neurological examination of icu patients -...
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NEUROLOGICAL EXAMINATION OF ICU PATIENTS
[email protected] Université de Versailles
Institut Pasteur Hôpital Raymond Poincaré
Garches - France
NEUROLOGICAL EXAMINATION • Component of the « localizing" approach
– Differentiate central from peripheral nervous disorders
– Spinal cord vs brainstem vs hemisphere – Motoneuron, nerve, NMJ and muscle
• Component of the « diagnosis » approach – Acute vs chronic course – Inflammatory (exacerbation) vs degenerative
(progressive) course – Congenital vs acquired disorders
• Component of the prognosis assessment
NEUROLOGICAL EXAMINATION
It is necessary for indicating and interpreting the complementary biological, neuroradiological and neurophysiological investigations
NEUROLOGICAL EXAMINATION
Admission 1. Neurological disease as cause for admission 2. Preexisting neurological disease (interpretation
of subsequent neurological complication)
Critical illness 1. Detection of ICU-neurological complication 2. Prevention of ICU-neurological complication
Recovery of critical illness
1. Diagnosis of ICU-neurological complication 2. Treatment of ICU-neurological complication
Discharge 1. Follow-up of ICU-neurological complication
CENTRAL NERVOUS SYSTEM
COMA
EPIDEMIOLGY
• Present in 25-60% of ICU patients • Leading predictor of
– Death – Length of mechanical ventilation – LOS
• Coma assessment (GCS) is an integral component in the most widely used intensive care scoring systems – APACHE – SAPS – SOFA
Stevens - Crit Care Med - 2006
• Comatose patients are not sleeping • Comatose patients do not speak, do not move spontaneously and do not follow
commands. • When provoked by a noxious stimulus, their eyes remain closed, vocalization is
limited or absent, and motor activity is absent or abnormal and reflexive rather than purposeful or defensive .
IMPAIRMENT OF WAKEFULNESS (absence of arousal) - Lack of eyes opening - Absence sleep-wake cycles IMPAIRMENT OF AWARENESS - Of self - Of environment
DEFINITION
NON-ORGANIC
Presence of avoidance - Blinking to threat - Do not let hand fall on his face
If any doubt, do an EEG
COMATOSE PATIENT
BRAINSTEM RESPONSES 1. Eyes spontaneous movement 2. Eyes position 3. Oculocephalogyre response 4. Oculovestibular response 5. Pupillar size 6. Pupillar light reflex 7. Corneal reflex 8. Grimace 9. Cough reflex 10. Oculocardiac response 11. Respiratory pattern
FOCAL SIGNS Comparison between right and left body 1. Motor responses to order or painful stimulation 2. Limbs tone 3. Tendon reflexes 4. Plantar reflex
Verbal response Eyes response Motor response
SCALE
MYOCLONUS 1. Limbs 2. Lids NECK STIFFNESS
APPROACH
1. Diagnosis 2. Severity 3. Causes 4. Prognosis
FOUR & GLASGOW COMA SCALES
Wijdicks et al – Ann Neurol - 2005
Patients with the lowest GCS score could be further distinguished using the FOUR score.
FOUR COMA SCORE
Wijdicks et al – Ann Neurol - 2005
EYE RESPONSES
MOTOR RESPONSES
FOUR COMA SCORE
Wijdicks et al – Ann Neurol - 2005
RESPIRATION
BRAINSTEM REFLEXES
COMATOSE PATIENT EYES POSITION
Wijdicks E.F.M. Plum and Posner
Skew deviation (Cajal nuclei)
Hemispheric /pons
Thalamus /mesenceph
Bilateral hemispheric
COMATOSE PATIENT
A: roving B: periodic alternating gaze (bi H., cereb.) C: ping pong (bi H., cereb.)
D: convergence nystagmus (mesenceph.) E: bobbing (pons) F: dipping (bi H.)
Wijdicks E.F.M.
PUPILS
Adapted from Plum and Posner's Diagnosis of Stupor and Coma
HERNIATION
CLAUDE BERNARD HORNER
Sympathetic nervous system
Dissection Catheter
Cancer
Spine
Medulla (Wallenberg)
78 years old woman, with hypertension and diabetes, treated by anticoagulant for an atrial fibrillatrion was referred to our ICU for a coma. Neurological examination showed: Glasgow coma scale at 7, myosi,s generalized hypotonia and a bilateral Babinski sign. Biological screening is normal, but PT of 49%.
