Borederline personality disorder - Nursing Case Study

Pathophysiology

• Primary mechanism: Abnormalities in brain structure and function, specifically areas that regulate emotions and impulse control, like the amygdala, hippocampus and frontal lobes. This leads to emotional instability, impulsivity and erratic behavior.

• Secondary mechanism: Imbalance in neurotransmitter systems (serotonin, dopamine, noradrenaline), contributing to mood swings, aggression, self-harm, and suicidal tendencies.

• Key complication: Chronic feelings of emptiness and fear of abandonment lead to unstable relationships, self-damaging behavior, and identity disturbance, increasing risk of suicide and comorbid psychiatric disorders.

Patient Profile

Demographics:

34, Female, Unemployed due to disability

History:

• Diagnosed with Borderline Personality Disorder at age 24; history of severe depression, panic disorder, and substance abuse (alcohol, cocaine)

• Current medications: Quetiapine, Topiramate, Fluoxetine, Clonazepam

• Allergies: Penicillin, Ibuprofen

Current Presentation:

• Chief complaint: Intense mood swings, suicidal ideation, self-harming behavior, frequent panic attacks

• Key symptoms: Extreme emotional instability, chronic feelings of emptiness, intense fear of abandonment, impulsive and risky behavior, unstable self-image, explosive anger, dissociative symptoms, difficulty controlling emotions

• Vital signs: Blood pressure 145/90 mmHg, heart rate 120 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 95% on room air

Section 1

Change in Patient Status:

The patient's condition deteriorated over the next 24 hours, characterized by an increased frequency of panic attacks and escalating self-harming behavior. Despite the administration of Clonazepam, the patient's anxiety remained uncontrolled, with a reported subjective rating of 9/10. Her blood pressure rose to 160/100 mmHg, heart rate increased to 130 bpm, and respiratory rate escalated to 26 breaths per minute. Oxygen saturation dropped to 93% on room air and the temperature spiked to 99.5°F.

Additionally, she began to exhibit signs of severe depression and an increased intensity of suicidal ideation. She showed an increased lack of interest in her surroundings, refused meals, and exhibited slow speech and delayed responses during interaction. She expressed feelings of hopelessness, worthlessness, and a persistent desire to die. She also reported experiencing hallucinations, claiming to hear voices telling her to harm herself. Her Glasgow Coma Scale (GCS) score was 14, indicating slight disorientation. Moreover, her pupils were noted to be dilated, indicative of possible substance use relapse, which she denied when questioned. Her urine toxicology screen has been sent and results are pending. The escalating severity of her symptoms suggests the need for immediate intervention and possibly a revision of her treatment plan.

Section 2

Change in Patient Status:

Despite the administration of a higher dosage of Clonazepam, her symptoms did not seem to improve. On the contrary, her anxiety escalated further, with her subjective rating rising to 10/10. Her vital signs continued to show signs of worsening; her blood pressure increased to 175/105 mmHg, heart rate spiked to 145 bpm, and respiratory rate was at 30 breaths per minute. Her oxygen saturation dropped further to 89% on room air, and she developed a fever of 101.3°F, suggesting a possible infection.

Alongside, her depressive symptoms also intensified. She continued refusing meals and showed further regression in her interactions. She was persistently tearful and expressed a heightened desire to die. She started seeing visual hallucinations along with auditory ones, which she described as 'demons' telling her to hurt herself. The GCS dropped to 13, indicating a worsening cognitive function. The patient’s responses to questioning were inconsistent, and she appeared increasingly agitated and confused. Her pupils were still dilated and the possibility of a substance use relapse could not be ruled out. The results from her urine toxicology screen returned positive for opioids, contradicting her earlier denial of substance use. This new development necessitates an immediate reconsideration of her treatment plan, given the complexity of managing her dual diagnosis of Borderline Personality Disorder and Substance Use Disorder.

Section 3

Change in Patient Status:

Despite our attempts to stabilize her, the patient's condition began to deteriorate rapidly. Her blood pressure increased to 190/110 mmHg, heart rate accelerated to 160 bpm, and her respiratory rate escalated to 36 breaths per minute. Her oxygen saturation levels continued to drop, now at 86% on room air, and her fever persisted at 101.5°F. Symptoms of a possible systemic infection were becoming more apparent - her white blood cell count was elevated (16,000 per mm3) with a left shift, and her procalcitonin levels were high (2.0 ng/mL). Blood cultures were ordered immediately to identify the source of infection.

Her cognitive and mental status also continued to decline. She became increasingly unresponsive and her GCS score dropped further to 11. She described her hallucinations as becoming more vivid and frightening, and her suicidal ideation increased in intensity. An urgent CT scan of the brain was ordered to rule out any possible neurological abnormalities. Concurrently, her opioid withdrawal symptoms worsened, marked by increasing agitation, severe muscle aches, profuse sweating, and tremors. This complex clinical scenario calls for a comprehensive, multisystem approach, with close monitoring and prompt interventions to manage her deteriorating physical and mental health conditions.

Section 4

New Diagnostic Results:

The results from the CT scan revealed cerebral edema without any evidence of a mass lesion or hemorrhage. Her blood cultures grew gram-negative bacilli, indicative of a systemic bacterial infection. Furthermore, her liver function tests showed elevated transaminases (ALT 150 U/L and AST 180 U/L) suggesting possible acute liver injury, a complication that could be attributed to the sepsis, drug toxicity, or both. Her D-dimer was also elevated (900 ng/mL), raising the concern for a possible thromboembolic event.

An urgent MRI was ordered to better visualize the extent of cerebral edema and a venous Doppler of her lower extremities was scheduled to rule out deep vein thrombosis. Meanwhile, her worsening sepsis and potential liver injury demanded immediate broad-spectrum antibiotics and careful monitoring of her liver enzymes. The escalating opioid withdrawal symptoms added another layer of complexity, requiring a delicate balance of her withdrawal management in the context of her unstable medical condition. This complex scenario necessitated a critical evaluation of her condition and a prompt, individualized intervention plan.

Section 5

Change in Patient Status:

As the patient's clinical picture grew increasingly complex, a sharp decline in her neurological status was noted overnight. She became lethargic with a Glasgow Coma Scale (GCS) score dropping to 10 from her previous score of 15 - a significant decrease indicating worsening cerebral edema. Her blood pressure escalated to a hypertensive crisis level of 180/110 mmHg, possibly due to the stress of her systemic infection and opioid withdrawal. Her oxygen saturation also dipped to 88% on room air, necessitating supplemental oxygen.

The patient's jaundice intensified, and her abdominal examination revealed a palpable, tender liver edge, suggestive of hepatomegaly. Her latest lab results showed a further increase in transaminases (ALT 200 U/L and AST 250 U/L) and a rising total bilirubin (3.5 mg/dL), indicating a worsening liver function. Her sepsis-induced coagulopathy was evident with a prolonged prothrombin time (PT) of 18 seconds and a partial thromboplastin time (PTT) of 45 seconds, both above the normal range. Her worsening clinical status necessitated an immediate reevaluation of her treatment plan and a multidisciplinary approach to manage her complex condition.