A patient with diabetic ketoacidosis (DKA) is receiving treatment with intravenous fluids and insulin. Her mental status has worsened, and she is now lethargic and confused. What is the most appropriate nursing action to take next?

C) Prepare the patient for a CT scan of the head

A) Increase the rate of insulin infusion

B) Administer 50% dextrose intravenously

C) Prepare the patient for a CT scan of the head

D) Increase the rate of intravenous fluids

A patient with diabetic ketoacidosis (DKA) is being treated with intravenous fluids and an insulin infusion. The patient becomes increasingly lethargic and confused, and a CT scan is ordered to rule out cerebral edema. Which of the following interventions is the priority for the nurse to implement while waiting for the CT scan results?

C) Monitor and adjust the infusion of potassium to maintain serum levels within normal range.

A) Increase the rate of intravenous fluids to improve cerebral perfusion.

B) Administer a bolus of 50% dextrose to counteract potential hypoglycemia.

C) Monitor and adjust the infusion of potassium to maintain serum levels within normal range.

D) Elevate the head of the bed to 30 degrees to reduce intracranial pressure.

A patient with diabetic ketoacidosis (DKA) presents with altered mental status, low blood pressure, tachycardia, and hyponatremia. After initiating broad-spectrum antibiotics and fluid resuscitation, which of the following interventions should the nurse prioritize to address the patient's clinical presentation?

C) Monitor for signs of fluid overload while continuing careful fluid replacement.

A) Increase the rate of intravenous saline infusion to rapidly correct hyponatremia.

B) Administer additional insulin to quickly reduce elevated glucose levels.

C) Monitor for signs of fluid overload while continuing careful fluid replacement.

D) Initiate a continuous EEG to assess for possible subclinical seizures.

A patient with diabetic ketoacidosis (DKA) is being monitored for complications. Her blood pressure is 92/60 mmHg, heart rate is 118 bpm, respiratory rate is 28 breaths per minute, and there is an altered mental status. Her serum sodium is 128 mEq/L and serum potassium is 3.4 mEq/L. Which nursing intervention should be prioritized to address the patient's current condition?

D) Monitor the patient's neurological status frequently and adjust interventions as needed.

A) Increase the rate of intravenous fluid infusion to address the low blood pressure.

B) Administer sodium bicarbonate to correct the metabolic acidosis.

C) Initiate seizure precautions in response to the altered mental status.

D) Monitor the patient's neurological status frequently and adjust interventions as needed.

A patient with worsening hyponatremia and an elevated respiratory rate is being closely monitored. Despite ongoing treatment, her mental status is deteriorating, and she presents with cool, clammy skin and delayed capillary refill. What is the priority nursing intervention in managing this patient's condition?

C) Conduct frequent neurological assessments to detect changes in mental status early.

A) Increase the rate of insulin infusion to better control blood glucose levels.

B) Administer a hypertonic saline solution to rapidly correct the sodium imbalance.

C) Conduct frequent neurological assessments to detect changes in mental status early.

D) Initiate a fluid restriction protocol to prevent further dilutional hyponatremia.

A 45-year-old female patient with a history of type 1 diabetes mellitus is being treated for suspected sepsis. Her current vital signs are: respiratory rate 32 breaths per minute, heart rate 116 bpm, blood pressure 94/58 mmHg, and she appears lethargic. Laboratory results show serum sodium of 126 mEq/L, potassium 3.5 mEq/L, and blood glucose 260 mg/dL. The anion gap has closed to 12. What is the priority nursing intervention in managing this patient's condition?

C) Administer a balanced crystalloid solution to address hyponatremia.

A) Administer a bolus of 500 mL normal saline to increase blood pressure.

B) Initiate a continuous insulin infusion to further control blood glucose levels.

C) Administer a balanced crystalloid solution to address hyponatremia.

D) Increase the frequency of neurological assessments to monitor mental status.

