A patient with diabetic ketoacidosis (DKA) is receiving treatment, but her confusion and lethargy persist despite interventions. Which nursing action should be prioritized to address the potential complication of cerebral edema?

A) Administer mannitol as prescribed

B) Increase the rate of IV insulin infusion

C) Restrict fluid intake to reduce cerebral swelling

D) Administer an antiemetic to prevent vomiting

A patient with diabetic ketoacidosis (DKA) presents with confusion and lethargy despite initial treatment interventions. Which of the following actions should the nurse prioritize to address the potential complication of cerebral edema?

C) Administer mannitol as prescribed to reduce intracranial pressure

A) Administer 50% dextrose to counteract hypoglycemia

B) Increase the rate of insulin infusion to quickly lower blood glucose levels

C) Administer mannitol as prescribed to reduce intracranial pressure

D) Initiate high-flow oxygen therapy to improve cerebral perfusion

A patient with diabetic ketoacidosis (DKA) is experiencing a drop in blood pressure and new neurological symptoms. The CT scan shows mild cerebral edema. Which of the following interventions should the nurse prioritize to address these findings?

A) Administer IV mannitol to reduce intracranial pressure

B) Increase the rate of insulin infusion to decrease blood glucose levels

C) Administer IV potassium to correct hypokalemia

D) Increase fluid replacement to address hypotension

A patient with diabetic ketoacidosis (DKA) and hypokalemia develops mild cerebral edema. Which of the following should be prioritized by the nurse to address the patient's current condition?

C) Initiating aggressive potassium replacement therapy while monitoring cardiac function

A) Administering intravenous mannitol to reduce cerebral edema

B) Increasing the rate of insulin infusion to rapidly correct blood glucose levels

C) Initiating aggressive potassium replacement therapy while monitoring cardiac function

D) Providing isotonic fluids to stabilize blood pressure and improve hydration

A patient with severe diabetic ketoacidosis (DKA) presents with a declining Glasgow Coma Scale score, persistent hypotension, decreased urine output, and fluctuating potassium levels. Which nursing intervention should be prioritized to address the patient's current condition?

D) Monitor neurological status closely and prepare for potential intubation if the level of consciousness continues to decline.

A) Increase the rate of intravenous fluids to improve blood pressure and renal perfusion.

B) Administer additional potassium supplements to correct the level and prevent cardiac complications.

C) Prepare for potential renal replacement therapy due to decreased urine output.

D) Monitor neurological status closely and prepare for potential intubation if the level of consciousness continues to decline.

A patient with severe diabetic ketoacidosis (DKA) is being treated with mannitol and electrolyte management. The patient's Glasgow Coma Scale score has dropped, blood pressure is unstable, and urine output is decreased. What is the priority nursing intervention to address the patient's current condition?

A) Increase the rate of intravenous fluid administration to improve blood pressure and renal perfusion.

B) Administer additional potassium supplements to correct the suboptimal potassium level.

C) Prepare the patient for potential renal replacement therapy as recommended by nephrology.

D) Initiate low-dose dopamine infusion as advised to enhance renal perfusion and monitor renal function.

A patient is experiencing increased intracranial pressure, acute kidney injury, and cardiac instability. As the nurse, which intervention should be prioritized to address these conditions effectively?

A) Administer hypertonic saline to reduce cerebral edema.

B) Initiate continuous renal replacement therapy (CRRT) to manage fluid balance.

C) Adjust the IV electrolyte replacement strategy to stabilize potassium levels.

D) Monitor for signs of further neurological deterioration before taking action.

A nurse is caring for a patient with worsening cerebral edema, acute kidney injury, and cardiac instability. Which intervention should the nurse prioritize when planning care for this patient?

B) Administer hypertonic saline to reduce cerebral edema.

A) Initiate continuous renal replacement therapy (CRRT) to improve renal function.

B) Administer hypertonic saline to reduce cerebral edema.

C) Adjust the IV electrolyte replacement to correct potassium levels.

D) Prepare for potential decompressive surgery to address increased intracranial pressure.

Which of the following nursing interventions is most critical to prioritize when managing this patient's care, considering the described complications and interventions?

A) Increase the frequency of neurological assessments to every hour.

B) Administer a bolus of IV potassium to quickly stabilize levels.

C) Prepare for immediate endotracheal intubation due to declining GCS.

D) Initiate a stat MRI to assess for potential new intracranial lesions.

A patient receiving continuous renal replacement therapy (CRRT) for acute kidney injury presents with fluctuating potassium levels and episodes of ventricular tachycardia. Which nursing intervention is most appropriate to address the cardiac complications associated with this patient's electrolyte imbalance?

B) Administer magnesium sulfate bolus and continue monitoring cardiac rhythm closely.

A) Increase the rate of potassium infusion to quickly correct hypokalemia.

