Keywords
encephalopathy, metals, neuropathy, neurotoxins, occupational disorders, organic solvents, organophosphates, pesticides, toxins
Occupationally related disorders may result from injury, which is not the focus of this chapter, or from exposure to toxins. Many of the chemical agents that are present or are being introduced into the workplace environment may produce behavioral, cognitive, motor, sensory, or autonomic disturbances resulting from disorders of the central or peripheral nervous system (CNS or PNS). In this chapter, attention is focused on some of the main neurotoxic agents to which exposure occurs in the workplace. These may affect workers using or involved in the manufacture of potentially neurotoxic substances and those subject to industrial, agricultural, horticultural, or military exposure.
In order to demonstrate that a particular chemical is neurotoxic or that a certain syndrome is due to neurotoxin exposure, it must be shown that the suspected neurotoxin causes neurologic dysfunction of a consistent nature in exposed humans. The dysfunction may vary in severity between individuals but—depending on their level of exposure—all exposed workers should have some signs of neurotoxicity. Involvement of a single worker suggests that the disorder is not due to a toxin, that toxin exposure did not occur at work, or that exposure resulted from some individual work habit, such as failure to use a protective mask. In practice, many disorders that are presumed to be occupationally related consist of nonspecific symptoms that are common and may occur for a variety of reasons. Furthermore, any publicity about the outbreak of a neurotoxic disorder may lead to identical symptoms in suggestible subjects with less or no exposure to the suspected toxin.
It is often difficult to reproduce a suspected neurotoxic syndrome in animals and thereby provide support for the belief that a substance is indeed neurotoxic. Failure to reproduce in animals a suspected human neurotoxic disorder does not exclude this possibility, as differences in species susceptibility may be responsible and certain impairments, such as of cognitive function, are anyway difficult to reproduce in animals. Moreover, human exposure is often to combinations of several chemicals, which individually may be harmless but in combination lead to neurologic dysfunction. This is because the effects of the different chemicals may be additive or one may potentiate the neurotoxic effects of another, as is illustrated by the effect of adding the nontoxic methyl ethyl ketone to a lowered concentration of the known neurotoxin n -hexane, a practice that led in the past to an outbreak of toxic neuropathy.
Ideally, to establish the toxic basis of a neurologic disorder, it should be possible to identify reproducible pathologic or pathophysiologic changes in the nervous system in humans or animals, and these should account for the clinical features of the disorder. In practice, this is often not possible or feasible.
The temporal profile of the clinical disorder may suggest a neurotoxic disorder. Depending on the toxic agent, there is often little or no latent period between the time of exposure and onset of symptoms, but certain toxic neuropathies (arsenic, thallium, organophosphates) occur after a delay on the order of 2 to 3 weeks. Although cessation of exposure may lead to clinical stabilization or improvement, deterioration may continue for some days to weeks after termination of exposure to certain neurotoxins, a phenomenon termed “coasting.”
Improvement of symptoms during periods away from work, such as at weekends or during vacations, may raise the possibility of a work-related exposure to a neurotoxin, but other factors may be responsible, such as anxiety or disputes with co-workers. These various points are summarized in Table 35-1 .
| History of exposure to a potential neurotoxin |
| Pattern of neurologic dysfunction accords with previously reported cases |
| Exposed co-workers also affected |
| A temporal relation exists between toxin exposure and onset of symptoms, and between cessation of exposure and arrest of progression (sometimes after coasting) |
| If the pathologic and pathophysiologic basis of the disorder have been identified, they should be reproducible and account for the clinical disturbance; an animal model of the disorder may exist |
| Other causes of the disorder have been excluded |
Manifestations of Occupational Neurotoxic Disorders
Acute Encephalopathy
An acute encephalopathy is a common but nonspecific manifestation that may consist solely of headache and malaise that settle shortly after exposure is discontinued. With more severe involvement, symptoms may come to include confusion, irritability, poor concentration, impaired judgment, drowsiness, vertigo, tinnitus, sensory complaints, ataxia, weakness or fatigue, and nausea and vomiting. Neurologic examination is usually normal. Neuropsychologic examination may be abnormal but, because recovery is rapid and complete (usually within 24 hours), is rarely performed. With continued exposure, level of consciousness becomes depressed, sometimes leading to coma; seizures may also occur. Recovery is then likely to be more protracted and may be incomplete. The cause of this acute syndrome usually is easy to determine because of the history of exposure, because many workers are affected, and because a variety of other manifestations are common, such as conjunctival, mucosal, and cutaneous irritation, and respiratory difficulties.