WHAT IS IT?
She is fine, she is sleeping…
• 27/11/10 : 74 years old and aplasic patient
• 1-2/12/11 : Pneumoniae and shock (Pseudomonas Aeruginosa et Stenotrophomonas Maltophilia)
• 5/12/11 : Non sedated. The patient is sleeping…
She is fine, she is sleeping…
ALGORITHM
Fever
Medical history (Alcohol, Epilepsia…)
Circumstances (CO…) Glycemia
Imaging,
± AB ± CSF
Neck stiffness Focal sign Trauma
Imaging
Seizure
Imaging
± AB ± CSF
Imaging
± CSF
EEG, Imaging
± CSF
OUTCOMES
COMA
BRAIN DEATH
PERSISTENT COMA
VEGETATIVE STATE (VS)
MINIMALLY CONSCIOUS STATE (MCS)
NEUROPSYCHOCOGNITIVE DYSFUNCTIONS
FULL RECOVERY
GLOBAL DISORDERS OF CONSCIOUSNESS
Stevens et al – Crit Care Med - 2006
RELEVANCE FOR DETECTING MCS?
• Errors: 40% ! – Schnakers et al. Diagnostic accuracy of the vegetative and minimally
conscious state: Clinical consensus versus standardized neurobehavioral assessment. BMC Neurology. 2009
• Better prognosis??
– Luauté et al. Long-term outcomes of chronic minimally conscious and vegetative states. Neurology. 2010 juill 20;75(3):246–52.
• Important for the family
VEGETATIVE AND MCS STATUS
1. Use appropriate scale 2. Redo the examination 3. Ask a neurologist to come 4. Usefulness of complementary investigation
PROGNOSIS
Wijdicks et al Crit Care Med 2014
N=1695 ICU patients Admission for coma
Prognosis value of brainstem assessment
Wijdicks et al - Neurology 2006
PREDICTION STudies: 1966-2006 Bad outcomes: at 1 month, death o consciousness impairment or at 6 mois, consciousness impairment or severe sequellae (daily nursing)
A
B
B
B
Am
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NEUROLOGICAL ASSESSMENt IN POST-CA COMATOSE PATIENTS
1. Arousal 2. Consciousness 3. Focal Neurological signs 4. Brainstem reflexes 5. Myoclonia
GCS FOUR EEG
Brain death Coma Status epilepticus
Acute stage Prediction phase
Motor response Brainstem reflexes SSEP (N20) EREP (MMN) EEG (Reactivity) ±MRI
Recovery phase
1. Full neurological examination 2. Motor assessment 3. Cognitive function 4. COnfusion
CRS-R CAM-ICU/NINDS MMS Neurocognitive tests Psychological tests
Withdrawal Support Unknown
Vegetative state MCS Lance Adams Sequellae
NEUROLOGICAL EXAMINATION
Booth et al - JAMA 2004
DELIRIUM
DELIRIUM DSM IV A. Alteration of consciousness: decreased interaction with the environment,
attention and concentration difficulties
B. Impairment of one or more cognitive functions: – Speech – Memory – Disorientation in space and time – Thinking/judgement
C. Onset sudden or rapidly progressive, fluctuating symptoms D. Secondary to:
– Medical illness – Drugs toxicity – Withdrawal
DELIRIUM TYPES
Hyperactive delirium: agitation, restlessness, emotional lability Hypoactive delirium: withdrawal, flat affect, lethargy and decreased responsiveness
All agitated patients are not confused All confused patients are not agitated
However, there are common causes and
risk factors between agitation and delirium
DELIRIUM SCALES Sedation/Agitation : - RAMSAY - Richmond Agitation Sedation Scale (RASS) - Adaptation to the Intensive Care Unit
Environment (ATICE) Delirium : - Confusion Assessment Method for the ICU
(CAM-ICU) - Intensive Care Delirium Screening Check-list
(ICDSC)
RA
SS
CAM-ICU FLOW SHEET
Items Altered level of consciousness (if A or B, do not complete patient evaluation for the
period) A: No response, score: none B: Response to intense and repeated stimulation (loud voice and pain), score: none D: Normal wakefulness, score: 0 E: Exaggerated response to normal stimulation, score: 1 Inattention (score: 0 to 1) Disorientation (score: 0 to 1) Hallucination-delusion-psychosis (score: 0 to 1) Psychomotor agitation or retardation (score: 0 to 1) Inappropriate speech or mood (score: 0 to 1) Sleep/wake cycle disturbance (score: 0 to 1) Symptom fluctuation (score: 0 to 1) Total (score: 0 to 8)
ICU Delirium Screening Checklist
RISK FACTORS
HOST FACTORS FACTORS OF CRITICAL ILLNESS IATROGENIC FACTORS Age (older) Acidosis Immobilization Alcoholism Anemia SEDATION (opioids, bzd)
APOE4 Fever/infection/SEPSIS Sleep disturbances
(Pre) Dementia Hypotension Dehydration, dyspnea
Depression Metabolic disturbances (for example, sodium, calcium, BUN, bilirubin) Drugs toxicity
Hypertension Withdrawal syndrome
