A patient with diabetic ketoacidosis (DKA) is receiving treatment in the emergency department. Despite aggressive fluid resuscitation and insulin therapy, the patient develops tachycardia and hypotension. Which of the following actions should the nurse prioritize to prevent cardiovascular collapse?

C) Initiate vasopressor support as prescribed.

A) Increase the rate of isotonic saline infusion.

B) Administer a bolus of hypertonic saline.

C) Initiate vasopressor support as prescribed.

D) Administer additional intravenous insulin.

A critically ill patient with diabetic ketoacidosis (DKA) is being treated with aggressive fluid resuscitation and intravenous insulin. Despite initial therapy, the patient develops tachycardia and hypotension. Which of the following actions should the nurse prioritize to prevent cardiovascular collapse?

B) Administer a bolus of isotonic saline and initiate vasopressor support.

A) Increase the rate of intravenous insulin infusion.

B) Administer a bolus of isotonic saline and initiate vasopressor support.

C) Discontinue potassium supplementation until hemodynamic stability is achieved.

D) Initiate sodium bicarbonate infusion to correct severe acidosis.

A patient in the ICU with diabetic ketoacidosis (DKA) and sepsis is experiencing worsening respiratory distress, severe hypokalemia, and hypotension. Considering these factors, which of the following interventions should be prioritized by the nurse to stabilize the patient's condition?

B) Administer potassium chloride intravenously to correct hypokalemia.

A) Increase fluid resuscitation to improve blood pressure.

B) Administer potassium chloride intravenously to correct hypokalemia.

C) Initiate vasopressor therapy to address hypotension.

D) Provide high-flow oxygen therapy to counteract hypoxemia.

A patient in the ICU is experiencing respiratory distress, pulmonary edema, severe hypokalemia, and hypotension despite ongoing fluid resuscitation and insulin therapy. The blood cultures are positive for Escherichia coli, indicating a systemic infection. What is the nurse's highest priority intervention at this time?

A) Administer potassium chloride intravenously to correct severe hypokalemia and prevent cardiac arrhythmias.

B) Initiate vasopressor therapy to stabilize blood pressure and support hemodynamic status.

C) Provide supplemental oxygen and consider non-invasive ventilation to improve oxygen saturation.

D) Start broad-spectrum antibiotics to address the systemic infection and reduce sepsis progression.

A patient with hypokalemia and pulmonary edema is receiving aggressive potassium replacement and vasopressor support. The patient's serum potassium level has risen to 3.5 mEq/L, but the mean arterial pressure remains below 65 mmHg despite vasopressor therapy. Which of the following interventions should the nurse prioritize to address this patient's hemodynamic instability while minimizing the risk of worsening pulmonary edema?

C) Adjust the non-invasive positive pressure ventilation settings to improve oxygenation and reduce cardiac workload.

A) Increase the dose of vasopressors to achieve a mean arterial pressure above 65 mmHg.

B) Administer intravenous fluids to improve blood pressure and renal perfusion.

C) Adjust the non-invasive positive pressure ventilation settings to improve oxygenation and reduce cardiac workload.

D) Initiate continuous renal replacement therapy to manage fluid overload and electrolyte imbalances.

A nurse is caring for a patient with corrected hypokalemia and persistent hemodynamic instability despite vasopressor support. The patient also exhibits pulmonary edema and altered mental status. Which of the following interventions should the nurse prioritize to address the patient's current condition?

D) Administer a diuretic to reduce pulmonary edema and improve respiratory status.

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

B) Adjust the vasopressor dosage to achieve a mean arterial pressure above 65 mmHg.

C) Initiate continuous renal replacement therapy (CRRT) to manage fluid overload.

D) Administer a diuretic to reduce pulmonary edema and improve respiratory status.

A patient with persistent metabolic acidosis, confirmed by arterial blood gas analysis and an elevated anion gap, shows no improvement despite insulin therapy. The patient also has elevated serum lactate levels and mild cerebral edema. Which of the following nursing interventions is most critical to prioritize to address the complex clinical picture?

C) Adjust fluid management to address cerebral edema and improve tissue perfusion.

A) Administer sodium bicarbonate to correct the acidosis immediately.

B) Initiate broad-spectrum antibiotics to target potential infectious sources.

C) Adjust fluid management to address cerebral edema and improve tissue perfusion.

