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Napoli 12-13 maggio2016
Presidente del Congresso: Prof. Carlo Di Iorio.
Coordinamento Scientifico: D.ssa Carla Maglione, Dr. Tullio Cafiero, Dr. Antonio Frangiosa, Dr. Federico Bilotta.
IL MONITORAGGIO NEUROLOGICO NEL PAZIENTE CON DEBOLEZZA MUSCOLARE Nicola Latronico Dipartimento di Specialità Medico-Chirurgiche, Scienze Radiologiche e Sanità Pubblica Università degli Studi di Brescia Dipartimento di Anestesia e Rianimazione Emergenza Urgenza ASST degli Spedali Civili di Brescia Paresis acquired in the intensive care unit: a
prospective multicenter study
De Jonghe B, et al. JAMA 2002; 288:2859-2867
• Among the 95 patients who achieved satisfactory awakening, the incidence of ICU-acquired paresis
was 25.3%.
• Duration of mechanical ventilation after day 1 was significantly longer in patients with ICUAP compared
with those without (18.2 vs 7.6 days).
A guided approach to diagnose severe muscle
weakness in the intensive care unit
Nicola Latronico and Rik Gosselink Rev Bras Ter Intensiva 2015; 27(3):199-201
In the ICU, severe muscle weakness is independently
associated with prolonged mechanical ventilation, ICU
stay, hospital stay and increased mortality.
Patients developing weakness during the ICU stay have
reduced quality of life and increased mortality 1 year
after ICU discharge.
normal CMAP & no weakness abnormal CMAP & no weakness normal CMAP & weakness abnormal CMAP & weakness Hermans G, et al. Predictive value for weakness and 1-year mortality of screening electrophysiology tests in the ICU.
Intensive Care Med 2015; 41(12):2138-48
• The term designates clinically detected
weakness in critically ill patients in whom there is no plausible etiology other than critical illness. Stevens R, et al. A framework for diagnosing and classifying intensive care unit-acquired weakness. Crit Care
Med
2009; 37[Suppl.]:S299 –S308
• The weakness must follow the onset of the critical illness. Guillain-Barré Syndrome (GBS)
• GBS is often considered in the differential diagnosis of CIP, but distinction is usually obvious. • GBS is a (rare) cause of ICU admission, whereas CIP arises as a complication of critical illness after ICU admission. • However, the differential diagnosis can be difficult in cases of rapid progression of respiratory failure in previously undiagnosed GBS ACUTE NEUROMUSCULAR RESPIRATORY FAILURE
Cabrera Serrano M, Rabinstein AA. Causes and Outcomes of Acute Neuromuscular Respiratory Failure. Arch
Neurol
2010;67(9):1089-1094
The weakness must follow the onset of the critical illness. • Physical examination shows diffuse, symmetric weakness involving all extremities and respiratory muscles. ICUAW is usually excluded if:
