I. Epidemiology and Incidence in Critically Ill Patients

AIS comprises the majority of strokes worldwide and carries distinct risks in ICU settings. Critically ill patients face higher incidence and mortality driven by complex comorbidities and atypical presentations.

• Global burden: AIS represents ~87% of all strokes; one of the leading causes of death and long-term disability.
• Trends: Age-adjusted stroke mortality has declined in high-income regions, but absolute stroke numbers are rising due to aging populations and improved survival after initial events.
• ICU incidence: Stroke rates in ICU cohorts exceed those in general wards as hemodynamic instability, arrhythmias, sepsis, and prothrombotic states precipitate cerebral ischemia.
• ICU mortality: Elevated due to delayed recognition, multisystem organ dysfunction, and overlapping critical illnesses.

Key Datasets

II. Pathophysiology of Acute Ischemic Stroke

AIS results from sudden arterial occlusion that creates an irreversibly damaged core surrounded by a salvageable penumbra. A cascade of excitotoxic, oxidative, and inflammatory processes drives tissue injury.

1. Arterial Occlusion Mechanisms

• Thromboembolism: Emboli from cardiac (e.g., atrial fibrillation, mural thrombus) or large-artery sources lodge in cerebral vessels, causing large territorial infarcts.
• In situ thrombosis: Plaque rupture or endothelial injury in intracranial/extracranial arteries triggers local clot formation; small penetrating arteries occlude in lipohyalinosis-mediated lacunar strokes.
• Vessel size: Large-vessel occlusions lead to severe deficits and risk of malignant edema; small-vessel (lacunar) infarcts present more subtly.

2. Ischemic Penumbra Dynamics

• Core vs. Penumbra:
  • Core: Tissue with perfusion below viability threshold—irreversible injury.
  • Penumbra: Hypoperfused but salvageable tissue reliant on collateral flow.
• Time dependency: Penumbral tissue evolves into core without reperfusion; early restoration of flow is paramount.

3. Neuronal Injury Cascade

• Excitotoxicity: Energy failure → excessive glutamate → NMDA receptor overactivation → calcium influx → cytotoxic damage.
• Oxidative stress: Mitochondrial dysfunction and reperfusion generate reactive oxygen species → lipid peroxidation, protein/DNA damage.
• Inflammation/apoptosis: Microglial activation, cytokine release, leukocyte infiltration amplify injury and trigger programmed cell death.

III. Impact of Pre-existing Chronic Diseases

Chronic comorbidities exacerbate vascular vulnerability, influence stroke phenotype, and inform both prevention and acute management strategies.

• Hypertension
  • Arterial remodeling and endothelial dysfunction accelerate atherogenesis.
  • Chronic hypertension shifts cerebral autoregulatory curve, increasing risk of hypoperfusion if BP is lowered precipitously.
  • Strict BP control reduces first and recurrent stroke risk; targets individualized per comorbidities.
• Atrial Fibrillation
  • Stasis in the left atrial appendage fosters thrombus formation and large embolic strokes.
  • Cardioembolic strokes are typically more disabling with higher mortality.
  • Guideline-directed oral anticoagulation reduces AIS risk; timing post-stroke balances hemorrhage vs. recurrence.
• Diabetes Mellitus
  • Endothelial dysfunction and basement membrane thickening impair collateral circulation.
  • Acute hyperglycemia worsens infarct expansion and reduces penumbral salvage.
  • Acute glucose targets: 140–180 mg/dL to optimize neurologic outcomes.
• Hyperlipidemia
  • LDL accumulation promotes plaque formation and instability.
  • Dyslipidemia increases platelet aggregation and thrombogenicity.
  • High-intensity statins for clinical atherosclerotic disease; add nonstatin agents if LDL goals unmet.

IV. Social Determinants of Health as Stroke Risk Factors

Nonclinical factors profoundly affect prevention, recognition, and access to acute stroke care, contributing to outcome disparities.

• Medication Access
  • Cost-related nonadherence for antihypertensives, anticoagulants, and statins elevates risk of uncontrolled factors.
  • Formularies and insurance hurdles delay initiation of evidence-based therapies.
• Health Literacy
  • Poor understanding of stroke signs prolongs prehospital delays and reduces reperfusion eligibility.
  • Low literacy undermines adherence to preventive lifestyle and pharmacologic measures.
• Socioeconomic Status
  • Lower SES correlates with reduced primary care access, delayed EMS activation, and lower rates of advanced therapies.
  • Disparities in acute care utilization contribute to higher morbidity and mortality.

V. Clinical Presentation Overview

AIS typically presents with sudden focal deficits but can fluctuate; prompt differentiation from mimics is crucial for timely therapy.

Focal Neurological Deficits

• Motor: Hemiparesis/hemiplegia, classic face-arm-leg distribution.
• Sensory: Numbness, paresthesia, proprioceptive loss.
• Speech: Aphasia (expressive/receptive), dysarthria.
• Vision: Homonymous hemianopia, gaze deviation, cortical blindness.

Temporal Dynamics

• Onset: Abrupt, maximal at onset.
• Progression: Fluctuating or stuttering deficits may herald evolving thrombosis.

Stroke Mimics and Differential