DKA

DKA 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

DKA 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.

DKA 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

DKA 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**.

DKA US Medical PG Question 3: 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

DKA 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.

DKA US Medical PG Question 4: 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)

DKA 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.

DKA US Medical PG Question 5: 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

DKA 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.

DKA US Medical PG Question 6: A previously healthy 14-year-old girl is brought to the emergency department by her mother because of abdominal pain, nausea, and vomiting for 6 hours. Over the past 6 weeks, she has also had increased frequency of urination, and she has been drinking more water than usual. She has lost 6 kg (13 lb) over the same time period despite having a good appetite. Her temperature is 37.1°C (98.8°F), pulse is 125/min, respirations are 32/min, and blood pressure is 94/58 mm Hg. She appears lethargic. Physical examination shows deep and labored breathing and dry mucous membranes. The abdomen is soft, and there is diffuse tenderness to palpation with no guarding or rebound. Urine dipstick is positive for ketones and glucose. Further evaluation is most likely to show which of the following findings?

• A. Excess water retention
• B. Serum glucose concentration > 800 mg/dL
• C. Increased arterial pCO2
• D. Increased arterial blood pH
• E. Decreased total body potassium (Correct Answer)

DKA Explanation: ***Decreased total body potassium*** - This is the correct answer. In **diabetic ketoacidosis (DKA)**, patients have **significant total body potassium depletion** due to osmotic diuresis and urinary losses. - **Serum potassium may initially appear normal or even elevated** due to acidosis-induced extracellular shift of potassium from cells. - However, **total body potassium stores are markedly depleted**, and during treatment with insulin and fluids, severe hypokalemia can develop as potassium shifts back intracellularly. *Excess water retention* - The patient's symptoms, including **polydipsia**, **polyuria**, and **dry mucous membranes**, indicate **dehydration**, not excessive water retention. - Her blood pressure of 94/58 mm Hg also suggests **volume depletion**. *Serum glucose concentration > 800 mg/dL* - While the patient has significant hyperglycemia (indicated by glucose in urine), **DKA** typically presents with glucose levels between **250-600 mg/dL**. - Glucose levels >800 mg/dL are more characteristic of **hyperosmolar hyperglycemic state (HHS)**, which is less common in children and usually lacks significant ketosis. *Increased arterial pCO2* - The patient exhibits **Kussmaul respirations** (deep and labored breathing) and an increased respiratory rate (32/min), which are compensatory mechanisms for **metabolic acidosis**. - This compensation leads to **decreased arterial pCO2** as the body tries to blow off CO2 to raise pH. *Increased arterial blood pH* - The symptoms, particularly **Kussmaul respirations** and the presence of **ketones** in the urine, strongly suggest **diabetic ketoacidosis (DKA)**. - DKA is characterized by **severe metabolic acidosis**, meaning the arterial blood pH would be **decreased**, not increased.

DKA 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

DKA 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.

DKA 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

DKA 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.

DKA 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

DKA 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.

DKA 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

DKA 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.

DKA Flashcard 1 of 5

Question: Medi-_____ is state/federal assistance for people with limited income/resources

Answer: caid

DKA Flashcard 2 of 5

Question: Is IDR a dynamic measure? _____

Answer: Yes

DKA Flashcard 3 of 5

Question: Which healthcare payment model involves patients paying for all expenses associated with a single incident of care with a single payment? _____

Answer: Global payment

DKA Flashcard 4 of 5

Question: Which major medical insurance plan denies payment for any service that does not meet evidence-based guidelines?_____

Answer: Health maintenance organization

DKA Flashcard 5 of 5

Question: Patients with abnormal blood glucose levels receive counseling on: _____

Answer: Healthy diet and physical activity

Extra Information:  https://onlinemeded.org?ref=anki