medication error - Nursing Case Study
Pathophysiology
• Primary mechanism: Disruption in drug metabolism due to incorrect dosage can overwhelm the liver's enzymatic pathways, leading to toxic accumulation of the medication in the bloodstream.
• Secondary mechanism: Altered receptor binding occurs when the administered drug interacts with unintended targets, causing adverse effects that can mimic or exacerbate existing conditions.
• Key complication: These mechanisms can lead to organ damage or failure, particularly in vulnerable populations like the elderly or those with pre-existing liver or kidney conditions, necessitating vigilant monitoring and timely intervention.
Patient Profile
Demographics:
45-year-old female, registered nurse
History:
• Key past medical history: Hypertension, Type 2 Diabetes
• Current medications: Lisinopril 20 mg daily, Metformin 500 mg twice daily
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Dizziness and shortness of breath
• Key symptoms: Palpitations, nausea, mild chest discomfort
• Vital signs: Blood pressure 95/60 mmHg, heart rate 110 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 92% on room air
Section 1
New Diagnostic Results:
Following the initial assessment, the medical team decided to conduct a series of diagnostic tests to determine the underlying cause of the patient's symptoms, given her history of medication use and chronic conditions. The primary concern was a potential medication error leading to an overdose or adverse drug reaction. Blood tests revealed elevated serum levels of Lisinopril, suggesting that the patient may have inadvertently taken a higher dose than prescribed. This was further supported by her low blood pressure of 95/60 mmHg and elevated heart rate of 110 bpm, both of which are consistent with Lisinopril's pharmacological effects at higher doses.
Additionally, the laboratory results indicated slightly elevated liver enzymes, which raised concerns about hepatic stress or dysfunction. The patient's renal function tests, including BUN and creatinine levels, were within normal limits, reducing the immediate concern for acute kidney injury. An ECG was performed to assess the chest discomfort and palpitations, revealing sinus tachycardia but no significant ischemic changes. Given her oxygen saturation of 92% on room air, a chest X-ray was obtained to rule out pulmonary causes for her symptoms, which showed no acute abnormalities.
These findings highlight the need to address the potential Lisinopril overdose and its systemic effects. The clinical team considered holding the Lisinopril dose and closely monitoring the patient's blood pressure and heart rate. The elevated liver enzymes warranted further evaluation to prevent progression to more severe hepatic complications. The team planned to recheck liver function tests in 24 hours and assess the need for additional interventions based on the patient's ongoing clinical status. This approach required careful monitoring and reassessment to prevent further complications and ensure a safe recovery.
Section 2
As the clinical team continued to monitor the patient, a notable change in her status was observed. Approximately 12 hours after the decision to hold the Lisinopril dose, the patient began to exhibit signs of increasing fatigue and confusion. Her blood pressure remained low at 90/58 mmHg, and her heart rate increased to 115 bpm. Despite these concerning cardiovascular parameters, the patient reported mild improvement in her chest discomfort. However, her oxygen saturation dropped further to 89% on room air, prompting the initiation of supplemental oxygen to maintain adequate oxygenation.
A repeat set of liver function tests showed a further increase in liver enzymes, with ALT rising to 85 U/L and AST to 90 U/L, indicating possible worsening hepatic stress. This prompted the team to consider additional causes of liver dysfunction beyond the potential Lisinopril overdose, such as drug-induced liver injury or exacerbation of a pre-existing liver condition. The patient's mental status changes also raised concerns about hepatic encephalopathy, requiring close neurological monitoring and consideration of further diagnostic imaging or consultation with a hepatologist for expert guidance.
In response to these developments, the clinical team initiated a more comprehensive assessment to address the multifactorial nature of the patient's condition. This included evaluating her medication regimen for any other potential hepatotoxic agents, reviewing her dietary intake and fluid balance, and considering the role of her chronic conditions in the current presentation. The team emphasized the importance of ongoing communication with the patient and her family to ensure a thorough understanding of the evolving clinical picture and to guide shared decision-making for future interventions. This approach aimed to stabilize the patient's condition while preventing further complications, paving the way for a thoughtful and deliberate plan of care.
Section 3
As the team delved deeper into the assessment, they prioritized a thorough review of the patient's medication history and potential interactions. A pharmacy consult was called to evaluate any hepatotoxic agents that might have contributed to the liver enzyme elevation. Notably, the patient had been taking acetaminophen for chronic pain management, raising concerns about cumulative hepatotoxicity, especially in the context of her existing liver dysfunction. The team decided to discontinue acetaminophen and explore alternative pain management strategies to mitigate further liver stress.
