Subarachnoid Hemorrhage Secondary to Mechanical Fall. 90 year old male that arrived to the ER from neurology clinic. longstanding known history of falls. Patient in ED for abcess to shoulder. Placed in fast track area. Went to bathroom without assistance, fell resulting in subarachnoid hemmorhage. - Nursing Case Study

Pathophysiology

• Primary mechanism: The mechanical fall caused a sudden acceleration-deceleration impact, leading to a rupture of cerebral blood vessels in the subarachnoid space, resulting in bleeding between the arachnoid membrane and the pia mater.

• Secondary mechanism: The bleeding increases intracranial pressure, which can disrupt normal cerebral blood flow and lead to further neuronal injury due to ischemia or compression.

• Key complication: The accumulation of blood in the subarachnoid space can cause irritation and inflammation of the meninges, potentially leading to vasospasm, further increasing the risk of cerebral ischemia and subsequent neurological deficits.

Patient Profile

Demographics:

90-year-old male, retired

History:

• History of frequent falls, hypertension, and osteoarthritis

• Current medications: Lisinopril, Acetaminophen, and Vitamin D supplements

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Fall resulting in subarachnoid hemorrhage

• Key symptoms: Headache, confusion, dizziness, and weakness on one side

• Vital signs: Blood pressure 160/95 mmHg, heart rate 98 bpm, respiratory rate 22 breaths per minute, temperature 37.8°C (100°F)

Section 1

As the medical team continued to monitor the patient, a change in his status became evident. Over the course of several hours, the patient began to exhibit increasing confusion and agitation, a sign that the intracranial pressure might be escalating. His headache intensified, and he started to develop a decreased level of consciousness, becoming less responsive to verbal stimuli. These changes prompted an urgent re-evaluation by the neurology team.

A repeat CT scan of the head was ordered to assess the progression of the subarachnoid hemorrhage. The imaging revealed an increase in the volume of blood in the subarachnoid space, suggesting that the bleeding had not yet stabilized. This finding was concerning for the potential development of cerebral vasospasm, a common and serious complication that could further compromise cerebral perfusion and exacerbate neurological deficits. In response, the team initiated nimodipine therapy, a calcium channel blocker, to help prevent vasospasm and mitigate the risk of secondary ischemic injury.

Laboratory results showed a mild hyponatremia, with the sodium level at 133 mmol/L, likely resulting from a syndrome of inappropriate antidiuretic hormone secretion (SIADH), a condition that can occur following subarachnoid hemorrhage. This electrolyte imbalance required careful correction to avoid exacerbating cerebral edema. The medical team implemented fluid restriction and closely monitored the patient's electrolyte levels to prevent further complications. This evolving clinical picture highlighted the complexity of managing subarachnoid hemorrhage in an elderly patient with multiple comorbidities, underscoring the need for vigilant monitoring and timely interventions. The next steps in the patient's care would focus on continued stabilization, prevention of further complications, and consideration of rehabilitation needs.

Section 2

As the medical team continued to manage the patient's condition, they closely monitored his response to the interventions, particularly the nimodipine therapy initiated to prevent cerebral vasospasm. Over the next 24 hours, the patient's vital signs showed some stabilization, with blood pressure readings normalizing at an average of 135/75 mmHg and heart rate maintaining at around 80 beats per minute. However, clinical assessment revealed that while the patient was no longer agitated, his level of consciousness remained diminished. The patient scored a Glasgow Coma Scale (GCS) of 9, indicating moderate impairment, and he continued to exhibit sluggish pupil reactions and mild right-sided weakness, necessitating further neurological evaluation.

In addition to the neurological concerns, the fluid restriction and careful electrolyte management began to show positive effects on the patient's hyponatremia. Sodium levels improved to 135 mmol/L, within the low-normal range, suggesting a stabilization of the SIADH. Despite this progress, the medical team remained cautious, as the risk of cerebral edema persisted, requiring ongoing vigilance in fluid and electrolyte balance. The team also initiated physical therapy consultations to assess the patient's mobility and potential for rehabilitation, recognizing the importance of early intervention in preventing complications associated with prolonged immobility, such as deep vein thrombosis or pressure ulcers.

This combination of clinical observations and responses to treatment underscored the complexity of the patient's condition. The team prepared for potential adjustments in the treatment plan, considering the need for possible escalation of care if the patient's neurological status failed to improve. The next phase of the patient's journey would focus on whether the stabilization observed would lead to cognitive and functional recovery, or if further interventions would be necessary to manage emerging complications. This ongoing assessment was crucial in forming a comprehensive, multidisciplinary approach to the patient's rehabilitation and overall care trajectory.

