary wedge pressure*
- **Pulmonary capillary wedge pressure (PCWP)** requires invasive monitoring via a pulmonary artery catheter, which is rarely indicated for routine fluid management in burn patients due to its invasiveness and associated risks.
- Less invasive and equally effective methods, like urinary output, are preferred for monitoring resuscitation.
*Heart rate*
- **Heart rate** is a sensitive but non-specific indicator of fluid status; it can be elevated due to pain, anxiety, or infection, not solely hypovolemia.
- While a decreasing heart rate can indicate improved fluid status, it is not as reliable or direct an indicator of end-organ perfusion as urinary output.
Replacement of ongoing losses US Medical PG Question 4: A 23-year-old man presents to the emergency department for altered mental status after a finishing a marathon. He has a past medical history of obesity and anxiety and is not currently taking any medications. His temperature is 104°F (40°C), blood pressure is 147/88 mmHg, pulse is 200/min, respirations are 33/min, and oxygen saturation is 99% on room air. Physical exam reveals dry mucous membranes, hot flushed skin, and inappropriate responses to the physician's questions. Laboratory values are ordered as seen below.
Hemoglobin: 15 g/dL
Hematocrit: 44%
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 199,000/mm^3
Serum:
Na+: 165 mEq/L
Cl-: 100 mEq/L
K+: 4.0 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 133 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L
Which of the following is the best next step in management?
- A. Lactated ringer
- B. Hypotonic saline
- C. 50% normal saline 50% dextrose
- D. Normal saline (Correct Answer)
- E. Dextrose solution
Replacement of ongoing losses Explanation: ***Normal saline***
- The patient presents with **heat stroke** (temperature 104°F, altered mental status after marathon) complicated by **severe hypernatremia (Na+ 165 mEq/L)** and **hypovolemia** (elevated BUN/Cr ratio, tachycardia, dry mucous membranes).
- In **hypovolemic hypernatremia**, the best initial step is to restore **intravascular volume** with **isotonic crystalloid** (normal saline or lactated Ringer's) to stabilize hemodynamics and organ perfusion.
- **Normal saline (0.9% NaCl, 154 mEq/L Na+)** is hypotonic relative to the patient's serum (165 mEq/L), so it will begin **gradual correction** of hypernatremia while providing volume resuscitation.
- After volume restoration, hypotonic fluids (0.45% saline or D5W) may be used for further correction, but they should NOT be given initially to a volume-depleted patient due to risk of worsening hypotension.
- Correction rate should be **≤10-12 mEq/L per 24 hours** to avoid cerebral edema.
*Hypotonic saline*
- While hypotonic saline (0.45% NaCl) is used to correct hypernatremia, it should **not** be the first-line choice in a **hypovolemic** patient.
- Administering hypotonic fluids to a volume-depleted patient can worsen hypotension and compromise organ perfusion before adequately restoring intravascular volume.
- Hypotonic saline is appropriate **after** volume status has been restored with isotonic fluids.
*Lactated ringer*
- **Lactated Ringer's solution** is an isotonic crystalloid (130 mEq/L Na+) and would be an equally acceptable choice for initial volume resuscitation.
- It is slightly more hypotonic than normal saline, which could provide marginally faster correction of hypernatremia.
- Either normal saline or lactated Ringer's is appropriate for initial management; normal saline is more commonly cited in USMLE resources for hypernatremia management.
*50% normal saline 50% dextrose*
- This mixture would create a **hypertonic solution** that could worsen hypernatremia rather than correct it.
- The patient's glucose is normal (133 mg/dL), so dextrose supplementation is not indicated.
- This option is inappropriate for managing hypernatremia.
*Dextrose solution*
- **D5W (5% dextrose in water)** provides free water and would correct hypernatremia by diluting serum sodium.
- However, in a **volume-depleted** patient, giving free water without adequate sodium can lead to rapid osmotic shifts, worsening hypotension, and potentially causing cerebral edema if correction occurs too rapidly.
- D5W is reserved for **euvolemic or hypervolemic hypernatremia**, not hypovolemic hypernatremia.