Based on the patient's clinical presentation and laboratory findings, which nursing intervention is the most critical to prioritize in addressing the underlying cause of her metabolic acidosis?

B) Increasing intravenous fluid administration to improve tissue perfusion

A) Administering sodium bicarbonate to correct the acidosis

B) Increasing intravenous fluid administration to improve tissue perfusion

C) Adjusting the insulin regimen to maintain blood glucose levels

D) Initiating vasopressor support to stabilize blood pressure

A patient is exhibiting signs of metabolic acidosis with partial respiratory compensation and hemodynamic instability, as evidenced by Kussmaul respirations, tachycardia, hypotension, and changes in mental status. In addition to initiating IV fluids and considering vasopressor support, which nursing intervention is most appropriate to address potential cerebral perfusion issues?

B) Administer oxygen via non-rebreather mask

A) Elevate the head of the bed to 30 degrees

B) Administer oxygen via non-rebreather mask

C) Perform frequent neurological assessments

D) Implement seizure precautions

A patient with sepsis is receiving intravenous fluids and vasopressor support. Despite improvements in blood pressure and heart rate, she continues to have elevated serum lactate levels and Kussmaul respirations. Which nursing intervention is most appropriate to address the persistent lactic acidosis?

D) Initiate broad-spectrum antibiotics as per the sepsis protocol.

A) Increase the rate of intravenous fluid administration.

B) Collaborate with the healthcare provider to adjust the vasopressor dose.

C) Administer sodium bicarbonate to correct the acidosis.

D) Initiate broad-spectrum antibiotics as per the sepsis protocol.

A nurse is caring for a patient showing signs of persistent lactic acidosis with stabilized hemodynamic parameters but elevated respiratory rate and Kussmaul respirations. Despite anion gap normalization, serum lactate levels remain high. What is the most appropriate nursing intervention to prioritize at this time?

C) Administer supplemental oxygen to enhance tissue oxygenation and reduce lactic acid production.

A) Increase the rate of intravenous fluid administration to address potential dehydration.

B) Initiate a strict fluid balance chart to monitor for signs of fluid overload due to potential acute kidney injury.

C) Administer supplemental oxygen to enhance tissue oxygenation and reduce lactic acid production.

D) Prepare for emergency hemodialysis to rapidly correct severe metabolic acidosis.

Diabetic ketoacidosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency leads to increased lipolysis, causing a surge in free fatty acids. The liver converts these fatty acids into ketones, resulting in ketonemia and metabolic acidosis.

• Secondary mechanism: Hyperglycemia from reduced glucose uptake and increased gluconeogenesis causes osmotic diuresis, leading to dehydration and electrolyte imbalances, notably hypokalemia.

• Key complication: Severe dehydration and acidosis can result in altered mental status and, if untreated, progress to coma or death.

Patient Profile

Demographics:

45-year-old female, accountant

History:

• Key past medical history: Type 1 diabetes mellitus diagnosed 15 years ago, hypertension

• Current medications: Insulin glargine, lisinopril, metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Nausea and abdominal pain for the past 24 hours

• Key symptoms: Vomiting, fruity-scented breath, increased thirst, fatigue, confusion

• Vital signs: Blood pressure 100/60 mmHg, heart rate 115 bpm, respiratory rate 28 breaths per minute, temperature 99.2°F, blood glucose 450 mg/dL

Section 1

As the patient was admitted to the emergency department, initial lab work was prioritized to confirm the suspected diagnosis of diabetic ketoacidosis (DKA) and to evaluate the severity of the condition. Blood tests revealed a pH of 7.25, confirming a state of metabolic acidosis. Serum ketones were significantly elevated, and the anion gap was 20, indicating an anion gap metabolic acidosis. Potassium levels initially measured at 3.0 mEq/L, highlighting a notable hypokalemia, which, despite the hyperkalemia commonly associated with DKA, results from the osmotic diuresis and insulin deficiency.

