Altered Sensorium in the ICU: A Bedside Clinical Approach
A State-of-the-Art Clinical Review for Intensivists
Dr Neeraj Manikath , claude.ai
Abstract
Altered sensorium represents one of the most challenging clinical scenarios in the intensive care unit, affecting up to 80% of mechanically ventilated patients and significantly impacting morbidity, mortality, and healthcare costs. This review provides a systematic, bedside-oriented approach to evaluating altered consciousness in critically ill patients, emphasizing practical clinical assessment techniques, diagnostic pearls, and evidence-based management strategies. We highlight the importance of differentiating delirium from other causes of altered mentation and provide actionable clinical hacks for real-world ICU practice.
Keywords: Delirium, Altered mental status, Critical care, Encephalopathy, ICU, Consciousness assessment
Introduction
Altered sensorium in the ICU is not a diagnosis but a clinical syndrome demanding systematic evaluation. The term encompasses a spectrum from subtle inattention to coma, with delirium being the most common manifestation. Despite its prevalence, altered consciousness remains underrecognized, with studies showing that non-delirium specialists miss the diagnosis in up to 75% of cases.(1) The implications are profound: each additional day of delirium increases mortality by 10% and is associated with long-term cognitive impairment comparable to mild Alzheimer's disease.(2,3)
The modern intensivist must approach altered sensorium with the rigor of a neurologist, the pragmatism of an emergency physician, and the holistic perspective of a geriatrician. This review provides a practical framework for bedside assessment and management.
Defining the Spectrum of Consciousness
The Consciousness Continuum
Normal consciousness requires both arousal (wakefulness) and awareness (content). Understanding this duality is fundamental:
- Arousal is mediated by the reticular activating system in the brainstem
- Awareness requires intact cortical function and connectivity
Clinical Pearl: A patient can be awake but unaware (vegetative state) or aware but not fully awake (minimally conscious state). This distinction guides both prognosis and family discussions.
Classification Framework
Quantitative disorders:
- Confusion: Disoriented but arousable
- Obtundation: Requires repeated stimulation
- Stupor: Responds only to vigorous stimulation
- Coma: Unresponsive to any stimulation
Qualitative disorders:
- Delirium: Fluctuating consciousness with inattention
- Encephalopathy: Global cerebral dysfunction
Bedside Hack: Use the mnemonic "COAT" - Confusion, Obtundation, Arousal deficit, Terminal (coma) to quickly categorize altered consciousness severity.
The Systematic Bedside Assessment
Step 1: Establish the Baseline
Critical First Question: "What was the patient's mental status before ICU admission?"
Obtaining collateral history from family, review of outpatient records, and nursing home documentation is mandatory. Pre-existing dementia is present in 40% of elderly ICU patients and profoundly affects assessment and prognosis.(4)
Oyster: Families often overestimate pre-ICU cognitive function. Probe specifically: "Could they manage their medications? Cook? Handle finances?" These instrumental activities of daily living reveal true baseline function.
Step 2: Rapid Consciousness Assessment
The Glasgow Coma Scale (GCS) remains the universal language but has limitations in ICU patients (intubation affects verbal score, sedation confounds assessment).
Better for ICU Use: The Richmond Agitation-Sedation Scale (RASS)
- +4: Combative
- +3: Very agitated
- +2: Agitated
- +1: Restless
- 0: Alert and calm
- -1: Drowsy
- -2: Light sedation
- -3: Moderate sedation
- -4: Deep sedation
- -5: Unarousable
Clinical Pearl: Always assess RASS before evaluating for delirium. You cannot assess delirium in a deeply sedated patient. Target RASS should be -1 to 0 for most ICU patients.(5)
Step 3: Delirium Screening
The Confusion Assessment Method for ICU (CAM-ICU) has 95% sensitivity and 89% specificity.(6)
Four Features (mnemonic: ABCD):
- Acute onset or fluctuating course
- Inattention (cannot squeeze hand on letter "A" in SAVEAHAART)
- Disorganized thinking (fails simple yes/no questions)
- Altered level of consciousness (RASS other than 0)
Delirium = Features 1 AND 2 AND (3 OR 4)
Bedside Hack: The "picture recognition test" is more sensitive than letter tests in mechanically ventilated patients. Show 5 pictures, remove them, then show 10 pictures and ask the patient to indicate which they saw before.(7)
Step 4: Delirium Subtyping
Three Motor Subtypes:
- Hyperactive (25%): Agitated, combative, easily recognized
- Hypoactive (45%): Withdrawn, quiet, often missed
- Mixed (30%): Alternating features
Critical Oyster: Hypoactive delirium has the worst prognosis but is missed 60-80% of the time because these patients are "easy" and don't disturb the ICU workflow.(8) Actively screen quiet patients.
