A 12-year-old patient with diabetic ketoacidosis (DKA) is receiving treatment in the emergency department. Which nursing intervention is most critical to prevent complications related to cerebral edema during the management of this patient?

A) Monitor for changes in level of consciousness and report immediately.

B) Administer a bolus of 5% dextrose in normal saline to prevent hypoglycemia.

C) Increase the insulin infusion rate to rapidly reduce blood glucose levels.

D) Encourage oral intake of fluids to promote hydration.

A 12-year-old patient with diabetic ketoacidosis (DKA) is being treated with fluid replacement therapy and insulin infusion. Given the need to monitor for potential complications, which clinical sign should the nurse prioritize to assess for the development of cerebral edema?

C) Change in level of consciousness

B) Decrease in blood glucose level

C) Change in level of consciousness

A patient with diabetic ketoacidosis (DKA) is experiencing a drop in Glasgow Coma Scale (GCS) score, tachycardia, tachypnea, and fluctuating blood pressure after initial fluid resuscitation. Laboratory results show persistent metabolic acidosis and electrolyte imbalances. What is the most appropriate nursing intervention to prioritize at this time?

B) Initiate mannitol administration to prevent cerebral edema.

A) Administer an additional bolus of isotonic saline to address hypotension.

B) Initiate mannitol administration to prevent cerebral edema.

C) Adjust insulin infusion to rapidly lower serum glucose levels further.

D) Prepare to assist with intubation due to respiratory distress.

A patient with a history of diabetic ketoacidosis demonstrates a declining Glasgow Coma Scale (GCS) score, persistent tachycardia, increased respiratory rate, and fluctuating blood pressure. Laboratory findings show a decreased serum glucose, low bicarbonate, elevated anion gap, hyponatremia, hyperkalemia, and decreased urine output. Which intervention should the nurse prioritize to address the patient's current condition?

A) Increase the rate of isotonic fluid replacement to improve blood pressure and urine output.

B) Administer sodium bicarbonate to correct metabolic acidosis and stabilize the anion gap.

C) Initiate mannitol infusion to prevent cerebral edema due to the declining neurological status.

D) Administer insulin bolus to rapidly decrease serum glucose and correct electrolyte imbalances.

A pediatric patient with diabetic ketoacidosis (DKA) is being treated for signs of cerebral edema with mannitol. Which nursing intervention is most critical in the first hour following the administration of mannitol?

D) Evaluate the patient's neurological status to determine the response to treatment.

A) Monitor urine output to assess the effectiveness of mannitol as a diuretic.

B) Assess the patient's blood glucose levels to ensure insulin therapy is effective.

C) Check the patient's serum sodium levels to monitor for hyponatremia.

D) Evaluate the patient's neurological status to determine the response to treatment.

A pediatric patient with diabetic ketoacidosis (DKA) is being treated for cerebral edema with mannitol. Her sodium is 126 mEq/L, potassium is 5.7 mEq/L, and her GCS score has improved from 9 to 10. What is the priority nursing intervention at this time?

C) Adjust insulin administration to address the elevated potassium levels while closely monitoring electrolyte changes.

A) Continue monitoring her neurological status while administering additional mannitol.

B) Initiate fluid resuscitation with hypotonic fluids to correct the sodium imbalance.

C) Adjust insulin administration to address the elevated potassium levels while closely monitoring electrolyte changes.

D) Prepare for immediate intubation due to the risk of impending respiratory failure.

A pediatric patient with diabetic ketoacidosis (DKA) has developed an irregular respiratory pattern and mixed respiratory and metabolic acidosis with a pH of 7.25. Which nursing intervention is most appropriate to address the patient's current respiratory status?

B) Prepare for intubation and mechanical ventilation.

A) Administer supplemental oxygen via nasal cannula.

B) Prepare for intubation and mechanical ventilation.

C) Increase the rate of intravenous fluid administration.

D) Administer a bronchodilator to ease breathing.

A pediatric patient with diabetic ketoacidosis (DKA) and mixed respiratory and metabolic acidosis is experiencing irregular breathing patterns, and her sodium and potassium levels are being closely monitored. What is the most appropriate nursing intervention to address these findings?

A) Initiate continuous pulse oximetry monitoring and prepare for potential intubation.

B) Discontinue the potassium-sparing diuretic to prevent further hyperkalemia.

C) Administer a high-dose bicarbonate infusion to correct the metabolic acidosis.

D) Increase the rate of intravenous insulin infusion to quickly lower blood glucose levels.

A patient with acute kidney injury is experiencing fluctuating oxygen saturation levels despite non-invasive positive pressure ventilation. The healthcare team has decided to intubate the patient. What is the nurse's priority intervention immediately following intubation?

