A nurse is caring for a patient diagnosed with SIADH who has been placed on a fluid restriction and oral salt tablets. The patient exhibits increased confusion and irritability. Which nursing intervention is the highest priority?

C) Monitor the patient's neurological status and report changes immediately.

A) Increase the patient's fluid restriction to prevent further water retention.

B) Administer an additional dose of oral salt tablets to quickly raise sodium levels.

C) Monitor the patient's neurological status and report changes immediately.

D) Educate the family about the importance of adhering to the fluid restriction plan.

A patient with SIADH is being managed with fluid restriction and oral salt tablets. They suddenly exhibit increased confusion and irritability. What is the priority nursing intervention?

C) Reassess the patient's vital signs and neurological status.

A) Increase the patient's fluid intake to improve hydration.

B) Administer a hypertonic saline solution as prescribed.

C) Reassess the patient's vital signs and neurological status.

D) Encourage the patient to consume more salt tablets.

A patient with hyponatremia is receiving treatment with hypertonic saline due to worsening neurological symptoms. Which nursing action is most critical in monitoring this patient?

B) Conducting neurological assessments every hour

A) Monitoring blood pressure every 4 hours

B) Conducting neurological assessments every hour

C) Measuring urine output every shift

D) Checking serum sodium levels every 48 hours

A patient with hyponatremia is receiving hypertonic saline infusion due to worsening neurological symptoms and a history of elevated urine osmolality. As the nurse, which assessment finding would warrant immediate notification to the healthcare provider?

C) Development of new-onset headache and confusion

A) Serum sodium level increased to 130 mEq/L

B) Neurological improvement with increased alertness

C) Development of new-onset headache and confusion

D) Stable urine output with clear yellow urine

A patient receiving hypertonic saline for hyponatremia develops signs of mild fluid overload. Which nursing intervention is most appropriate to prioritize at this time?

A) Administer a low-dose loop diuretic as prescribed

B) Increase the rate of the hypertonic saline infusion

C) Restrict oral fluid intake to prevent further fluid overload

D) Place the patient in a supine position to improve comfort

A patient with hyponatremia is receiving hypertonic saline and has developed mild fluid overload. The nursing team observes slight peripheral edema and mild shortness of breath. Which nursing intervention is most appropriate to prioritize in this scenario?

B) Administer a low-dose loop diuretic as prescribed and monitor urine output closely.

A) Increase the infusion rate of hypertonic saline to quickly correct the sodium level.

B) Administer a low-dose loop diuretic as prescribed and monitor urine output closely.

C) Restrict the patient's oral fluid intake to reduce fluid overload.

D) Position the patient in a Trendelenburg position to improve circulation.

A patient with SIADH is experiencing increased respiratory effort and decreased oxygen saturation despite supplemental oxygen. The patient's serum osmolality remains low, and they are receiving loop diuretics. What is the priority nursing intervention at this time?

B) Restrict fluid intake to manage fluid overload.

A) Increase the oxygen flow rate to 4 liters per minute.

B) Restrict fluid intake to manage fluid overload.

C) Administer an additional dose of loop diuretics.

D) Encourage the patient to perform deep breathing exercises.

A patient with SIADH is experiencing increased respiratory effort, fine crackles at the lung bases, and decreased oxygen saturation. The healthcare team has initiated supplemental oxygen and continued loop diuretic therapy with an adjusted dose. Given these clinical findings, which nursing intervention is most appropriate to prioritize at this time?

B) Monitor the patient's neurological status and report any changes immediately.

A) Encourage the patient to increase oral fluid intake to promote diuresis.

B) Monitor the patient's neurological status and report any changes immediately.

C) Increase the supplemental oxygen flow rate to improve oxygen saturation.

D) Discontinue the loop diuretic to prevent further electrolyte imbalances.

A patient with SIADH is being treated for fluid overload with loop diuretics and fluid restriction. The patient’s oxygen saturation is 92%-94% despite supplemental oxygen, respiratory rate is 26 breaths per minute, and fine crackles are present. The chest X-ray shows mild bilateral pulmonary infiltrates. Which nursing intervention is most crucial at this time?

B) Monitor the patient’s electrolyte levels and adjust loop diuretic dosage as needed.

A) Increase the flow rate of supplemental oxygen.

B) Monitor the patient’s electrolyte levels and adjust loop diuretic dosage as needed.

C) Encourage deep breathing exercises to improve lung expansion.

D) Assess for signs of neurological changes related to hyponatremia.

A patient with suspected SIADH and pulmonary edema has been initiated on loop diuretics and fluid restriction. Despite treatment, the patient exhibits increased respiratory rate and more pronounced crackles. Which of the following interventions should the nurse prioritize to effectively manage the patient's condition?