D) Re-evaluate and potentially increase the insulin dosing regimen.

A patient with ketoacidosis, potential lactic acidosis, and signs of infection is being managed in the intensive care unit. The arterial blood gas shows a persistent metabolic acidosis with an elevated anion gap. Given the current findings, which of the following interventions should be the immediate focus for the nursing team to address the underlying metabolic disturbance and prevent further complications?

C) Adjust the insulin dosing regimen to more effectively reduce ketone production and manage hyperglycemia.

A) Increase the rate of intravenous fluid administration to improve tissue perfusion and reduce lactate levels.

B) Administer sodium bicarbonate to correct the severe metabolic acidosis and improve blood pH.

C) Adjust the insulin dosing regimen to more effectively reduce ketone production and manage hyperglycemia.

D) Initiate vasopressor therapy to maintain blood pressure and ensure adequate cerebral perfusion.

A patient with diabetic ketoacidosis and suspected sepsis is experiencing hemodynamic instability despite aggressive fluid resuscitation and vasopressor support. They exhibit a worsening anion gap metabolic acidosis and elevated serum lactate levels. What is the most appropriate nursing intervention to prioritize, considering the need to stabilize the patient's condition and address the underlying issues?

D) Optimize antibiotic therapy by ensuring cultures are obtained and reviewed for appropriate adjustments.

A) Increase the rate of insulin infusion to rapidly lower blood glucose and correct ketoacidosis.

B) Initiate continuous renal replacement therapy (CRRT) to manage acidosis and support renal function.

C) Administer a sodium bicarbonate bolus to immediately correct the severe metabolic acidosis.

D) Optimize antibiotic therapy by ensuring cultures are obtained and reviewed for appropriate adjustments.

A patient with diabetic ketoacidosis and suspected sepsis is being closely monitored. Despite aggressive fluid resuscitation and initiation of norepinephrine, the patient remains hypotensive and tachycardic. The patient's lab results show a worsening anion gap metabolic acidosis and elevated serum lactate levels. Which nursing intervention is most crucial to prioritize at this stage to address the patient’s hemodynamic instability and metabolic state?

C) Titrate norepinephrine to achieve a target mean arterial pressure above 65 mmHg.

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

B) Initiate continuous renal replacement therapy to manage acute kidney injury.

C) Titrate norepinephrine to achieve a target mean arterial pressure above 65 mmHg.

D) Administer sodium bicarbonate to correct the metabolic acidosis.

DKA - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency leads to uncontrolled lipolysis, causing excess free fatty acids to be converted into ketones by the liver, resulting in ketonemia and metabolic acidosis.

• Secondary mechanism: Hyperglycemia from impaired glucose uptake and increased gluconeogenesis induces osmotic diuresis, causing severe dehydration and electrolyte imbalances.

• Key complication: Severe acidosis and dehydration can precipitate cardiovascular collapse and cerebral edema, posing significant life-threatening risks if not rapidly addressed.

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Key past medical history: Type 1 Diabetes Mellitus (diagnosed 20 years ago), hypertension, chronic kidney disease stage 3

• Current medications: Insulin glargine, lisinopril, metformin, atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain and confusion

• Key symptoms: Nausea, vomiting, polyuria, polydipsia, fatigue, shortness of breath

• Vital signs: Temperature 101.3°F (38.5°C), heart rate 128 bpm, respiratory rate 32 breaths per minute, blood pressure 88/54 mmHg, SpO2 89% on room air

Section 1

The initial assessment reveals a critically ill patient presenting with signs of severe dehydration and metabolic acidosis. Physical examination shows dry mucous membranes, decreased skin turgor, and altered mental status, indicative of significant fluid loss and electrolyte imbalance. Lung auscultation reveals Kussmaul respirations, a compensatory mechanism for the metabolic acidosis. His abdomen is tender to palpation, without rebound tenderness, suggesting pain potentially related to the acidosis or electrolyte disturbance rather than an acute surgical abdomen. Neurological assessment indicates confusion and disorientation, with a Glasgow Coma Scale score of 13, showing a decline in cognitive function likely due to the metabolic derangements and dehydration.

