Exhibits

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A. Narrowed pulse pressure, presence of 3+ femoral pulses, apneic episodes. Narrowed pulse pressure is consistent with hypovolemic shock, but 3+ femoral pulses are not expected, as shock leads to weak, thready pulses due to reduced perfusion. Apneic episodes typically occur in the late stages of shock, not in the early or progressive stages.
B. Widening pulse pressure, muffled heart sounds, presence of atrial gallop. A widening pulse pressure and muffled heart sounds are more indicative of cardiac tamponade, not hypovolemic shock. Hypovolemic shock is characterized by a narrowing pulse pressure due to a drop in systolic blood pressure while diastolic pressure remains relatively stable.
C. Increased heart rate, lowered systolic reading, peripheral extremity mottling. Tachycardia is an early compensatory response to hypovolemia as the body attempts to maintain cardiac output. As shock progresses, systolic blood pressure drops due to inadequate circulating volume. Peripheral extremity mottling occurs as the body shunts blood to vital organs, reducing perfusion to the skin. These signs are characteristic of progressive hypovolemic shock.
D. Irregular heart rate, elevated diastolic reading, increased respiratory rate. An irregular heart rate is not a primary indicator of hypovolemic shock. While respiratory rate increases in response to decreased oxygen delivery, an elevated diastolic reading is uncommon, as diastolic pressure tends to stay stable or decrease slightly with ongoing hypovolemia.

A. White blood cell differential. Although infection is a common precipitating factor for DKA, an elevated WBC count is common in DKA due to stress, dehydration, and inflammation rather than infection itself. While a WBC differential may be done if infection is suspected, it is not a primary test for DKA management.
B. Hemoglobin A1C. Hemoglobin A1C (HbA1c) reflects long-term glucose control (past 2-3 months) but does not provide immediate information about the current metabolic status or severity of DKA. While it may be useful in assessing overall diabetes management, it is not essential for acute DKA treatment.
C. Serum electrolytes. Patients with DKA experience significant electrolyte imbalances, particularly potassium depletion due to osmotic diuresis and insulin deficiency. Monitoring serum sodium, potassium, and bicarbonate is crucial for guiding fluid and electrolyte replacement therapy. Potassium levels may appear normal or high initially due to acidosis but typically drop with insulin administration.
D. Urine culture. A urine culture is only indicated if a urinary tract infection (UTI) is suspected as a trigger for DKA. However, routine urine culture is not required in every case of DKA unless there are symptoms of infection such as fever, dysuria, or pyuria.
E. Anion gap. DKA is a form of high anion gap metabolic acidosis, caused by the accumulation of ketones. The anion gap (AG) is calculated as (Na⁺ - [Cl⁻ + HCO₃⁻]), with a value >12 mEq/L indicating metabolic acidosis. Monitoring the anion gap helps assess the severity of acidosis and guide treatment progress, as a decreasing anion gap suggests resolution of ketosis.
F. Urine ketones. Urine ketone testing helps confirm the presence of ketoacidosis, particularly in the initial stages of DKA diagnosis. While serum beta-hydroxybutyrate is a more accurate indicator of ketone levels, urine ketones remain useful for initial screening and monitoring treatment response as they decrease with appropriate management.