Critical illness polyneuropathy-1

Critical illness polyneuropathy-1 - Critical illness...

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Unformatted text preview: Critical illness polyneuropathy Critical illness polyneuropathy From = Critical care medicine 2002 ,8 , 302—310 Authors = Walther N.K.A. van Mook, MD, and Riquette P.M.G. Hulsewé­Evers, MD 報報報 : 趙趙趙 Abstract **Critical illness polyneuropathy(CIP) = first extensively described in the early 1980s, mainly in patients with failure to wean from mechanical ventilation **limb muscle weakness, usually more distally than proximally **The facial musculature is often strikingly spared. **Reduced DTR and loss of peripheral sensation to light touch and pin prick often accompanied **Involvement of the phrenic nerve will cause delayed weaning. **electrophysiologic studies= predominantly motor and, often to a lesser extent, sensory axonal polyneuropathy. **incidence =>50% of patients in major medical and surgical critical care units **The systemic inflammatory response syndrome(SIRS) is strongly associated with CIP and, among the multiorgan failure often seen in SIRS, CIP is thought to represent a neurologic manifestation of SIRS. **Mechanism = cytokines and free radicals, affecting the microcirculation of the nervous system **Examination of the peripheral nervous system is often unreliable **the only way to establish a definitive diagnosis =electrophysiologic studies. **Onset = 80% within 72hrs after SIRS/sepsis **recovery was very slow = weeks to months Epidemiology Epidemiology Diagnosis Clinical presentation Laboratory parameters Electrophysiologic studies Nerve and muscle biopsies Additional techniques Differential diagnosis Clinical presentation **early stages = PE unreliable due to encephalopathy or sedation. **Even after the encephalopathy disappears, a proper and complete neurologic examination can be difficult to perform **The discrepancy between grimacing of facial musculature in response to a painful stimulus and the complete absence of limb movement is often striking. **weakness usually more pronounced distally than proximally and is often accompanied by muscle atrophy. **DTR are usually absent or decreased. **Loss of peripheral sensation to light touch and pin prick and relative preservation of cranial nerve function also result from the syndrome. Lab **mostly not diagnostic, CK only marginally raised or normal in most pts Electrophysiologic studies Electrophysiologic **1.sensitive tools 2.could be quantified **NCV = unchanged. **relatively pure axonal polyneuropathy **Reduced action potential both in motor and sensory nerve. (However,reduction of the CMAP may also be the result of severe muscle atrophy(motor) or tissue edema (sensory) **spontaneous activity with fibrillations and positive sharp waves in a widespread distribution as signs of denervation **Apart from involvement of the chest wall muscles, diaphragmatic denervation in patients with CIP seems to play a role in ventilator dependency. **One study = 60% patients showed evidence of diaphragmatic denervation as determined by diaphragmatic needle EMG **Another study = 54% exhibited diaphragmatic denervation as determined by phrenic nerve conduction studies in combination with electromyography (However, this denervation is frequently attributable to causes other than CIP (eg, mediastinal pathology)) Nerve and muscle Bx ## Nerve Bx **In 1994 review Bx of 19 pts *15/19(79%) nerve biopsies =axonal pathology with primary axonal degeneration without demyelinization was found *Distal nerves to be more severely involved, whereas the more central nerves like the vagal and was relatively spared *No inflammatory changes have been reported in nerve biopsies **Latronico et al. 22 Pts /c CIP =14 normal nerves and only 8 had axonal neuropathy **sepsis­related CIP may caused impairment of axonal transport and transmembrane potential in early stage which could not be detected by nerve biopsy. **If sepsis persistented , significant axonal neuropathy may be seen **Thus, the absence of histologic indicators of nerve damage does not exclude significant functional impairment Muscle Bx **Atrophy of predominantly type II fibers as evidence of innervation loss is the most commonly found abnormality and is almost always present **In several studies, muscle biopsy examination yielded striking abnormalities *One prosepctive study = Muscle fiber necrosis occurred in 30% of cases == the myopathic changes secondary or primary **Coakley et al. performed muscle biopsies in 24 pts == No clear relation between changes in these biopsies and the observed neurophysiologic abnormalities was found. Histologic normal muscle was found only in patients with normal electrophysiologic results ** In a study by Latronico et al. *muscle alterations were found in 23/24 pts, with abnormalities ranging from primary myopathic, neurogenic, or both. **in a study by De Letter et al.