Smoking Respiratory disease/ congestive heart failure
Vision/hearing impairment High severity of illness
A 55 years old man was hospitalised for a septic shock. Blood culture were positive to Staphylococcus aureus and CSF analysis showed an aseptic meningitis. At admission, neurological examination was normal as well as MRI of the brain and spine. Transoesophageal cardiac ultrasound only showed a thrombus in the left atria. He also underwent surgery for a septic arthritis of the right knee. A right jugular catheter could not be put. A goitre was also noticed. Vasopressor and mechanical ventilation were discontinued the 3rd and 5th days from admission. The patient was treated with methicillin and heparin. Day 8, the patient developed agitation and delirium. Neurological examination showed a weakness of the right arm and slight right central facial palsy as well a ptosis and miosis of the right eye. The right arm was also oedematous. The brain CT scan and CSF analysis were normal. EEG showed a slow cortical activity. Biochemical screening showed a moderate renal insufficiency. Blood culture were negative.
CASE REPORT 2
CASE REPORT 2
1. Left pre-rolandic lesion 2. Thrombosis of right jugular vein 3. Orbenin overdose
CASE REPORT
• Mme X…, 53 years old, traited with CS et I- for LED, is admitted for ARF related to a thrombotic microangiopathy. Occurrence of a hyperactive delirium: « on me vole mon enfant, les médecins me vole mon enfant… »
NEUROLOGICAL EXAMINATION OF SEDATED
PATIENTS
EFFECTS OF SEDATION
• Most severe critically ill patients often require sedation
• Sedation is a risk factor for brain dysfunction (delirium or delayed awakening) and can mask the occurrence of a brain dysfunction
• How to detect acute brain dysfunction in sedated critically ill patients?
DESIGN
[12-24h] Every day Discontinuation of sedation
1st N.E N.E Coma/Delirium
Within 3 days
Reproducibility of neurological examination was satisfactory
Sharshar et al – Crit Care Med – 2011
Non brain injured critical ill patients
NEUROLOGICAL ASSESSMENT
BRAINSTEM RESPONSES 1. Eyes spontaneous movement 2. Eyes position 3. Oculocephalogyre response 4. Pupillar size 5. Pupillar light reflex 6. Corneal reflex 7. Grimace 8. Cough reflex
FOCAL SIGNS Comparison between right and left body 1. Motor responses to order or painful stimulation 2. Limbs tone 3. Tendon reflexes 4. Plantar reflex
Verbal response Eyes response Motor response
GLASGOW COMA SCALE
NEUROLOGICAL EXAMINATION 12-24H OF SEDATION Fitting set Validation set Number of patients 72 72 Midazolam (mg/kg) 0.9 (0.6 to 1.8) 1.3 (0.8 to 2.0) Subfentanyl (µg/kg) 2.0. (0.8 to 4.0) 2.0 (0.7 to 4.6) sedation to inclusion (hours) 12 (12-24) 12 (12-24) ATICE (from 0 to 20) 9 (9 to 10) 9 (9 to 10) RASS Not tested -4 (-4 to -2) Blinking to strong light (%) 31 (43) 28 (39) Absent eye movement (%) 66 (93) 67 (93) Myosis (%) 45 (63) 38 (54) Pupillary light response (%) 51 (71) 58 (82) Corneal reflex (%) 65 (90) 66 (92) Oculocephalic response (%) 32 (47) 33 (46) Cough response (%) 36 (51) 60 (83) Grimacing (%) 41 (57) 48 (69)
Multiple logistic model
28-DAYS MORTALITY
Sharshar et al – Crit Care Med - 2011
Fitting set Validation set
OR (95%CI) P OR (95%CI) P SAPS-II at inclusion 1.06 (1.02 to 1.09) 0.003 1.03 (1.00 to 1.07) 0.051 Absent cough response 7.80 (2.00 to 30.4) 0.003 5.44 (1.35 to 22.0) 0.017 C-index (SE) 0.836 (0.055) 0.743 (0.067)
RESPONSES ASSESSED BETWEEN THE 12Th AND 24th H OF SEDATION
ALTERED MENTAL STATUS (after discontinuation of sedation)
Fitting set Validation set
Criteria Confusion or coma Delirium or coma OR (95%CI) P OR (95%CI) P
SAPS-II at inclusion 1.04 (1.00 to 1.07) 0.058 1.03 (0.99 to 1.08) 0.10
Absent oculocephalic response 4.49 (1.34 to 15.1) 0.015 5.64 (1.63 to 19.5) 0.006
RESPONSES ASSESSED BETWEEN THE 12Th AND 24th hours of sedation
Multiple logistic model
Sharshar et al – Crit Care Med - 2011
NEUROLOGICAL EXAMINATION
1. Feasible, reproducible and interpretable 2. Enables to detect focal neurological sign 3. Enables to estimate critical illness severity (cough
reflex) 4. Enables to identify patient at risk to develop
delirium after sedation discontinuation (Oculocephalogyre response) – Titration of sedation?