B) Administer a higher dose of loop diuretics as prescribed and monitor urine output closely.

A) Increase the rate of oxygen delivery to improve oxygen saturation.

B) Administer a higher dose of loop diuretics as prescribed and monitor urine output closely.

C) Encourage the patient to take deep breaths and perform incentive spirometry to improve lung expansion.

D) Elevate the head of the bed to improve ventilation and facilitate breathing.

SAIDH - Nursing Case Study

Pathophysiology

• Primary mechanism: Syndrome of Inappropriate Antidiuretic Hormone (SIADH) involves excessive release of antidiuretic hormone (ADH) despite normal or low plasma osmolality, leading to water retention and dilutional hyponatremia. This inappropriate secretion often stems from ectopic production by tumors or pulmonary disorders.

• Secondary mechanism: The continuous presence of high ADH levels enhances renal water reabsorption via aquaporin channels in the collecting ducts, decreasing urine output and concentrating urine, which exacerbates the dilution of serum sodium.

• Key complication: The resulting hyponatremia can lead to neurological symptoms due to cerebral edema, such as confusion, seizures, or coma, underscoring the importance of early recognition and management in clinical settings.

Patient Profile

Demographics:

54-year-old female, school teacher

History:

• Key past medical history: Hypertension, hypothyroidism

• Current medications: Lisinopril 10 mg daily, Levothyroxine 75 mcg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Confusion and fatigue

• Key symptoms: Headache, nausea, muscle cramps, decreased urine output

• Vital signs: Blood pressure 135/85 mmHg, heart rate 92 bpm, respiratory rate 18 breaths per minute, temperature 98.6°F, oxygen saturation 96% on room air

Section 1

New Diagnostic Results:

After the initial assessment and suspicion of SIADH, laboratory tests were conducted to confirm the underlying condition and evaluate the extent of electrolyte imbalance. The serum sodium level returned at 122 mEq/L, significantly below the normal range, confirming profound hyponatremia. Urine osmolality was elevated at 600 mOsm/kg, suggesting concentrated urine despite the low serum osmolality, which is consistent with SIADH. Serum osmolality was measured at 260 mOsm/kg, further supporting the diagnosis. These findings indicate inappropriate water retention and dilutional hyponatremia, which aligns with the patient's presenting symptoms of confusion, fatigue, and muscle cramps.

In response to these diagnostic results, the medical team initiated a fluid restriction regimen to manage the water retention and gradual correction of hyponatremia. Additionally, the patient was started on oral salt tablets to aid in increasing serum sodium levels. However, the patient began exhibiting increased confusion and irritability over the next few hours. This change in mental status raises concerns about the possibility of worsening cerebral edema due to the persistent low sodium levels. Continuous monitoring of neurological status and frequent reassessment of electrolyte levels were ordered to guide further interventions.

These diagnostic findings and subsequent changes in the patient's condition necessitate close observation and adjustment of therapeutic strategies. The medical team must balance correcting the hyponatremia without causing rapid shifts in sodium levels, which could lead to osmotic demyelination syndrome. As the patient's journey progresses, the focus will be on carefully titrating interventions, monitoring for potential complications, and addressing any new clinical developments.

Section 2

Response to Interventions

Following the initiation of fluid restriction and administration of oral salt tablets, the medical team closely monitored the patient's response to these interventions. Despite these measures, the patient's serum sodium level showed only a modest increase to 124 mEq/L after the first 24 hours, indicating a slow correction. However, the patient’s neurological status continued to decline, with increased lethargy and disorientation noted during hourly neuro checks. Vital signs remained stable, with a blood pressure of 118/76 mmHg, heart rate of 82 bpm, and oxygen saturation at 97% on room air. Despite stable hemodynamics, the persistent decline in mental status prompted further evaluation.

A repeat set of laboratory tests revealed that the urine osmolality remained elevated at 610 mOsm/kg, and the serum osmolality was still low at 262 mOsm/kg, indicating persistent inappropriate secretion of antidiuretic hormone. The team was particularly cautious of rapid sodium correction due to the risk of osmotic demyelination syndrome. Given the worsening neurological symptoms, the decision was made to cautiously add hypertonic saline infusion under strict monitoring to gradually increase serum sodium levels more effectively.

The interdisciplinary team, including neurology and nephrology, was consulted to refine the management strategy. The team emphasized the importance of monitoring for signs of osmotic shifts, and neurological assessments were increased in frequency. The patient's ongoing fluid status, electrolyte levels, and neurological condition would be pivotal in guiding further intervention adjustments. The medical team remained vigilant, recognizing that the balance between correcting hyponatremia and preventing new complications would be critical in the patient’s recovery trajectory.