B) Administer magnesium sulfate bolus and continue monitoring cardiac rhythm closely.

C) Delay electrolyte replacement until potassium levels are critically low.

D) Reduce the frequency of electrolyte monitoring to prevent unnecessary interventions.

Diabetic ketoacidosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency leads to elevated blood glucose levels as cells cannot uptake glucose effectively. This prompts the liver to produce more glucose through gluconeogenesis and glycogenolysis, further increasing blood glucose.

• Secondary mechanism: The lack of insulin triggers lipolysis, breaking down fat stores into free fatty acids. The liver converts these fatty acids to ketones, resulting in ketoacidosis—a state that acidifies the blood due to excessive ketone bodies.

• Key complication: The combination of hyperglycemia and ketoacidosis causes osmotic diuresis, leading to dehydration and electrolyte imbalances, notably hypokalemia, which can result in cardiac and muscular dysfunction if not promptly corrected.

Patient Profile

Demographics:

45-year-old female, office manager

History:

• Key past medical history: Type 1 Diabetes Mellitus diagnosed 20 years ago, hypertension, and hyperlipidemia

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

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing fatigue and abdominal pain over the past two days

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

• Vital signs: Temperature 100.4°F (38°C), heart rate 115 bpm, respiratory rate 28 breaths per minute, blood pressure 105/65 mmHg, oxygen saturation 95% on room air

Section 1

During the initial assessment, the clinical team focused on evaluating the severity of the patient's diabetic ketoacidosis (DKA) and identifying any emergent complications. Notably, the patient's blood glucose level was critically elevated at 550 mg/dL. Arterial blood gas analysis revealed a pH of 7.24, indicating significant acidosis, and serum ketones were markedly elevated. Electrolyte analysis highlighted a potassium level of 3.2 mEq/L, confirming hypokalemia, a common complication of DKA. The patient's anion gap was also widened at 18 mEq/L, further supporting the diagnosis of metabolic acidosis. Despite the administration of regular insulin via an intravenous infusion, the patient's mental status showed little improvement, with persistent confusion and lethargy, suggesting possible cerebral edema or other neurological involvement.

The healthcare team initiated aggressive fluid resuscitation with isotonic saline to address the severe dehydration and correct electrolyte imbalances. Concurrently, potassium supplementation was administered to prevent cardiac complications from hypokalemia. As the treatment proceeded, the patient's heart rate remained elevated at 110 bpm, and her respiratory rate increased to 32 breaths per minute, reflecting ongoing respiratory compensation for metabolic acidosis. Given the potential for worsening complications, including cardiac arrhythmias and neurological deterioration, the team closely monitored her cardiac rhythm and neurological status.

Despite initial interventions, the patient's condition did not stabilize as expected. Her confusion intensified, and she exhibited signs of distress, prompting a reevaluation of her treatment plan. The clinical team considered the possibility of additional complications, such as cerebral edema or acute kidney injury, which could exacerbate her current state. A computed tomography (CT) scan of the head was ordered to rule out cerebral edema, and nephrology was consulted to assess renal function, considering the risk of acute tubular necrosis in the setting of severe dehydration and prolonged hyperglycemia. These steps aimed to identify and address any underlying issues impeding her recovery, ensuring a comprehensive approach to her complex clinical presentation.

Section 2

As the clinical team awaited the results of the CT scan and nephrology consult, they continued to monitor the patient's vital signs and laboratory values closely. Despite efforts to stabilize her condition, the patient developed new complications. Her blood pressure, which had previously been stable, began to trend downward, with readings dropping to 88/60 mmHg, raising concerns for potential hypovolemic shock due to ongoing dehydration and fluid shifts associated with DKA.

Simultaneously, the results from the CT scan revealed mild cerebral edema, necessitating immediate intervention to prevent further neurological compromise. The team initiated osmotherapy with intravenous mannitol to reduce intracranial pressure while maintaining a delicate balance in fluid management to avoid exacerbating her electrolyte imbalances. The patient's neurological status required constant assessment, with frequent checks for changes in her level of consciousness and pupil reactivity.

Lab results indicated a further drop in potassium levels to 2.8 mEq/L despite ongoing supplementation, highlighting the need for more aggressive electrolyte replacement and reevaluation of her insulin infusion rate. Continuous cardiac monitoring showed occasional premature ventricular contractions, suggesting increased cardiac irritability secondary to hypokalemia. This prompted the team to implement a more focused regimen to address electrolyte repletion while ensuring that her blood glucose levels were gradually corrected to mitigate the risk of further complications. These adjustments aimed to stabilize her hemodynamic status and improve her overall prognosis, paving the way for potential recovery from the complex interplay of conditions affecting her health.

