Insulin therapy protocols US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Insulin therapy protocols. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Insulin therapy protocols US Medical PG Question 1: A 27-year-old man with a past medical history of type I diabetes mellitus presents to the emergency department with altered mental status. The patient was noted as becoming more lethargic and confused over the past day, prompting his roommates to bring him in. His temperature is 99.0°F (37.2°C), blood pressure is 107/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Laboratory values are ordered as seen below.
Serum:
Na+: 144 mEq/L
Cl-: 100 mEq/L
K+: 6.3 mEq/L
HCO3-: 16 mEq/L
BUN: 20 mg/dL
Glucose: 599 mg/dL
Creatinine: 1.4 mg/dL
Ca2+: 10.2 mg/dL
Which of the following is the appropriate endpoint of treatment for this patient?
- A. Clinically asymptomatic
- B. Normal anion gap (Correct Answer)
- C. Normal glucose
- D. Vitals stable
- E. Normal potassium
Insulin therapy protocols Explanation: ***Normal anion gap***
- A **normal anion gap** (approximately 8-12 mEq/L) indicates resolution of the **metabolic acidosis** characteristic of diabetic ketoacidosis (DKA). The current anion gap is high (Na - (Cl + HCO3) = 144 - (100 + 16) = 28 mEq/L).
- The patient's presentation with **type 1 diabetes** and **altered mental status**, coupled with **hyperglycemia** (599 mg/dL) and **low bicarbonate** (16 mEq/L), is highly suggestive of DKA, for which anion gap normalization is a key treatment endpoint.
*Clinically asymptomatic*
- While a desirable outcome, resolution of symptoms occurs gradually and is not the primary biochemical endpoint for DKA treatment.
- Patients may have residual symptoms even after metabolic derangements have significantly improved.
*Normal glucose*
- In DKA treatment, glucose is allowed to drop to a level (e.g., <200 mg/dL) but not necessarily to normal range, before initiating **dextrose-containing intravenous fluids** to prevent hypoglycemia while continuing insulin.
- **Normal glucose** alone does not guarantee resolution of ketoacidosis, which is the main life-threatening aspect of DKA.
*Vitals stable*
- **Stable vital signs** indicate hemodynamic stability, which is crucial but does not confirm the resolution of the underlying DKA metabolic derangements.
- Vitals can stabilize or worsen independently of acidosis resolution, especially if complications arise.
*Normal potassium*
- **Potassium levels** are critical to monitor and correct during DKA treatment, as insulin administration drives potassium into cells, potentially causing **hypokalemia**.
- While important for patient safety, achieving a normal potassium level is part of supportive care and not the primary endpoint for resolving the ketoacidotic state itself.
Insulin therapy protocols 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
Insulin therapy protocols 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**.
Insulin therapy protocols US Medical PG Question 3: A 61-year-old female with congestive heart failure and type 2 diabetes is brought to the emergency room by her husband because of an altered mental status. He states he normally helps her be compliant with her medications, but he had been away for several days. On physical exam, her temperature is 37.2 C, BP 85/55, and HR 130. Serum glucose is 500 mg/dL. Which of the following is the first step in the management of this patient?
- A. IV ½ NS
- B. IV insulin
- C. Subcutaneous insulin injection
- D. IV NS (Correct Answer)
- E. IV D5W
Insulin therapy protocols Explanation: ***IV NS***
- The patient presents with **hypotension (85/55 mmHg)** and **tachycardia (130 bpm)**, indicating significant **volume depletion** despite a history of congestive heart failure.
- **Isotonic intravenous fluids (e.g., normal saline)** are crucial in the initial management of **diabetic ketoacidosis (DKA)** or **hyperosmolar hyperglycemic state (HHS)** to restore intravascular volume and improve tissue perfusion.
*IV ½ NS*
- **Hypotonic solutions** such as IV ½ NS are typically used later in DKA/HHS management, once the patient's **hemodynamic stability** has been achieved and serum sodium levels are stable or elevated.
