Acid-base disorders in surgical patients US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Acid-base disorders in surgical patients. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Acid-base disorders in surgical patients US Medical PG Question 1: A 65-year-old man is brought to the emergency department from his home. He is unresponsive. His son requested a wellness check because he had not heard from his father in 2 weeks. He reports that his father was sounding depressed during a telephone call. The paramedics found a suicide note and a half-empty bottle of antifreeze near the patient. The medical history includes hypertension and hyperlipidemia. The vital signs include: blood pressure 120/80 mm Hg, respiratory rate 25/min, heart rate 95/min, and temperature 37.0°C (98.5°F). He is admitted to the hospital. What do you expect the blood gas analysis to show?
- A. Non-anion gap metabolic acidosis
- B. Metabolic alkalosis
- C. Respiratory acidosis
- D. Anion gap metabolic acidosis (Correct Answer)
- E. Mixed acid-base disorder
Acid-base disorders in surgical patients Explanation: ***Anion gap metabolic acidosis***
- The patient's history of **antifreeze ingestion** indicates likely exposure to **ethylene glycol**, which is metabolized into toxic acids (glycolic and oxalic acid).
- These accumulating acids lead to an **increased anion gap metabolic acidosis**.
*Non-anion gap metabolic acidosis*
- This type of acidosis typically results from **bicarbonate loss** (e.g., severe diarrhea) or **excessive chloride intake**, which is not indicated by the antifreeze ingestion.
- It involves a normal anion gap because other unmeasured anions do not accumulate.
*Metabolic alkalosis*
- This imbalance is characterized by an **increase in bicarbonate** or a significant loss of acid, often due to vomiting or diuretic use.
- Antifreeze poisoning directly leads to acid accumulation, precisely the opposite of metabolic alkalosis.
*Respiratory acidosis*
- This occurs due to **hypoventilation** and subsequent buildup of CO2, leading to increased carbonic acid.
- While respiratory rate is elevated, the primary problem here is metabolic due to toxin ingestion, not respiratory CO2 retention.
*Mixed acid-base disorder*
- While a mixed disorder is possible in complex cases, the presentation with antifreeze poisoning is classically dominated by a **severe anion gap metabolic acidosis**.
- There is no clear indication of a separate primary respiratory or alkalotic disorder at onset to warrant a "mixed" label as the primary anticipated finding.
Acid-base disorders in surgical patients US Medical PG Question 2: A 24-year-old woman presents to the emergency department after she was found agitated and screaming for help in the middle of the street. She says she also has dizziness and tingling in the lips and hands. Her past medical history is relevant for general anxiety disorder, managed medically with paroxetine. At admission, her pulse is 125/min, respiratory rate is 25/min, and body temperature is 36.5°C (97.7°F). Physical examination is unremarkable. An arterial blood gas sample is taken. Which of the following results would you most likely expect to see in this patient?
- A. pH: increased, HCO3-: increased, Pco2: increased
- B. pH: decreased, HCO3-: decreased, Pco2: decreased
- C. pH: decreased, HCO3-: increased, Pco2: increased
- D. pH: increased, HCO3-: decreased, Pco2: decreased (Correct Answer)
- E. pH: normal, HCO3-: increased, Pco2: increased
Acid-base disorders in surgical patients Explanation: ***pH: increased, HCO3-: decreased, Pco2: decreased***
- The patient's presentation with **agitation**, **dizziness**, **paresthesias** (tingling in lips and hands), and **tachypnea** (respiratory rate 25/min) is highly suggestive of **hyperventilation** due to an anxiety attack.
- **Hyperventilation** leads to excessive **CO2 expulsion**, causing a decrease in Pco2, which results in respiratory alkalosis (increased pH) and a compensatory decrease in HCO3-.
*pH: increased, HCO3-: increased, Pco2: increased*
- An **increased pH** coupled with **increased HCO3-** and **increased Pco2** would suggest a **metabolic alkalosis with respiratory compensation**, which is not consistent with the patient's acute hyperventilation.
- While pH is increased, the other values contradict the primary respiratory cause suggested by the symptoms.
*pH: decreased, HCO3-: decreased, Pco2: decreased*
- This profile describes **metabolic acidosis with respiratory compensation**, which would typically present with **Kussmaul breathing** and other signs of acidosis, not acute hyperventilation and agitation.
- Symptoms such as dizziness and tingling are associated with alkalosis, not acidosis.
*pH: decreased, HCO3-: increased, Pco2: increased*
- This pattern is characteristic of **respiratory acidosis with metabolic compensation**, often seen in conditions like **COPD exacerbation** or **opioid overdose** with hypoventilation.
- The patient's rapid breathing and clinical picture are not consistent with respiratory acidosis.
