Posted: February 28th, 2022

A 19-year old marine was brought to the infirmary after passing

“A 19-year old marine was brought to the infirmary after passing…
“A 19-year old marine was brought to the infirmary after passing out during basic training. He had repeatedly complained of severe weakness, dizziness, and sleepiness during the preceding 4 weeks of boot camp. In a previous episode 3 weeks earlier, he had drowsiness and generalized tiredness, and was brought to the infirmary, where after IV administration of saline, he was returned to duty with the diagnosis of dehydration. Upon questioning, he reported unquenchable thirst, and the repeated need to urinate. On the last day, he complained of vague abdominal pain, which was worse on the morning of admission. He had vomited once. During examination, he was oriented but tachypneic. He appeared pale, dehydrated with dry mucous membranes, and poor skin turgor.

His respiratory rate was 36/minute with deep, laborious breathing; his heart rate was 138/minute regular, and his blood pressure was 90/60. His chest was clear, heart tones were normal. There was an ill-defined generalized abdominal tenderness, which was otherwise soft to palpation and showed no rebound. There was a generalized muscular hypotonia; his deep tendon reflexes were present but very weak.

Laboratory, on admission, showed glucose of 560 mg/dl, sodium 154, potassium 6.5, pH 7.25, bicarbonate 10 mM/liter, chloride 90, BUN 38 mg/dl, creatinine 2.5 mg/dl. (Normal values: glucose, 70-114 mg/dl; Na = 136-146; K, 3.5-5.3; Cl, 98-108; bicarbonate, 20-32 [all in mM/l]; BUN, 7-22mg/dl; creatinine, 0.7-1.5 mg/dl). A urine sample was 4+ for glucose and had “large” acetone. HbA1c was 14% (n=4-6.2%). Serum acetone was 4+ undiluted, and still positive at the 4th dilution. Beta-Hydroxybutyrate level was 20 millimols/liter (normal=0.0-0.3 mM/l).

He was treated with insulin and saline I.V. By the 4th hour of treatment, potassium chloride was added to the IV at a rate of 15 mEq/hour. Sixteen hours later, he was active, alert, well hydrated and cheerful, indicating he felt extremely well. He requested that his IV be discontinued. His physician decided to switch his insulin to subcutaneous injections and to start a liquid diet. He was later put on a diabetes maintenance diet and treated with one injection of Human Lente insulin in the morning. Although his blood sugars the next morning were 100-140 mg/dl, he had frequent episodes of hypoglycemia during the day, and his HbA1c was 9%. Eventually, he was put on 3 injections of regular insulin/day, and a bedtime intermediate duration (Lente) insulin.”

—-revised from https://lcu.edu/

Questions:

Interprete patient’s lab results:
His respiratory rate was 36/minute with deep–name this condition______
his heart rate was 138/minute regular–name this condition___
his blood pressure was 90/60–name this condition___
Glucose of 560 mg/dl ___–name this condition___
sodium 154–name this condition___
potassium 6.5–name this condition___
pH 7.25, bicarbonate 10 mM/liter, CO2 normal–Name this acid/base imbalance___
chloride 90_______
BUN 38 mg/dl, creatinine 2.5 mg/dl –What condition is indicated by these two? ____

(Normal values: glucose, 70-114 mg/dl; Na = 136-146; K, 3.5-5.3; Cl, 98-108; bicarbonate, 20-32 [all in mM/l]; BUN, 7-22mg/dl; creatinine, 0.7-1.5 mg/dl).

A urine sample was 4+ for glucose and had “large” acetone. Serum acetone was 4+ undiluted, and still positive at the 4th dilution. Beta-Hydroxybutyrate level was 20 millimols/liter (normal=0.0-0.3 mM/l). —What condition is indicated by this?

HbA1c was 14% (n=4-6.2%) —What condition is indicated by this?

Which evidence in the case supports the diagnosis of Diabetes? Which type of diabetes do you suspect the patient has? How would you confirm this type of DM?
What is the diagnosis of the marine when he was brought to the infirmary? All evidence
Why did the patient improve after being given Insulin and IV saline?
He was hyperkalemic on admission, and yet, why was potassium later added to the IV infusion? (hint: acidosis and alkalosis)

________________________________

Interpreting patient’s lab results:

His respiratory rate was 36/minute with deep, laborious breathing–name this condition: This condition is known as Kussmaul respirations, which are deep and rapid breathing patterns associated with metabolic acidosis.

His heart rate was 138/minute regular–name this condition: This condition is known as tachycardia, which is an abnormally fast heart rate.

His blood pressure was 90/60–name this condition: This condition is known as hypotension, which refers to low blood pressure.

Glucose of 560 mg/dl–name this condition: This condition is known as hyperglycemia, which indicates high blood sugar levels.