Sharshar et al – Crit Care Med - 2011
SYNDROMIC APPROACH
0
20
40
60
80
100GCS Eyes response
GCS Motorresponse
Myosis
Pupillar lightreflex
Corneal reflex
Oculocephalogyrereflex
Grimace
Cough reflex
Class AClass B
Abolition of brainstem reflexes is not at random Do not correpond to: 1. Particular lesion of the BT 2. To a reported BT syndrome Do not in agreement with 1. Jacksonian paradigm
Rohaut et al - Submitted
Abolition of oculocephalic response
Neuronal apoptosis of LC
Multifocal necrotizing leukoencephalopathy
Death
Abolition of cough reflex
Impaired HR/BP variability
Neuronal apoptosis
RAAS dysfunction Delirium
Maladaptative immune response
Autonomic dysfunction Hemodynamic
failure
CONCEPT OF BRAINSTEM DYSFUNCTION
Sharshar et al – CCM – 2002; Sharshar et al – Lancet – 2004; Pandharipande et al – CC -2011; Annane et al – AJRCCM – 1999; Tracey et al – Nature Review Neuroci
Inf cerebellar peduncle
XII nerves Vestibular n.
Spinothalamic tract
Noyau ambiguus IX/X
Sympathetic fibers
Corticospinal tract
- Medial Lemniscus
- Sympathetic fibers - Facial nerve
- Nerve VIII
- Spinothalamic tract
- Trigeminal Nerve
- Medial longitudinal fascilulus
- Cortico spinal tract - Cerebellar connections
Red nucleus
Medial lemniscus
Spinothalamic tract
Cortico spinal tract
BRAINSTEM SYNDROMES
Pons
Midbrain
Medulla
CASE REPORT A 65 years old man was hospitalised for
an acute respiratory failure that required invasive mechanical ventilation and sedation. Respiratory failure was ascribed to amiodarone interstitial pneumonia, which was given with anticoagulant a month ago for an atrial fibrillation. He had also a severe arteritis and coronary disease.
A week later, while the patient was
ventilated and lightly sedated, neurological examination showed no response of the left arm to painful stimulation, a greater hypotonia of the left arm and leg but also a decreased contraction of the right face to painful stimulation and right ptosis with small pupil.
Weakness
Facial palsy
CASE REPORT
Three days after discontinuation of sedation, the patient developed agitation and delirium. General and neurological examination was not changed. EEG was normal. Agitation and delirium was ascribed to discontinuation of sedation. Three days later, patient complained of pain of the legs and ankles that turned to be due to bacterial and ischemic myositis.
DELIRIUM WITHOUT (new) FOCAL NEUROLOGICAL SIGN IN A RECENTLY NON SEDATED PATIENT
CASE REPORT
Abolition of the left patellar reflex in 72 years old man who needed to be sedated for a very severe ARDS
Non sedated
EXAMINATION Normal
Focal sign
Delirium Agitation
Coma
Myoclonus
Brain imaging
EEG - Biochemistry - Drugs Brain imaging
EEG - Biochemistry - Drugs Brain imaging
Biochemistry - Drugs Brain imaging EEG
LUMBAR PUNCTURE IF ANY DOUBT
UNCONTROLLED SEPSIS?