The patient was started on intravenous fluids immediately to address her dehydration, and an insulin infusion was initiated to correct the hyperglycemia and halt ketone production. Despite these interventions, the patient's mental status began to worsen; she became increasingly lethargic and confused, raising concerns about potential cerebral edema, a rare but serious complication of DKA, especially in adults. Her blood pressure dropped to 90/58 mmHg, and heart rate increased to 120 bpm, indicating potential worsening of her hemodynamic status.

Given the new complication of altered mental status, the clinical team decided to perform a CT scan of the head to rule out cerebral edema or other intracranial processes. Concurrently, electrolyte replacement, particularly potassium, was carefully managed to prevent cardiac arrhythmias due to hypokalemia. The team was faced with the challenge of balancing fluid resuscitation to avoid exacerbating any potential cerebral edema while ensuring adequate correction of the acidosis and dehydration. These developments required vigilant monitoring and rapid adjustments to the treatment plan, highlighting the complexity and dynamic nature of managing DKA with evolving complications.

Section 2

As the clinical team awaited the results of the CT scan, they focused on closely monitoring the patient's vital signs and laboratory values to assess her response to the current interventions. The initial infusion of intravenous fluids had improved her hydration status, but the patient's blood pressure remained low at 92/60 mmHg, and her heart rate persisted at 118 bpm, suggesting ongoing hemodynamic instability. Her respiratory rate slightly increased to 28 breaths per minute, which, coupled with her altered mental status, pointed towards a potential respiratory compensation for the metabolic acidosis. The patient's oxygen saturation was maintained at 95% on room air, indicating adequate oxygenation.

New laboratory results revealed that serum sodium levels had decreased to 128 mEq/L, raising concerns about potential dilutional hyponatremia secondary to aggressive fluid resuscitation. Potassium replacement therapy had been carefully titrated, resulting in a modest improvement in serum potassium levels to 3.4 mEq/L, though still below normal. Despite these adjustments, the patient's glucose levels remained elevated at 280 mg/dL, necessitating continued insulin therapy. The anion gap had decreased to 16, a positive sign of resolving acidosis, yet the persistence of her neurological symptoms warranted further investigation and cautious management.

The CT scan ruled out significant cerebral edema, reassuring the team but not fully explaining the patient's mental status changes. Given the complexity of her presentation, the team considered other factors contributing to her altered mental state, including electrolyte imbalances, persistent acidosis, and potential infection. A blood culture was ordered to rule out sepsis as a complicating factor, and broad-spectrum antibiotics were initiated as a precaution. The team remained vigilant, ready to adjust the treatment course based on the evolving clinical picture and any new information that might arise, demonstrating the need for continuous clinical reasoning and adaptability in managing DKA with complications.

Section 3

As the clinical team continued to monitor the patient, they noted a subtle change in her status. Her respiratory rate had increased further to 32 breaths per minute, and she appeared more lethargic, struggling to keep her eyes open and respond appropriately to questions. Her heart rate remained elevated at 116 bpm, and her blood pressure had not improved significantly, staying at 94/58 mmHg. These changes were concerning, prompting a detailed reassessment of her condition. Physical examination revealed cool, clammy skin and delayed capillary refill, indicating possible peripheral vasoconstriction and poor perfusion.

The latest laboratory results provided additional insights into her deteriorating condition. Her serum sodium had fallen further to 126 mEq/L, confirming worsening hyponatremia, while potassium levels had stabilized at 3.5 mEq/L. Despite ongoing insulin therapy, her blood glucose level had decreased only slightly to 260 mg/dL, suggesting a need to reassess her insulin regimen. The anion gap had closed to 12, yet the patient's mental status had not improved as expected, raising suspicions of an underlying issue that might have been missed. The team considered the possibility of hypoglycemia, cerebral hypoperfusion, or a more insidious infection process, despite the broad-spectrum antibiotics already initiated.