Replacement of ongoing losses US Medical PG Question 5: A 48-year-old woman is transferred from her primary care physician's office to the emergency department for further evaluation of hypokalemia to 2.5 mEq/L. She was recently diagnosed with hypertension 2 weeks ago and started on medical therapy. The patient said that she enjoys all kinds of food and exercises regularly, but has not been able to complete her workouts as she usually does. Her temperature is 97.7°F (36.5°C), blood pressure is 107/74 mmHg, pulse is 80/min, respirations are 15/min, and SpO2 is 94% on room air. Her physical exam is unremarkable. Peripheral intravenous (IV) access is obtained. Her basic metabolic panel is obtained below.
Serum:
Na+: 135 mEq/L
Cl-: 89 mEq/L
K+: 2.2 mEq/L
HCO3-: 33 mEq/L
BUN: 44 mg/dL
Glucose: 147 mg/dL
Creatinine: 2.3 mg/dL
Magnesium: 2.0 mEq/L
What is the next best step in management?
- A. Obtain an electrocardiogram (Correct Answer)
- B. Obtain urine sodium and creatinine
- C. Administer isotonic saline 1 liter via peripheral IV
- D. Administer potassium chloride 40mEq via peripheral IV
- E. Administer potassium bicarbonate 50mEq per oral
Replacement of ongoing losses Explanation: ***Obtain an electrocardiogram***
- The patient has severe **hypokalemia** (K+ 2.2 mEq/L), which requires urgent assessment for cardiac complications before initiating treatment.
- An **ECG is the mandatory first step** in severe hypokalemia (K+ <2.5 mEq/L) to evaluate for life-threatening arrhythmias and ECG changes including U waves, T wave flattening, ST depression, and QT prolongation.
- The patient is **hemodynamically stable** with only mild symptoms (exercise intolerance), so immediate potassium administration is not required before obtaining an ECG.
- ECG findings will guide the urgency and route of potassium repletion and determine the need for cardiac monitoring during treatment.
*Administer potassium chloride 40mEq via peripheral IV*
- While **IV potassium chloride** will be needed for repletion, it should be administered after ECG assessment in a stable patient.
- IV potassium administration carries risks including phlebitis, infiltration, and potential cardiac complications if given too rapidly without monitoring.
- In severe hypokalemia without cardiac arrest or documented life-threatening arrhythmias, obtaining an ECG first is standard practice.
*Obtain urine sodium and creatinine*
- Measuring **urine electrolytes** helps identify the cause of hypokalemia (likely diuretic-induced given recent hypertension treatment with metabolic alkalosis and hypochloremia).
- However, this diagnostic workup should follow the immediate assessment and treatment of severe hypokalemia.
- While useful for long-term management, it does not take priority over assessing cardiac risk with an ECG.
*Administer potassium bicarbonate 50mEq per oral*
- **Potassium bicarbonate** is contraindicated in this patient with **metabolic alkalosis** (HCO3- 33 mEq/L), as it would worsen the alkalosis.
- The correct form for repletion in metabolic alkalosis is **potassium chloride**, which addresses both the hypokalemia and hypochloremia.
- Oral repletion is also too slow for severe hypokalemia and may cause gastrointestinal side effects.
*Administer isotonic saline 1 liter via peripheral IV*
- While the patient shows signs of volume depletion (elevated BUN/Cr ratio, likely prerenal azotemia from diuretic use), the immediate priority is assessing the cardiac impact of severe hypokalemia.
- **Isotonic saline** without potassium supplementation could potentially worsen hypokalemia through dilution and increased renal potassium excretion.
- Volume resuscitation should be considered after ECG assessment and in conjunction with potassium repletion.
Replacement of ongoing losses US Medical PG Question 6: A 78-year-old male with history of coronary artery disease, status post coronary stent placement currently on aspirin and clopidogrel was found down in his bathroom by his wife. His GCS score was 3 and an accurate physical exam is limited. A stat non-contrast CT scan of his brain demonstrated a large right parietal intracranial hemorrhage with surrounding edema. He was promptly transferred to the intensive care unit (ICU) for monitoring. Over the next day, his mental status continues to worsen but repeat CT scan shows no new bleeding. In addition, the patient’s urinary output has been >200 cc/hr over the last several hours and increasing. His temperature is 99.0 deg F (37.2 deg C), blood pressure is 125/72 mmHg, pulse is 87/min, and respirations are 13/min. Which of the following values would most likely correspond to the patient’s urine specific gravity, urine osmolality, plasma osmolality, and serum sodium?