- Administering hypotonic fluids to an already **hypotensive and volume-depleted patient** could worsen hypotension and potentially lead to cerebral edema if not carefully monitored.
*IV insulin*
- While insulin is essential for correcting hyperglycemia, it is administered **after or concurrently with fluid resuscitation** to avoid worsening hypovolemia as it drives glucose and potassium into cells, potentially causing **hypokalemia** and further **hemoconcentration**.
- **Fluid resuscitation** should always precede or be initiated simultaneously with insulin therapy, especially in cases of hemodynamic instability.
*Subcutaneous insulin injection*
- **Subcutaneous insulin** is not appropriate for initial management in this critically ill patient due to its **slower onset of action** and potentially **erratic absorption** in hypotensive and poorly perfused states.
- **Intravenous insulin** is preferred in DKA/HHS for its rapid, titratable effect.
*IV D5W*
- **Dextrose 5% in water (D5W)** is a hypotonic solution primarily used when **blood glucose levels fall below 250 mg/dL** during DKA/HHS treatment to prevent hypoglycemia.
- Administering D5W in a patient with a **serum glucose of 500 mg/dL** would further elevate blood sugar and worsen the hyperosmolar state.
Insulin therapy protocols US Medical PG Question 4: A 19-year-old man with a history of type 1 diabetes presents to the emergency department for the evaluation of a blood glucose level of 492 mg/dL. Laboratory examination revealed a serum bicarbonate level of 13 mEq/L, serum sodium level of 122 mEq/L, and ketonuria. Arterial blood gas demonstrated a pH of 6.9. He is admitted to the hospital and given bicarbonate and then started on an insulin drip and intravenous fluid. Seven hours later when his nurse is making rounds, he is confused and complaining of a severe headache. Repeat sodium levels are unchanged, although his glucose level has improved. His vital signs include a temperature of 36.6°C (98.0°F), pulse 50/min, respiratory rate 13/min and irregular, and blood pressure 177/95 mm Hg. What other examination findings would be expected in this patient?
- A. Hypoglycemia
- B. Pupillary constriction
- C. Papilledema (Correct Answer)
- D. Pancreatitis
- E. Peripheral edema
Insulin therapy protocols Explanation: ***Papilledema***
- This patient's symptoms (confusion, severe headache, bradycardia, irregular respiration, hypertension) following treatment for **diabetic ketoacidosis (DKA)** are highly suggestive of **cerebral edema**.
- **Papilledema** is a retinal finding resulting from increased intracranial pressure (ICP), which is a characteristic sign of cerebral edema.
*Hypoglycemia*
- While the patient's glucose level has improved, it is not described as being low enough to cause hypoglycemia, and the symptoms are more consistent with **increased ICP**.
- Symptoms of hypoglycemia (e.g., tremors, sweating, hunger, anxiety) are different from the patient's current presentation of confusion and severe headache.
*Pupillary constriction*
- **Pupillary constriction** (miosis) is typically not associated with cerebral edema; instead, **pupillary dilation** (mydriasis) can occur with severe increase in ICP due to uncal herniation.
- The combination of bradycardia, irregular respiration, and hypertension (Cushing's triad) is indicative of increased ICP, which would likely cause pupillary changes related to brainstem compression.
*Pancreatitis*
- Pancreatitis is a known complication of DKA, but it typically presents with **severe abdominal pain**, nausea, and vomiting, rather than cerebral symptoms.
- Although the patient had DKA, the current neurological symptoms point directly to an intracranial process rather than an abdominal issue.
*Peripheral edema*
- **Peripheral edema** results from fluid accumulation in peripheral tissues and is not a direct consequence or expected finding in cerebral edema.
- While fluid administration can cause some peripheral fluid retention, it typically does not lead to the acute neurological deterioration seen in this patient.
