A patient with diabetic ketoacidosis (DKA) presents with a blood glucose level of 550 mg/dL, serum potassium of 5.9 mmol/L, and metabolic acidosis with a pH of 7.15. The ECG shows peaked T waves and a widened QRS complex. What is the nurse's priority intervention to address the patient's current condition?

C) Administer calcium gluconate to stabilize the cardiac membrane.

A) Administer intravenous insulin to decrease blood glucose levels.

B) Initiate fluid resuscitation with isotonic saline to correct dehydration.

C) Administer calcium gluconate to stabilize the cardiac membrane.

D) Provide sodium bicarbonate to correct the metabolic acidosis.

A patient with diabetic ketoacidosis (DKA) presents with severe hyperkalemia, evidenced by peaked T waves and a widened QRS complex on ECG. Which of the following is the most immediate nursing intervention to prevent life-threatening cardiac complications?

C) Administer intravenous calcium gluconate to stabilize the cardiac membrane.

A) Administer intravenous sodium bicarbonate to correct metabolic acidosis.

B) Initiate continuous intravenous insulin infusion to reduce hyperglycemia and shift potassium intracellularly.

C) Administer intravenous calcium gluconate to stabilize the cardiac membrane.

A patient with diabetic ketoacidosis has been receiving aggressive fluid resuscitation and insulin therapy. The patient now exhibits confusion, agitation, a heart rate of 120 bpm, blood pressure of 90/60 mmHg, and oxygen saturation of 88% on room air. Considering the clinical presentation and potential complications, what is the priority nursing intervention at this time?

B) Initiate non-invasive ventilation to improve oxygenation and prevent further respiratory compromise.

A) Administer a rapid bolus of hypertonic saline to address potential cerebral edema.

B) Initiate non-invasive ventilation to improve oxygenation and prevent further respiratory compromise.

C) Increase the rate of isotonic saline infusion to support blood pressure and perfusion.

D) Administer an additional dose of insulin to further decrease blood glucose levels and monitor closely.

A patient with diabetic ketoacidosis is receiving treatment, including fluid resuscitation and insulin infusion. The patient develops new onset confusion, agitation, increased heart rate, low blood pressure, and low oxygen saturation, with concerns for pulmonary edema or ARDS. What is the most appropriate nursing intervention to address these evolving complications?

C) Prepare for the initiation of non-invasive ventilation or possible intubation to manage respiratory compromise.

A) Increase the rate of isotonic saline infusion to improve blood pressure and renal function.

B) Administer a diuretic to reduce pulmonary edema and improve oxygenation.

C) Prepare for the initiation of non-invasive ventilation or possible intubation to manage respiratory compromise.

D) Administer hypertonic saline to rapidly correct cerebral edema and improve mental status.

A patient with diabetic ketoacidosis (DKA) and suspected acute respiratory distress syndrome (ARDS) is showing signs of altered mental status and respiratory compromise, with an arterial blood gas analysis indicating respiratory acidosis. After adjusting the fluid resuscitation rate to prevent cerebral edema, what should be the nurse's next priority action to manage the patient's condition effectively?

A) Increase the rate of insulin infusion to rapidly lower blood glucose levels.

C) Administer a diuretic to reduce potential cerebral edema from fluid overload.

D) Initiate continuous renal replacement therapy (CRRT) to manage metabolic acidosis.

A patient with diabetic ketoacidosis (DKA) is experiencing sudden confusion and respiratory compromise. Arterial blood gas analysis indicates both metabolic and respiratory acidosis, and the patient's oxygen saturation remains low despite supplemental oxygen. What is the most appropriate initial nursing intervention to prioritize in this scenario?

B) Prepare for the insertion of an endotracheal tube and initiation of mechanical ventilation.

A) Administer a bolus of normal saline to address potential hypovolemia.

B) Prepare for the insertion of an endotracheal tube and initiation of mechanical ventilation.

C) Increase the rate of insulin infusion to rapidly correct hyperglycemia.

D) Elevate the head of the bed and initiate non-invasive positive pressure ventilation.

A patient with diabetic ketoacidosis is receiving an insulin infusion and has developed significant hypokalemia with a potassium level of 2.8 mEq/L. The patient also shows signs of acute kidney injury with a serum creatinine of 2.1 mg/dL and BUN of 45 mg/dL. What is the most appropriate nursing action to prioritize in managing this patient’s care?