- A. Low, High, High, High
- B. Low, Low, High, High (Correct Answer)
- C. High, High, Low, Low
- D. Low, Low, High, Low
- E. High, Low, Low, High
Replacement of ongoing losses Explanation: ***Low, Low, High, High***
- This patient's presentation, particularly the **large intracranial hemorrhage**, worsening mental status despite no new bleeding, and especially the **high urinary output (>200 cc/hr)**, is classic for **diabetes insipidus (DI)**, often neurogenic DI, due to damage to the posterior pituitary or hypothalamus.
- In DI, there is a deficiency of **ADH (vasopressin)**, leading to the kidneys' inability to reabsorb water. This results in the excretion of large volumes of **dilute urine** (low urine specific gravity, low urine osmolality) and concentration of the plasma (high plasma osmolality and hypernatremia, which means high serum sodium).
*Low, High, High, High*
- This pattern would indicate concentrated urine alongside concentrated plasma and high sodium, which contradicts the presence of **polyuria** and the underlying pathology of **diabetes insipidus (DI)**.
- High urine osmolality and specific gravity would suggest intact ADH function and water reabsorption in the kidneys, which is not what occurs in DI.
*High, High, Low, Low*
- This profile describes a state of **concentrated urine** but **dilute plasma** and **hyponatremia**, which is characteristic of the **Syndrome of Inappropriate Antidiuretic Hormone (SIADH)**.
- SIADH is the opposite of diabetes insipidus, involving excessive ADH leading to water retention, not excessive water excretion.
*Low, Low, High, Low*
- While **low urine specific gravity** and **low urine osmolality** are consistent with diabetes insipidus, a **low serum sodium** (hyponatremia) is not.
- In diabetes insipidus, the loss of free water typically leads to **hypernatremia** as the body becomes dehydrated.
*High, Low, Low, High*
- This combination is inconsistent with any common clinical scenario. A **high urine specific gravity** with a **low urine osmolality** is contradictory, as specific gravity is a measure of urine concentration, which correlates with osmolality.
- Furthermore, a **low plasma osmolality** with a **high serum sodium** is physiologically improbable.
Replacement of ongoing losses US Medical PG Question 7: Three days after being admitted to the hospital because of a fall from the roof of a two-story building, a 27-year-old man is being monitored in the intensive care unit. On arrival, the patient was somnolent and not oriented to person, place, or time. A CT scan of the head showed an epidural hemorrhage that was 45 cm3 in size and a midline shift of 7 mm. Emergency surgery was performed with craniotomy and hematoma evacuation on the day of admission. Perioperatively, a bleeding vessel was identified and ligated. Postoperatively, the patient was transferred to the intensive care unit and placed on a ventilator. His temperature is 37°C (98.6°F), pulse is 67/min, and blood pressure is 117/78 mm Hg. The ventilator is set at a FiO2 of 55%, tidal volume of 520 mL, and positive end-expiratory pressure of 5.0 cm H2O. In addition to intravenous administration of fluids, which of the following is the most appropriate next step in managing this patient's nutrition?
- A. Enteral feeding via nasogastric tube (Correct Answer)
- B. Oral feeding
- C. Keep patient NPO
- D. Total parenteral nutrition
- E. Enteral feeding using a percutaneous endoscopic gastrostomy (PEG) tube
Replacement of ongoing losses Explanation: ***Enteral feeding via nasogastric tube***
- This patient has been **somnolent** and on a ventilator for 3 days after a significant head injury, indicating a prolonged period without oral intake and an inability to protect his airway for oral feeding. **Early enteral nutrition** via a nasogastric tube is preferred in critically ill patients, especially those with head injuries, as it helps maintain gut integrity and reduces complications compared to parenteral nutrition.
- The patient's **hemodynamic stability** (blood pressure and pulse are within a reasonable range for a ventilated patient) suggests he can tolerate enteral feeding, and there are no signs of gut ischemia or ileus that would contraindicate it.