Chronic Encephalopathy
The occurrence of a chronic encephalopathy relating to long-term low-level neurotoxin exposure is widely reported but of uncertain validity. Its symptoms include headache, “dizziness,” poor concentration, memory impairment, irritability, affective disorders, various sleep disturbances, loss of libido, numbness and paresthesias, and “weakness.” Such symptoms are nonspecific in nature, usually mild in degree, but may lead to surprising disability. Examination is typically normal, but ataxia and nystagmus are sometimes found; the results of laboratory and electrophysiologic studies are generally unhelpful or of questionable significance or relevance. Neurobehavioral studies may be abnormal, but often the findings are inconsistent, difficult to interpret in the absence of premorbid baseline studies, and of uncertain relevance. At present, then, whether such an entity truly exists—and its pathophysiologic basis—remains unclear.
Peripheral Neuropathy
Peripheral neuropathy is a better understood consequence of toxin exposure in the workplace. It may occur as a delayed effect of single high-dose exposure or after short-term repeated exposure to certain organophosphates, arsenic, or thallium. Chronic exposure to these and other neurotoxins, such as acrylamide and many organic solvents, also leads to neuropathy, causing that portion of the axon farthest from the cell body to degenerate, a phenomenon described as a distal axonal neuropathy or axonopathy , or a dying-back neuropathy. Symptoms and signs begin distally in the legs and then progress proximally depending on the severity of exposure. Sensory axons pass both peripherally to the limbs and centrally into the spinal cord; both degenerate toward the cell body. Some of the central sensory fibers ascend in the posterior columns to the cuneate and gracile nuclei in the medulla and, because of their length, are often among the first to degenerate. As regeneration does not occur in the CNS, recovery after axonal degeneration will be incomplete despite effective regeneration of the peripheral nerves.
In subjects who are chronically exposed to other neurotoxins in the workplace but who have no clinical deficit, minor electrodiagnostic abnormalities are sometimes found. Although these will not necessarily progress to clinical neuropathy, such subjects need careful monitoring to limit exposure and minimize any risk of progression.
Screening AT-Risk Workers
Screening workers for signs of toxicity may help to identify individuals with incipient or subclinical neurologic dysfunction or exposure to low levels of a neurotoxin, and thereby limit further exposure. Screening of fellow workers may also be diagnostically helpful when a subject with a suspected, occupationally related, neurotoxic disorder is encountered, because similarly exposed workers are likely to have at least some symptoms and signs of intoxication, although to a varying degree that probably relates to differences in age, gender, ethnicity, genetic background, health status, and other factors. In general, however, screening techniques are insensitive, nonspecific, time-consuming, costly, or poorly tolerated by patients.
Clinical Evaluation
An occupational history is an important part of the medical record, especially when patients with obscure neurologic disorders are encountered. Job titles may need clarification for the nature of an occupation to be appreciated. If exposure to toxins is suspected, a detailed list of chemicals used in the workplace—and at previous places of employment, if symptoms are longstanding—should be obtained. Details of the work environment are also important, such as whether it is well ventilated, the nature of any protective measures (such as a requirement to wear special clothing and gloves, and the use of other devices including masks and goggles), and the provisions made for washing after exposure and for storage of food. The most common routes of occupational exposure are inhalation and through the skin.
It may be necessary to question co-workers to determine whether they have similar symptoms to those of a subject with a suspected neurotoxic disorder, and even to examine those working in a similar environment. When asymptomatic but exposed co-workers are screened, questioning may be focused, based on the clinical features in recognized cases; self-administered, standardized symptom questionnaires may be especially helpful.
Neurotoxin exposure may also relate to environmental factors (such as a subject’s residence or its location close to, for example, an industrial plant) and to social and personal factors (such as hobbies, other recreational activities, or dietary peculiarities) rather than to the workplace. The history must therefore exclude these possibilities.
Routine neurologic examination is of limited utility for screening purposes, its principal role being to exclude other conditions that might underlie the patient’s symptoms. Generalized rather than focal neurologic abnormalities are the expected finding in many neurotoxic disorders. In some instances, however, focal findings—such as parkinsonism from manganese exposure—may be conspicuous. Techniques have been developed for quantifying aspects of the neurologic—especially the sensory—examination for screening purposes and for following changes over time. These include quantitative tests of muscle strength, coordination, body sway, balance, vibration and discriminative tactile sensibility, cold and warm thermal thresholds, and heat pain thresholds.
Electrodiagnostic Testing and Neuroimaging
Electroencephalography (EEG) and evoked potential studies can be used to assess CNS function. The EEG is commonly slowed diffusely—but occasionally more focally—in patients with acute toxic or metabolic encephalopathies, but may be normal in chronic encephalopathies. It is therefore of little use in screening patients for neurotoxic injury. Changes are nonspecific and do not distinguish between toxic and other encephalopathies or between different toxic disorders. Evoked potentials provide some measure of the functional integrity of certain afferent CNS pathways, but normal responses may show marked amplitude variation between subjects and on the two sides of the same subject. Because most neurotoxins produce axonal degeneration, which causes changes in amplitude rather than latency of responses, evoked potentials are of limited utility in evaluating patients with suspected neurotoxicity.