Simultaneously, the patient underwent an abdominal ultrasound to assess liver architecture and blood flow, which revealed mild hepatic steatosis but no significant obstruction or focal lesions. This finding, coupled with the elevated liver enzymes and altered mental status, reinforced the suspicion of hepatic encephalopathy. Subsequently, lactulose was initiated to help reduce ammonia levels, targeting the neurological symptoms. The patient’s fluid balance was meticulously monitored, given her low blood pressure and the potential for fluid shifts affecting hepatic and renal function.
Over the next 24 hours, the patient’s condition showed a mixed response. Her oxygen saturation improved with supplemental oxygen, stabilizing at 93%, and her confusion began to resolve slightly, suggesting a positive response to lactulose. However, her blood pressure remained low, now at 88/56 mmHg, despite cautious fluid resuscitation. The heart rate persisted at 112 bpm, indicating ongoing cardiovascular stress. These findings prompted a reevaluation of her cardiovascular status, considering potential underlying issues such as adrenal insufficiency or autonomic dysfunction. The team prepared to conduct further endocrine assessments, ensuring a comprehensive approach to unravel the multifaceted nature of her clinical deterioration while maintaining open communication with the patient’s family about the evolving plan of care.
Section 4
As the team continued to monitor the patient's progress, new diagnostic results revealed significant insights into her condition. The recent laboratory tests indicated a marked increase in ammonia levels, now at 105 µmol/L, which was concerning despite the initiation of lactulose therapy. Additionally, the latest liver function tests showed further elevation of liver enzymes, with AST at 95 U/L and ALT at 110 U/L. These results suggested ongoing hepatic stress and potential worsening of liver function. Contributing to the clinical picture, the patient's renal function was also beginning to show signs of compromise, with creatinine levels rising to 1.8 mg/dL, suggesting possible hepatorenal syndrome. The team recognized the need for a multidisciplinary approach, including nephrology, to address these evolving complications.
Clinically, the patient's status had changed subtly yet significantly. Although her confusion had slightly improved, she now exhibited mild asterixis during neurological examination, reinforcing the diagnosis of hepatic encephalopathy. Her blood pressure remained low, and lactate levels were elevated at 3.5 mmol/L, indicating a possible shift towards metabolic instability. In response, the team adjusted her fluid management strategy and initiated a low-dose norepinephrine infusion to support her hemodynamics cautiously. This intervention required close monitoring to avoid exacerbating her renal impairment.
The evolving nature of the patient's condition necessitated a re-evaluation of her treatment plan. The team considered the introduction of rifaximin as an adjunct therapy to lactulose, aiming to further reduce ammonia production and absorption. Concurrently, they planned to initiate a low-protein diet to decrease nitrogenous load, considering the delicate balance required in managing her nutritional needs. These steps, combined with ongoing assessments and support from the interdisciplinary team, aimed to stabilize the patient's condition, reduce complications, and ultimately improve her overall prognosis.
Section 5
Response to Interventions
Over the next 48 hours, the healthcare team closely monitored the patient's response to the adjusted treatment regimen. Encouragingly, the combination of lactulose and rifaximin began to show positive effects, reflected by a gradual decrease in ammonia levels, now at 85 µmol/L. Despite this improvement, the patient's liver function continued to deteriorate; AST and ALT levels rose to 110 U/L and 125 U/L, respectively, indicating ongoing hepatic inflammation or injury. The nephrology team, now actively involved, adjusted her fluid management to prevent further renal compromise, yet her creatinine remained elevated at 1.9 mg/dL, underscoring the complexity of her condition.
Clinically, the patient showed mixed responses. Her episodes of confusion decreased, and she was more oriented, a promising sign of improving hepatic encephalopathy. However, her blood pressure remained labile, necessitating careful titration of norepinephrine to maintain adequate perfusion without worsening renal function. Additionally, the patient developed mild tachycardia, with heart rates consistently in the range of 100-110 beats per minute, suggesting a compensatory response to her metabolic demands, possibly exacerbated by the norepinephrine infusion.
The interdisciplinary team recognized that while the interventions were beginning to address some aspects of her condition, new challenges were emerging. They discussed the need for further diagnostic imaging to evaluate the structural integrity of the liver and kidneys, and potential adjustments to her medication regimen to better balance her hemodynamic status. The team also contemplated the possibility of requiring more invasive monitoring or support, such as central venous pressure monitoring or temporary renal replacement therapy, to better manage her complex clinical picture. This careful balancing act between therapeutic interventions and potential complications required ongoing vigilance and adaptation of her care plan.