*pH: normal, HCO3-: increased, Pco2: increased*
- A **normal pH** with **increased HCO3-** and **increased Pco2** would indicate a **compensated metabolic alkalosis**.
- Her acute symptoms point to an uncompensated or acutely compensated respiratory disorder, not a compensated metabolic issue.
Acid-base disorders in surgical patients US Medical PG Question 3: A 27-year-old man presents to the emergency department with his family because of abdominal pain, excessive urination, and drowsiness since the day before. He has had type 1 diabetes mellitus for 2 years. He ran out of insulin 2 days ago. The vital signs at admission include: temperature 36.8°C (98.2°F), blood pressure 102/69 mm Hg, and pulse 121/min. On physical examination, he is lethargic and his breathing is rapid and deep. There is a mild generalized abdominal tenderness without rebound tenderness or guarding. His serum glucose is 480 mg/dL. Arterial blood gas of this patient will most likely show which of the following?
- A. ↑ pH, ↑ bicarbonate, and normal pCO2
- B. ↓ pH, ↓ bicarbonate and ↑ anion gap (Correct Answer)
- C. ↑ pH, normal bicarbonate and ↓ pCO2
- D. ↓ pH, ↓ bicarbonate and normal anion gap
- E. ↓ pH, normal bicarbonate and ↑ pCO2
Acid-base disorders in surgical patients Explanation: ***↓ pH, ↓ bicarbonate and ↑ anion gap***
- The patient's symptoms (abdominal pain, excessive urination, drowsiness, rapid and deep breathing, hyperglycemia) and history of Type 1 diabetes with missed insulin are highly suggestive of **diabetic ketoacidosis (DKA)**.
- DKA is characterized by **metabolic acidosis** due to the accumulation of ketone bodies, leading to a **decreased pH**, consumption of bicarbonate and thus a **decreased bicarbonate level**, and an **increased anion gap**.
*↑ pH, ↑ bicarbonate, and normal pCO2*
- This pattern suggests a **metabolic alkalosis**, which is inconsistent with the patient's presentation of DKA.
- Metabolic alkalosis is typically seen in conditions like severe vomiting or diuretic use, not uncontrolled diabetes.
*↑ pH, normal bicarbonate and ↓ pCO2*
- This profile describes **respiratory alkalosis**, often caused by primary hyperventilation.
- While the patient has rapid and deep breathing (Kussmaul respiration), this is a compensatory mechanism for metabolic acidosis, not a primary respiratory alkalosis.
*↓ pH, ↓ bicarbonate and normal anion gap*
- This indicates a **normal anion gap metabolic acidosis**, also known as hyperchloremic acidosis.
- This is typically seen in conditions like renal tubular acidosis or severe diarrhea, where bicarbonate is lost or chloride is retained, which is not the case for DKA.
*↓ pH, normal bicarbonate and ↑ pCO2*
- This presentation indicates **respiratory acidosis**, which is caused by hypoventilation and retention of CO2.
- The patient's rapid and deep breathing (Kussmaul breathing) is a compensatory mechanism to blow off CO2 and would decrease pCO2, not increase it.
Acid-base disorders in surgical patients US Medical PG Question 4: What is the primary mechanism for maintaining acid-base balance during prolonged vomiting?
- A. Increased chloride reabsorption
- B. Increased potassium excretion
- C. Increased bicarbonate excretion (Correct Answer)
- D. Decreased hydrogen secretion
Acid-base disorders in surgical patients Explanation: ***Increased bicarbonate excretion***
- Prolonged vomiting leads to the loss of **gastric acid (HCl)**, causing **metabolic alkalosis**. The kidneys compensate by increasing the excretion of **bicarbonate (HCO3-)** to restore acid-base balance.
- This renal compensation is the primary mechanism to eliminate the excess alkali from the body.
*Increased chloride reabsorption*
- In **metabolic alkalosis** due to vomiting, the body tends to reabsorb less chloride, not more, in an attempt to excrete bicarbonate.
- **Chloride depletion** can actually hinder bicarbonate excretion by promoting sodium reabsorption with bicarbonate.
*Increased potassium excretion*
- **Hypokalemia** can occur with prolonged vomiting due to increased aldosterone activity and direct renal loss associated with metabolic alkalosis.
- However, increased potassium excretion itself is not the primary mechanism for correcting the acid-base disorder; rather, it is a consequence or a contributing factor to the imbalance.
*Decreased hydrogen secretion*
- In response to alkalosis, the kidneys would typically decrease, not increase, **hydrogen ion (H+) secretion** in an effort to retain H+ and normalize pH.
- Decreased H+ secretion is a compensatory mechanism, but the direct excretion of bicarbonate is more crucial for correcting the metabolic alkalosis.
