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Introduction to Neurological Intensive Care M. S. Damian, Cambridge/Ipswich Medical neurointensive care issues deal primarily with: • • • • Altered conscious states Coma and failure to awaken Seizures and status epilepticus Acute paralysis causing respiratory distress or failure of airways protection What are the prime issues for neurological assessment in critical care? • Are there focal neurological abnormalities? – Focal findings = structural lesion – No focal findings = metabolic disease • How long since consciousness lost? – Outcome in come is linked to duration – Every condition is reversible at the beginning – “Time is brain” Altered Consciousness and Coma 2 main components of consciousness: Arousal or wakefulness = “level of consciousness“: The ascending reticular activating system (ARAS) extends through the dorsal brainstem at the floor of the 4th ventricle, then branches out through the thalamus and diencephalon to both hemispheres. Awareness and responsiveness = ”contents of consciousness“ includes attention, orientation, motivation, sensation, perception, self-awareness, memory and cognition. Causes of Impaired Consciousness 500 consecutive cases - Plum & Posner Metabolic/diffuse disorders: 63% • Intoxications 30% • Anoxia/Ischemia 17% • Hepatic Coma 3.5% • Endocrine Coma 2.5% • Acid-base disturbance 2.5% • Encephalitis 2.8% • Hypothermia 1.8% • Uremia 1.6% • Pulmonary diseases, malnutrition, psychiatric disorders, others 2.5% Hemispheric Disorders: 24% • ICH 9% • Subdural hematomas 5% • SAH 2.6% • Epidural hematomas 1% • Cerebral infarction 1.8% • Brain tumor, abscess, pituitary apoplexy, thalamic infarct 3.4% Infratentorial Disorders: 13% • Brain stem infarction 8% • Brain stem hemorrhage 2.2% • Others: 2.8% Causes of Impaired Consciousness 500 consecutive cases - Plum & Posner Metabolic/diffuse disorders: 63% • Intoxications 30% • Anoxia/Ischemia 17% • Hepatic Coma 3.5% • Endocrine Coma 2.5% • Acid-base disturbance 2.5% • Encephalitis 2.8% • Hypothermia 1.8% • Uremia 1.6% • Pulmonary diseases, malnutrition, psychiatric disorders, others 2.5% Hemispheric Disorders: 24% • ICH 9% • Subdural hematomas 5% • SAH 2.6% • Epidural hematomas 1% • Cerebral infarction 1.8% • Brain tumor, abscess, pituitary apoplexy, thalamic infarct 3.4% Infratentorial Disorders: 13% • Brain stem infarction 8% • Brain stem hemorrhage 2.2% • Others: 2.8% 29 y/o university student, 1 day confused and somnolent: Vague history → emergency CT considered normal → skew deviation was missed → neurologist advised “MR tomorrow” in phone consultation. Patient is now demented and dystonic Phone advice without seeing the patient is never a Good Call! Phone consultations: Bad call! Assessment of metabolic encephalopathy • • • • Search for subtle focal clinical signs Make sure laboratory tests are complete Analyse acid-base abnormalities Look for clinical characteristics of specific conditions Hepatic encephalopathy and coma Hepatic encephalopathy is clinically classified in 4 stages: Stage 1 features anxiety and restlessness, or apathy, shortened attention span, and altered sleep patterns. Altered handwriting is an indicator Stage 2 features personality change, disorientation, and psychosis. Asterixis, ataxia, dysarthria and abnormalities of muscle tone appear. Stage 3 features delirium, bizarre behaviour, drowsiness or stupor. Seizures, myoclonus, and hyperreflexia appear. Stage 4 is hepatic coma with flexor or extensor responses, and commonly increased tone, brain swelling progressing to deep coma and brain death. Hepatic coma results from the combined effects of electrolyte disturbance and neurotoxins, including benzodiazepine analogs, glutamate, and ammonia, most often arterial value exceeding 120 micromols/L, and of a systemic inflammatory