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An acute or subacute symmetrical polyneuropathy is a frequent development in critically ill and septic patients, particularly in those with failure of multiple organs (Zochodne et al) This type of neuropathy causes dif culty in weaning a patient from the ventilator, even as the underlying critical illness comes under control The neuropathic process, predominantly of motor type, varies in severity from an electrophysiologic abnormality without obvious clinical signs to a pronounced quadriparesis with respiratory failure Sensory symptoms and signs are variable but tend to be mild Usually the cranial nerves are spared and there are no overt dysautonomic manifestations In general, the disease appears after several days or more of profound sepsis (now called systemic in ammatory response syndrome SIRS) and multiple organ failure and is preceded in most instances by a confusional state or a depressed state of consciousness ( septic encephalopathy ) The EMG ndings of a primary axonal process with early denervation and a normal CSF distinguish this entity from the typical demyelinative form of GBS Autopsy material has usually disclosed no in ammatory changes in the peripheral nerves As mentioned, differentiating critical illness polyneuropathy from the axonal form of GBS is dif cult and depends on the context in which the illness occurs The toxic effects of drugs and antibiotics and nutritional de ciency must be considered in causation, but rarely can they be established Perhaps some of the many systemic mediators of sepsis are toxic to the peripheral nervous system; tumor necrosis factor has been proposed as one such endogeneous toxin This form of polyneuropathy must also be distinguished from a poorly understood acute quadriplegic myopathy that sometimes complicates critical illness (page 1237) High doses of corticosteroids, particularly in combination with neuromuscular blocking agents, have been implicated The acute myopathy, which affects both distal and proximal muscles, is usually heralded by an elevation in the serum creatine kinase (CK) concentration (at times up to several thousand units) and myopathic potentials in the EMG, and there is a unique degeneration of myo laments in all the muscles This illness is described in more detail in Chap 51.

Table 11-3

Acute Sensory Neuronopathy (Sensory Ganglionopathy)

Once you have a table and have added data, you can send a SQL query to look into a table and pull out whatever you want The first SQL command for making queries is SELECT It specifies the fields that you want to query, that is, to find out what their values are The SELECT command needs a FROM clause to specify the table where the query will occur The basic format is

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If you want to look at all of them, you can use the * wildcard symbol For example,

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Attention was drawn to this entity by Sterman and colleagues in a report of three adult patients with rapidly evolving sensory ataxia, are exia, numbness, and pain, beginning in the face and spreading to involve the entire body In each instance, the symptoms began within 4 to 12 days following the institution of penicillin therapy for a febrile illness (antibiotics were subsequently shown not to be the cause) Proprioception was profoundly reduced, but there was no weakness or muscle atrophy, despite generalized are exia The sensory de cit attained its maximum severity within a week, after which it stabilized and improved very little Electrophysiologic studies showed absent or slowed sensory conduction but there were no abnormalities of motor nerve conduction or signs of denervation In two of these patients, the CSF protein content was elevated to 126 and 175 mg/dL Follow-up observations (for up to 5 years) disclosed no neoplastic or immunologic disorder, the usual causes of such a sensory neuronopathy Lacking pathology, it was assumed, from the permanence of the condition, that sensory neurons were destroyed (sensory neuronopathy) In all likelihood, these cases were postinfectious and immune mediated A subsequent series of 42 patients reported by Windebank and colleagues emphasized an asymmetrical and brachial pattern of symptoms in some patients and an initial affection of the face in others In contrast to Sterman s cases, the CSF was usually normal and most patients had some improvement or a spontaneous resolution of symptoms These authors viewed the process as a sensory neuropathy In this and subsequent reports, as mentioned, antibiotics were not implicated At present, this clinical pattern should be viewed as a syndrome rather than as a disease Probably, some instances are immune-postinfectious in nature The same pattern of sensory loss evolving in a subacute or chronic manner is well known to occur as a paraneoplastic illness, described further on in this chapter, or in association with the Sjogren syndrome, scleroderma, lupus erythematosus, paraproteinemia, and HTLV-I infection Certain drugs and other agents, especially cisplatin and excessive intake of pyridoxine, are also causes of a sensory neuronopathy Also to be distinguished from sensory neuronopathy is a rare form of GBS that involves solely the large sensory bers and produces ataxia In the latter, there is usually some degree of proximal weakness, and the sensory changes do not normally extend to the face and trunk.

examines all of the columns in the table, including the SupID field that was not specified in the first query of the table

a the processextendsthe curve extrapolationrepresents step into the unknown because beyondthe known regionAs such,the true curve could easilydivergeliom the prediction Extreme care should, therefore,be exercisedwhenever a case arises where one mu$ extrapolate

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