The Etiological Detective Work
The "DELIRIUM WATCH" Framework
A comprehensive mnemonic for ICU-specific causes:
Drugs (sedatives, anticholinergics, steroids) Electrolytes (Na, Ca, Mg, PO4 abnormalities) Lack of drugs (withdrawal from alcohol, benzodiazepines) Infection/Inflammation (sepsis, encephalitis) Respiratory (hypoxia, hypercarbia) Intracranial (stroke, hemorrhage, seizure) Uremia/Metabolic (hepatic, renal failure) Myocardial (shock, hypoperfusion)
Withdrawal of essential medications Alcohol/Substance intoxication or withdrawal Trauma (traumatic brain injury) CNS infection (meningitis, encephalitis) Hypoglycemia/Hyperglycemia
The Physical Examination Renaissance
In our technology-dependent era, bedside examination remains irreplaceable.
The Focused Neurological Examination:
1. Pupillary Examination
- Pinpoint pupils: Opiate toxicity, pontine lesion
- Dilated, fixed pupils: Anticholinergic toxicity, severe hypoxia, herniation
- Unilateral dilated pupil: Uncal herniation, third nerve palsy
- Hippus (oscillating pupils): Suggests diencephalic dysfunction
Pearl: Use a bright smartphone light in a dark room if a formal pupil gauge is unavailable. Normal pupils constrict briskly; sluggish response suggests pathology.
2. Eye Movement Assessment
- Spontaneous roving movements: Intact brainstem, cortical dysfunction
- Dysconjugate gaze: Brainstem lesion, metabolic disorder
- Oculocephalic reflex (doll's eyes): Tests brainstem integrity in comatose patients
- Cold caloric testing: Definitive brainstem assessment (contraindicated if tympanic membrane perforation)
Hack: The "three-step test" for ophthalmoplegia can be done at bedside with a penlight and helps distinguish peripheral from central causes.
3. Motor Examination
- Asterixis (flapping tremor): Metabolic encephalopathy (hepatic > renal > hypercapnia)
- Myoclonus: Uremia, hypoxia, drug toxicity
- Tremor: Alcohol withdrawal, lithium toxicity, hyperthyroidism
- Focal weakness: Structural lesion until proven otherwise
Pearl: True asterixis requires the patient to be cooperative enough to hold arms extended. In obtunded patients, look for multifocal myoclonus instead.
4. Meningismus
- Neck stiffness, Kernig's sign, Brudzinski's sign
- Oyster: Absence of meningismus does NOT exclude meningitis in the elderly, immunosuppressed, or deeply comatose. Maintain high suspicion.
5. Respiratory Pattern
- Cheyne-Stokes: Bihemispheric dysfunction, heart failure
- Central neurogenic hyperventilation: Midbrain/pontine lesion
- Apneustic breathing: Pontine damage
- Ataxic breathing: Medullary dysfunction (pre-terminal)
Laboratory Investigation Strategy
Tier 1 (Everyone):
- Complete blood count
- Comprehensive metabolic panel (glucose, electrolytes, BUN, creatinine, liver enzymes)
- Arterial blood gas
- Urinalysis and culture
- Chest X-ray
- ECG
Tier 2 (High clinical suspicion):
- Thyroid function tests
- Cortisol level (especially if on chronic steroids or septic)
- Ammonia level (if liver disease)
- Toxicology screen and specific drug levels (digoxin, lithium, anticonvulsants)
- Vitamin B12, thiamine levels (alcoholics, malnutrition)
- Blood cultures
Tier 3 (Specific scenarios):
- Lumbar puncture (unexplained fever, immunocompromised, seizure)
- CT/MRI brain
- EEG (if suspecting non-convulsive status epilepticus)
- Autoimmune encephalitis panel (young patient, psychiatric features, refractory seizures)
- HIV testing, syphilis serology (appropriate risk factors)
Clinical Hack: The "Rule of 120s" - If Na >120, glucose >120, and no obvious toxic-metabolic cause, get brain imaging. Don't wait.