response, mitochondrial failure, BBB failure, and altered brain perfusion. Flumazenil infusion may improve the conscious state where brain swelling is not the cause of coma. Causes of Anion Gap Metabolic Acidosis Anion gap =Na+ - (Cl- + HCO3-); normal = 12-15 • • • • • • • • Exogenous Salicylates Methanol Ethylene glycol Iron Paraldehyde Cyanide Carbon monoxide Isoniazid Endogenous • Uremia • Ketoacidosis • Lactic acidosis Hypertensive encephalopathy and posterior white matter disease Endocrine Derangement Left: cortical damage in hypoglycemia; Right: Hashimotos encephalopathy Septic encephalopathy Disease outside the brain must be considered: critical illness myoneuropathy, other neuromuscular disease, or myelopathy? Careful review for toxicity: cumulative effects of sedative drugs are underestimated (prolonged half-lives; third-spacing). Endogenous toxins through organ failure? Left: mutifocal bleeding (ECMO patient); Right: septic emboli with endocarditis Bihemispheric brain injury must be excluded (endocarditis, multiple infarcts, abscesses; multifocal haemorrhage; anoxic injury; brain swelling). Nonconvulsive status epilepticus is underdiagnosed. The septic process itself may cause persistent cognitive deficits and brain atrophy after recovery ( images bottom left and right). A 51 year old patient with cognitive loss following severe sepsis. MRI on left during sepsis; MRI right performed 3 months later shows enlarging CSF spaces Medication effects Left: Leukoencephalopathy due to 5FU-Metimazole (chemotherapy for bowel cancer) Below: PRES and hemorrhage with tacrolimus after stem cell transplantation Anoxic-ischaemic coma after resuscitation • 50-100 per 100 000 per year undergo CPR • 25% are admitted to hospital • 10% are discharged alive • 5% are alive after 1 year Pathophysiology of hypoxic brain injury y cit i x o c Ex t ito ATP deficit NA/K pump failure Energy failure Depolarisation Glutamate release Metabotropic Ca++ channels open Voltage-gated Ca++ channels open ROS Intracellular Ca-influx Phospholipase Mi dy tocho CPR sfu n nct drTia Mitochondrial i l injury + swelling on Reperfusion r Aquaporin(AQP8/9) e channels activated →H2O influx a Inflammation t Cytokine Cytochrome C release m Caspase activation e ROS n Apoptosis t Secondary Ischaemia / Hypoxia ROS Protease Cell Death hypoperfusion Diencephalic hypoxic injury after asthma attack causing respiratory arrest. Prolonged coma with prominent autonomic dysregulation. Neurological complications in known medical conditions Complications of systemic infection (septic encephalopathy; critical illness myoneuropathy; endocarditis) Anoxia and cardiac arrest Endocrine disorders Renal disease (uremic encephalopathy, disequilibrium syndrome; hypertensive encephalopathy) Hepatic encephalopathy and fulminant liver failure Disorders of hemostasis and coagulation Acute vasculitic complications Complications of organ transplantation Tests: Laboratory How severe must laboratory abnormalities be to explain coma? • Hyponatremia: <110 mmol/L coma, <120 mmol/L may cause drowsiness if rapid onset • Hypernatremia: >160 mmol/L • Hypercalcemia: >3.4 mmol/L • Hypermagnesemia: >3 mmol/L • Hypercapnia: >70 mm Hg pCO² (9.3kPa) • Hypoglycemia: < 2.5 mmol/L • Hyperglycemia: > 40mmol/L • Hypophosphatemia < 0.2mmol/L Individual toleration varies substantially, and severely ill patients may have multiple coexisting abnormalities Tests : Electrophysiology Seizure? EEG during right facial twitch Neurological Assessment of the Unresponsive Patient: 4 components • Inspection • Brain stem reflexes • Motor function • Sensory testing 1. Inspection • Tone: Normal – spastic/rigid – symmetric or asymmetric – flaccid – varies • Posture: Normal – decorticate – decerebrate hemiparetic • Movements: repetitive – simple – complex – spontaneous or