1. clinical signs suggest a CNS disease (i.e. Babinski signs, increased deep tendon reflexes, spasticity, widespread muscle fasciculation, and focal neurological signs); 2. facial muscles are involved (i.e. drooping of the eyelids, weakness of extraocular muscles with diplopia, facial nerve palsy with altered patient's expression, and difficulty in speech, chewing or swal owing); 3. distribution of muscle weakness is asymmetrical (i.e. monoparesis or hemiparesis); 4. progression of muscle weakness suggests a specific diagnosis, for example, the pattern is ascending (Guil ain–Barre´ syndrome) or descending (botulin intoxication); 5. muscle weakness is fluctuating and worsens after brief exercise indicating muscle fatigability and neuromuscular transmission defect (myasthenia gravis) or improves after exercise indicating pre-synaptic neuromuscular defect (Lambert–Eaton syndrome); 6. there are associated abnormalities such as skin rash or abdominal pain pointing to dermatomyositis, vasculitis, porphyria, or diabetes; 7. there are dysautonomic signs (i.e. dilated pupils poorly reactive to light suggesting botulin intoxication, and cardiac arrhythmias or fluctuations in blood pressure as seen in GBS); 8. pharmacological side effects are suspected (i.e. after prolonged administration of neuromuscular blocking agents, steroids, or cancer chemotherapy). Sharshar T, et al. Neurological examination of critically ill patients: a pragmatic approach. Report of an ESICM expert
panel. Intensive Care Med 2014;40:484-495
The weakness must follow the onset of the critical illness. Physical examination shows diffuse, symmetric weakness involving all extremities and respiratory muscles. • MRC sumscore <48/60, or mean MRC score 4 in all testable muscle groups noted on 2 occasions separated by 24 hrs. Medical Research Council - MRC
complete paralysis minimal contraction active movement with gravity eliminated weak contraction against gravity active movement against gravity and resistance MRC-sumscore (0-60)
Abduction of the arm (0-5) Significant weakness
Flexion of the forearm (0-5) Extension of the wrist (0-5) Flexion of the leg or hip flexion (0-5) Severe weakness
Extension of the knee (0-5) Dorsal flexion of the foot (0-5) Muscle groups (right and left) assessed in the measurement of the MRC-sumscore Kleyweg RP, et al. Muscle Nerve 1991; 14: 1103–09.
De Jonghe B, et al. JAMA 2002; 288: 2859–67.
Hermans G, et al. Muscle Nerve 2012; 45: 18–25


MRC SUM SCORE
Abduction of the arm (0-5) Flexion of the forearm (0-5) Extension of the wrist (0-5) Flexion of the leg (0-5) or hip flexion Extension of the knee (0-5) Dorsal flexion of the foot (0-5) Muscle groups (right and left) assessed in the measurement of the MRC-sumscore De Jonghe B , et al. JAMA 2002; 288:2859-67
Ali NA , et al. Am J Respir Crit Care Med 2008; 178:261-268
Acquired Muscle Weakness in the Surgical Intensive Care
Unit. Nosology, Epidemiology, Diagnosis, and Prevention
Farhan H, et al. Anesthesiology 2016; 124:207-34
Subject cooperation
Technical
Pain, anxiety and its Testing position (preload) treatment effects Training level of the Sensory abnormalities Muscle fatigability Joint-related injury Regional barriers
paralysis
Sensory impairment


Acquired Weakness, Handgrip Strength, and Mortality
in Critically Ill Patients
Am J Respir Crit Care Med 2008; 178:261-268
• MRC & handgrip dynamometry. • 25.7% had ICUAP (a force value of <11 kg-
force for males and <7 kg-force for females). • ICUAP was independently associated with hospital mortality (OR 7.8; 95% CI 2.4 -
25.3).
ICU- and hospital-free days were also
significantly reduced in ICUAP subjects.