Sedated
Discontinuation of sedation
What strategy?
Sedation necessary
Monitoring
Antagonist?
SPINAL CORD SYNDROMES
Syringomyelic
Complete transection
Brown Séquard Anterior spinal artery
Posterior spinal artery
Subacute combined degeneration
ALS
Poliomyelitis
PERIPHERAL NERVOUS SYSTEM
PERIPHERAL NERVOUS SYSTEM Neurono -
neuropathy Neuropathy Myasthenic
syndrome Myopathy
Symmetry Bilateral ± symmetrical
Variable MM: asymmetrical
PN: symmetrical PRN: symmetrical
Bilateral and symmetrical
Bilateral and symmetrical
Proximal vs distal
Proximal or distal
MM: distal PN: distal
PRN: proximal
Proximal ++
Proximal ++
Topography
Limbs, Bulbar,
respiratory
MM: ≥ 1 nerve PN: limbs ± respiratory
PRN: limbs, trunk, bulbar, facial,
respiratory
Variable Limbs, facial,
bulbar, trunk or respiratory Ptosis (often
unilateral) and diplopia
Variable
Limbs, facial, bulbar, trunk,
respiratory
MM: mononeuropathy multiplex; PN: polyneuropathy; polyradiculoneuropathy
PERIPHERAL NERVOUS SYSTEM
Neurono- Neuropathy
Neuropathy Myasthenic syndrome Myopathy
Tone flaccidity flaccidity flaccidity flaccidity
Tendon reflexes Lost or
pyramidal signs (ALS)
Lost or decreased Preserved Preserved
Idio-muscular response Preserved Preserved Preserved Absent
Atrophy Pronounced Pronounced No Variable
Other motor signs Fasiculation - Fatigability Fluctuation
Myalgia Myotonia
Other neurological signs Cramps
± sensory loss ± dysautonomia
No sensory loss (except L.
Eaton) No sensory loss
PERIPHERAL NERVOUS SYSTEM
A 67 years old man, without pre-existing neurological disease and who was referred to our ICU for a severe ARDS and septic shock complicated by multiple organ failure developed a flaccid quadriplegia. There was no Babinski sign, fasiculations or evidence for a sensory deficit. Tendon reflexes were abolished. Examination of cranial nerves was normal. There was diffuse edema. The patient had been treated by steroids and neuromuscular blocking agent.
?
MRC SUM SCORE
Kleyweg et al. - Muscle Nerve - 1991 0
60
48
36
Pare
sis
Nor
mal
Se
vere
DETECTION Advantages Inconvenients
CLINICAL EXAMINATION
(ICU-AP)
Simple Relevant
Due to CINM
Awareness Delayed
diagnosis
ENMG (CIP/CIM/CINM)
Neuropathy Myopathy
Early detection
Availability Artefacts
Correlation?
Muscle biopsy (CIM)
Myopathy Physiopathology
Invasive
Other techniques: ultasound, MRI
SEMIOLOGY
• Weakness – Bilateral et symmetric – Four limbs – Essentially proximal – Sparing the face
• ± sensory deficit • ± Areflexia • ± Amyotrophic
RIGHT LEFT
SHOULDER
ELBOW
WRIST
HIP
KNEE ANKLE
0,0 0,5 1,0
1,5 2,0
2,5
3,0
3,5
4,0
4,5
5,0
NM score
De Jonghe et al JAMA 2002
CSF: not helpful CK: normal, slightly or highly increased (Status asthmaticus)
ICU-ACQUIRED PARESIS
Frequent and severe complication associated with 1. Increased mortality 2. Prolonged weaning and reintubation 3. Increased length of stay in ICU 4. Disability
ENTRAPMENT NEUROPATHY
Peroneal nerve
Radial nerve
Hypoesthesia in green area
Hypoesthesia
University of Versailles Raymond Poincaré
Service de Réanimation Pr Djillali Annane
MERCI
Institut Pasteur Fabrice Chrétien
Human Histopathology and Animal Models
DIFFERENTIAL DIAGNOSIS OF PARAPLEGIA
Areflexic and flaccid paraplegia
Think about injury of the spinal cord, conus medullaris syndrome or a cauda equina syndrome, especially if there is a sensory level, urinary retention or pelvic hypoesthesia
Doubt: usefulness of MRI, electrophysiological testing