Updated October 2025

Neurocritical Care

Neurologic Complications of Systemic Illness and Critical Care

Systemic critical illnesses—especially sepsis, multiorgan failure, hypoxia, and metabolic derangements—are tightly linked to acute and chronic neurologic complications. High-value care focuses on early detection of encephalopathy and ICU-acquired weakness, prevention of delirium, meticulous avoidance of secondary brain injury, and structured neuroprognostication. Evidence supports protocolized delirium prevention, sedation minimization, glycemic safety, and early mobilization while recognizing prognostic uncertainty in the ICU.

Clinical question

What neurologic complications arise from systemic critical illnesses, how should clinicians prevent, detect, and manage them in the ICU, and what are the key prognostic and systems-level considerations?

SepsisDeliriumICU-acquired weaknessHypoxic-ischemic brain injuryMetabolic encephalopathyNeuroprognosticationCritical care

Key points

Recognize early encephalopathy

Screen all critically ill patients for delirium and decreased arousal; evaluate for hypoxemia, sepsis, metabolic derangements, sedative accumulation, and nonconvulsive seizures ^[4], ^[5], ^[1].

Detect ICU-acquired weakness

Suspect critical illness polyneuropathy/myopathy when weaning failure or diffuse weakness occurs; perform bedside MRC sum score and consider NCS/EMG if persistent ^[4], ^[1], ^[2].

Prevent secondary brain injury

Optimize oxygenation, perfusion, glucose, temperature, and sedation; avoid deep sedation when possible and use structured delirium prevention bundles ^[1], ^[6], ^[7].

Structured prognostication

Time prognostic conversations appropriately; use multimodal assessments and avoid sedative confounding, especially after cardiac arrest and severe sepsis ^[8], ^[1].

Advance systems and equity

Implement multidisciplinary neurocritical care education, standardized quality indicators, and palliative integration to reduce disparities and improve outcomes ^[9], ^[6], ^[7].

Evidence highlights

30–80% in mechanically ventilated adults ^[1]

ICU delirium prevalence

25–50% in prolonged ventilation/sepsis ^[1], ^[2]

ICU-acquired weakness

Common; associated with ↑ mortality and long-term cognitive impairment ^[3], ^[4], ^[1]

Sepsis-associated encephalopathy

Pathophysiology and Phenotypes

Major Neurologic Complications from Systemic Critical Illness

Systemic inflammation, hypoxia, microvascular dysfunction, metabolic disarray, and iatrogenesis converge to impair the central and peripheral nervous systems.

Sepsis-Associated Encephalopathy (SAE)

Characterized by fluctuating inattention, altered arousal, and EEG slowing without overt CNS infection. Mechanisms include cytokine-mediated neuroinflammation, endothelial dysfunction, BBB disruption, and mitochondrial injury. SAE is linked to higher mortality and long-term cognitive decline ^[3], ^[4], ^[1].

Delirium and Long-term Cognitive Impairment

Delirium is common in ICU and predicts worse functional outcomes. Risk is amplified by benzodiazepines, deep sedation, sepsis, hypoxia, and metabolic abnormalities. Persistent cognitive deficits are reported months after discharge ^[1].

ICU-Acquired Weakness (Critical Illness Polyneuropathy/Myopathy)

Presents with diffuse, symmetric limb weakness and difficulty weaning from ventilation. Risk factors: sepsis, multiorgan failure, hyperglycemia, corticosteroids/neuromuscular blockers. EMG/NCS can differentiate neuropathy vs myopathy. Recovery may be prolonged ^[4], ^[1], ^[2].

Hypoxic–Ischemic Brain Injury (HIBI)

Follows respiratory failure, shock, or cardiac arrest. Secondary injury arises from reperfusion, edema, seizures, and dysautonomia. Neuroprognostication must avoid sedative confounding and is multimodal ^[8], ^[1].

Metabolic/Toxic Encephalopathies

Uremia, hepatic failure, hypo/hypernatremia, hypo/hyperglycemia, hypercapnia, and medication toxicity commonly precipitate encephalopathy or seizures. Rapid correction of severe derangements is essential, with careful avoidance of overcorrection (e.g., osmotic demyelination) ^[5], ^[1].