Dodds RM, et al. Grip Strength across the Life Course: Normative Data from Twelve British Studies. PLoS ONE 2014; Dec 4;9(12):e113637
TWO-TIER STRENGTH ASSESSMENT APPROACH
(≥ 11 Kg males; ≥ 7 Kg in females) HANDGRIP DYNAMOMETRY
(< 11 Kg males; <7 Kg in females) UNABLE TO PERFORM HGD (no antigravity strength in their elbow Parry SM, et al. A new two-tier strength assessment approach to the diagnosis of weakness in intensive care: an
observational study. Crit Care 2015; 19:52
AWAKENING TIME
Days 9 [IQR 5-12] Parry SM, et al. Crit Care 2015; 19:52
The weakness must follow the onset of the critical illness. Physical examination shows diffuse, symmetric weakness involving all extremities and respiratory muscles. MRC sumscore <48/60, or mean MRC score 4 in all testable muscle groups noted on 2 occasions separated by 24 hrs. • Dependence on mechanical ventilation. Perren A, Brochard L. Intensive Care Med 2013;39(11):1885-95
WEANING & MV
• CIP is an independent risk factor for failed weaning from the ventilator and prolonged mechanical ventilation Latronico N, Bolton CF. Lancet Neurol 2011; 10: 931-41
The weakness must follow the onset of the critical Physical examination shows diffuse, symmetric weakness involving all extremities and respiratory MRC sumscore <48/60, or mean MRC score 4 in all testable muscle groups noted on 2 occasions separated by 24 hrs. Dependence on mechanical ventilation. • Causes of weakness not related to the underlying critical illness have been excluded. Question 7: how should patients be evaluated for ICU-acquired muscle weakness? Differential diagnosis includes concurrent complications:
• electrolyte abnormalities • rhabdomyolysis • nerve compression or entrapment • status epilepticus • use of drugs Sharshar T, et al. Neurological examination of critically ill patients: a pragmatic approach. Report of an ESICM
expert panel. Intensive Care Med 2014;40:484-495
Previously Undiagnosed/New Onset ICU Complication Brain cortex and
Acute disseminated encephalomyelitis Post-cardiac arrest encephalopathy brainstem
Encephalitis (including paralytic form of rabies) Status epilepticus (including nonepileptic) Multiple sclerosis Multiple sclerosis Vascular causes (brainstem infarction or haemorrhage; cerebral haemorrhage; ischaemic stroke) Post-cardiac arrest encephalopathy Status epilepticus Tetanus Vascular causes Spinal cord (including
Amyotrophic lateral sclerosis Compression (tumour, infection, haematoma) Hopkins syndrome anterior horn cells) Malformations (Arnold-Chiari) Transverse myelitis Post-polio syndrome Spinal muscular atrophy Trauma West Nile virus poliomyelitis Peripheral nerve
Acute intermittent porphyria Entrapment neuropathy Chronic inflammatory demyelinating polyneuropathy Entrapment neuropathy Critical illness polyneuropathy Drugs* (bortezomib, cisplatin, dichloroacetate, epothilone, isoniazid, ixabepilone, leflunomide, Guillain-Barré syndrome linezolid, nitrofurantoin, oxaliplatin, pyridoxine, reverse transcriptase inhibitors, statins, taxanes, thalidomide, tumour necrosis factor-alpha blockers, vincristine) Guillain-Barré syndrome Hormonal disorders (acromegaly, hypothyroidism) Infections (diphtheria, HIV, Lyme disease) Tumours (carcinoma, lymphoma, multiple myeloma) Metabolic (diabetes, porphyria, tyrosinaemia, uraemia) Nutritional (thiamine deficiency) Sarcoidosis Toxic (acrylamide; heavy metals: arsenic, thallium, lead, gold; organophosphates; hexacarbons) Vasculitis (polyarteritis nodosa, lupus erythematous, rheumatoid arthritis, Churg-Strauss) Botulism. Lambert-Eaton syndrome. Myasthenia gravis Hypermagnesaemia Hypermagnesaemia junction
Drugs*. ANESTHETIC AGENTS (desflurane, enflurane, halothane, isoflurane, nitrous oxide, opioids, Myasthenia gravis Prolonged neuromuscular propofol, sevoflurane). ANTIBIOTICS: amynoglycosides+ (amikacin, clindamycin, gentamycin, kanamycin,
Snake, scorpion and spider bites lincomycin, neomycin, streptomycin, tobramycin); fluoroquinolones (ciprofloxacin, gemifloxacin, fish, shellfish, jellyfish and crab toxins levofloxacin, lomefloxacin, moxifloxacin, norfloxacin, ofloxacin, and trovafloxacin); macrolides (azithromycin, erythromycin, telithromycin), other antibiotics (ampicillin, bacitarcin, polymyxins,
tetracyclin, imipenem/cilastatin, penicillin, vancomycin). ANTI-ARRHYTHMIC AGENTS (etafenone,
peruvoside, procainamide, propafenone). ANTIEPILEPTICS (carbamazepine, gabapentin, phenytoin,
trimethadione). BETA-BLOCKERS** (atenolol, nadolol, oxprenolol, practolol, propranolol, sotalol,
ophthalmic timolol). CALCIUM-CHANNEL BLOCKERS** (amlodipine, felodipine, nifedipine, verapamil).