Insulin therapy protocols US Medical PG Question 5: A 22-year-old woman with a history of type I diabetes mellitus presents to the emergency department with nausea, vomiting, and drowsiness for the past day. Her temperature is 98.3°F (36.8°C), blood pressure is 114/74 mmHg, pulse is 120/min, respirations are 27/min, and oxygen saturation is 100% on room air. Physical exam is notable for a confused and lethargic young woman. Initial laboratory values are notable for the findings below.
Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 2.9 mEq/L
HCO3-: 9 mEq/L
BUN: 20 mg/dL
Glucose: 599 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L
An initial ECG is notable for sinus tachycardia. Which of the following is the best initial step in management for this patient?
- A. Normal saline and insulin
- B. Insulin and potassium
- C. Normal saline and potassium
- D. Normal saline, insulin, and potassium (Correct Answer)
- E. Normal saline, insulin, potassium, and sodium bicarbonate
Insulin therapy protocols Explanation: ***Normal saline, insulin, and potassium***
- This patient presents with signs and symptoms consistent with **diabetic ketoacidosis (DKA)**, including hyperglycemia (glucose 599 mg/dL), metabolic acidosis (HCO3- 9 mEq/L, respiratory compensation with elevated respiratory rate), and altered mental status. The initial management of DKA involves aggressive **intravenous fluid resuscitation** (normal saline), **insulin administration** to correct hyperglycemia and acidosis, and **potassium replacement** due to total body potassium depletion and anticipated further drop with insulin therapy.
- Her **hypokalemia (2.9 mEq/L)**, even before insulin administration, necessitates immediate potassium repletion as insulin drives potassium intracellularly, which could worsen hypokalemia and lead to arrhythmias.
*Normal saline and insulin*
- While fluid resuscitation and insulin are crucial for DKA management, omitting **potassium replacement** in a patient with initial hypokalemia (K+ 2.9 mEq/L) would be inappropriate and potentially dangerous.
- Failure to correct hypokalemia before or with insulin administration can precipitate life-threatening **cardiac arrhythmias**.
*Normal saline, insulin, potassium, and sodium bicarbonate*
- **Sodium bicarbonate** is generally not recommended for DKA unless pH is extremely low (typically <6.9), as it can worsen cerebral edema and hypokalemia. The patient's bicarbonate of 9 mEq/L and presumably higher pH does not warrant bicarbonate administration.
- While fluids, insulin, and potassium are essential, the addition of sodium bicarbonate is usually reserved for severe, life-threatening acidosis (pH < 6.9).
*Normal saline and potassium*
- Administering only normal saline and potassium would address dehydration and hypokalemia but would fail to correct the underlying **hyperglycemia** and **ketoacidosis**, which are the core pathologies of DKA.
- **Insulin** is critical to stop ketogenesis and lower blood glucose.
*Insulin and potassium*
- Administering insulin and potassium without **fluid resuscitation** would be inadequate. The patient is likely significantly dehydrated due to osmotic diuresis from hyperglycemia and vomiting.
- **Fluid administration** is paramount in restoring circulating volume, improving renal perfusion, and reducing hyperglycemia by enhancing glucose excretion.
Insulin therapy protocols US Medical PG Question 6: An 8-year-old boy is brought to the emergency department with severe dyspnea, fatigue, and vomiting. His mother reports that he has been lethargic for the last several days with an increase in urine output. She thinks he may even be losing weight, despite eating and drinking more than normal for the last couple weeks. Laboratory results are notable for glucose of 440, potassium of 5.8, pH of 7.14 and HCO3 of 17. After administrating IV fluids and insulin, which of the following would you expect?
- A. Increase in anion gap
- B. Increase in serum glucose
- C. Decrease in serum potassium (Correct Answer)
- D. Decrease in pH
- E. Decrease in serum bicarbonate
Insulin therapy protocols Explanation: ***Decrease in serum potassium***
- **Insulin therapy** drives **potassium** into cells, as it stimulates the **Na+/K+ ATPase pump**, leading to a decrease in serum potassium levels.
- The initial **hyperkalemia** (potassium 5.8) is due to extracellular fluid shifts and acidosis, which will correct as **DKA** resolves with treatment.