Neuroimaging: When and What
Indications for Emergent CT Head
Absolute indications:
- Focal neurological deficits
- GCS <13 without clear reversible cause
- Head trauma (even seemingly minor in anticoagulated patients)
- Severe hypertension with headache
- Suspected herniation (blown pupil, posturing)
- New-onset seizure without known epilepsy
Relative indications:
- Age >60 with undifferentiated altered sensorium
- Persistent altered consciousness despite correction of metabolic abnormalities
- Anticoagulated patients with any change in mental status
- Immunocompromised patients (opportunistic CNS infections)
Pearl: Non-contrast CT is the first-line study in acute settings. It excellently identifies hemorrhage, hydrocephalus, mass effect, and large strokes. CT is fast, available, and doesn't require patient cooperation.
When to Upgrade to MRI
- Suspected posterior fossa pathology (CT has artifacts)
- Clinical picture suggests stroke but CT is negative (MRI with diffusion-weighted imaging)
- Encephalitis (temporal lobe enhancement in HSV encephalitis)
- Suspected venous sinus thrombosis (MR venography)
- Demyelinating disease
- Metabolic encephalopathies may show characteristic patterns (posterior reversible encephalopathy syndrome, osmotic demyelination)
Oyster: MRI requires 30-60 minutes of patient immobility. Agitated, hypoxic, or hemodynamically unstable patients are poor candidates. Don't delay treatment for imaging.
The EEG Decision
When to Consider EEG
Strong indications:
- Suspected non-convulsive status epilepticus (subtle movements, eye deviation, persistent altered consciousness post-seizure)
- Unexplained coma after cardiac arrest
- Persistent encephalopathy without clear cause
- Monitoring burst suppression during barbiturate coma
Supporting evidence: Non-convulsive seizures occur in 10-20% of ICU patients with unexplained altered consciousness.(9) The only way to diagnose is EEG.
Clinical Pearl: "Twitching" in ICU patients is seizure until proven otherwise. Even subtle rhythmic movements (finger twitching, eye deviation, chewing) warrant EEG.
Hack: Continuous EEG monitoring is ideal but resource-intensive. A 30-minute routine EEG captures seizures in 50% of cases, 24-hour monitoring increases yield to 80%.(10)
Special Scenarios and Diagnostic Pearls
The Post-Cardiac Arrest Patient
Avoid premature prognostication. The 2021 American Heart Association/European Resuscitation Council guidelines recommend multimodal assessment at ≥72 hours post-arrest in normothermic patients.(11)
Favorable prognostic signs:
- Early motor response better than extensor posturing
- Intact pupillary and corneal reflexes at 72 hours
- Absence of myoclonic status epilepticus
- EEG with continuous background activity
Unfavorable but not definitive:
- Bilateral absence of N20 somatosensory evoked potential
- Status myoclonus in first 72 hours
- Highly malignant EEG patterns
Pearl: Sedation, hypothermia, and neuromuscular blockade can all confound neurological examination. Wait until these effects have cleared.
Alcohol Withdrawal Delirium (Delirium Tremens)
Timing is diagnostic:
- Minor symptoms: 6-12 hours
- Seizures: 12-48 hours
- Delirium tremens: 48-96 hours
Clinical features:
- Autonomic hyperactivity (tachycardia, hypertension, fever, diaphoresis)
- Tremor
- Hallucinations (classically visual)
- Agitation
Oyster: Alcohol withdrawal can be superimposed on other causes of altered sensorium. Don't assume withdrawal explains everything in a chronic alcoholic.
Management Pearl: CIWA-Ar score guides benzodiazepine dosing, but in severe DT, phenobarbital loading may be superior.(12) Consider ICU-level monitoring and continuous benzodiazepine infusions.
Hepatic Encephalopathy
Grading (West Haven Criteria):
- Grade 1: Trivial lack of awareness, short attention span
- Grade 2: Lethargy, disorientation, inappropriate behavior
- Grade 3: Somnolent but arousable, gross disorientation, bizarre behavior
- Grade 4: Coma
Bedside Test: Number connection test (connect numbers 1-25 in order as fast as possible; >30 seconds abnormal)
Management Hack: Lactulose titrated to 2-3 soft bowel movements daily remains first-line. Rifaximin added for refractory cases. Zinc and L-ornithine-L-aspartate are adjuncts with some evidence.(13)
Pearl: Always search for precipitants: GI bleeding, infection, constipation, hypokalemia, excessive protein intake, medications (benzodiazepines, opioids).
Septic Encephalopathy
Most common cause of delirium in ICU. May precede other signs of sepsis.
