altered mental status - Nursing Case Study

Pathophysiology

• Primary mechanism: Cerebral hypoperfusion - Reduced blood flow to the brain leads to inadequate oxygen and glucose delivery, impairing neuronal function and causing confusion or stupor. Common in shock or severe dehydration.

• Secondary mechanism: Neurotransmitter imbalance - Disruption in neurotransmitter systems (e.g., dopamine, serotonin) due to metabolic derangements or toxin exposure (e.g., hepatic encephalopathy) alters synaptic transmission, affecting cognition and consciousness.

• Key complication: Increased intracranial pressure - Resulting from trauma, infection, or hemorrhage, can compress brain structures, leading to herniation and potential fatality if unaddressed.

Patient Profile

Demographics:

72-year-old female, retired chemist

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Chronic Kidney Disease Stage 3, Atrial Fibrillation

• Current medications: Metformin, Lisinopril, Warfarin, Metoprolol, Insulin glargine

• Allergies: Penicillin, Sulfa drugs

Current Presentation:

• Chief complaint: Altered mental status

• Key symptoms: Confusion, agitation, slurred speech, disorientation to time and place

• Vital signs: Blood pressure 86/54 mmHg, heart rate 124 bpm, respiratory rate 24 breaths per minute, temperature 101.3°F, oxygen saturation 88% on room air

Section 1

As the medical team initiates the initial assessment for the 72-year-old female patient with altered mental status, several critical findings emerge that require immediate attention. On physical examination, the patient appears lethargic with fluctuating levels of consciousness, failing to respond appropriately to verbal stimuli. Neurological assessment reveals right-sided weakness suggesting possible focal neurological deficit, and pupils are found to be unequal with sluggish reaction to light, raising concern for intracranial pathology. Auscultation of the lungs reveals crackles at the bases, indicating potential pulmonary congestion or infection, possibly contributing to her hypoxemia.

Laboratory results return, revealing significant metabolic derangements: serum glucose is elevated at 320 mg/dL, yet there is evidence of anion gap metabolic acidosis with a bicarbonate level of 14 mEq/L, suggesting possible diabetic ketoacidosis (DKA) despite her type 2 diabetes history. Her serum creatinine is elevated at 2.4 mg/dL, showing a worsening of her chronic kidney disease, potentially exacerbated by dehydration or acute kidney injury. Furthermore, her INR levels are elevated at 3.5, indicating supratherapeutic anticoagulation, which raises the risk of bleeding complications, particularly in the context of her altered mental status and potential for intracranial hemorrhage.

Given these findings, the medical team must employ advanced critical thinking and clinical judgment to prioritize interventions. Immediate actions include stabilizing the patient's hemodynamic status with careful fluid resuscitation, considering her renal impairment, and addressing potential diabetic ketoacidosis with insulin therapy while closely monitoring blood glucose and electrolyte levels. Simultaneously, urgent neuroimaging is warranted to evaluate for intracranial hemorrhage or other acute neurological events. These interventions aim to correct metabolic imbalances, optimize cerebral perfusion, and prevent further neurological deterioration while balancing the risks of her complex medical background.

Section 2

As the medical team proceeds with fluid resuscitation and insulin therapy, the patient’s status is closely monitored. Despite initial interventions, her condition takes a concerning turn. The patient becomes increasingly tachypneic with a respiratory rate climbing to 30 breaths per minute, and her oxygen saturation drops to 88% on room air. A repeat auscultation of her lungs reveals worsening crackles, now extending to the mid-lung fields, suggesting pulmonary edema secondary to aggressive fluid administration in the context of her compromised renal function. Simultaneously, her mental status deteriorates further; she becomes unresponsive to painful stimuli, necessitating immediate intubation and mechanical ventilation to secure the airway and manage her respiratory distress.

Concurrent with these developments, the results of her urgent neuroimaging return, revealing a small left-sided subdural hematoma with surrounding edema, likely exacerbated by her supratherapeutic INR levels. This finding underscores the critical need to reverse her anticoagulation promptly, but given the risk of worsening her metabolic acidosis and renal function, the team must deliberate carefully on the best course of action. The decision is made to administer prothrombin complex concentrate (PCC) for rapid INR reversal, alongside close monitoring of her neurological status and consideration for neurosurgical consultation should her intracranial pressure increase.

As these complications unfold, the patient's laboratory results show a slight improvement in her anion gap metabolic acidosis, with bicarbonate levels rising to 18 mEq/L, indicating a partial response to insulin therapy. However, her renal function continues to decline, as evidenced by a serum creatinine level now at 3.0 mg/dL, necessitating nephrology input for potential renal replacement therapy. The clinical picture is complex, requiring a multidisciplinary approach to manage the evolving challenges while anticipating further complications that may arise from her intertwined medical conditions.