D) Collaborate with the healthcare team to adjust the potassium replacement protocol and monitor for cardiac arrhythmias via telemetry.

A) Administer potassium chloride intravenously at a rapid rate to quickly correct hypokalemia.

B) Hold the insulin infusion temporarily until potassium levels are corrected to prevent further hypokalemia.

C) Initiate a fluid restriction to mitigate the risk of fluid overload due to renal insufficiency.

D) Collaborate with the healthcare team to adjust the potassium replacement protocol and monitor for cardiac arrhythmias via telemetry.

A patient with diabetic ketoacidosis is receiving an insulin infusion and has developed significant hypokalemia with a potassium level of 2.8 mEq/L. The patient's renal function tests indicate acute kidney injury with a serum creatinine of 2.1 mg/dL and BUN of 45 mg/dL. Considering these lab results, which of the following nursing interventions is most critical to prioritize for this patient?

C) Initiate continuous cardiac monitoring and prepare for potential emergency interventions.

A) Increase the rate of insulin infusion to manage hyperglycemia more effectively.

B) Administer oral potassium supplements to address the hypokalemia.

C) Initiate continuous cardiac monitoring and prepare for potential emergency interventions.

D) Restrict fluid intake to prevent further renal overload and worsening of kidney function.

A patient with a worsening metabolic acidosis and signs of respiratory distress is being assessed for potential intubation and mechanical ventilation. Considering the patient's compromised renal function and the use of accessory muscles for breathing, which nursing intervention is most critical to implement prior to intubation?

D) Prepare for rapid sequence intubation (RSI) by ensuring all necessary equipment and medications are readily available.

A) Administer a bolus of intravenous sodium bicarbonate to quickly correct the acidosis.

B) Initiate continuous renal replacement therapy (CRRT) to manage electrolyte imbalances.

C) Start high-flow nasal cannula (HFNC) therapy to improve oxygenation and reduce respiratory effort.

D) Prepare for rapid sequence intubation (RSI) by ensuring all necessary equipment and medications are readily available.

A patient in the ICU is experiencing worsening metabolic acidosis with partial respiratory compensation, as evidenced by an arterial blood gas result of pH 7.22, HCO3- 12 mmol/L, and PaCO2 28 mmHg. The patient shows signs of respiratory distress, including tachypnea and accessory muscle use, and has an oxygen saturation of 88% on room air. Considering the patient's condition and the potential need for intubation, which of the following nursing interventions is most critical to prioritize at this time?

A) Initiate high-flow nasal cannula oxygen therapy to improve oxygenation and monitor the patient's response.

B) Prepare for immediate intubation and mechanical ventilation to address the patient's respiratory failure.

C) Administer sodium bicarbonate intravenously to correct the metabolic acidosis rapidly.

D) Conduct a thorough reassessment of the patient's fluid and electrolyte status to guide further treatment decisions.

diabetic ketoacidosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency leads to increased hepatic gluconeogenesis and decreased glucose uptake by tissues, causing hyperglycemia and osmotic diuresis.

• Secondary mechanism: Lack of insulin results in unopposed glucagon activity, promoting lipolysis and subsequent free fatty acid oxidation in the liver, generating excessive ketone bodies, and causing metabolic acidosis.

• Key complication: Severe dehydration and electrolyte imbalances from osmotic diuresis and acidosis can precipitate hypovolemic shock and potentially life-threatening arrhythmias, necessitating urgent medical intervention.

Patient Profile

Demographics:

45-year-old female, nurse

History:

• Key past medical history: Type 1 diabetes mellitus diagnosed at age 15, history of hypertension, chronic kidney disease stage 3, and recurrent urinary tract infections

• Current medications: Insulin glargine, insulin aspart, lisinopril, metoprolol, atorvastatin

• Allergies: Penicillin (rash)

Current Presentation:

• Chief complaint: Severe abdominal pain and difficulty breathing

• Key symptoms: Nausea and vomiting, extreme fatigue, polyuria, fruity-smelling breath, and confusion

• Vital signs: Blood pressure 90/50 mmHg, heart rate 130 bpm, respiratory rate 28 breaths per minute, temperature 101.2°F, oxygen saturation 90% on room air

Section 1

New Diagnostic Results:

