Initial assessment and risk stratification US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Initial assessment and risk stratification. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Initial assessment and risk stratification US Medical PG Question 1: 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
Initial assessment and risk stratification 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.
Initial assessment and risk stratification US Medical PG Question 2: A 14-year-old female with no past medical history presents to the emergency department with nausea and abdominal pain. On physical examination, her blood pressure is 78/65, her respiratory rate is 30, her breath has a fruity odor, and capillary refill is > 3 seconds. Serum glucose is 820 mg/dL. After starting IV fluids, what is the next best step in the management of this patient?
- A. Intravenous Dextrose in water
- B. Subcutaneous insulin glargine
- C. Intravenous regular insulin (Correct Answer)
- D. Intravenous glucagon
- E. Subcutaneous insulin lispro
Initial assessment and risk stratification Explanation: ***Intravenous regular insulin***
- The patient presents with **diabetic ketoacidosis (DKA)**, characterized by **hyperglycemia**, **fruity breath** (due to ketones), and **hypotension**. Prompt administration of **intravenous regular insulin** is crucial to lower blood glucose and resolve ketoacidosis.
- **Regular insulin** is preferred intravenously due to its **rapid onset** and short duration of action, allowing for precise titration and continuous adjustment based on glucose levels.
*Intravenous Dextrose in water*
- **Dextrose** would further increase the already severely elevated blood glucose level in a patient with DKA, worsening the metabolic derangements.
- Dextrose is typically initiated only after blood glucose drops to safe levels (<200 mg/dL) to prevent **hypoglycemia** during insulin infusion.
*Subcutaneous insulin glargine*
- **Insulin glargine** is a **long-acting insulin** designed for basal insulin coverage, not for acute management of severe hyperglycemia or DKA.
- Its **slow onset of action** and prolonged effect make it unsuitable for the urgent and rapid glucose reduction required in DKA.
*Intravenous glucagon*
- **Glucagon** is a hormone that **raises blood glucose levels**, counteracting the effects of insulin.
- Administering glucagon would exacerbate the severe hyperglycemia present in DKA and is used only in cases of severe hypoglycemia.
*Subcutaneous insulin lispro*
- **Insulin lispro** is a **rapid-acting insulin analog** but is typically given subcutaneously.
- While faster than regular insulin subcutaneously, the **subcutaneous route** has variable absorption in critically ill patients, and the immediate and precisely controllable effect of intravenous regular insulin is needed in DKA.
Initial assessment and risk stratification US Medical PG Question 3: A 27-year-old diabetic male rushes to the emergency department after finding his blood glucose level to be 492 mg/dL which is reconfirmed in the ED. He currently does not have any complaints except for a mild colicky abdominal pain. His temperature is 37°C (98.6°F), respirations are 15/min, pulse is 67/min, and blood pressure is 122/88 mm Hg. Blood is drawn for labs the result of which is given below:
Serum:
pH 7.0
pCO2 32 mm Hg
HCO3- 15.2 mEq/L
Sodium 122 mEq/L
Potassium 4.8 mEq/L
Urinalysis is positive for ketone bodies. He is admitted to the hospital and given intravenous bicarbonate and then started on an insulin drip and normal saline. 7 hours later, he is found to be confused and complaining of a severe headache. His temperature is 37°C (98.6°F), pulse is 50/min, respirations are 13/min and irregular, and blood pressure is 137/95 mm Hg. What other examination findings would be expected in this patient?
- A. Pancreatitis
- B. Pupillary constriction
- C. Hypoglycemia
- D. Peripheral edema
- E. Papilledema (Correct Answer)
Initial assessment and risk stratification Explanation: ***Papilledema***
- The patient's presentation with **confusion**, **severe headache**, **bradycardia**, **irregular respirations**, and **elevated blood pressure** (Cushing's triad) 7 hours after treatment for **diabetic ketoacidosis (DKA)** suggests increased intracranial pressure due to **cerebral edema**.
- **Papilledema** is a key ophthalmoscopic finding in significant cerebral edema, resulting from increased intracranial pressure transmitted to the optic nerve sheath.
*Pancreatitis*
- Pancreatitis can cause abdominal pain and may be associated with DKA, but the acute neurological deterioration with signs of increased intracranial pressure after initial treatment points away from pancreatitis as the primary expected finding at this stage.
- While initial mild colicky abdominal pain could suggest pancreatitis, the late-onset confusion, headache, and vital sign changes following DKA treatment are not characteristic of pancreatitis, but rather of a severe neurological complication.
*Pupillary constriction*
- **Pupillary constriction** (miosis) can be associated with opioid overdose, pontine lesions, or certain medications, but it is not a direct or expected finding in cerebral edema causing increased intracranial pressure.
- In cerebral edema, pupils are more likely to be dilated or unequal, especially if there is uncal herniation.