= 30patients with CIP, and neuropathic changes were found in 11 of 30(37%), myopathic changes in 12 of 30 (40%), and both in 7 of 30 (30%). ** Thus sepsis­ and SIRS related myopathies occur more frequently than previously recognized and sometimes in combination with CIP. **Perhaps the term critical illness myo­ and (poly)neuropathy is more applicable in many patients. Additional techniques **NCV and conventional EMG = hard to d/d neuropathy and myopathy = Both low CMAP and frequently show spontaneous activity in the form of fibrillation potentials and positive sharp waves. **Measurement of muscle fiber excitability by direct muscle stimulation and quantitativ electromyography is valuable in differentiating myopathy and neuropathy. Differential diagnosis 1.Weakness before ICU admission * Brain and spinal cord dysfunction resulting from trauma, neoplasm, infection, or systemic illness * worseningof preexisting diseases and occurrence of new diseasesof motor neurons, nerves, neuromuscular junction, 2.Weakness after ICU admission *CIP, other ICU­acquired neuropathies,disorders of neuromuscular transmission, and myopathies Table 2 and Fig 1 Neuromuscular disorders of critical illness Neuromuscular Critical illness polyneuropathy. Critical Delayed reversal of neuromuscular blockade. Delayed Acute myopathy, Acute divided into two pathogenetically distinct syndromes divided 1. critical illness myopathy critical 2.myopathy associated with combined use of a 2. corticosteroid and a neuromuscular blocking drug. Delayed reversal of neuromuscular blockade. Delayed **pancuronium and vecuronium, are normally cleared from the circulation within several hours, primarily by the liver. **In patients with poor renal function ,functionally active 3­hydroxy metabolites of these drugs accumulate and persist in the blood. **As a result, NM block effect may lasted one week after drugs DC . **Dx = 1.EMG = Train of four twitch 2. anticholinesterase inhibitor test Acute myopathy, =critical illness myopathy Acute ** As with critical illness polyneuropathy, this form of acute muscle injury is strongly associated with sepsis and MOF **Mechanism effects of microorganism­associated toxins, as is observed in toxic shock syndrome and in occasional infections with influenza or other viruses .(SARS) 2.inflammatory mediators that are implicated generally in the systemic inflammatory response syndrome. **Whether peripheral nerve and muscle are injured simultaneously by the same process, or independently by separate processes in the SIRS , remains to be determined. Myopathy associated with steroid and NM blocking agent **s/s = symmetrical weakness , reduced DTR ,reserved sensory function ,and elevated CK + myoglobinuria for several days . days ** Bx = selective loss of thick (myosin) ** filaments filaments **First observed in asthma patient with **First steroid and NM block 1.weakness only in the patients who were treated simultaneously with both types of drugs drugs 2.Muscle weakness increased dramatically in frequency and severity with the duration of NM block **Mechanism = unknown >in rats= favor acute form of corticosteroid-induced myopathy. myopathy. Risk factors of CIP SIRS and/or sepsis Steroids Neuromuscular blocking agents Aminoglycoside antibiotics Total parenteral nutrition Vasopressor support Immune mechanisms Neurologic failure Renal replacement therapy Low albumin and elevated glucose levels SIRS and/or sepsis SIRS **in a cohort of open­heart surgery patients, sepsis occurred more in patients with CIP, and patients with CIP suffered longer from sepsis than patients without CIP. **Bacteremia was found to be an independent risk factor for polyneuropathy in a study by van den Berghe Steroid Steroid **The steroid and muscle relaxants have also **The steroid and muscle relaxants have also been implicated as a cause of prolonged weakness. **No study found evidence of a role for steroids in CIP Neuromuscular blocking agents **NMBAs were found to be a risk factor on multivariate analysis in one study, but most studies did not find evidence for a role of NMBAs in CIP Aminoglycoside antibiotics **Aminoglycoside antibiotics administration was the only significant difference between the group the with and the group without CIP (59% vs 19 %) in 2 studies studies Total parenteral nutrition **Total parenteral nutrition has