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A client is admitted to the neurological intensive care unit after having just sustained a C5 spinal cord injury (SCI). Which assessment finding for this client warrants immediate intervention by the nurse?

A.

Respirations are shallow, labored, and 14 breaths/minute.

B.

Has flaccid upper and lower extremities.

C.

Blood pressure is 110/70 mm Hg and the apical heart rate is 68 beats/minute.

D.

Is unable to feel sensation in the arms and hands.

Answer and Explanation

The Correct Answer is A

A. Respirations are shallow, labored, and 14 breaths/minute. A C5 spinal cord injury can impair diaphragmatic function and respiratory effort, leading to respiratory failure. Shallow and labored breathing suggests that the client is experiencing respiratory compromise, which can quickly progress to hypoventilation, hypoxia, and respiratory arrest. Immediate intervention, such as assisted ventilation or intubation, may be necessary to maintain adequate oxygenation and prevent further complications.
B. Has flaccid upper and lower extremities. Flaccid paralysis is an expected finding immediately after a high spinal cord injury due to spinal shock. While this condition requires ongoing monitoring, it is not an immediate life-threatening emergency like respiratory distress.
C. Blood pressure is 110/70 mm Hg and the apical heart rate is 68 beats/minute. These vital signs are within normal limits and do not indicate hemodynamic instability. Neurogenic shock, which can occur with high spinal injuries, typically presents with hypotension and bradycardia, but this client’s current BP and HR are stable.
D. Is unable to feel sensation in the arms and hands. Loss of sensation is expected with a cervical spinal cord injury due to nerve pathway disruption. While this finding is significant, it does not require immediate intervention compared to respiratory distress, which is the most urgent priority.
 


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Related Questions

Correct Answer is {"A":{"answers":"A"},"B":{"answers":"B"},"C":{"answers":"C"},"D":{"answers":"A"},"E":{"answers":"B"}}

Explanation

  • Increase the fraction of inspired oxygen (FiO₂). The client has severe COVID pneumonia and is on mechanical ventilation with high inspiratory pressures, suggesting acute respiratory distress syndrome (ARDS). Increasing FiO₂ is indicated if oxygenation is inadequate (e.g., low PaO₂ or SpO₂). However, oxygen toxicity should be avoided, so adjustments should be made based on arterial blood gases (ABGs) and oxygen saturation.
  • Collect equipment for a needle aspiration. Needle aspiration is typically used for pneumothorax management, but there is no mention of clinical signs such as sudden hypotension, absent breath sounds, or tracheal deviation. While ventilated COVID-19 patients are at risk for barotrauma, this procedure is not justified without evidence of pneumothorax.
  • Replace the ventilator. There is no indication that the ventilator is malfunctioning or that the settings are inappropriate. If ventilation issues arise (e.g., high plateau pressures, auto-PEEP, or ventilator asynchrony), adjustments to settings, sedation, or lung-protective strategies should be considered before replacing the ventilator.
  • Measure the nasogastric tube output. The client is intubated and sedated, meaning they cannot protect their airway or tolerate oral intake. A nasogastric (NG) tube is commonly placed for gastric decompression and feeding. Monitoring NG output is essential to assess for gastrointestinal bleeding, ileus, or high residual volumes, which can affect feeding tolerance.
  • Place the client in Trendelenburg. The Trendelenburg position increases the risk of aspiration, impairs lung expansion, and worsens ventilation-perfusion mismatch, especially in ARDS patients. Instead, prone positioning is often preferred in severe COVID pneumonia to improve oxygenation and alveolar recruitment.

Correct Answer is {"dropdown-group-1":"B","dropdown-group-2":"D"}

Explanation

  • Compensated respiratory acidosis occurs when the lungs retain CO₂, causing acidosis, but the kidneys compensate by increasing bicarbonate (HCO₃⁻) levels. In this case, the pH is low, and the PaCO₂ is within normal limits, which does not indicate a respiratory issue or compensation. Compensation would require an elevated HCO₃⁻, which is not provided in the lab results.
  • Compensated metabolic acidosis would require a low pH with a decreased PaCO₂, as the respiratory system compensates by increasing ventilation (hyperventilation) to "blow off" CO₂. Since the PaCO₂ in this case is within normal limits, no significant respiratory compensation has occurred yet, making this uncompensated metabolic acidosis instead.
  • Uncompensated respiratory acidosis would present with a low pH and an elevated PaCO₂ (>45 mmHg) due to inadequate ventilation and CO₂ retention. Since the PaCO₂ here is 37 mmHg (within normal range), respiratory acidosis is unlikely. The metabolic component, rather than a respiratory problem, is driving the acidosis.
  • Uncompensated metabolic acidosis is characterized by a low pH (7.23) and a normal PaCO₂ (37 mmHg), indicating a primary metabolic problem without sufficient respiratory compensation. In diabetic ketoacidosis (DKA), the lack of insulin results in fat breakdown and ketone production, leading to a drop in pH and metabolic acidosis. This client likely has DKA due to their history of type 1 diabetes and the lack of insulin administration.
  • Kussmaul respirations are a compensatory response to metabolic acidosis, seen in conditions like DKA. However, they do not cause acidosis; instead, they are the body's attempt to correct it by exhaling CO₂. Since the ABG shows normal PaCO₂, there is no strong evidence of hyperventilation, suggesting compensation has not yet occurred.
  • Starvation can lead to ketoacidosis due to prolonged fasting and fat metabolism, producing ketones. However, in type 1 diabetes, the primary issue is no insulin production, not caloric deprivation. The severity of metabolic acidosis in this client is more likely due to insulin deficiency rather than starvation.
  • Tissue hypoxia leads to lactic acidosis, which results from anaerobic metabolism. This can be seen in conditions like sepsis or shock. However, in this case, the client has type 1 diabetes, and the more likely cause of acidosis is ketoacidosis due to insulin deficiency rather than hypoxia.
  • A lack of insulin in type 1 diabetes prevents glucose uptake, forcing the body to break down fat, leading to ketone formation and metabolic acidosis. This matches the clinical scenario of a patient with a history of type 1 diabetes, hyperglycemia >500 mg/dL, and metabolic acidosis.

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