Laboratory diagnostics reveal a blood glucose level of 620 mg/dL, serum bicarbonate of 10 mEq/L, and an anion gap of 35, confirming high anion gap metabolic acidosis. Blood gases display a pH of 7.09, indicating severe acidosis, and elevated serum ketones corroborate the diagnosis of diabetic ketoacidosis (DKA). Serum electrolytes highlight critical imbalances: potassium at 2.8 mEq/L, sodium at 128 mEq/L, and a markedly elevated blood urea nitrogen (BUN) of 54 mg/dL and creatinine at 3.2 mg/dL, reflecting acute renal impairment exacerbated by dehydration. These findings necessitate immediate intervention to rectify life-threatening disturbances.

The patient is initiated on aggressive fluid resuscitation with isotonic saline and intravenous insulin therapy to manage hyperglycemia and halt ketogenesis. Close monitoring ensues for signs of cerebral edema, a feared complication in the context of rapid fluid shifts and correction of hyperglycemia. Potassium supplementation is cautiously administered, given the initial low serum levels and the risk of potential cardiac arrhythmias. Despite initial interventions, the patient develops tachycardia and a further drop in blood pressure, raising concerns for impending cardiovascular collapse, necessitating reevaluation and potential escalation of care, including vasopressor support and transfer to an intensive care unit for advanced hemodynamic monitoring and management.

Section 2

As the patient remains in the intensive care unit under close observation, new complications emerge, necessitating immediate attention and advanced clinical reasoning. Despite ongoing fluid resuscitation and insulin therapy, the patient exhibits a sudden increase in respiratory distress, with a rise in respiratory rate to 36 breaths per minute and oxygen saturation dropping to 88% on room air. Auscultation now reveals crackles at the lung bases, suggesting the development of pulmonary edema, a potential consequence of aggressive fluid administration in a patient with compromised renal function. Concurrently, the patient’s mental status deteriorates further, with a Glasgow Coma Scale score dropping to 10, indicating a deepening level of consciousness impairment.

Laboratory results reveal worsening electrolyte imbalances with a precipitous drop in serum potassium to 2.2 mEq/L, raising the alarm for severe hypokalemia, which poses a significant risk for life-threatening cardiac arrhythmias. Electrocardiogram findings confirm this risk, showing prominent U waves and flattened T waves, indicative of electrolyte-induced cardiac instability. The patient's blood pressure remains critically low at 78/42 mmHg, despite increased fluid volume, pointing towards a distributive shock likely exacerbated by sepsis, secondary to the underlying infection that precipitated the DKA episode. Blood cultures return positive for Escherichia coli, confirming the presence of a urinary tract infection that has likely progressed to systemic involvement.

This multifaceted deterioration demands a reassessment of the therapeutic approach, emphasizing the need for a delicate balance between ongoing fluid management to prevent further pulmonary edema and the administration of vasopressors to stabilize hemodynamics. The critical priority is to address the severe hypokalemia with aggressive potassium replacement, closely monitoring cardiac function to avert arrhythmias. Concurrently, broad-spectrum antibiotics are initiated to combat the identified infection source. The evolving scenario challenges the healthcare team to exercise advanced critical thinking in navigating the intricate interplay of metabolic, respiratory, and infectious processes, ensuring timely interventions that align with the patient's dynamic clinical status.

Section 3

As the healthcare team intensifies the management of this complex case, the focus shifts toward the patient's response to the interventions, particularly the aggressive potassium replacement and vasopressor support. Over the next few hours, the patient's serum potassium levels are cautiously corrected, rising to 3.5 mEq/L. This improvement is accompanied by a stabilization of the electrocardiogram, where U waves become less prominent, and T waves show signs of normalization, suggesting a reduction in the immediate risk of cardiac arrhythmias. Despite these positive trends, the patient's blood pressure remains a challenge. Vasopressors are titrated with care to avoid exacerbating the pulmonary edema, yet the mean arterial pressure struggles to maintain above 65 mmHg, indicating ongoing hemodynamic instability.

Simultaneously, attention is directed toward the patient's respiratory status, as the development of pulmonary edema remains a pressing concern. The introduction of non-invasive positive pressure ventilation (NIPPV) aids in improving oxygenation, with oxygen saturation levels gradually increasing to 92% on FiO2 of 40%. However, the patient's respiratory rate remains elevated at 30 breaths per minute, indicating persistent respiratory distress. A repeat chest X-ray confirms bilateral pulmonary infiltrates, underscoring the delicate balance required in fluid management to prevent further exacerbation of respiratory compromise.