*Hypoglycemia*
- While **hypoglycemia** can occur with insulin therapy, leading to confusion and neurological symptoms, the patient's blood pressure is elevated and heart rate is low (bradycardia), which are not typical signs of hypoglycemia.
- Hypoglycemia usually presents with sympathetic activation (tachycardia, diaphoresis) before progressing to bradycardia in severe cases, but the associated hypertension and irregular breathing pattern are more indicative of increased intracranial pressure.
*Peripheral edema*
- **Peripheral edema** is swelling in the extremities and is generally due to fluid overload, heart failure, kidney disease, or liver disease.
- While fluid administration during DKA treatment could potentially lead to some fluid retention, it does not explain the acute neurological deterioration, headache, and vital sign changes (Cushing's triad) seen in this patient, which are far more characteristic of cerebral edema.
Initial assessment and risk stratification US Medical PG Question 4: An 8-year old boy is brought to the emergency department because he has been lethargic and has had several episodes of nausea and vomiting for the past day. He has also had increased thirst over the past two months. He has lost 5.4 kg (11.9 lbs) during this time. He is otherwise healthy and has no history of serious illness. His temperature is 37.5 °C (99.5 °F), blood pressure is 95/68 mm Hg, pulse is 110/min, and respirations are 30/min. He is somnolent and slightly confused. His mucous membranes are dry. Laboratory studies show:
Hemoglobin 16.2 g/dL
Leukocyte count 9,500/mm3
Platelet count 380,000/mm3
Serum
Na+ 130 mEq/L
K+ 5.5 mEq/L
Cl- 99 mEq/L
HCO3- 16 mEq/L
Creatinine 1.2 mg/dL
Glucose 570 mg/dL
Ketones positive
Blood gases, arterial
pH 7.25
pCO2 21 mm Hg
Which of the following is the most appropriate next step in management?
- A. Intravenous hydration with 0.45% normal saline and insulin
- B. Intravenous hydration with 5% dextrose solution and 0.45% normal saline
- C. Intravenous sodium bicarbonate
- D. Intravenous hydration with 0.9% normal saline and insulin (Correct Answer)
- E. Intravenous hydration with 0.9% normal saline and potassium chloride
Initial assessment and risk stratification Explanation: ***Intravenous hydration with 0.9% normal saline and insulin***
- This patient presents with **diabetic ketoacidosis (DKA)**, characterized by hyperglycemia (glucose 570 mg/dL), metabolic acidosis (pH 7.25, HCO3- 16 mEq/L, ketones positive), and dehydration (dry mucous membranes, increased thirst, weight loss).
- Initial management of DKA involves aggressive **volume expansion** with **0.9% normal saline** to restore perfusion and reduce hyperglycemia; subsequently, **insulin infusion** is started to correct hyperglycemia and halt ketogenesis.
*Intravenous hydration with 0.45% normal saline and insulin*
- While insulin is crucial, **0.45% normal saline (hypotonic saline)** is generally not the initial fluid of choice for DKA due to the risk of exacerbating cerebral edema, especially in children.
- **Isotonic saline (0.9% normal saline)** is preferred for initial resuscitation to rapidly restore extracellular fluid volume.
*Intravenous hydration with 5% dextrose solution and 0.45% normal saline*
- **5% dextrose solution** should only be added to intravenous fluids when the blood glucose level falls to around 200-250 mg/dL, to prevent hypoglycemia while continuing insulin to resolve ketosis.
- Administering dextrose initially would worsen the existing severe hyperglycemia.
*Intravenous sodium bicarbonate*
- **Sodium bicarbonate** is generally not recommended for mild to moderate DKA due to potential risks like cerebral edema and metabolic alkalosis, and potential paradoxical worsening of CNS acidosis.
- Bicarbonate therapy is reserved for **severe acidosis (pH < 6.9 or 7.0)** with hemodynamic instability or impaired cardiac contractility, which is not the case here.
*Intravenous hydration with 0.9% normal saline and potassium chloride*
- While **0.9% normal saline** is appropriate, this option lacks **insulin therapy**, which is essential for treating DKA by halting ketogenesis and correcting hyperglycemia.
- Although potassium supplementation will be necessary during DKA treatment (as insulin drives K+ into cells and can cause hypokalemia), the most appropriate **next step** is to initiate both fluid resuscitation and insulin therapy together.
- The patient's current potassium level of 5.5 mEq/L is at the upper limit of normal, but reflects total body potassium depletion; potassium should be added to maintenance fluids once adequate urine output is established.
Initial assessment and risk stratification US Medical PG Question 5: A 35-year-old patient with a history of diabetes presents to the ED with a myriad of systemic complaints. An arterial blood gas shows serum pH = 7.3, HCO3- = 13 mEq/L, PCO2 = 27 mmHg. Which of the following would you LEAST expect to observe in this patient?