CORTICOSTEROIDS***. CHEMOTHERAPICS (doxorubicin, etoposide, cisplatin). H-2 RECEPTOR ANTAGONISTS
(cimetidine, ranitidine, roxatidine). QUINOLONE DERIVATIVES (chloroquine, quinidine, quinine).
NONCOMPETITIVE NEUROMUSCULAR BLOCKING AGENTS+. Psychotropic medications (amitriptyline,
chlorpromazine, haloperidol, imipramine, lithium). OTHER DRUGS (interferon, penicillamine).
Metabolic/congenital Adult-onset acid maltase deficiency Corticosteroid myopathy Mitochondrial myopathies Hypo- and hyperkalaemia Critical illness myopathy Muscular dystrophies Hypophosphataemia Hypo- and hyperkalaemia Periodic paralyses (muscle channelopathiyes) Muscular dystrophies Hypophosphataemia Propofol infusion syndrome Toxic myopathies Latronico N, Fagoni N. Neuromuscular Disorders & Acquired Neuromuscular Weakness. In: Oxford Textbook of Neurocritical Care. Smith M, CITERIO G, Kofke A W (Eds). Oxford University Press, 2016 ICU-ACQUIRED WEAKNESS (ICUAW)
Disuse atrophy
(with muscle deconditioning) Critical Illness
Critical Illness
Myopathy
ICU-ACQUIRED WEAKNESS (ICUAW)
Disuse atrophy
(with muscle deconditioning) Critical Illness
Critical Illness
Myopathy
DISUSE MUSCLE ATROPHY
In healthy adults, muscle strength declines by 1% per day of strict bed rest. Limb immobilization by casting results in a faster decline in muscle strength — about 25% within 7 days. Chambers MA, et al. Physical inactivity and muscle weakness in the critically ill. Crit Care Med 2009; 37(10 Suppl.): S337-46 33
ICU-ACQUIRED WEAKNESS (ICUAW)
Disuse atrophy
(with muscle deconditioning) Critical Illness
Critical Illness
Myopathy
CRITICAL ILLNESS POLYNEUROPATHY
• CIP is a distal axonal sensory-motor polyneuropathy affecting limb and respiratory muscles Latronico N, Bolton CF. Lancet Neurol 2011; 10: 931-41
CRITICAL ILLNESS POLYNEUROPATHY
Latronico N, et al. Lancet 1996; 347:1579-1582
ICU-ACQUIRED WEAKNESS (ICUAW)
Disuse atrophy
(with muscle deconditioning) Critical Illness
Critical Illness
Myopathy
CRITICAL ILLNESS MYOPATHY
• CIM is a primary myopathy that is not secondary to muscle denervation, with distinctive electrophysiological and morphological findings Latronico N, Bolton CF. Lancet Neurol 2011; 10: 931-41
CRITICAL ILLNESS MYOPATHY
Condition
Incidence
Clinical features
Electrophysiologic Serum
Muscle biopsy
Prognosis
findings
creatine kinase
Thick-filament myopathy Common with steroids, Flaccid limbs; respiratory Abnormal spontaneous neuromuscular blocking (myosin) filaments agents, and sepsis Acute myopathy with scattered Common Flaccid limbs; respiratory Mildly or moderately Scattered necrosis Acute myopathy with diffuse Flaccid weakness; Markedly elevated, necrosis (necrotising myopathy of intensive care) Disuse (cachectic) myopathy Normal or type II Markedly elevated Latronico N, Bolton CF. Lancet Neurol 2011; 10: 931-41
THICK FILAMENT MYOPATHY
Latronico N, Tomelleri G, Filosto M. Curr Opin Rheumatol 2012; 24:616–622
MUSCLE FIBER NECROSIS
Latronico N, Tomelleri G, Filosto M. Curr Opin Rheumatol 2012; 24:616–622
• Combined CIP and CIM could be the most common manifestation of neuromuscular weakness in the ICU. Latronico N, Bolton CF. Lancet Neurol 2011; 10: 931-41