Section 3

As the team closely monitored the patient's response to the interventions, they noticed a change in her status that warranted further attention. Despite the administration of mannitol and aggressive electrolyte management, the patient's neurological examination demonstrated new findings. Her level of consciousness deteriorated, with a Glasgow Coma Scale score dropping from 13 to 10, indicating a decline in her neurological function. Pupillary assessment revealed sluggish reaction to light bilaterally, suggesting that the cerebral edema might not be fully controlled.

Concurrently, the patient's blood pressure remained unstable, with readings fluctuating between 85/58 mmHg and 90/62 mmHg. This persistent hypotension raised concerns about the adequacy of her fluid replacement therapy, prompting the team to adjust her intravenous fluid composition and rate. Despite these efforts, the patient's urine output decreased to less than 20 mL/hour, hinting at possible acute kidney injury, a common complication in severe DKA cases. The nephrology consult recommended the initiation of low-dose dopamine to enhance renal perfusion, while the team continued to closely monitor her renal function tests.

Laboratory data showed a slight improvement in potassium levels, now at 3.2 mEq/L, but this remained suboptimal, necessitating continued vigilant potassium replacement. The patient's cardiac monitoring still showed sporadic premature ventricular contractions, reinforcing the need for precise electrolyte and fluid management to prevent further cardiac complications. The team prepared for potential escalation of care, considering the possibility of renal replacement therapy if the patient's condition did not improve, while maintaining a focus on stabilizing her hemodynamic and neurological status. This evolving scenario demanded comprehensive clinical reasoning to anticipate further complications and adapt the treatment plan accordingly.

Section 4

As the medical team continued to monitor the patient, new diagnostic results provided critical insights into her condition. A repeat CT scan of the brain was performed to assess the extent of cerebral edema, revealing a slight increase in midline shift, indicating worsening intracranial pressure. This finding corroborated the neurological decline observed in the patient and prompted an urgent discussion among the team regarding the need for more aggressive interventions to manage the cerebral edema, such as the potential administration of hypertonic saline or consideration of decompressive surgery if her condition continued to worsen.

In parallel, the laboratory results showed an increase in serum creatinine levels, now at 2.1 mg/dL, confirming the suspicion of acute kidney injury. The patient's blood urea nitrogen (BUN) also rose to 40 mg/dL, further indicating compromised renal function. This development required immediate attention to balance fluid management without exacerbating the cerebral edema. The nephrology team discussed the initiation of continuous renal replacement therapy (CRRT) as a gentle means of managing the patient's fluid status and electrolytes, given her fragile hemodynamic state.

The patient's cardiac monitoring continued to reveal instability, with an increase in frequency and severity of premature ventricular contractions, now accompanied by occasional runs of ventricular tachycardia. The team recognized the urgency of stabilizing the patient's electrolyte levels, particularly potassium, which had only marginally improved. This situation necessitated a reassessment of her IV electrolyte replacement strategy and close cardiac monitoring to preempt potentially life-threatening arrhythmias. As the team prepared for these interventions, they remained vigilant for any further changes in the patient's status that could necessitate additional modifications to her treatment plan.

Section 5

As the medical team continued to implement the revised treatment plan, close monitoring of the patient's response to interventions revealed new complications that required immediate attention. Despite aggressive management with IV electrolyte replacement, the patient's potassium levels remained unstable, fluctuating between 3.0 and 3.5 mEq/L, contributing to continued cardiac irritability. The cardiac monitor showed more frequent runs of ventricular tachycardia, and the patient experienced an episode of sustained ventricular tachycardia lasting 15 seconds, prompting an urgent response from the team. A bolus of magnesium sulfate was administered to stabilize myocardial function, and an amiodarone infusion was initiated to reduce the risk of further arrhythmias. The team recognized the importance of achieving optimal electrolyte balance and decided to increase the frequency of potassium checks to every two hours, ensuring more precise adjustments to supplementation.

Simultaneously, the patient's neurological status exhibited further decline. She became increasingly somnolent, with a Glasgow Coma Scale score dropping to 8, indicating a shift from a verbal to a non-verbal state. Pupillary response was sluggish, and there was decreased motor response to painful stimuli on her right side, suggesting further exacerbation of cerebral edema. The decision was made to administer hypertonic saline to reduce intracranial pressure while carefully monitoring serum sodium levels to prevent rapid shifts that could cause additional complications. The neurosurgical team was on standby, ready to assess the need for surgical intervention should her condition not improve with medical management.

In this challenging scenario, the medical team faced a complex balancing act, requiring careful integration of multiple clinical concepts. Continuous renal replacement therapy was initiated to address the acute kidney injury and manage fluid balance without worsening cerebral edema. However, this intervention required meticulous monitoring of fluid shifts and electrolytes to support both renal and cardiac function. The team remained vigilant, ready to reassess and modify the treatment plan as necessary, understanding that the patient's journey required a dynamic and responsive approach to her evolving clinical picture.