- A. Increased anion gap
- B. Increased urine output
- C. Increased serum potassium
- D. Decreased respiratory rate (Correct Answer)
- E. Increased serum ketones
Initial assessment and risk stratification Explanation: ***Decreased respiratory rate***
- This patient has **diabetic ketoacidosis (DKA)**, which causes a metabolic acidosis. The body compensates for acidosis by increasing the respiratory rate (**Kussmaul respirations**) to blow off CO2, thus decreasing serum acidity.
- A decreased respiratory rate would worsen the acidosis by retaining CO2, which is contrary to the body's compensatory mechanism in DKA.
- This is what you would **LEAST expect** to observe in a patient with DKA.
*Increased anion gap*
- The patient's **pH of 7.3** and **HCO3- of 13 mEq/L** indicate a metabolic acidosis with a PCO2 of 27 mmHg showing respiratory compensation.
- DKA is characterized by the accumulation of **ketoacids** (acetoacetate, beta-hydroxybutyrate), which are unmeasured anions, leading to an **elevated anion gap**.
- This is an **expected finding** in DKA.
*Increased urine output*
- In DKA, **hyperglycemia** leads to an osmotic diuresis as excess glucose is filtered by the kidneys and draws water out, resulting in **polyuria** (increased urine output).
- This excessive urination contributes to **dehydration**, a common finding in DKA.
- This is an **expected finding** in DKA.
*Increased serum potassium*
- Despite total body potassium depletion, patients in DKA often present with **normal or elevated serum potassium** due to intracellular potassium shifting out of cells in exchange for hydrogen ions (to buffer acidosis).
- **Insulin deficiency** also contributes to this shift by impairing potassium uptake into cells.
- This is an **expected finding** in DKA, though potassium will drop with insulin treatment.
*Increased serum ketones*
- **Diabetic ketoacidosis (DKA)** is fundamentally caused by insulin deficiency, leading to increased **lipolysis** and subsequent overproduction of **ketone bodies** (acetoacetate, beta-hydroxybutyrate) by the liver.
- These ketones accumulate in the blood, causing the characteristic metabolic acidosis and are measurable in serum and urine.
- This is an **expected finding** and diagnostic of DKA.
Initial assessment and risk stratification US Medical PG Question 6: A 20-year-old male is brought by ambulance to the emergency room in extremis. He is minimally conscious, hypotensive, and tachypneic, and his breath gives off a "fruity" odor. An arterial blood gas and metabolic panel show anion gap metabolic acidosis. This patient is most likely deficient in which of the following metabolic actions?
- A. Glucagon production
- B. Cortisol secretion
- C. Formation of ketone bodies
- D. Glucose production
- E. Cellular uptake of glucose (Correct Answer)
Initial assessment and risk stratification Explanation: ***Cellular uptake of glucose***
- The patient's symptoms, including **fruity odor breath**, **anion gap metabolic acidosis**, and being found in extremis, are classic signs of **diabetic ketoacidosis (DKA)**.
- DKA results from a profound lack of **insulin**, which is essential for cells (especially muscle and adipose tissue) to take up glucose from the bloodstream, leading to hyperglycemia and a shift to fat metabolism.
*Glucagon production*
- **Glucagon** is a counter-regulatory hormone that *raises* blood glucose levels, and its production is often *increased* in DKA as the body attempts to provide fuel to cells in the absence of insulin's effect.
- A deficiency in glucagon production would more likely lead to **hypoglycemia**, not the profound hyperglycemia seen in DKA.
*Cortisol secretion*
- **Cortisol** is another counter-regulatory hormone that *increases* blood glucose, and its secretion is typically *elevated* in stress states like DKA.
- A deficiency in cortisol (e.g., in adrenal insufficiency) would present with different symptoms such as **hypoglycemia**, **hyponatremia**, and **hyperkalemia**, without the classic DKA picture.
*Formation of ketone bodies*
- The patient's **fruity odor breath** and **anion gap metabolic acidosis** are direct consequences of the *overproduction* of **ketone bodies**.
- This overproduction occurs when the body, lacking glucose for fuel due to insulin deficiency, switches to **fat metabolism**, leading to excessive formation of acetoacetate, beta-hydroxybutyrate, and acetone.
*Glucose production*
- **Glucose production** (gluconeogenesis and glycogenolysis) is typically *increased* in DKA as the liver tries to supply glucose to the body due to perceived cellular starvation (despite high blood glucose).
- A deficiency in glucose production, such as in certain glycogen storage diseases or severe liver failure, would lead to **hypoglycemia**, not the hyperglycemia characteristic of DKA.
Initial assessment and risk stratification 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
Initial assessment and risk stratification 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.
Initial assessment and risk stratification 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
Initial assessment and risk stratification 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.
Initial assessment and risk stratification 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
Initial assessment and risk stratification 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.
Initial assessment and risk stratification 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
Initial assessment and risk stratification 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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