B) Monitor the patient's end-tidal CO2 and adjust ventilator settings as needed

A) Begin administration of prescribed diuretics to manage fluid overload

B) Monitor the patient's end-tidal CO2 and adjust ventilator settings as needed

C) Prepare the patient for possible renal replacement therapy

D) Increase the patient's fluid intake to address dehydration

A patient with acute kidney injury and respiratory distress has been intubated for ventilation support. Her creatinine levels have increased, indicating declining renal function, and her potassium levels remain elevated. What is the most appropriate nursing intervention to prevent further complications in this patient?

B) Prepare the patient for potential renal replacement therapy while monitoring electrolyte levels closely.

A) Administer a potassium-sparing diuretic to manage fluid overload.

B) Prepare the patient for potential renal replacement therapy while monitoring electrolyte levels closely.

C) Increase the patient's fluid intake to compensate for dehydration.

D) Discontinue all medications that affect renal function immediately.

pediatric DKA - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency leads to decreased glucose uptake by cells, resulting in hyperglycemia and the utilization of fat as an alternative energy source, which increases ketone production and causes metabolic acidosis.

• Secondary mechanism: Osmotic diuresis occurs due to hyperglycemia, leading to dehydration and electrolyte imbalances, which can exacerbate acidosis and impair cellular function.

• Key complication: Severe dehydration and acidosis can lead to hypovolemic shock and impaired tissue perfusion, increasing the risk of cerebral edema, a critical concern in pediatric DKA.

Patient Profile

Demographics:

12-year-old female, student

History:

• Type 1 Diabetes diagnosed 2 years ago

• Insulin therapy (Lispro and Glargine)

• No known drug allergies

Current Presentation:

• Chief complaint: Abdominal pain and vomiting

• Key symptoms: Rapid breathing, fatigue, increased thirst, frequent urination

• Vital signs: Temperature 99.1°F, Heart rate 130 bpm, Respiratory rate 28 breaths/min, Blood pressure 95/60 mmHg, Blood glucose 350 mg/dL

Section 1

As the pediatric team continues to manage the 12-year-old patient with diabetic ketoacidosis (DKA), an initial assessment reveals concerning signs of moderate dehydration. Her mucous membranes are dry, skin turgor is decreased, and she exhibits delayed capillary refill time of four seconds, indicative of compromised peripheral perfusion. Her heart rate remains elevated at 134 bpm, and respiratory rate has increased to 32 breaths per minute, suggesting worsening metabolic acidosis and compensatory respiratory alkalosis. The patient is lethargic but responsive to verbal stimuli, with a Glasgow Coma Scale (GCS) score of 13, raising concerns about her neurological status.

Laboratory results return with critical findings: arterial blood gas shows a pH of 7.22, indicating significant acidosis, with a bicarbonate level of 10 mEq/L. Serum ketones are markedly elevated, and her anion gap is 22, confirming metabolic acidosis with an anion gap. Electrolyte imbalances are evident, with a sodium level of 130 mEq/L, potassium at 5.0 mEq/L, and chloride at 95 mEq/L, reflecting the osmotic diuresis and dehydration. These results, combined with her clinical presentation, suggest that the patient is in a moderate to severe state of DKA and at risk for further complications, such as cerebral edema.

The healthcare team initiates a carefully monitored fluid replacement therapy, starting with normal saline to address hypovolemia and improve tissue perfusion. Insulin infusion is commenced to gradually lower blood glucose levels and suppress ketone production. The team remains vigilant for signs of cerebral edema, prioritizing neurological assessments and cautious fluid administration. As the patient's condition is closely monitored, the focus is on stabilizing her hemodynamic status and correcting metabolic derangements to prevent further deterioration.

Section 2

As the team continues to manage the patient, close monitoring reveals a change in her status, prompting immediate attention. Despite initial fluid resuscitation, the patient's mental status begins to deteriorate further; she becomes less responsive, with a Glasgow Coma Scale (GCS) score dropping to 11. Her heart rate remains elevated at 140 bpm, and her respiratory rate increases to 36 breaths per minute, indicating persistent compensation for metabolic acidosis. Notably, her blood pressure begins to fluctuate, showing episodes of hypotension with systolic readings dropping to 86 mmHg, suggesting inadequate fluid replacement or potential vasodilation due to acidosis.

Repeat laboratory tests show the patient's serum glucose has decreased from 450 mg/dL to 320 mg/dL, which is a positive trend. However, the bicarbonate level remains low at 12 mEq/L, and the anion gap is still elevated at 20, indicating that acidosis has not yet resolved. Electrolyte imbalances persist, with a sodium level now at 128 mEq/L, and potassium has increased to 5.5 mEq/L, likely due to the effects of insulin therapy on potassium shifting back into cells and renal impairment from dehydration. Importantly, the team notes a decrease in urine output, raising concerns about kidney function and prompting further evaluation.

Given the patient's declining neurological status and laboratory findings, there is an urgent need to reassess the fluid management strategy, considering the risk of cerebral edema. The team discusses the possibility of adding mannitol or hypertonic saline if signs of increased intracranial pressure develop. It is crucial to adjust the fluid and insulin therapy carefully to avoid rapid shifts in osmolality, which could exacerbate her condition. The situation calls for continued vigilance and frequent reassessment to ensure that the interventions are effectively addressing the underlying pathophysiology without precipitating new complications.