*Increase in anion gap*
- The presented patient has **diabetic ketoacidosis (DKA)**, which is characterized by a **high anion gap metabolic acidosis** (evidenced by low pH and bicarbonate).
- Treatment with **IV fluids and insulin** aims to resolve the ketoacidosis, which would consequently lead to a **decrease** in the **anion gap**, not an increase.
*Increase in serum glucose*
- The primary goal of **IV fluids and insulin** in **DKA** is to lower the critically high **serum glucose** levels by promoting glucose uptake into cells and inhibiting hepatic glucose production.
- Therefore, one would expect a **decrease** in serum glucose, not an increase, as treatment progresses.
*Decrease in pH*
- The patient's initial pH of 7.14 indicates **acidosis**, a hallmark of **DKA**.
- **Insulin therapy** and **fluid resuscitation** will resolve the ketoacidosis, leading to an **increase** in **pH** towards normal, not a further decrease.
*Decrease in serum bicarbonate*
- The patient already presents with **decreased serum bicarbonate** (17 mEq/L), which is consistent with **metabolic acidosis** due to DKA.
- Treatment with **fluids and insulin** will correct the acidosis by reducing ketone production, leading to an **increase** in **serum bicarbonate**, not a further decrease.
Insulin therapy protocols US Medical PG Question 7: A 48-year-old man presents with DKA. Initial treatment is initiated with fluids and insulin infusion. Labs show glucose 460 mg/dL, pH 7.18, bicarbonate 10 mEq/L, potassium 4.5 mEq/L, and creatinine 2.8 mg/dL (baseline 1.0). After 4 hours, glucose decreases to 380 mg/dL but pH worsens to 7.12, bicarbonate drops to 8 mEq/L, and lactate is 5.2 mmol/L (initially 1.8). Blood pressure is 85/50 mmHg. Evaluate the clinical situation and necessary intervention.
- A. Administer additional fluid bolus for persistent hypotension
- B. Evaluate for sepsis or other concurrent illness causing lactic acidosis (Correct Answer)
- C. Increase insulin infusion rate to accelerate ketone clearance
- D. Add bicarbonate therapy for worsening acidosis
- E. Continue current management as DKA takes time to resolve
Insulin therapy protocols Explanation: ***Evaluate for sepsis or other concurrent illness causing lactic acidosis***
- While the blood glucose is responding to insulin, the **worsening metabolic acidosis** and significantly elevated **lactate (5.2 mmol/L)** indicate a secondary process such as **sepsis** or tissue hypoperfusion.
- **Diabetic Ketoacidosis (DKA)** often has a precipitating factor; the combination of **hypotension** and rising lactate suggests **septic shock** or organic ischemia that requires urgent investigation and targeted treatment.
*Administer additional fluid bolus for persistent hypotension*
- Although fluid resuscitation is vital, simply giving more fluids without diagnosing the **underlying cause** of the rising lactate and refractory shock is insufficient.
- **Hypotension** in this context may be secondary to **septic shock** or systemic inflammatory response rather than simple volume depletion from DKA.
*Increase insulin infusion rate to accelerate ketone clearance*
- The current insulin infusion is successfully lowering the blood glucose, but the acidosis is worsening due to **lactic acid**, not just ketones.
- Increasing insulin will not resolve **Type A lactic acidosis** caused by **inadequate tissue oxygenation** or sepsis.
*Add bicarbonate therapy for worsening acidosis*
- **Bicarbonate therapy** is generally not recommended in DKA unless the pH is <6.9, as it can cause **paradoxical cerebral acidosis** and hypokalemia.
- Administering bicarbonate would provide a temporary buffer but would fail to address the **rising lactate** and underlying hemodynamic instability.
*Continue current management as DKA takes time to resolve*
- While DKA resolution is gradual, a **rising lactate** and **falling pH** despite therapy are red flags that indicate the clinical condition is deteriorating.