been suggested as a risk factor for CIP risk **Recently, a Garnacho-Montero et al. found TPN et to be independently associated with CIP development on multivariate analysis (P = 0.02). development Vasopressor support **Vasopressor support for more than 3 days was **Vasopressor days an independent predictor of polyneuropathy on an multivariate analysis in study by van den Berghe et al. et **In another prospective study, patients who **In developed CIP used significantly more epinephrine and norepinephrine and less epinephrine dobutamine than patients who did not develop dobutamine CIP. **The presence of Anti­GM1­ganglioside IgG of Immune mechanisms patients with CIP has been demonstrated **The supposed autotoxin may disturb enzymatic processes of the neuron and affect axonal transport of nutrients and degrading products, causing a functional axonopathy. **Many autotoxins have been considered candidates, but TNF has been of special interest because it plays a pivotal role in the activation of other cytokines in the cascade. **However, patients with CIP had no significantly elevated TNF or IL6 compared with control subjects . Neurologic failure In a study by Garnacho­Montero et al. ==GCS < 10 is an independent risk factor for development of CIP. Renal replacement therapy **in the study conducted by Garnacho­Montero et al.= Patients who had undergone renal replacement therapy had a lower risk of developing CIP on multivariate analysis **In the most recent study = renal replacement therapy was found to be an independent predictor of CIP on multivariate analysis Low albumin and elevated glucose levels **Low albumin and elevated glucose levels were mentioned in both retrospective and prospective studies as risk factors for CIP **in another study(large, prospective, randomized ,trial ) ,intensive insulin therapy in critically ill patients reduced the incidence of CIP by 44%, provided strong evidence in favor of a role for hyperglycemia in the pathogenesis of CIP Treatment ** Successful treatment of the underlying sepsis/SIRS remains crucial in the prevention of CIP ** Prevention now seems possible in many cases with intensive glycemic control with insulin in critically ill patients **Immunoglobulins have been used as an adjuvant therapy for sepsis and septic shock and are effective in patients with Guillain­ Barre syndrome **A retrospective study on the effects of early treatment with immunoglobulins in 33 patients who survived MOF or GNB sepsis suggested that this strategy may prevent or mitigate CIP **But high­dose immunoglobulin dministration failed to alter the clinical course Prognosis and outcome Short-term prognosis **recovery will take weeks in mild cases and months in severe cases **Mortality in the ICU was 2 to 3.5 times higher for patients with CIP versus patients without CIP **CIP also have a negative influence on prognosis by causing weaning difficulty. Long term prognosis **Most investigators agree that there is a 50% chance of complete recovery depending on the severity of the initial symptoms **After 1 year of follow­up of 24 pts ,improvements were reported in all patients ,but severe functional handicap was noted in 5/24 patients (22%) **Zifko determined the clinical and electrophysiologic profile of 13 survivors (median f/u 17 Ms) == only two (15%) were clinically normal ,but All patients still had neurophysiologic abnormalities **in one 2­year f/u study analysis in 19 patients with CIP = 10% died 58% recovered completely 32% had remaining quadriparesis = Three parameters were significantly correlated with poor recovery: longer length of stay in ICU, longer duration of sepsis greater body weight loss Conclusions: **Sepsis and/or SIRS are the most important risk factors for CIP. **CIP is a common disorder in surgical patients. **Critical illness myopathy is increasingly recognized and can occur together with CIP. **Direct muscle stimulation and quantitative EMG are valuable in the d/d between CIP and critical illness myopathy. Suxamethonium should be used with caution ** in patients with CIP because of the possibility of the occurrence of life­ threatening hyperkalemia. **Intensive insulin therapy in the ICU to achieve tight glucose control can reduce the incidence of CIP by 44%. **Prospective research with longer follow­up (>3yrs) to determine long­term outcome is necessary to describe rehabilitation problems encountered in CIP patients. Thanks for your attentions ...
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This note was uploaded on 01/02/2012 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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