Cerebrovascular Events Triggered by Systemic Illness

Sepsis, DIC, AF, and ECMO can precipitate ischemic or hemorrhagic stroke through coagulopathy and embolism. Vigilance for focal deficits or unexplained coma is critical ^[5], ^[1].

Iatrogenic/Sedation-Related Effects

Benzodiazepines and deep sedation increase delirium and prolong ventilation. Analgosedation strategies and daily sedation interruption may mitigate harm ^[1].

Bedside Application

Prevention, Detection, and Management

Prioritize early recognition and bundle-based prevention while individualizing diagnostic testing.

Screening & Monitoring

Use RASS for arousal and CAM-ICU or ICDSC for delirium each shift ^[1].

Consider continuous EEG for persistent coma, fluctuating mental status, or suspected nonconvulsive seizures ^[1].

MRC sum score for strength when cooperative; trend handgrip or diaphragm ultrasound for weaning failure ^[1], ^[2].

Track glucose, sodium, ammonia, urea, PaCO2, thyroid/adrenal axes if unexplained encephalopathy ^[5], ^[1].

Delirium Prevention Bundle

Promote daytime wakefulness: lights, mobilization, eyeglasses/hearing aids ^[1].

Minimize benzodiazepines; prefer dexmedetomidine/propofol for ventilated patients when appropriate ^[1].

Daily sedation interruption and spontaneous breathing trials when safe ^[1].

Sleep hygiene: noise reduction, clustered care, melatonin as institutional practice ^[1].

ICU-Acquired Weakness Mitigation

Early mobilization and PT/OT when hemodynamically stable ^[1], ^[2].

Avoid persistent deep sedation and unnecessary NMBA exposure ^[1].

Maintain euglycemia; avoid both severe hyper- and hypoglycemia ^[1].

Assess nutrition and protein adequacy; address vitamin D deficiency per local protocols.

Red Flags Requiring Escalation/Imaging

New focal deficits, acute severe headache, papilledema, or seizures ^[5], ^[1].

Coma unexplained by sedation, or asymmetric pupils/posturing ^[5], ^[1].

Rapid sodium shifts, hyperammonemia, or severe hypercapnia with altered mental status ^[5], ^[1].

Diagnostic Workup Pearls

CT head initially for structural lesions; MRI for diffuse axonal injury, HIBI patterns, PRES, or encephalitis ^[5], ^[1].

LP when CNS infection suspected; do not delay antimicrobials in septic shock ^[5], ^[1].

EEG: diffuse slowing in SAE; triphasic waves in metabolic encephalopathy; look for nonconvulsive status ^[4], ^[1].

NCS/EMG: axonal sensorimotor neuropathy (CIP) vs myopathic MUAPs (CIM) ^[4], ^[2].

Prognostication & Follow-up

Use multimodal approach: exam off sedation, EEG reactivity, SSEP, neuroimaging, and biomarkers when available ^[8], ^[1].

After cardiac arrest, defer final prognostication ≥72 h after normothermia and sedative clearance; avoid self-fulfilling bias ^[8].

Plan post-ICU cognitive and neuromuscular rehabilitation; screen for depression, PTSD, and cognitive impairment ^[1].

Quality and Systems

Service Delivery and Equity in Neurocritical Care

Structured neurocritical programs and quality indicators reduce variation and improve outcomes.

Multidisciplinary Neuro-ICU Teaming

Specialized units and trained teams improve processes and outcomes, but gaps persist in education, individualized therapy, and access in underserved regions ^[9], ^[7].

Standardization and Quality Metrics

Emerging quality indicators and consensus guidance target sedation, analgesia, hemodynamics, and neuromonitoring to reduce complications and disparities ^[6], ^[7].

Palliative Integration

Early palliative involvement aligns care with values, especially where prognostication carries uncertainty and potential long-term disability ^[9], ^[7], ^[8].

References

Source material

Primary literature that informs this article.