- Ignoring the **acute kidney injury** (Creatinine 2.8) and persistent **hypotension** increases the risk of multi-organ failure and mortality.
Insulin therapy protocols US Medical PG Question 8: A 25-year-old woman with type 1 diabetes presents with DKA. She admits to intentionally withholding insulin to lose weight. This is her fifth DKA admission in 8 months. Current pH is 7.14, glucose 520 mg/dL, bicarbonate 11 mEq/L. Medical costs exceed $150,000 for recurrent admissions. The team is frustrated. Evaluate the comprehensive management approach beyond acute DKA treatment.
- A. Referral to ethics committee for discussion of resource allocation
- B. Involuntary psychiatric commitment for non-compliance
- C. Insulin pump placement to prevent future manipulation
- D. Multidisciplinary approach including psychiatry, eating disorder specialist, diabetes educator, and close outpatient follow-up (Correct Answer)
- E. Standard DKA treatment with discharge to outpatient endocrinology
Insulin therapy protocols Explanation: ***Multidisciplinary approach including psychiatry, eating disorder specialist, diabetes educator, and close outpatient follow-up***
- This patient presents with **diabulimia**, a life-threatening eating disorder where Type 1 diabetics restrict insulin for weight control, requiring a **comprehensive care team** to address both physiologic and psychological needs.
- A **multidisciplinary strategy** is essential to reduce the high risk of mortality and frequent **recurrent DKA admissions** by targeting the root cause of non-compliance.
*Referral to ethics committee for discussion of resource allocation*
- While medical costs are high, **withholding treatment** based on cost or resource allocation for a life-threatening condition like DKA is generally unethical.
- The **ethics committee** may assist in complex care plans, but it does not address the primary clinical need for specialized psychiatric and nutritional intervention.
*Involuntary psychiatric commitment for non-compliance*
- **Involuntary commitment** typically requires the patient to be a danger to themselves or others due to a mental illness; insulin omission, while dangerous, often does not meet legal criteria if the patient has **decision-making capacity**.
- Simple **non-compliance** in an adult with capacity is not usually grounds for commitment, and long-term behavioral change is better achieved through voluntary therapeutic engagement.
*Insulin pump placement to prevent future manipulation*
- An **insulin pump** is not a solution as it can still be easily manipulated, disconnected, or the settings altered by a patient determined to restrict insulin.
- Introducing a medical device without addressing the **underlying eating disorder** may actually complicate management and increase the risk of device-related complications.
*Standard DKA treatment with discharge to outpatient endocrinology*
- Given five DKA admissions in 8 months, standard management has already proven **insufficient** and fails to address the unique psychiatric etiology of her condition.
- Discharging to **standard outpatient endocrinology** without specialized eating disorder support ignores the behavioral triggers that lead to recurrent life-threatening metabolic crises.
Insulin therapy protocols US Medical PG Question 9: A 55-year-old man with type 2 diabetes and end-stage renal disease on hemodialysis presents with DKA. Initial glucose is 580 mg/dL, pH 7.12, bicarbonate 10 mEq/L, and potassium 6.2 mEq/L. He is fluid overloaded with bilateral crackles and peripheral edema. His last dialysis was 3 days ago. Evaluate the optimal management strategy addressing both DKA and renal failure.
- A. Standard DKA protocol with furosemide for fluid management
- B. Bicarbonate therapy to correct acidosis without fluids
- C. Subcutaneous insulin with no IV fluids due to volume overload
- D. Insulin infusion with limited fluids and urgent hemodialysis (Correct Answer)
- E. Standard DKA protocol with aggressive fluid resuscitation
Insulin therapy protocols Explanation: ***Insulin infusion with limited fluids and urgent hemodialysis***
- Patients with **ESRD** and **DKA** who are **fluid overloaded** require **urgent hemodialysis** to safely correct metabolic acidosis, hyperkalemia, and volume status.
- **Continuous insulin infusion** is essential to stop ketone production, but fluid resuscitation must be severely **restricted** to avoid worsening pulmonary edema.