to stimuli – none – face or limbs? • Respiration: – rate and pattern (see below) • Pupils: – size – shape – equal or anisocor • Fundoscopy 2. Brainstem reflexes: • • • • • • Pupillary examination and pupillary reflexes Corneal reflex Eye movements and Oculocephalic Reflex Gag reflex Cough Respiratory pattern Pupillary Abnormalities in Coma From: Wijdicks EFM 2001 The corneal reflex (CN 3 and 7) Brain Control of Eye Movements: 3 separate types of eye movement represent a large area of the brain Saccades (frontal control) Smooth pursuit (parietal) http://cnx.org/contents/29ea21c4-4625-4e86-82be [email protected]:15 1.) Nuclei of oculomotor nerve 2.) Trochlear nucleus 3.) Pons 4.) Fourth ventricle 5.) Abducent nucleus 6.) Vestibular nucleus 7.) Medial longitudinal fasciculus Oculomotor Assessment in Coma •Very reliable for identifying lesion location •Supratentorial lesions cause conjugated abnormalities of eye movements Vergence towards or away from lesion Abnormalities of saccadic gaze (frontal lesions) Abnormalities of smooth pursuit (ipsilateral parietal lesions) Preserved passive ocular motility •Metabolic disorders cause slowed passive movements and mild divergence •Asymmetric/disconjugate eye positions always signify brain stem dysfunction •Characteristic oculomotor syndromes exist for some specific lesions (INO, abnormal vertical motility, ocular bobbing, skew deviation) Rotate the head while observing the movements of both eyes. Exclude cervical trauma first! Respiratory Patterns in Craniocaudal Progression of Coma • Cheyne-Stokes respiration: slow periods of hyperventilation that alternate gradually with periods of hypoventilation (bihemispheric / metabolic) • Central neurogenic hyperventilation: rapid breathing 40-70 respirations/min (midbrain lesion) without variation • Apneustic breathing: slow with prolonged pauses between inspiration and expiration (pontine lesion) • Rapid cycle breathing (uncertain localization, but unfavourable) • Cluster breathing: clusters of breaths followed by apneic periods of variable duration (caudal pontine) • Ataxic breathing (Biot’s): irregular respiratory rate and rhythm (medullary; soon to followed by apnoea) The gag (pharyngeal) reflex (CN 9 and 10) and assessment of the tongue (CN12 3. Motor Function in the Assessment of Coma • Brain stem reflexes • Motor function (tone, response to pain, tendon reflexes and plantars, note especially symmetry left-to-right and arms-to-legs) • Sensory testing • Scores 4. Sensory Function in the Assessment of Coma • Brain stem reflexes • Motor function • Sensory testing Test pain Elicit maximum response Examine for sensory levels • Score Eyes 4 = open + tracking 3 = open spontaneously 2 = to speech 1 = to pain 0 = closed Brainstem 4 = Pupil + corneals + 3 = one pupil dilated 2 = pupil or corneals absent 1 = pupil and corneals absent 0 = cough absent Motor 4 = obeys 3 = localizes 2 = flexion 1 = extends 0 = none or myoclonus Respiration 4 = normal pattern 3 = Cheyne Stokes 2 = irregular 1 = breathes above ventilator 0 = breathes at ventilator Scores in the Assessment of Coma: The FOUR Score [EFM Wijdicks 2005] STANDARDISED NEUROLOGICAL ASSESSMENT of the COMATOSE PATIENT Inspection: Speech Facial (droop R/L; grimacing) Tone Posture Movements (complex/repet/stereo) Respiration (rate and pattern) On Admission Date__________ Review Date___________ Review Date___________ Speech Oriented Confused Inappropriate words Incomprehensible No sounds Tone Normal Spastic Rigid Flaccid Posture Normal Decorticate Decerebrate Hemiplegic Symmetrical Asymmetrical Variable Fundoscopy (R/L) Autonomic findings Notable other observations Brain stem reflexes: Pupils (size and reflexes) Spontaneous eye movements Eye movements to pain Oculocephalic reflex FOUR score criteria Eye response (E) 4 = eyelids open/opened/tracking/blinking 