Section 3

As the hypertonic saline infusion was initiated, the medical team meticulously monitored the patient's response, recognizing the delicate balance required in managing the patient's condition. Over the next 12 hours, the patient's serum sodium levels increased to 128 mEq/L, a cautious yet deliberate improvement. However, the increase in serum sodium levels was accompanied by a new complication: the patient began exhibiting signs of mild fluid overload, noted by slight peripheral edema and mild shortness of breath upon exertion. Despite this, the patient's vital signs remained largely stable, with a blood pressure of 122/78 mmHg, heart rate of 85 bpm, and oxygen saturation dipping slightly to 95% on room air, prompting the team to maintain vigilant respiratory monitoring.

The interdisciplinary team reconvened to address these developments, considering the potential need for diuretics to manage the fluid overload while continuing to correct the hyponatremia cautiously. The nephrology consultant recommended a low-dose loop diuretic to facilitate water excretion and potentially enhance the correction of hyponatremia, while ensuring serum sodium levels were closely monitored to prevent overly rapid correction. The neurology team remained focused on the patient's neurological status, which, although slightly improved, still showed lingering confusion and disorientation.

The nursing team played a critical role in ongoing assessments, noting subtle changes in the patient's mental status and fluid balance that could indicate further complications. They reported these findings promptly, allowing the medical team to make timely adjustments to the treatment plan. As the patient's journey continued, the healthcare team remained acutely aware of the need to balance fluid management and electrolyte correction, with the ultimate goal of stabilizing the patient's condition without precipitating additional complications.

Section 4

As the nursing team continued their vigilant monitoring of the patient, they observed a notable change in the patient's status. Over the next 24 hours, the patient's respiratory effort began to increase, with a respiratory rate rising to 24 breaths per minute. Auscultation revealed fine crackles at the lung bases, suggesting a progression of fluid overload. Concurrently, the patient's oxygen saturation decreased further to 92% on room air, warranting the initiation of supplemental oxygen at 2 liters per minute via nasal cannula to maintain adequate oxygenation.

Laboratory tests were promptly repeated, revealing that while serum sodium had increased further to 130 mEq/L, indicative of ongoing improvement of hyponatremia, the patient's serum osmolality remained low at 270 mOsm/kg, and BUN had decreased to 8 mg/dL. These findings suggested dilutional effects consistent with the fluid overload. The decision was made to continue the loop diuretic therapy at an adjusted dose, carefully balancing the risks of over-diuresis and the potential for further electrolyte imbalances.

The interdisciplinary team reconvened to evaluate the patient's evolving condition. The nephrology consultant emphasized the importance of maintaining a cautious approach to sodium correction, as the risk of central pontine myelinolysis remains a concern. Meanwhile, the neurology team noted that, while the patient's confusion had not worsened, it had not significantly improved, prompting a discussion on whether to pursue additional neurological imaging or assessments. The team's strategic focus remained on fine-tuning fluid management to mitigate the risk of pulmonary edema while ensuring the patient’s neurological status continued to trend towards stabilization. This evolving clinical picture underscored the importance of continuous, dynamic reassessment and collaborative care in managing the complexities of SIADH.

Section 5

As the nursing team proceeded with their vigilant care, they noted that the patient's respiratory status remained a key concern. Despite the initiation of supplemental oxygen, the patient's oxygen saturation showed only marginal improvement, fluctuating between 92% and 94%. Additionally, the respiratory rate slightly increased to 26 breaths per minute, and the fine crackles heard during auscultation became more pronounced. This raised the suspicion of worsening pulmonary edema, prompting an urgent review of the patient's fluid balance and diuretic therapy.

A chest X-ray was ordered and revealed mild bilateral pulmonary infiltrates, consistent with fluid overload. This finding prompted the team to re-evaluate the patient's fluid management strategy. The nephrology consultant recommended a cautious escalation of loop diuretic dosage to enhance diuresis while closely monitoring electrolyte levels to prevent complications such as hypokalemia. Concurrently, the decision was made to restrict fluid intake further, setting a limit of 800 mL per day, to assist in managing the fluid overload more effectively.

The interdisciplinary team remained focused on the delicate balance of correcting the patient's electrolyte disturbances and managing fluid status. While the patient's serum sodium level showed a gradual improvement, now at 132 mEq/L, the team stayed vigilant for any signs of neurological changes. The neurology team was consulted to assess whether any subtle changes in cognitive function could be attributed to the ongoing treatment or if they warranted further investigation. This strategic approach underscored the complexity of managing SIADH, highlighting the need for continuous assessment and adjustment of the treatment plan to address emerging complications effectively.