Critical illness polyneuromyopathy after artificial respiration

Coul, A. A. W. Op De; Verheul, G. A. M.; Leyten, A. C. M.; Schellens, Ronald L. L. A.; Teepen, Johannes L.

doi:10.1016/0303-8467(91)90005-a

Cited by 112 publications

(61 citation statements)

References 11 publications

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“…Abnormal spontaneous electrical activity presenting as fibrillation potentials or positive sharp waves may be due to denervation in CIP but also may occur in CIM due to muscle sodium channel dysfunction (580,581) Fiber atrophy with abnormal variation in size of muscle fibers, angulated fibers, fatty degeneration, fibrosis; mostly affecting both fiber types, may be limited to type II fibers or secondary involvement of nerve endings in primary myopathy (126,403,577,742). Terms such as critical illness polyneuromyopathy or the acronym CRIMYNE subsequently emerged (401,405,528). To emphasize the clinical problem of muscle weakness, regardless of its cause, descriptive terminology such as ICU acquired paresis, critical illness neuromuscular abnormalities, acquired neuromuscular disorders, or ICU-acquired (muscle) weakness was launched (145,618).…”

Section: History Time Course and Clinical Features Of Icu-relatmentioning

confidence: 99%

“…The presence of sodium channelopathy in both muscle and nerve might provide a mechanism to explain why critical illness myopathy and critical illness neuropathy often coexist (43, 44, 64,147,361,403,413,528,614). When patients with co-occurrence of neuropathy and myopathy are studied longitudinally, many evolve into either CIP or CIM (43, 273,361).…”

Section: Are Electrically Active Tissues Other Than Skeletal Muscle Amentioning

confidence: 99%

“…These conditions are the primary cause of muscle weakness and paralysis during and following critical illness (402). Weakness appears to be triggered by critical illness and the ICU course regardless of the underlying primary condition (382,453,528). The chance of developing muscle weakness correlates with the severity of critical illness, as assessed by several organ dysfunction scores (149,181,370,763), and represents a pathophysiological process that cannot be explained by immobilization alone (181).…”

Section: Introductionmentioning

confidence: 99%

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The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

291

329

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Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

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Section: History Time Course and Clinical Features Of Icu-relatmentioning

confidence: 99%

Section: Are Electrically Active Tissues Other Than Skeletal Muscle Amentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

291

329

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“…Outros autores obttiveram achados semelhantes. Em 1990, Op-de-Coul et al 11 descreveram 22 pacientes com tetraparesia flácida importante, arreflexia e atrofia muscular depois de duas semanas de respiração artificial e com evolução favorável. Ebeling et al 12 relataram cinco pacientes com falência de múltiplos órgãos e fraqueza muscular, com alterações da ENMG eletromiográficas compatíveis com degeneração axonal.…”

Section: Discussionunclassified

Polineuropatia do paciente crítico: registro de caso

Alvim¹,

Freitas

Nascimento

et al. 1999

Arq. Neuro-Psiquiatr.

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RESUMO -A polineuropatia do paciente crítico é de natureza axonal, aguda e de predomínio motor, desenvolvendo-se em pacientes sépticos ou com falência de múltiplos órgãos que geralmente necessitam de ventilação mecânica em unidade de tratamento intensivo. Seu diagnóstico é corroborado por achados eletroneuromiográficos e, geralmente, a evolução é satisfatória e rápida. Relatamos o caso de uma paciente de 35 anos que, após internação em unidade de tratamento intensivo devido a septicemia e retirada de feto morto, desenvolveu tetraparesia com melhora importante em quatro meses. A eletroneuromiografia mostrou diminuição de amplitudes de potenciais sensitivos e motores, ondas positivas e fibrilações. A biópsia de nervo sural evidenciou neuropatia axono-mielínica em atividade. Estando esses achados condizentes com os da literatura, acreditamos tratar-se de caso de polineuropatia do paciente crítico.PALAVRAS-CHAVE: polineuropatia, axonal, sepsis. Critical illness polyneuropathy: case reportABSTRACT -The critical illness polyneuropathy has an acute onset and an axonal predominantly motor nature. It occurs in sepsis or in multiple organ failure usually requiring mechanical ventilation in critical care units. Electroneuromyography corroborates the diagnosis. Usually it courses satisfactorily. We report on a 35-year-old female patient who, after a permanence in a critical care unit due to sepsis and removal of a dead phetus, developed tetraparesis. She had an important improvement in four months. Electromyography showed reduction of amplitude of motor and sensory action potentials, positive waves and fibrillations. The sural nerve biopsy showed axonmyelinic neuropathy. These findings are consistent with those in literature and we believe they support the diagnosis of critical illness neuropathy. KEY-WORDS: polyneuropathy, axonal, sepsis.A polineuropatia do paciente crítico é de natureza axonal, predominantemente motora, simétrica e aguda 1,2 . Foi primeiramente reconhecida por Bolton et al.1,3-5 em pacientes em unidades de tratamento intensivo que apresentavam dificuldade no desmame da ventilação mecânica e nos quais se verificava tetraparesia e reflexos profundos abolidos. Está associada a sepsis ou falência de múltiplos órgãos [1][2][3][4][5][6][7][8] . Zochodne et al. 4 definem a sepsis como septicemia ou infecção localizada com efeitos sistêmicos. A falência de múltiplos órgãos pode ocorrer eventualmente sem sepsis, como resultado de doença primária grave. Isso tudo pode ser englobado dentro da síndrome da resposta inflamatória sistêmica (SIRS). Sugere-se que a patogenia desta polineuropatia esteja relacionada com a própria sepsis 3,4,6,9 , durante a qual há distúrbios na microcirculação, perda da autorregulação dos vasos sanguíneos que suprem os nervos periféricos e liberação de citocinas que também aumentam a permeabilidade dos vasos, tudo

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“…Early studies of CIP revealed a high frequency of concurrent myopathic changes suggesting that, at least in some patients, CIP may occur concomitantly with CIM [16]. It was later suggested that neuropathy and myopathy might be acquired in tandem during critical illness [17]. Multiple prospective studies subsequently reported combined myopathic and neuropathic findings in individual patients on the basis of either electrophysiologic or biopsy specimens [12,18,19].…”

Section: Incidence Of Acquired Neuromuscular Dysfunction In the Icumentioning

confidence: 99%

Mechanisms of Neuromuscular Dysfunction in Critical Illness

Khan

Harrison

Rich

2008

Critical Care Clinics

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The development of neuromuscular dysfunction (NMD) during critical illness is increasingly recognized as a cause of failure to wean from mechanical ventilation and is associated with significant morbidity and mortality. At times it is difficult to identify the presence of NMD and distinguish the etiology of the weakness in patients with critical illness, but subtle clinical findings and bedside electrophysiological testing are helpful in establishing the diagnosis. The purpose of this review is to describe the clinical spectrum of acquired neuromuscular weakness in the setting of critical illness, provide an approach to diagnosis, and to discuss its pathogenesis. Finally, we propose defective sodium channel regulation as a unifying mechanism underlying NMD in critically ill patients.

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Critical illness polyneuromyopathy after artificial respiration

Cited by 112 publications

References 11 publications

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Polineuropatia do paciente crítico: registro de caso

Mechanisms of Neuromuscular Dysfunction in Critical Illness

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