*Enteral feeding using a percutaneous endoscopic gastrostomy (PEG) tube*
- While a PEG tube provides enteral nutrition, it is typically reserved for patients requiring **long-term enteral support** (usually more than 4-6 weeks) or those who cannot tolerate a nasogastric tube.
- Given that it has only been 3 days post-injury, a **less invasive method** like a nasogastric tube is initially preferred.
*Oral feeding*
- The patient is described as **somnolent** and on a ventilator, meaning he is not awake enough or able to protect his airway to safely receive oral feeding.
- Attempting oral feeding in this state carries a high risk of **aspiration pneumonia**.
*Keep patient NPO*
- Keeping the patient NPO (nil per os) for an extended period in critical illness is associated with several negative outcomes, including **gut mucosal atrophy, increased infection risk**, and poorer clinical outcomes.
- After 3 days, initiating nutritional support is crucial to prevent these complications.
*Total parenteral nutrition*
- **Total parenteral nutrition (TPN)** is generally considered a last resort when the gastrointestinal tract is non-functional or enteral feeding is contraindicated.
- TPN is associated with a **higher risk of complications**, such as central line infections, liver dysfunction, and metabolic disturbances, compared to enteral feeding.
Replacement of ongoing losses US Medical PG Question 8: 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?
- A. 5% albumin 6-8 grams per liter of ascites removed (Correct Answer)
- B. Normal saline bolus 2 liters
- C. Octreotide and midodrine for hepatorenal syndrome
- D. Vasopressors to maintain blood pressure
- E. Re-infusion of filtered ascitic fluid
Replacement of ongoing losses Explanation: ***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.
Replacement of ongoing losses US Medical PG Question 9: 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?
- A. Secondary hyperaldosteronism from volume depletion
- B. Insufficient potassium replacement dose
- C. Ongoing losses from continued vomiting
- D. Metabolic alkalosis promoting intracellular potassium shift
- E. Hypomagnesemia preventing potassium retention (Correct Answer)
Replacement of ongoing losses Explanation: ***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.
Replacement of ongoing losses US Medical PG Question 10: 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?
- A. Conivaptan infusion for water diuresis
- B. Normal saline infusion with fluid restriction
- C. Rapid correction to 135 mEq/L with 3% hypertonic saline over 4 hours
- D. Increase sodium by 6-8 mEq/L in first 24 hours with 3% saline boluses
- E. 3% saline to increase sodium by 4-6 mEq/L in first 2-4 hours, then slower correction (Correct Answer)
Replacement of ongoing losses Explanation: ***3% saline to increase sodium by 4-6 mEq/L in first 2-4 hours, then slower correction***
- For **acute symptomatic hyponatremia** (seizures, confusion) in **TURP syndrome**, a rapid initial rise of **4-6 mEq/L** is required to reverse cerebral edema and prevent herniation.
- After the initial stabilization, the rate is slowed to stay within **6-8 mEq/L per 24 hours** to mitigate the risk of **Osmotic Demyelination Syndrome (ODS)**.
*Conivaptan infusion for water diuresis*
- **Vaptans** are Vasopressin receptor antagonists typically used for **euvolemic hyponatremia** (SIADH) rather than acute, life-threatening hyponatremia.
- This treatment is too slow for a patient presenting with **seizures** and severe neurological compromise.
*Normal saline infusion with fluid restriction*
- **Normal saline (0.9%)** may worsen hyponatremia in high ADH states or be insufficient to rapidly increase sodium in a **hypervolemic** post-TURP state.
- **Fluid restriction** alone is an appropriate long-term strategy for mild cases but is contraindicated as primary therapy for **acute, symptomatic seizures**.
*Rapid correction to 135 mEq/L with 3% hypertonic saline over 4 hours*
- Correcting sodium to **normal levels (135 mEq/L)** too quickly represents an overcorrection that carries an extremely high risk of **pontine myelinolysis**.
- The goal of emergency treatment is **symptom reversal**, not immediate normalization of laboratory values.
*Increase sodium by 6-8 mEq/L in first 24 hours with 3% saline boluses*
- While 6-8 mEq/L is a safe 24-hour target, it does not prioritize the necessary **early rapid rise** needed in the first few hours for a patient having **seizures**.
- This approach lacks the specific **2-4 hour urgency** required to manage active intracranial pressure increases from acute hypotonicity.
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