PATIENT ADMITTED WITH SEIZURE - Nursing Case Study

Pathophysiology

• Primary mechanism: Imbalance between excitatory and inhibitory neurotransmission leads to excessive neuronal firing. The primary excitatory neurotransmitter, glutamate, becomes overly active, while inhibitory signals via GABA are deficient, disrupting normal brain function.

• Secondary mechanism: Altered ion channel function, particularly sodium, calcium, and potassium channels, causes abnormal electrical activity. This dysregulation can result from genetic mutations or acquired changes, contributing to the hyperexcitability of neurons.

• Key complication: Uncontrolled seizures can lead to neuronal injury and potential progression to status epilepticus, a life-threatening condition requiring immediate medical intervention.

Patient Profile

Demographics:

35-year-old male, software engineer

History:

• Key past medical history: Epilepsy diagnosed 5 years ago, hypertension

• Current medications: Levetiracetam, Lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Seizure episode

• Key symptoms: Generalized tonic-clonic seizures, confusion, fatigue, headache

• Vital signs: Blood pressure 150/95 mmHg, heart rate 110 bpm, respiratory rate 22 breaths per minute, temperature 37.8°C, oxygen saturation 94% on room air

Section 1

Change in patient status:

During the second day of hospitalization, the patient experiences a change in status that raises concern among the healthcare team. Despite initial stabilization, he begins exhibiting subtle signs of neurological deterioration. Nurses note that he is becoming increasingly lethargic and disoriented, struggling to follow simple commands. His speech becomes slurred, and he demonstrates a new onset of right-sided weakness. Repeat vital signs show a persistent elevation in blood pressure at 160/100 mmHg, a heart rate that has increased to 120 bpm, and oxygen saturation that has dropped slightly to 92% on room air. These changes suggest potential complications, such as a possible postictal state or evolving neurological event, necessitating further evaluation.

The attending physician orders an urgent CT scan of the brain to rule out any acute intracranial pathology, such as hemorrhage or cerebral edema, that might explain the neurological changes. Additionally, electrolyte levels are reassessed given the potential impact of imbalances on seizure activity and neurological function. The results reveal hyponatremia with a sodium level of 128 mEq/L, which could be contributing to the patient's altered mental status and increased seizure susceptibility. This electrolyte disturbance may be related to the use of levetiracetam, which has been known in some cases to affect sodium balance.

The healthcare team is now faced with the challenge of addressing both the immediate neurologic changes and the underlying electrolyte imbalance. They initiate a cautious correction of the hyponatremia to avoid rapid shifts that could provoke further seizures or cerebral complications. The scenario emphasizes the importance of continuous monitoring and reassessment in patients with epilepsy, recognizing that even well-managed conditions can experience significant fluctuations that require timely intervention.

Section 2

As the healthcare team works to address the patient's hyponatremia with careful infusion of hypertonic saline, the patient’s neurological status is closely monitored. However, despite these efforts, the patient begins to exhibit further deterioration. He becomes increasingly difficult to arouse, requiring a painful stimulus to elicit any response. The right-sided weakness progresses to a complete hemiparesis, and his speech is reduced to incoherent mumbling. Repeat vital signs indicate continued hypertension with a blood pressure of 170/105 mmHg, a heart rate that has risen further to 130 bpm, and oxygen saturation that has decreased to 90% on room air. These alarming signs suggest worsening cerebral pathology.

A follow-up CT scan reveals evidence of cerebral edema, particularly in the left hemisphere, which correlates with the patient's right-sided weakness. This finding suggests that the initial seizure may have been more severe than previously appreciated, leading to complications such as increased intracranial pressure. Additionally, the persistence of hyponatremia, now slightly improved to 130 mEq/L, continues to be a concern as it can exacerbate cerebral edema. The multidisciplinary team, including neurology and nephrology consultants, is convened to develop an integrated management plan that addresses both the neurological and electrolyte challenges.

The team decides to escalate care by transferring the patient to the intensive care unit for closer monitoring and potential intervention. They implement strategies to reduce cerebral edema, including elevating the head of the bed, administering mannitol, and considering hypertonic saline boluses. The patient's fluid status is meticulously managed to avoid exacerbating the hyponatremia while addressing the cerebral swelling. The unfolding complexity of this case underscores the critical importance of dynamic clinical reasoning, as each new development requires reevaluation and adjustment of the therapeutic approach. As the patient's condition is stabilized, the healthcare team remains vigilant for new complications that may arise on this challenging clinical journey.