Pathophysiology: Blood-brain barrier disruption, neuroinflammation, neurotransmitter dysregulation, microvascular dysfunction.
Diagnosis: Exclusion diagnosis. Requires systemic infection and absence of other explanations.
Pearl: Correction of sepsis resolves encephalopathy. Persistence despite sepsis control mandates reassessment for other causes.
Non-Convulsive Status Epilepticus (NCSE)
High index of suspicion required:
- Subtle facial twitching
- Eye deviation
- Altered consciousness in known epileptic
- Post-ictal confusion lasting >30 minutes
Diagnostic Gold Standard: EEG showing continuous or recurrent seizure activity
Management: Treat as status epilepticus with benzodiazepines, then antiepileptic drug loading. Neurology consultation essential.(14)
Medication-Related Altered Consciousness
The Prime Suspects
Anticholinergics:
- Diphenhydramine, promethazine, scopolamine
- Features: Dilated pupils, dry mucous membranes, urinary retention, absent bowel sounds, agitation
- Mnemonic: "Blind as a bat, red as a beet, hot as a hare, dry as a bone, mad as a hatter"
Benzodiazepines/Propofol:
- Dose-dependent sedation
- Paradoxical agitation possible, especially in elderly
- Propofol infusion syndrome: Metabolic acidosis, rhabdomyolysis, cardiac dysfunction
Opioids:
- Pinpoint pupils, respiratory depression
- Pearl: Pupil dilation occurs with severe hypoxia/anoxia; don't dismiss opioid toxicity if pupils are mid-sized
Steroids:
- Can cause delirium, psychosis, or mania
- More common with higher doses and longer duration
Oyster: Medication withdrawal is as dangerous as intoxication. Sudden cessation of benzodiazepines, baclofen, or beta-blockers can precipitate delirium.
The Anticholinergic Burden
Many ICU medications have anticholinergic properties. The cumulative effect is often underappreciated.
Common culprits:
- H2 blockers (ranitidine > famotidine)
- Antiemetics (promethazine, metoclopramide)
- Antipsychotics (quetiapine, olanzapine)
- Antidepressants (amitriptyline, paroxetine)
- Antihistamines
- Muscle relaxants (cyclobenzaprine)
Hack: Use the Anticholinergic Cognitive Burden Scale. Score ≥3 significantly increases delirium risk.(15)
Non-Pharmacological Prevention and Management
The ABCDEF Bundle (Evidence-Based Delirium Prevention)
Assess, prevent, and manage pain Both spontaneous awakening and breathing trials Choice of analgesia and sedation Delirium: assess, prevent, and manage Early mobility and exercise Family engagement and empowerment
Evidence: Implementation of the ABCDEF bundle reduces delirium incidence by 50%, decreases ICU length of stay, and improves survival.(16)
Practical Implementation Pearls:
1. Optimize the environment:
- Windows for natural light (regulates circadian rhythm)
- Minimize nighttime noise and interruptions
- Remove unnecessary lines and catheters
- Clocks and calendars for orientation
2. Sensory aids:
- Ensure patients have glasses and hearing aids
- Simple intervention, often overlooked, profoundly improves orientation
3. Early mobilization:
- Even in mechanically ventilated patients
- Reduces delirium duration and improves functional outcomes
- Safety first: exclude contraindications (unstable fractures, active bleeding, hemodynamic instability)
4. Sleep promotion:
- Consolidate nighttime care
- Reduce alarm volumes at night
- Consider melatonin or ramelteon (evidence for prevention, not treatment)
- Avoid benzodiazepines for sleep
5. Family presence:
- Liberalized visitation policies
- Familiar voices and faces provide orientation
- Family can identify subtle changes in baseline
Pharmacological Management of Delirium
The Uncomfortable Truth
No medication has been proven to reduce delirium duration, ICU length of stay, or mortality.(17)
Antipsychotics may reduce agitation and allow nursing care but do not treat underlying delirium.