Upon admission to the emergency department, the initial laboratory results revealed a blood glucose level of 550 mg/dL, a serum potassium level of 5.9 mmol/L, and a blood pH of 7.15, confirming severe metabolic acidosis. The anion gap was markedly elevated at 25 mEq/L, indicating an increased presence of ketone bodies. The serum bicarbonate was critically low at 10 mEq/L, and the blood urea nitrogen (BUN) and creatinine levels were elevated to 45 mg/dL and 2.8 mg/dL, respectively, suggesting significant renal impairment likely exacerbated by dehydration. The arterial blood gas (ABG) analysis showed partial pressure of carbon dioxide (PCO2) at 20 mmHg, correlating with Kussmaul respirations as a compensatory mechanism for the metabolic acidosis.

The urinalysis indicated significant ketonuria and glucosuria, further supporting the diagnosis of diabetic ketoacidosis (DKA). An electrocardiogram (ECG) was performed due to concerns about potential life-threatening arrhythmias, given the patient's electrolyte imbalances. The ECG revealed peaked T waves and a widened QRS complex, indicative of hyperkalemia, which posed an immediate risk of cardiac instability. Additionally, a chest X-ray was conducted to assess the cause of the patient's difficulty breathing, which showed bilateral infiltrates suggestive of possible pulmonary edema, complicating the clinical picture.

These diagnostic findings necessitate urgent interventions to address the severe hyperglycemia, electrolyte disturbances, and potential respiratory compromise. The healthcare team must prioritize aggressive fluid resuscitation, careful electrolyte management, and insulin therapy to stabilize the patient. Given the complexity of her condition, continuous monitoring for any further deterioration in renal function or cardiac status is critical. This comprehensive assessment underscores the need for advanced clinical judgment to navigate the intertwined complications of DKA, acute kidney injury, and potential cardiac events.

Section 2

As the healthcare team initiated treatment for the patient with diabetic ketoacidosis, they focused on aggressive fluid resuscitation with isotonic saline to address the profound dehydration and subsequent renal impairment. Concurrently, an insulin infusion was started to gradually reduce the patient's blood glucose levels and suppress ketogenesis. Continuous cardiac monitoring was implemented due to the ECG findings indicative of hyperkalemia, with plans to administer calcium gluconate and insulin with glucose to stabilize the cardiac membrane potential and facilitate intracellular potassium shift, respectively.

Within the first two hours of treatment, the patient's condition began to evolve. Repeat laboratory tests showed a slight decrease in blood glucose to 480 mg/dL, a serum potassium level that had fallen to 5.2 mmol/L, and a marginal improvement in blood pH to 7.20. However, despite these small improvements, the patient developed a new onset of confusion and agitation, complicating her management. Vital signs revealed a heart rate increase to 120 beats per minute, blood pressure at 90/60 mmHg, and an oxygen saturation of 88% on room air, indicating potential respiratory compromise. The bilateral infiltrates noted on the initial chest X-ray and these new symptoms raised concerns for evolving pulmonary edema or Acute Respiratory Distress Syndrome (ARDS), necessitating a more invasive respiratory support strategy, possibly progressing to non-invasive ventilation or intubation.

This change in patient status prompted further evaluation and a reassessment of the treatment strategy. The team considered the delicate balance between aggressive fluid administration to correct dehydration and the risk of exacerbating pulmonary edema. They also explored the possibility of cerebral edema given the patient's altered mental status, which could result from rapid shifts in osmolarity during treatment. These complexities underscored the necessity for advanced clinical reasoning to anticipate and mitigate these potential complications, guiding the next steps in the patient's critical care management.

Section 3

As the healthcare team carefully considered the patient's sudden confusion and potential respiratory compromise, they decided to prioritize further diagnostic testing and reassessment. An arterial blood gas analysis was promptly performed, revealing a pH of 7.18, a PaCO2 of 55 mmHg, and a PaO2 of 60 mmHg, confirming the presence of respiratory acidosis in addition to the metabolic acidosis already identified. This finding, along with the chest X-ray that now showed worsening bilateral infiltrates, suggested the development of Acute Respiratory Distress Syndrome (ARDS). The patient's oxygen saturation continued to hover around 88% despite supplemental oxygen, indicating an urgent need for enhanced respiratory support. Given the progression of respiratory failure, the team prepared for potential endotracheal intubation and mechanical ventilation to ensure adequate oxygenation and ventilation.