Section 3

As the patient settles into the intensive care unit, the healthcare team maintains a careful watch over his evolving condition. Despite the initial interventions, there is a notable change in the patient’s status. Over the next few hours, his neurological function continues to decline. The patient becomes unresponsive to verbal commands and only responds minimally to painful stimuli. GCS has decreased to 6, confirming a significant deterioration in his level of consciousness. His vital signs remain concerning, with a blood pressure of 165/100 mmHg, heart rate elevated at 135 bpm, and oxygen saturation dropping further to 88% despite supplemental oxygen. These clinical indicators suggest a potentially worsening cerebral insult.

New diagnostic results reveal further complexities. A repeat CT scan shows not only persistent cerebral edema but also a midline shift of 5 mm, indicating increased intracranial pressure and potential herniation risk. The serum sodium level has improved marginally to 132 mEq/L, but the patient’s condition raises suspicion for additional complications such as a possible intracerebral hemorrhage or an evolving ischemic stroke, given his rapid neurological decline. Arterial blood gas analysis shows a respiratory acidosis with a pH of 7.28, PaCO2 of 55 mmHg, and bicarbonate of 24 mEq/L, reflecting insufficient ventilation, likely due to decreased neurological drive.

In response to these developments, the multidisciplinary team intensifies their approach. They initiate mechanical ventilation to manage the respiratory acidosis and ensure adequate oxygenation. Mannitol and hypertonic saline are adjusted to optimize the patient's osmolar balance and reduce intracranial pressure. The team also contemplates the need for surgical intervention, such as decompressive craniectomy, given the risk of herniation. Continuous EEG monitoring is set up to detect any subclinical seizure activity that may further compromise the patient's cerebral function. This phase of care demands precise clinical reasoning, as the team must balance aggressive management of cerebral edema with the risks of rapid osmotic shifts, while vigilantly monitoring for new complications that could alter the course of treatment.

Section 4

As the healthcare team continues to closely monitor the patient, a shift in his status becomes apparent, necessitating immediate re-evaluation of their strategies. Despite the aggressive interventions to control intracranial pressure, the patient's neurological status further deteriorates. His Glasgow Coma Scale (GCS) score has now dropped to 4, with no eye-opening response and decerebrate posturing observed in response to painful stimuli. These findings suggest a worsening brain injury and an increasing risk of brainstem involvement.

Concurrently, new diagnostic results reveal an alarming development. An urgent MRI scan identifies a small intracerebral hemorrhage in the left temporal lobe, likely exacerbating the cerebral edema and contributing to the midline shift. The presence of the hemorrhage complicates the management plan, as it introduces the risk of expansion with aggressive osmotic therapy. Additionally, laboratory tests indicate a worsening electrolyte imbalance, with serum sodium dropping to 128 mEq/L, raising concerns for hyponatremia-induced cerebral edema.

In response to these complications, the team pivots their approach to stabilize the patient. The neurosurgical team is consulted for an emergent decompressive craniectomy, a decision necessitated by the cumulative evidence of increased intracranial pressure and herniation risk. The medical team adjusts the hypertonic saline infusion to cautiously correct the hyponatremia, aiming for a gradual increase in serum sodium to avoid osmotic demyelination syndrome. Meanwhile, the patient remains on mechanical ventilation, with adjustments made to optimize ventilation parameters and address the ongoing respiratory acidosis. As the team implements these critical interventions, they remain vigilant for further neurological decline or cardiovascular instability, which would demand rapid reassessment and adaptation of the treatment strategy.

Section 5

As the healthcare team monitors the patient's response to the interventions, they observe a change in his status that prompts further action. After the decompressive craniectomy, the patient's intracranial pressure shows a modest decrease, yet his neurological status remains critical. His Glasgow Coma Scale score remains unchanged at 4, and the decerebrate posturing persists, indicating severe neurological impairment. Continuous EEG monitoring reveals intermittent bursts of epileptiform activity, suggesting ongoing subclinical seizures that could further exacerbate the brain injury.

Meanwhile, the patient's vital signs show a concerning trend. His blood pressure has become labile, with fluctuations between hypertensive episodes of 180/110 mmHg and hypotensive readings of 90/60 mmHg, indicating possible autonomic instability. Heart rate remains tachycardic at 120 bpm, and the patient has developed a low-grade fever of 100.4°F (38°C), raising concerns for potential infection or neurogenic fever. The respiratory rate, although supported by mechanical ventilation, is erratic, reflecting the ongoing challenges in maintaining effective gas exchange.

Laboratory results reveal an improvement in serum sodium, now at 132 mEq/L, but the patient develops hyperchloremic metabolic acidosis, with a chloride level of 115 mEq/L and a pH of 7.29. This metabolic derangement complicates the clinical picture, necessitating cautious electrolyte management to prevent further deterioration. The team considers the possibility of renal involvement or an adverse effect of the saline therapy. As these challenges unfold, the healthcare team must reevaluate their therapeutic strategies, balancing the need for aggressive intervention with the potential risks of further destabilizing the patient.