CIP (denervation)
CIM (primary myopathy)

Latronico N, et al. Curr Opin Crit Care 2005; 11:381-390
SMALL NERVE FIBER PATHOLOGY IN
CRITICAL ILLNESS
• Of the 14 patients recruited, 13 (93%) had infections, sepsis or multiple organ failure. • All had degeneration of small nerve fibers, and reduced sweat gland innervation. • Of the 7 patients available for follow-up visit, three complained of diffuse sensory loss and burning pain, and another three showed clinical dysautonomia. Latronico N, et al. PLoS One 2013 Sep 30;8(9):e75696
Critical y il patient Severe depletion of intra-
epidermal nerve fibers
Severe reduction in the
density of dermal nerve
bundles
Severe reduction of sweat
gland
innervation
SIMPLIFIED ELECTROPHYSIOLOGICAL TESTS
Latronico N, Smith M. Intensive Care Med 2014;40(5):746-8
Validation of the peroneal nerve test to diagnose critical illness
polyneuropathy and myopathy in the intensive care unit:
the multicentre Italian CRIMYNE-2 diagnostic accuracy study.
Latronico N, Nattino G, Guarneri B, Fagoni N, Amantini A, Bertolini G, and GiVITI Study Investigators F1000Research 2014; 3:127
Objectives: accuracy of PENT compared
to complete NCS-EMG.
Patients: 121 pts (neurologic 106 and
non-neurologic 15, LOS ≥ 3 days in 9
Italian ICUs.
Measurements and main results: Same
day, independent clinicians, blind
assessment.
CRIMYNE-2
• Sensitivity and specificity of PENT were 100% (95% CI 96.1-100.0) and 85.2% (95%
CI 66.3-95.8).
• The median time needed to perform PENT and the complete NCS-EMG was 10
minutes
(IQR 8.0-10.5) and 50 minutes (40-
60)
SIMPLIFIED ELECTROPHYSIOLOGICAL TESTS
van den Berghe G, et al. Intensive insulin therapy in the critical y il patients. N Engl J Med 2001;
Van den Berghe G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med 2006; 354:449-461
Latronico N, et al. Simplified electrophysiological evaluation of peripheral nerves in critically ill patients: the Italian multi-centre CRIMYNE study. Crit Care 2007; 11(1):R11
Weber-Carstens S, et al. Nonexcitable muscle membrane predicts intensive care unit-acquired paresis in mechanical y ventilated, sedated patients. Crit Care Med 2009; 37:2632-2637
Moss M, et al. Screening for critical il ness polyneuromyopathy with single nerve conduction studies. Intensive Care Med 2014; 40(5):683-90
Latronico N, et al. Validation of the peroneal nerve test to diagnose critical il ness polyneuropathy and myopathy in the intensive care unit: the multicentre Italian CRIMYNE-2 diagnostic accuracy study. F1000Research 2014; 3:127
Hermans G, et al. Predictive value for weakness and 1-year mortality of screening electrophysiology tests in the ICU. Intensive Care Med 2015; 41(12):2138-48
Impression of muscle weakness Critical illness Consider other diagnoses Reassess the patient at later • CIP and/or CIM Diagnosis useful assessment valid electrophysiologic test Consider Increased CMAP duration or direct muscle stimulation in non collaborative patients Rehabilitation (1-2 weeks) • CIP • CIM • Combined CIP and CIM Latronico N, Gosselink RF. Rev Bras Ter Intensiva 2015; 27(3):199-201

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