In parallel, an urgent CT scan of the brain was ordered to evaluate the risk of cerebral edema contributing to the patient's altered mental status. The imaging revealed no clear evidence of cerebral edema, but the clinical suspicion remained due to the rapid osmotic shifts associated with the aggressive treatment of diabetic ketoacidosis. The team decided to adjust the rate of fluid administration, opting for a more cautious approach to avoid further exacerbating potential cerebral complications. Neurological assessments were intensified, with regular monitoring of Glasgow Coma Scale scores to detect any subtle changes in consciousness.

The patient's evolving clinical picture demanded constant vigilance and adaptive management strategies. The team faced the challenge of balancing fluid resuscitation to support renal function and hemodynamics while preventing fluid overload and its respiratory implications. Furthermore, they needed to carefully titrate insulin therapy to avoid precipitous declines in blood glucose, which could exacerbate cerebral edema. This case highlighted the necessity for dynamic clinical reasoning and interdisciplinary collaboration to navigate the intricate landscape of diabetic ketoacidosis with multi-system involvement, setting the stage for further critical care interventions.

Section 4

As the healthcare team continued to manage the patient's complex condition, they shifted their focus to the recent changes in laboratory results, which unveiled a new set of challenges. The latest electrolyte panel revealed a potassium level of 2.8 mEq/L, indicative of significant hypokalemia. This development raised immediate concerns due to the patient's ongoing insulin infusion, which could further exacerbate potassium depletion. Recognizing the potential for cardiac arrhythmias, the team promptly initiated potassium replacement therapy, carefully monitoring cardiac rhythms via continuous telemetry and adjusting the rate of potassium supplementation to prevent rapid shifts that could destabilize the patient's cardiac status.

Simultaneously, the patient's renal function tests showed a concerning trend. Serum creatinine had risen to 2.1 mg/dL, and blood urea nitrogen (BUN) was now at 45 mg/dL, suggesting acute kidney injury likely secondary to both the underlying diabetic ketoacidosis and the recent aggressive diuresis. This renal insufficiency not only complicated fluid management strategies but also necessitated a reevaluation of medication dosages to prevent potential nephrotoxicity. The nephrology team was consulted to provide input on optimizing renal support while balancing the critical need for metabolic stabilization.

In response to these new complications, the healthcare team intensified their interdisciplinary collaboration, bringing together expertise from critical care, nephrology, and cardiology to refine the management plan. The delicate interplay between correcting metabolic derangements, managing fluid balance, and supporting organ function required meticulous coordination and frequent reassessment. The evolving clinical scenario underscored the importance of dynamic decision-making and the need for ongoing vigilance to anticipate and address potential sequelae in this multifaceted case. As the team continued to adapt their strategies, they remained acutely aware of the fragility of the patient's condition and the potential for further complications, setting the stage for the next phase of critical care interventions.

Section 5

As the healthcare team continued to monitor the patient's progress, a change in the patient's status became evident. Despite initial improvements in metabolic parameters, the patient began exhibiting signs of respiratory distress. Arterial blood gas analysis revealed a worsening metabolic acidosis with a pH of 7.22, bicarbonate of 12 mmol/L, and a PaCO2 of 28 mmHg, suggesting a partial respiratory compensation but an overall deterioration in acid-base balance. Concurrently, the patient developed an increased respiratory rate of 32 breaths per minute and was using accessory muscles to breathe, indicative of the body's increased demand to compensate for the severe acidosis.

The patient's oxygen saturation had dropped to 88% on room air, necessitating supplemental oxygen to maintain adequate saturation levels. This development raised concerns about potential progression to respiratory failure, prompting the team to reassess ventilatory support needs. The intensivist considered the possibility of intubation and mechanical ventilation to stabilize the patient's respiratory status, particularly given the ongoing metabolic challenges and risk of further decompensation.

As the team deliberated on the best course of action, they remained acutely aware of the need to balance interventions with the patient's overall hemodynamic stability. The decision to potentially escalate respiratory support was weighed against the risks associated with sedation and intubation in a patient with compromised renal function and electrolyte imbalances. This scenario required expert-level clinical reasoning and an integrated approach to manage the interconnected complexities of the patient's condition, setting the stage for further adjustments in the critical care plan and the anticipation of additional challenges in the patient's treatment journey.