Section 3

As the medical team continues to navigate the complexities of the patient's condition, new diagnostic results add another layer of urgency and complexity. A repeat complete blood count reveals a marked leukocytosis, with the white blood cell count now elevated to 18,000/mm³, alongside a left shift that suggests an underlying infectious process. Blood cultures are drawn to identify a potential source, and broad-spectrum antibiotics are initiated empirically, given the patient's rapidly deteriorating status. Despite these measures, her temperature spikes to 39.5°C, and her heart rate climbs to 130 beats per minute, further complicating her hemodynamic status.

Amidst these developments, the patient's metabolic panel shows a worsening hyperkalemia, with serum potassium rising to 6.2 mEq/L, likely exacerbated by her declining renal function. This poses a significant risk for cardiac arrhythmias, necessitating immediate intervention with calcium gluconate for cardiac membrane stabilization, along with insulin and dextrose to drive potassium intracellularly, and consideration for renal replacement therapy becomes increasingly pressing.

The critical care team now faces the challenging task of balancing aggressive interventions to stabilize the patient's hemodynamics and metabolic derangements while vigilantly monitoring for signs of sepsis and managing the delicate state of her intracranial pressure. The convergence of these complications requires precise coordination across specialties, as the team anticipates the next steps in this precarious clinical scenario, including potential vasopressor support and continuous renal replacement therapy, to navigate the intertwined pathophysiological challenges while maintaining a focus on optimizing the patient's overall prognosis.

Section 4

As the medical team continues to manage the patient's precarious condition, new diagnostic results arrive, revealing significant alterations in her coagulation profile. The prothrombin time (PT) and activated partial thromboplastin time (aPTT) are both markedly prolonged, with the international normalized ratio (INR) elevated at 2.5. These findings suggest a coagulopathy, likely secondary to evolving disseminated intravascular coagulation (DIC), a complication often associated with severe infection and sepsis. The associated drop in platelets to 75,000/mm³ further corroborates the suspicion of DIC, complicating the patient's clinical picture and increasing the risk of bleeding.

In parallel, the latest arterial blood gas analysis displays a worsening metabolic acidosis, with a pH of 7.28 and a bicarbonate level of 18 mEq/L. The lactate level is critically elevated at 5.6 mmol/L, indicating tissue hypoperfusion and further supporting the diagnosis of septic shock. The patient's oxygenation status is also compromised, with a PaO2 of 60 mmHg on a high-flow nasal cannula, necessitating consideration for advanced airway management to ensure adequate oxygen delivery and prevent respiratory failure.

The convergence of these findings demands an immediate multidisciplinary approach. The hematology team is consulted to initiate targeted treatment for DIC, including possible administration of fresh frozen plasma and cryoprecipitate, while the intensivists deliberate on escalating circulatory support with norepinephrine and potential mechanical ventilation. These interventions aim to stabilize the patient's rapidly deteriorating condition while providing a critical window to address the underlying infectious etiology and prevent further organ dysfunction. As the team navigates this complex clinical scenario, they remain vigilant for any additional complications that may arise, poised to adapt their strategy to optimize the patient's chances of recovery.

Section 5

As the medical team implements the initial interventions, including the administration of fresh frozen plasma and cryoprecipitate, alongside norepinephrine titration for circulatory support, the patient's condition remains critical. Despite these efforts, a new set of diagnostic results reveals further complications. A follow-up complete blood count shows a continued decline in platelet count, now at 55,000/mm³, exacerbating concerns regarding bleeding risks. Concurrently, the patient's renal function has deteriorated, evidenced by a serum creatinine level that has increased to 2.8 mg/dL from a baseline of 1.0 mg/dL, indicating acute kidney injury possibly secondary to sepsis-related hypoperfusion and nephrotoxic exposure from ongoing antibiotic therapy.

In addition, the patient's neurological status worsens, with a decrease in Glasgow Coma Scale (GCS) score from 10 to 8, indicating a significant decline in consciousness. This change prompts an urgent need for reevaluation of her neurological status and potential neuroimaging to rule out intracranial hemorrhage, given the existing coagulopathy. Meanwhile, bedside echocardiography is performed to assess cardiac function and reveals a severely reduced ejection fraction of 30%, suggesting the development of septic cardiomyopathy, further complicating hemodynamic management.

The team faces a challenging decision-making process, needing to balance the risks of anticoagulation therapy for DIC against the potential for bleeding, while also considering renal replacement therapy options for acute kidney injury. The patient's oxygenation continues to deteriorate, warranting intubation and mechanical ventilation to prevent respiratory failure. As these complexities unfold, the team's coordinated approach remains critical, with close monitoring and frequent reassessment of the patient's evolving status to guide further therapeutic adjustments.