Section 3

As the medical team continued to monitor the 90-year-old patient, a significant change in his status was observed. Around 36 hours post-admission, the patient began to exhibit signs of increased intracranial pressure (ICP). His Glasgow Coma Scale (GCS) score dropped to 7, indicating a decline in his neurological status. In conjunction with the diminished consciousness, his pupils became more anisocoric, with the right pupil now sluggish and larger than the left. The patient's blood pressure increased to 160/90 mmHg, and his heart rate rose to 95 beats per minute, suggesting a Cushing's response indicative of rising ICP. These changes prompted the medical team to conduct an urgent CT scan to assess for potential complications such as cerebral edema or worsening hemorrhage.

The CT scan revealed a slight expansion of the subarachnoid hemorrhage with early signs of cerebral edema, raising concerns about the possibility of herniation if not addressed promptly. In response to these findings, the medical team initiated osmotherapy with mannitol to reduce the elevated ICP and adjusted the patient's positioning to optimize venous drainage. Additionally, they increased the frequency of neurological checks to every hour and consulted with the neurosurgery team for potential surgical intervention should the conservative measures fail to stabilize the patient's condition.

This development highlighted the critical need for ongoing, dynamic assessment and intervention. The medical team was now tasked with balancing the management of the patient's ICP while continuing to support his overall recovery. They also faced the challenge of maintaining vigilance for other potential complications such as seizures or further electrolyte imbalances. This phase of the patient's care underscored the necessity of a multidisciplinary approach, integrating neurology, neurosurgery, and critical care to navigate the complexities of his condition and optimize his outcomes.

Section 4

As the medical team closely monitored the patient’s response to the interventions, they began to observe a change in his status approximately 48 hours post-admission. Despite the administration of mannitol and optimized positioning, the patient’s intracranial pressure remained elevated, and his GCS showed minimal improvement, fluctuating between 7 and 8. His vital signs indicated an ongoing sympathetic response, with blood pressure persistently elevated at 165/92 mmHg and a heart rate that had increased further to 102 beats per minute. In addition to these findings, the patient began to exhibit irregular breathing patterns, characterized by periods of deep, rapid respirations followed by pauses, known as Cheyne-Stokes respiration.

Given these developments, the medical team decided to perform another CT scan to evaluate any progression of cerebral edema or hemorrhage. The new imaging revealed a slight increase in cerebral edema and the development of a small midline shift, suggesting an increased risk of potential brain herniation. Concurrently, laboratory results returned, showing a sodium level of 132 mEq/L, indicating a mild hyponatremia, which could further complicate the patient’s neurological status. In light of these findings, the neurology and neurosurgery teams convened to discuss the possibility of surgical intervention to alleviate the intracranial pressure, while also considering the risk-benefit ratio given the patient’s advanced age and overall frailty.

This change in the patient's condition emphasized the need for swift and decisive action. The medical team was now faced with the challenge of preventing imminent complications such as herniation while managing the underlying causes of the increased ICP. This situation called for a thorough reassessment of the patient’s treatment plan, including the potential adjustment of osmotherapy, consideration of hypertonic saline for sodium correction, and exploring surgical options. The unfolding scenario underscored the critical role of timely diagnostics and the importance of a proactive, multidisciplinary approach in managing complex patient cases.

Section 5

As the neurology and neurosurgery teams deliberated on the best course of action, the patient's condition necessitated immediate attention to his electrolyte imbalance. The decision was made to initiate a carefully monitored administration of hypertonic saline to correct the mild hyponatremia and potentially reduce cerebral edema. The patient was transferred to the intensive care unit for closer observation and management, where continuous cardiac monitoring and frequent neurological assessments were implemented.

Within hours of the hypertonic saline intervention, the patient's sodium levels began to stabilize, rising to 135 mEq/L. However, the patient's neurological status remained largely unchanged, with his Glasgow Coma Scale (GCS) score persisting at 8. His blood pressure showed slight improvement, decreasing to 158/88 mmHg, but his heart rate continued to hover around 100 beats per minute. Despite the sodium correction, the patient continued to exhibit Cheyne-Stokes respiration, prompting concerns about the potential deterioration of his respiratory function.

As the medical team processed these developments, they remained vigilant for signs of further neurological decline. A decision was made to prepare for a potential decompressive craniectomy should the patient's intracranial pressure continue to rise despite medical management. This proactive stance was crucial, as the slight midline shift observed on the CT scan posed an imminent risk of brain herniation. The team recognized the delicate balance between aggressive intervention and the patient's overall prognosis, emphasizing the necessity of constant communication and collaboration among the multidisciplinary team to navigate the complexities of the patient's evolving condition.