Acid-base disorders in surgical patients US Medical PG Question 5: A 37-year-old G1P0 woman presents to her primary care physician for a routine checkup. She has a history of diabetes and hypertension but has otherwise been healthy with no change in her health status since the last visit. She is expecting her first child 8 weeks from now. She also enrolled in a study about pregnancy where serial metabolic panels and arterial blood gases are obtained. Partial results from these studies are shown below:
Serum:
Na+: 141 mEq/L
Cl-: 108 mEq/L
pH: 7.47
pCO2: 30 mmHg
HCO3-: 21 mEq/L
Which of the following disease processes would most likely present with a similar panel of metabolic results?
- A. Diarrheal disease
- B. Loop diuretic abuse
- C. Living at high altitude (Correct Answer)
- D. Ingestion of metformin
- E. Anxiety attack
Acid-base disorders in surgical patients Explanation: ***Living at high altitude***
- Chronic exposure to **high altitude** leads to sustained **hypoxia**, which stimulates **hyperventilation** as a compensatory mechanism.
- This persistent hyperventilation causes a **respiratory alkalosis** (high pH, low pCO2) and a compensatory **metabolic acidosis** (low HCO3-) to normalize pH, mimicking the presented metabolic panel.
*Diarrheal disease*
- Severe **diarrhea** leads to the loss of bicarbonate from the gastrointestinal tract, causing a **non-anion gap metabolic acidosis**.
- This would present with a **low pH**, **low HCO3-**, and a **compensatory drop in pCO2**, not a respiratory alkalosis with a high pH.
*Loop diuretic abuse*
- Chronic abuse of **loop diuretics** can cause **metabolic alkalosis** due to increased renal excretion of hydrogen ions and potassium, leading to volume contraction.
- This would typically present with a **high pH**, high HCO3-, and a compensatory rise in pCO2, which is different from the given values.
*Ingestion of metformin*
- **Metformin** can cause **lactic acidosis** (a type of high anion gap metabolic acidosis), especially in patients with renal impairment.
- This would manifest as a **low pH**, **low HCO3-**, and a **compensatory decrease in pCO2**, along with an elevated anion gap, not the respiratory alkalosis seen here.
*Anxiety attack*
- An **anxiety attack** causes acute **hyperventilation**, leading to **acute respiratory alkalosis** (high pH, low pCO2).
- However, in an acute setting, there is insufficient time for significant renal compensation, so the HCO3- would remain near normal, unlike the compensated state shown in the panel.
Acid-base disorders in surgical patients US Medical PG Question 6: A 29-year-old woman presents to the emergency department with a broken arm after she tripped and fell at work. She says that she has no history of broken bones but that she has been having bone pain in her back and hips for several months. In addition, she says that she has been waking up several times in the middle of the night to use the restroom and has been drinking a lot more water. Her symptoms started after she fell ill during an international mission trip with her church and was treated by a local doctor with unknown antibiotics. Since then she has been experiencing weight loss and muscle pain in addition to the symptoms listed above. Urine studies are obtained showing amino acids in her urine. The pH of her urine is also found to be < 5.5. Which of the following would most likely also be seen in this patient?
- A. Hyperkalemia
- B. Hypernatremia
- C. Metabolic alkalosis
- D. Hypocalcemia (Correct Answer)
- E. Decreased serum creatinine
Acid-base disorders in surgical patients Explanation: ***Hypocalcemia***
- The patient's clinical presentation (bone pain, pathologic fracture, polyuria, polydipsia, aminoaciduria, and urine pH <5.5) is characteristic of **Fanconi syndrome**, a generalized proximal tubule dysfunction.
- Fanconi syndrome leads to urinary wasting of **phosphate**, resulting in **hypophosphatemia**, which impairs bone mineralization and causes rickets/osteomalacia.
- Chronic hypophosphatemia triggers **secondary hyperparathyroidism**, and in severe cases or with concomitant vitamin D deficiency, **hypocalcemia** can develop, contributing to the bone disease and neuromuscular symptoms.
- While hypophosphatemia is the more direct and consistent finding, hypocalcemia may occur in this clinical context.
*Hyperkalemia*
- Fanconi syndrome causes impaired proximal tubule reabsorption of **potassium**, leading to **hypokalemia**, not hyperkalemia.
- Urinary potassium wasting is a hallmark feature of this proximal tubulopathy.
*Hypernatremia*
- Fanconi syndrome does not typically cause hypernatremia; the polyuria may lead to volume depletion, but **hypernatremia** is not a consistent or direct feature.
- Sodium reabsorption can be affected, but this does not reliably produce hypernatremia.