3 = eyelids open but not tracking 2 = eyelids closed but open to loud voice 1 = eyelids closed but open to pain 0 = eyelids remain closed with pain Corneal reflex (R/L) Masseter reflex Pharyngeal sensation (gag) Tracheal sensation (cough) Eye response Motor response Pupillary (Y/N) FOUR score Brainstem reflexes Corneal (Y/N) Cough (Y/N) Score Respiration Total FOUR score Imaging results Motor response (M) 4 = thumbs-up, fist or peace sign 3 = localising to pain 2 = flexion response to pain 1 = extension response to pain 0 = no response to pain, or myoclonic status epilepticus Brainstem reflexes (B) 4 = pupil and corneal reflexes present 3 = one pupil wide and fixed 2 = pupil or corneal reflexes absent 1 = pupil and corneal reflexes absent 0 = absent pupil, corneal and cough reflexes Respiration (R) 4 = not intubated, regular breathing pattern 3 = not intubated, Cheyne-Stokes breathing 2 = not intubated, irregular breathing 1 = breathes above ventilator rate 0 = breathes at ventilator rate, or apnoea What are epileptic seizures? • • Clinical manifestations of abnormal hypersynchronous discharges of cortical neurons Symptoms depend on the location of the epileptic discharges in the cortex and on the pattern how they propagate in the brain (Cavazos 2010) Why is optimal seizure management important? • Convulsive status epilepticus is life-threatening • Seizures elevate ICP • Seizures may provoke cardiac failure • Nonconvulsive status alters conscious state • Antiepileptic drugs may affect consciousness • Drug interactions may affect other treatment Seizures drive up CBF and rSO2 elevate ICP Approach to Suspected Seizures on ICU Unexplained impaired consciousness or recurrent episodic stereotypies 1. Document the clinical features: – Duration of event (more than seconds?) – Pattern of movement (stereotyped episodes?) – Complex or elementary movements – Externally triggered events? (normally not) – Tremor or clonic movements? (not tremor) 2. Seek EEG confirmation – Preferably before medication – Only EEG changes during a clinical episode are proof Caveat: – Negative interictal EEG is not an exclusion – EEG “epileptiform” changes are not absolutes 3 main groups of patients with neuromuscular disease may require treatment in the ICU I. Patients with severe new onset acquired neuromuscular disease (eg. GBS) II. Patients with pre-existing chronic neuromuscular diseases who develop acute complications (eg. Myasthenia) III. Patients whose neuromuscular condition arises in the ICU (eg. ICUAW / critical illness neuromyopathy) M. S. Damian, Addenbrookes Hospital, Cambridge Patient found to be weak in the ICU (slow wean; ptosis; limb weakness) Clinical examination: Consciousness affected? Muscle tone increased? Plantars up? → 3x “No” suggests neuromuscular disease ↓ MRI: Exclude brain (if face affected) or spinal (limbs only) disease ↓ CSF and baseline labs: protein? Cell count? CK? Tox screen? ↓ NCV, RepStim and EMG: Nerve root vs. nerve vs. NMJ vs. Muscle? ↓ Special labs: Anti-GM1/GM2/GD1a/GQ1b; Anti-AchR/MuSK/VGKC; DNA tests ↓ Muscle/Nerve biopsy: If NCV and RepStim inconclusive M. S. Damian, Addenbrookes Hospital, Cambridge 3 major subtypes of ICUAW: 1.) Acute myosin loss myopathy – Also in steroids without neuromuscular blocking drugs – Selective loss of the thick (myosin) filaments – Recovery is normally good, but takes several months Absent A-band M. S. Damian, Addenbrookes Hospital, Cambridge ICUAW 2. Acute type 2 fibre atrophy 3. Acute necrotizing myopathy M. S. Damian, Addenbrookes Hospital, Cambridge Beware of your limitations! Specialised Neurointensive Care improves outcomes ▲ Neurocritical care unit; ▲ General ICU with full-time neurological support; Δ General ICU with limited neurological support Questions? M. S. Damian, Addenbrookes Hospital, Cambridge