In response to these findings, the team decided to adjust the fluid management strategy, opting for a more balanced crystalloid solution to address the sodium imbalance while maintaining vigilant monitoring for signs of fluid overload. They also consulted with the infectious disease team to review and refine the antibiotic regimen based on preliminary blood culture results, which showed gram-positive cocci. The team emphasized the importance of frequent neurological assessments, recognizing that the patient's evolving condition required continuous reevaluation and a dynamic approach to her treatment plan. Through careful observation and timely interventions, they aimed to stabilize her clinical status and prevent further complications, underscoring the critical nature of adaptability and clinical reasoning in complex cases like this.

Section 4

As the clinical team continued their vigilant monitoring, they noted a further change in the patient's status that warranted immediate attention. Her respiratory rate had increased to 36 breaths per minute, accompanied by a deep, labored breathing pattern consistent with Kussmaul respirations. This signaled a potential worsening of her metabolic acidosis, despite the closing of the anion gap. Her heart rate had climbed to 124 bpm, and her blood pressure remained precariously low at 90/54 mmHg, reflecting persistent hemodynamic instability. The patient's level of consciousness had deteriorated, now fluctuating between stupor and a barely responsive state, raising significant concerns about cerebral perfusion.

Further laboratory diagnostics provided critical insights into her current condition. The arterial blood gas analysis revealed a pH of 7.25, a bicarbonate level of 14 mEq/L, and a partial pressure of CO2 at 28 mmHg, highlighting a metabolic acidosis with partial respiratory compensation. Her serum lactate was elevated at 4.5 mmol/L, suggesting potential tissue hypoxia and anaerobic metabolism. The team hypothesized that inadequate tissue perfusion and oxygenation might be contributing to lactic acidosis, compounding her already complex metabolic derangements.

In response to these alarming findings, the clinical team initiated a series of targeted interventions. They increased the rate of intravenous fluid administration, opting for a combination of isotonic saline and sodium bicarbonate to address both volume status and acidosis. The insulin regimen was carefully adjusted to optimize glucose control without precipitating hypoglycemia, and vasopressor support was considered to enhance hemodynamic stability. The team also planned to perform a head CT scan to rule out cerebral edema or other intracranial processes, given the patient's persistent altered mental status. These strategic decisions were guided by a thorough understanding of the intricate interplay between metabolic, hemodynamic, and neurological factors, and underscored the need for precise clinical reasoning in managing her evolving condition.

Section 5

As the clinical team closely monitored the patient's response to the interventions, they observed a subtle yet significant improvement in her hemodynamic parameters. Her blood pressure had stabilized at 100/60 mmHg, and her heart rate decreased slightly to 116 bpm, suggesting a positive response to the increased intravenous fluid administration and vasopressor support. Despite these promising changes, her respiratory rate remained elevated at 34 breaths per minute, and she continued to exhibit Kussmaul respirations. This persistent respiratory pattern, coupled with her unchanged mental status, prompted further investigation into the underlying causes of her ongoing metabolic derangements.

Repeat laboratory tests revealed that while the anion gap had normalized, the serum lactate levels remained elevated at 4.3 mmol/L. This persistent lactic acidosis indicated ongoing tissue hypoxia, possibly aggravated by a developing sepsis or other systemic inflammatory response. In light of these findings, the team expanded their diagnostic approach to include a comprehensive infectious workup, initiating broad-spectrum antibiotics to preemptively address any potential infectious source. Blood cultures, urinalysis, and chest X-ray were ordered to identify any covert infection that might be contributing to her condition.

Simultaneously, the head CT scan was performed, revealing no signs of cerebral edema or acute intracranial pathology. This ruled out immediate neurological complications, yet the patient's fluctuating consciousness remained a puzzle, likely multifactorial in origin. The team considered the potential for concurrent acute kidney injury, given her metabolic state and fluid shifts, which could further exacerbate her acidosis and mental status changes. With these considerations in mind, the clinical team prepared to initiate renal function tests and adjusted her electrolyte management to prevent further complications, underscoring the dynamic and integrative nature of her care.