Sodium 154–name this condition: This condition is known as hypernatremia, which indicates high sodium levels in the blood.

Potassium 6.5–name this condition: This condition is known as hyperkalemia, which indicates high potassium levels in the blood.

pH 7.25, bicarbonate 10 mM/liter, CO2 normal–Name this acid/base imbalance: This condition indicates metabolic acidosis, characterized by low pH and low bicarbonate levels.

Chloride 90: This indicates hypochloremia, which refers to low chloride levels in the blood.

BUN 38 mg/dl, creatinine 2.5 mg/dl–What condition is indicated by these two? These findings indicate impaired kidney function and suggest acute kidney injury or renal dysfunction.

A urine sample was 4+ for glucose and had “large” acetone. Serum acetone was 4+ undiluted, and still positive at the 4th dilution. Beta-Hydroxybutyrate level was 20 millimols/liter (normal=0.0-0.3 mM/l)–What condition is indicated by this? These findings indicate diabetic ketoacidosis (DKA), a serious complication of uncontrolled diabetes characterized by high blood glucose, ketones in the urine and blood, and metabolic acidosis.

HbA1c was 14% (n=4-6.2%)–What condition is indicated by this? An HbA1c level of 14% indicates poor long-term glucose control and suggests uncontrolled diabetes.

The evidence in the case that supports the diagnosis of diabetes includes the presence of hyperglycemia (high blood glucose levels), glucosuria (glucose in the urine), large acetone in the urine, positive serum acetone, and elevated beta-hydroxybutyrate levels. The HbA1c level of 14% further confirms the presence of poorly controlled diabetes. Based on these findings, it is likely that the patient has Type 1 diabetes, as the symptoms and laboratory results are consistent with diabetic ketoacidosis (DKA) and the patient’s young age.

To confirm the type of diabetes, additional tests such as autoantibody testing (e.g., anti-islet cell antibodies, anti-glutamic acid decarboxylase antibodies) can be conducted. These tests help differentiate between Type 1 diabetes, which is characterized by autoimmune destruction of pancreatic beta cells, and Type 2 diabetes, which typically involves insulin resistance.

The diagnosis of the marine when he was brought to the infirmary is diabetic ketoacidosis (DKA). All the evidence, including symptoms (polydipsia, polyuria, unquenchable thirst, weakness), physical examination findings (dehydration, tachypnea, pale appearance), laboratory results (hyperglycemia, ketones in urine and blood, metabolic acidosis), and the presence of acetone and elevated beta-hydroxybutyrate levels, points towards the diagnosis of diabetic ketoacidosis (DKA). DKA is a life-threatening complication of uncontrolled diabetes, particularly Type 1 diabetes. It occurs when there is a severe insulin deficiency, leading to the breakdown of fats for energy, resulting in the production of ketones and the development of metabolic acidosis.

The patient’s improvement after being given insulin and IV saline is due to the correction of the underlying metabolic derangements. Insulin helps to lower blood glucose levels by facilitating the uptake of glucose into cells, reducing the production of ketones, and promoting the utilization of glucose as an energy source. IV saline administration helps to restore hydration and correct electrolyte imbalances, such as dehydration and electrolyte disturbances commonly seen in DKA.

Despite being hyperkalemic on admission, potassium was later added to the IV infusion because the initial treatment with insulin and IV saline can cause a shift of potassium from the extracellular space back into the cells. This shift, along with increased urinary excretion of potassium, can lead to a rapid decrease in serum potassium levels, potentially resulting in hypokalemia. To prevent hypokalemia and maintain appropriate potassium levels, potassium supplementation is added to the IV infusion. Additionally, as insulin therapy progresses and glucose levels normalize, cellular uptake of potassium is further enhanced, necessitating potassium replacement to avoid hypokalemia. The addition of potassium helps maintain the balance of electrolytes and prevents complications associated with potassium imbalances.

In summary, the marine’s presentation, including symptoms, physical examination findings, and laboratory results, indicates diabetic ketoacidosis (DKA). Prompt treatment with insulin and IV saline corrected the metabolic abnormalities and restored the patient’s condition. The addition of potassium to the IV infusion was necessary to prevent hypokalemia and maintain appropriate potassium levels during the course of treatment.

References
American Diabetes Association. (2020). Standards of medical care in diabetes – 2020. Diabetes Care, 43(Supplement 1), S1-S212.

Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes: A consensus statement from the American Diabetes Association. Diabetes Care, 32(7), 1335-1343.

Pasquel, F. J., & Umpierrez, G. E. (2014). Hyperosmolar hyperglycemic state: A historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care, 37(11), 3124-3131.

Savage, M. W., Dhatariya, K. K., Kilvert, A., Rayman, G., Rees, J. A., Courtney, C. H., & Hilton, L. (2016). Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine, 33(10), 1303-1308.

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