*Metabolic alkalosis*
- The urine pH <5.5 with systemic symptoms indicates **Type 2 (proximal) renal tubular acidosis**, which is an integral component of Fanconi syndrome.
- Loss of bicarbonate in the proximal tubule leads to **metabolic acidosis**, not alkalosis, though the distal tubule can still acidify urine (hence pH <5.5).
*Decreased serum creatinine*
- Fanconi syndrome is a **tubulopathy** affecting reabsorption, not a glomerulopathy affecting GFR.
- Serum creatinine typically remains **normal** unless there is concurrent glomerular or interstitial kidney disease; decreased creatinine is not an expected finding.
Acid-base disorders in surgical patients US Medical PG Question 7: Three days after undergoing an open cholecystectomy, a 73-year-old man has fever and abdominal pain. He has hypertension, type 2 diabetes mellitus, chronic obstructive pulmonary disease, and benign prostatic hyperplasia. He had smoked one pack of cigarettes daily for 40 years but quit 1 year ago. He does not drink alcohol. Prior to admission to the hospital, his medications included lisinopril, metformin, ipratropium, and tamsulosin. He appears acutely ill and lethargic. His temperature is 39.5°C (103.1°F), pulse is 108/min, respirations are 18/min, and blood pressure is 110/84 mm Hg. He is oriented only to person. Examination shows a 10-cm subcostal incision that appears dry and non-erythematous. Scattered expiratory wheezing is heard throughout both lung fields. His abdomen is distended with tenderness to palpation over the lower quadrants. Laboratory studies show:
Hemoglobin 10.1 g/dl
Leukocyte count 19,000/mm3
Serum
Glucose 180 mg/dl
Urea Nitrogen 25 mg/dl
Creatinine 1.2 mg/dl
Lactic acid 2.5 mEq/L (N = 0.5 - 2.2 mEq/L)
Urine
Protein 1+
RBC 1–2/hpf
WBC 32–38/hpf
Which of the following is the most likely underlying mechanism of this patient's current condition?
- A. Wound contamination
- B. Peritoneal inflammation
- C. Impaired alveolar ventilation
- D. Intraabdominal abscess formation (Correct Answer)
- E. Bladder outlet obstruction
Acid-base disorders in surgical patients Explanation: ***Intraabdominal abscess formation***
- The patient presents with **fever**, **leukocytosis**, **abdominal pain** and **distension** three days post-cholecystectomy. These symptoms, coupled with signs of systemic illness (lethargy, altered mental status, tachycardia, elevated lactic acid), are highly suggestive of an **intraabdominal infection** such as an abscess.
- The surgical site incision appears dry and non-erythematous, making a superficial wound infection less likely to explain the systemic symptoms and deep abdominal pain.
*Wound contamination*
- While wound contamination can cause infection, the incision site is described as **dry and non-erythematous**, suggesting that a superficial surgical site infection is not the primary cause of the patient's systemic illness and deep abdominal pain.
- A simple wound infection generally would not lead to such significant systemic symptoms, including **lethargy** and **altered mental status**, within three days post-surgery, especially without local signs of inflammation.
*Peritoneal inflammation*
- Peritoneal inflammation (peritonitis) is a consequence of an intraabdominal process like an abscess or anastomotic leak, rather than the primary underlying mechanism itself.
- The symptoms of **localized tenderness** and **distension** are more indicative of a contained process like an abscess rather than diffuse peritoneal inflammation as the initial cause.
*Impaired alveolar ventilation*
- While the patient has COPD and scattered expiratory wheezing, suggesting some degree of respiratory compromise, **impaired alveolar ventilation** alone does not explain the fever, elevated leukocyte count, abdominal pain, and an elevated lactic acid (though respiratory distress can contribute to lactic acidemia, an infection is a more direct cause here).
- Post-operative pulmonary complications are common, but the abdominal findings and systemic signs of infection point away from a purely respiratory origin for this acute deterioration.
*Bladder outlet obstruction*
- The patient has BPH and is on tamsulosin, but his current symptoms of fever, leukocytosis, abdominal pain, and elevated lactic acid are not typical for **bladder outlet obstruction**.
- Although the urine analysis shows pyuria (WBC 32-38/hpf), which could suggest a urinary tract infection (UTI), a UTI alone is less likely to cause this degree of systemic illness with **significant abdominal distension** and **tenderness** in the lower quadrants shortly after abdominal surgery; it's more probable that the pyuria is a secondary finding or contributing factor in a patient with a more severe intraabdominal process.
Acid-base disorders in surgical patients 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
Acid-base disorders in surgical patients 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.
Acid-base disorders in surgical patients 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)
Acid-base disorders in surgical patients 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.
Acid-base disorders in surgical patients 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)
Acid-base disorders in surgical patients 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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