Section 3

As the medical team continues to closely monitor the pediatric patient with diabetic ketoacidosis (DKA), further changes in her condition warrant immediate intervention. Despite previous treatment efforts, her neurological status continues to decline. Her Glasgow Coma Scale (GCS) score drops further to 9, indicating a potentially life-threatening level of altered consciousness. Her vital signs reveal persistent tachycardia, with a heart rate now at 145 bpm, and her respiratory rate remains elevated at 38 breaths per minute. Blood pressure readings fluctuate between 80/50 mmHg and 90/60 mmHg, underscoring the need for careful fluid management to avoid exacerbating potential cerebral edema while ensuring adequate perfusion.

In light of these developments, the team conducts a bedside ultrasound to evaluate for signs of cerebral edema. The examination reveals subtle signs of increased intracranial pressure, prompting the decision to administer mannitol to reduce the risk of further neurological compromise. This intervention is carefully weighed against the risk of worsening her electrolyte imbalances and is accompanied by meticulous monitoring of her sodium and potassium levels. Repeat laboratory tests show sodium has decreased further to 126 mEq/L, while potassium remains elevated at 5.7 mEq/L, necessitating close observation and possible electrolyte correction.

The patient's response to the administration of mannitol is critical. Over the next hour, her GCS score improves slightly to 10, suggesting a modest improvement in her neurological status. However, her electrolyte derangements and persistent anion gap metabolic acidosis require ongoing attention. The team decides to adjust her insulin infusion rate and consider additional electrolyte supplementation to address the underlying metabolic disturbances. As they navigate these complex clinical decisions, the importance of interdisciplinary collaboration and continuous reassessment becomes evident to ensure her safe recovery and prevent further complications.

Section 4

Despite the initial response to mannitol, the team faces a new complication as the patient's respiratory pattern becomes increasingly irregular. Her previously elevated respiratory rate of 38 breaths per minute now fluctuates, with periods of rapid breathing followed by shallow breaths. This change raises concern for potential respiratory fatigue or impending respiratory failure. A repeat arterial blood gas (ABG) analysis is performed, revealing a pH of 7.25, PaCO2 of 30 mmHg, and a bicarbonate level of 12 mEq/L, indicating a mixed respiratory and metabolic acidosis. The persistent acidosis and altered breathing pattern prompt the team to consider the need for respiratory support to prevent further deterioration.

Concurrently, her electrolyte imbalances continue to pose a challenge. The sodium level, which had decreased to 126 mEq/L, shows a slight improvement to 128 mEq/L following careful electrolyte management. However, the potassium level remains elevated at 5.6 mEq/L despite ongoing insulin therapy. The team decides to initiate a low-dose potassium-sparing diuretic to address the hyperkalemia, monitoring closely for any adverse effects on her renal function and electrolyte balance. The balance between correcting her acidosis and managing her electrolyte status highlights the complexity of care in pediatric DKA, necessitating continuous evaluation and adjustment of treatment strategies.

As the team navigates these challenges, they emphasize the importance of maintaining a multidisciplinary approach. Collaboration between pediatric intensivists, endocrinologists, and critical care nurses becomes crucial to anticipate potential complications and adapt the treatment plan promptly. With her neurological status showing slight improvement, the focus now shifts to stabilizing her respiratory function and resolving the biochemical imbalances. The team remains vigilant, prepared to escalate care as needed to ensure a positive outcome for the patient.

Section 5

As the team continues to monitor the patient closely, a change in her status becomes apparent. Despite the initiation of respiratory support with non-invasive positive pressure ventilation (NIPPV), her oxygen saturation begins to fluctuate, dipping as low as 88% on occasion. Her breathing pattern remains irregular, with intermittent periods of apnea. The decision is made to intubate the patient to provide more stable ventilation and prevent further respiratory compromise. This escalation in respiratory support necessitates careful coordination among the team to ensure seamless management of her airway and ventilation.

Concurrently, new diagnostic results reveal that the patient's renal function is beginning to decline. Her creatinine level has risen from 0.6 mg/dL to 1.1 mg/dL, indicating acute kidney injury, likely exacerbated by the diuretic therapy and ongoing dehydration. This development prompts the team to adjust the fluid management plan, balancing the need for hydration with the risk of fluid overload. The importance of maintaining her hemodynamic stability becomes paramount, and close monitoring of her urine output and fluid status is prioritized.

The persistent elevation in potassium levels, despite these interventions, suggests an underlying issue with renal excretion. The team considers the potential need for renal replacement therapy if the situation does not improve. In light of these complications, the multidisciplinary team remains focused on a holistic approach, integrating input from nephrologists and respiratory therapists to optimize care. The primary goal remains to stabilize her condition, allowing for gradual correction of her metabolic derangements while preventing further organ dysfunction.