Despite these focused interventions, the patient's mental status shows minimal improvement, maintaining a Glasgow Coma Scale score of 10. This persistent alteration in consciousness prompts a re-evaluation of potential etiologies, including the unresolved metabolic derangements, possible cerebral edema, and the effects of systemic infection. The healthcare team anticipates the need for further diagnostic imaging and laboratory tests to refine their understanding of the patient's condition. Through this complex clinical scenario, the team must continue to employ advanced critical thinking to prioritize and adapt their interventions, ensuring a comprehensive approach to the multifaceted challenges presented by the patient's evolving status.

Section 4

As the healthcare team continues to manage the patient's complex condition, new diagnostic results shed light on the underlying challenges. A repeat arterial blood gas analysis reveals a persistent metabolic acidosis with a pH of 7.25, HCO3- of 14 mEq/L, and a PaCO2 of 28 mmHg, suggesting ongoing ketoacidosis despite insulin therapy. An elevated anion gap of 23 mEq/L further confirms this, indicating the need for an intensified focus on resolving the metabolic disturbance. Concurrently, serum lactate levels are measured at 4.5 mmol/L, raising concerns about tissue hypoperfusion and the potential for lactic acidosis contributing to the patient's condition.

Simultaneously, a CT scan of the head is performed to assess for cerebral edema, given the patient's persistently altered mental status. The imaging reveals mild cerebral swelling without significant midline shift or herniation, emphasizing the need for careful management of the patient's fluid status and intracranial pressure. These findings, combined with the elevated inflammatory markers—C-reactive protein at 150 mg/L and white blood cell count at 18,000/mm³—suggest a superimposed infectious process, possibly sepsis, that could be further complicating the clinical picture.

Faced with these new diagnostic insights, the healthcare team refines their treatment strategy. The need to address the metabolic acidosis is prioritized, with a re-evaluation of the insulin dosing regimen and consideration of bicarbonate therapy to aid in correcting the severe acidosis. The potential infectious source is also targeted, with broad-spectrum antibiotics initiated early, pending culture results, to mitigate the risk of sepsis. The team remains vigilant, understanding that their clinical reasoning and judgment will be crucial in navigating the complex interplay of the patient's metabolic, respiratory, and neurological challenges to improve overall outcomes.

Section 5

As the healthcare team intensifies their management of the patient's diabetic ketoacidosis and suspected sepsis, they closely monitor for any changes in the patient’s status. Over the next few hours, the patient exhibits fluctuations in vital signs: blood pressure drops to 85/55 mmHg, heart rate increases to 118 beats per minute, and respiratory rate rises to 30 breaths per minute, with oxygen saturation decreasing to 90% on room air. This hemodynamic instability prompts concerns about evolving septic shock, necessitating immediate intervention. The team initiates aggressive fluid resuscitation with isotonic crystalloids to counteract the hypotension and improve tissue perfusion. Despite these efforts, the patient remains tachycardic and hypotensive, leading to the initiation of vasopressor support with norepinephrine to maintain adequate mean arterial pressure.

Simultaneously, repeat laboratory tests reveal a worsening anion gap metabolic acidosis with a pH now at 7.20 and bicarbonate level at 12 mEq/L, indicating insufficient resolution of the ketoacidosis. The serum lactate has risen further to 5.8 mmol/L, confirming persistent lactic acidosis, likely exacerbated by both the metabolic derangements and potential septic process. This compels the team to re-evaluate the insulin infusion rate, ensuring optimal glycemic control while considering adjunctive bicarbonate therapy to assist in buffering the acidosis. Broad-spectrum antibiotics are continued, and cultures are prioritized to identify the infectious source and tailor antimicrobial therapy accordingly.

As the patient’s neurological status remains compromised, with a Glasgow Coma Scale score of 9, the team remains vigilant for signs of increased intracranial pressure. Neuroprotective strategies are employed, including head elevation and careful monitoring of fluid balance, to mitigate cerebral edema. The complexity of the case underscores the importance of dynamic clinical reasoning, as the healthcare team must continuously integrate evolving data to guide therapeutic decisions, monitor for potential complications such as acute kidney injury or respiratory failure, and adjust their management plan to optimize the patient’s recovery trajectory.