*Standard DKA protocol with furosemide for fluid management*
- **Furosemide** is ineffective in patients with **end-stage renal disease** (ESRD) as they have minimal to no residual renal function.
- Standard DKA protocols prioritize aggressive IV fluids, which would be **life-threatening** for a patient already showing signs of volume overload and crackles.
*Bicarbonate therapy to correct acidosis without fluids*
- **Bicarbonate therapy** is generally not recommended for DKA unless the pH is below 6.9, and it can cause a **rebound worsening** of intracellular acidosis.
- It does not address the underlying **insulin deficiency** or the patient's massive **volume overload** and hyperkalemia.
*Subcutaneous insulin with no IV fluids due to volume overload*
- **Subcutaneous insulin** is inappropriate for severe DKA (pH 7.12); **intravenous insulin** is the standard for rapid titration and metabolic control.
- Complete avoidance of fluids may prevent correction of the **osmotic shift**, but the primary failure here is the omission of dialysis for a symptomatic ESRD patient.
*Standard DKA protocol with aggressive fluid resuscitation*
- Aggressive fluid administration is **contraindicated** in ESRD patients with clinical signs of **congestive heart failure** like crackles and peripheral edema.
- This approach carries a high risk of inducing **acute respiratory failure** or flash pulmonary edema.
Insulin therapy protocols US Medical PG Question 10: A 38-year-old pregnant woman at 28 weeks gestation with type 1 diabetes presents with nausea and vomiting. Labs show glucose 310 mg/dL, pH 7.27, bicarbonate 15 mEq/L, and positive urine ketones. Fetal monitoring shows reactive non-stress test. She has been taking her insulin but unable to eat for 24 hours due to hyperemesis. Analyze the optimal management approach considering maternal and fetal risks.
- A. Standard DKA protocol with standard glucose targets (200-250 mg/dL)
- B. Aggressive DKA treatment with lower glucose targets (100-150 mg/dL) and close fetal monitoring (Correct Answer)
- C. Immediate cesarean delivery followed by DKA treatment
- D. Conservative management with oral intake and subcutaneous insulin
- E. Standard DKA protocol with delivery planning after stabilization
Insulin therapy protocols Explanation: ***Aggressive DKA treatment with lower glucose targets (100-150 mg/dL) and close fetal monitoring***
- In pregnancy, **Diabetic Ketoacidosis (DKA)** often presents with lower blood glucose levels due to increased **glucose utilization** by the fetus and placenta.
- Successful management requires **aggressive hydration**, **intravenous insulin**, and maintaining blood glucose between **100-150 mg/dL** to prevent fetal complications.
*Standard DKA protocol with standard glucose targets (200-250 mg/dL)*
- Standard targets for non-pregnant adults are too high for pregnancy and can lead to prolonged **fetal acidosis** and increased morbidity.
- Pregnancy-specific protocols prioritize tighter glycemic control to optimize the **maternal-fetal environment** during acute metabolic distress.
*Immediate cesarean delivery followed by DKA treatment*
- Surgery during **untreated DKA** carries extremely high maternal and fetal risk; the fetus should only be delivered for **obstetric indications** after maternal stabilization.
- **Fetal heart rate** abnormalities often resolve once the mother's **acidosis** and electrolyte imbalances are corrected with medical therapy.
*Conservative management with oral intake and subcutaneous insulin*
- Maternal **acidemia (pH 7.27)** and **ketonuria** indicate a medical emergency that cannot be safely managed with subcutaneous insulin or oral fluids.
- **Nausea and vomiting** from hyperemesis or the DKA itself necessitate **intravenous fluid resuscitation** and specialized inpatient monitoring.
*Standard DKA protocol with delivery planning after stabilization*
- While maternal stabilization is the primary goal, following a "standard" protocol ignores the need for **lower glucose targets** unique to pregnancy.
- **Delivery planning** at 28 weeks should only be considered if fetal distress persists after maternal metabolic status has returned to baseline.
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