When to Consider Pharmacotherapy
Indications:
- Safety threat to self or staff
- Severe agitation interfering with necessary care (mechanical ventilation, life-sustaining treatments)
- Severe distress to patient
NOT indicated:
- Quiet hypoactive delirium
- Prophylaxis in non-delirious patients
- Convenience of staff
Medication Options
Haloperidol:
- 0.5-2 mg IV/PO q4-6h PRN
- Typical antipsychotic, fewer anticholinergic effects than atypicals
- Risk: QTc prolongation, extrapyramidal symptoms, neuroleptic malignant syndrome
- Pearl: Check baseline QTc; avoid if >500 ms
Quetiapine:
- 12.5-50 mg PO BID
- Atypical antipsychotic
- Advantage: May improve sleep
- Disadvantage: Significant anticholinergic effects, cannot be given IV
Dexmedetomidine:
- Alpha-2 agonist, provides sedation without respiratory depression
- May reduce delirium duration compared to benzodiazepines(18)
- Limitation: Expensive, requires continuous infusion, can cause bradycardia and hypotension
- Sweet spot: Post-extubation agitation, difficult ventilator weaning
Avoid:
- Benzodiazepines (except alcohol/benzodiazepine withdrawal): Worsen delirium, increase duration
- Physical restraints unless absolutely necessary: Increase agitation and risk of injury
Hack: Start with lowest effective dose. Delirium medications are for agitation control, not delirium cure. Minimize duration of use.
Prognosis and Long-Term Outcomes
The Sobering Reality
Delirium is not a benign, reversible condition. It has profound long-term consequences:
- Cognitive impairment: 40% of delirium survivors have cognitive deficits at 1 year, equivalent to moderate traumatic brain injury(19)
- Functional decline: Decreased ability to perform activities of daily living
- Increased mortality: Persists up to 1 year post-discharge
- Post-ICU syndrome: Cognitive, psychiatric, and physical impairments
Family Counseling Pearl: Prepare families for the possibility of persistent cognitive changes. Early cognitive rehabilitation and structured follow-up may help.
Clinical Hacks and Practical Tips
The "Eyeball Test"
Before touching the chart, observe:
- Is the patient tracking you with their eyes?
- Are they reaching for lines/tubes?
- What is the respiratory pattern?
- Do they respond to their name?
This 10-second assessment provides more information than many realize.
The "MOVE" Protocol for Rapid Assessment
Motor: Any spontaneous movement? Purposeful? Ocular: Pupil size, light reflex, tracking Verbal: Any sounds, words, following commands? Emotional: Flat, agitated, fearful, appropriate?
Communication with Non-Verbal ICU Patients
The "Squeeze Technique":
- "Squeeze my hand if you understand me"
- "Squeeze once for yes, twice for no"
- "Squeeze my right hand if you have pain"
Oyster: Inconsistent responses don't always mean delirium. Weakness, language barriers, and hearing impairment can interfere.
The "Sedation Vacation" Checklist
Before daily sedation interruption, ensure:
- No active seizures
- No escalating vasopressor requirements
- No ongoing neuromuscular blockade
- No active myocardial ischemia
- Adequate oxygenation
Documentation Essentials
Record daily:
- RASS score
- CAM-ICU result
- GCS (in non-sedated patients)
- Delirium type (hyperactive/hypoactive/mixed)
- Contributing factors identified
- Interventions implemented
Summary: The 10 Commandments of ICU Altered Sensorium
- Assume nothing: Always establish true baseline cognitive function
- Screen systematically: Use validated tools (RASS, CAM-ICU) consistently
- Don't miss the quiet ones: Hypoactive delirium is common and dangerous
- Search for reversible causes: Use the DELIRIUM WATCH framework
- Examine, don't just scan: Physical exam findings are irreplaceable
- Image appropriately: CT for acute/focal findings; MRI for diagnostic dilemmas
- Consider EEG liberally: Non-convulsive seizures are more common than appreciated
- Prevent aggressively: ABCDEF bundle, non-pharm interventions first
- Medicate judiciously: Antipsychotics control agitation but don't cure delirium
- Think long-term: Counsel families about persistent cognitive effects
Conclusion
Altered sensorium in the ICU demands a systematic, evidence-based approach combined with clinical acumen honed through experience. While technology and imaging play important roles, the foundation remains a thorough history, meticulous examination, and critical thinking. The modern intensivist must be a diagnostic detective, recognizing that each case of altered consciousness is a puzzle requiring patience, persistence, and clinical wisdom.
As we continue to understand the devastating long-term consequences of ICU delirium, prevention through evidence-based bundles, early recognition through systematic screening, and aggressive treatment of underlying causes become imperative. The quality of our assessment today determines not just survival, but the cognitive future of our patients.
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Conflict of Interest: None declared
Funding: None
Author Contributions: This review represents synthesis of clinical experience and current evidence-based practice in critical care medicine.
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