Electromyography (EMG) and nerve conduction studies evaluate the function of the PNS, neuromuscular junctions, and muscle. The findings help to identify subclinical disease, follow the progression of disorders, and characterize the pathophysiologic basis of symptoms. Nerve conduction studies are useful in studying both axonal and demyelinating neuropathies. Needle EMG can indicate the cause of weakness and localize pathologic processes to different regions of the motor units (spinal cord, nerve root, plexus, peripheral nerve, neuromuscular junction, or muscle). When evaluating exposed workers, comparison with appropriate control subjects is important. For example, sedentary office workers should not be used as controls for manual workers, who frequently develop minor abnormalities of nerve conduction as a result of occupationally related, repeated minor trauma or subclinical entrapment neuropathies.
Neuroimaging of the CNS, when normal, does not exclude a neurotoxic disorder. In some instances, however, the findings may show characteristic abnormalities, such as in manganese poisoning, discussed later.
Neuropsychologic Evaluation
Advances in neuropsychologic test procedures in recent years have improved their utility as a screening device. Such test procedures may reveal subtle cognitive dysfunction but the findings are not diagnostic of toxic encephalopathy. Moreover, testing is time-consuming even when self-administered questionnaires and computerized test procedures are used, and thus costly and impractical for screening large numbers of subjects. Careful matching for age, gender, ethnicity, and social, cultural, and educational background is necessary when making comparisons between groups.
Other Laboratory Testing
With the exception of screening for heavy metal excretion in the urine or their presence in other tissues, laboratory studies are generally unhelpful in screening for neurotoxic disorders.
Selected Neurotoxic Disorders
Only a limited number of neurotoxins and the disorders that they produce can be discussed in the space available here, and readers seeking more specialized information should consult standard textbooks or compendia on neurotoxicology.
Organic Solvents
Organic solvents, either individually or in combinations, are widely used in the workplace, for example, as cleaners, degreasers, and thinners, and in manufacturing other chemicals. Most are highly volatile liquids. Accordingly, exposure occurs primarily by inhalation, so the risk of toxicity is greatest in poorly ventilated areas. Some absorption also takes place through the skin, especially of those solvents that are both lipid and water soluble and are somewhat less volatile.
Ridgway and co-workers assessed the published evidence that industrial organic solvents as a generic group can induce long-term neurologic damage detectable by brain imaging, neurophysiologic testing, or postmortem studies of exposed workers. Some of the studies provided evidence for marginal atrophic abnormalities in the brain or deficits in nerve conduction velocity in solvent-exposed workers. However, methodologic limitations, absence of a consistently strong association between exposure and effect, lack of a dose–response relationship, the nonspecific nature of the reported changes, and the lack of coherence between the human and experimental animal data were problematic. Overall they were unable to draw reliable conclusions with respect to the presence or absence of nervous system damage related to the common properties of organic solvents.
Central Effects
Most organic solvents have high lipid solubility, so that they rapidly enter the brain and act as nonspecific depressants of the CNS. Acute exposure can cause the syndrome of acute encephalopathy described earlier. The exposed individual must be removed from exposure; recovery after mild exposure occurs rapidly (minutes to hours), usually without sequelae, although headache may continue for longer. When exposure has led to coma, however, recovery may be incomplete, perhaps because of hypoxic brain damage.
Several epidemiologic studies have suggested that neuropsychologic dysfunction has an increased prevalence in spray painters, who are chronically exposed to solvents used as thinners. Both level and duration of exposure may be important in its development. Using sophisticated imaging techniques, pronounced disturbances within the frontostriatothalamic circuitry were found in subjects with painters’ encephalopathy and in asymptomatic but exposed house painters, and related to the clinical findings and to exposure severity to solvents. However, it is unclear whether the entity of painters’ encephalopathy truly exists, because it is based on studies, mainly from the 1970s, which are so methodologically flawed that they are invalid. These studies were primarily epidemiologic in nature. Objections to them include concerns about the manner in which neuropsychologic tests were conducted and that other factors (such as alcohol, medications, or the residual effect of acute solvent exposure) may have caused the encephalopathic features ascribed to chronic exposure. Details concerning work conditions and extent of solvent exposure were often not provided or based on subjective recall. Some studies failed to allow for the influence of various confounding factors on neuropsychologic test results. In others, inappropriate controls may have confounded any comparisons that were made. This is well exemplified by the study of Gade and co-workers, in which 20 solvent-exposed workers, mostly painters, were re-examined 2 years after the diagnosis of chronic toxic encephalopathy was made. Neuropsychologic test results were unchanged, but the earlier impression of significant cognitive decline was not confirmed when comparison was now made to a non-exposed control group and allowance was made for age, educational background, and level of intelligence.
Nevertheless, the concept of painters’ encephalopathy has come to be accepted by many authorities even though no scientific consensus has been reached to establish it as a diagnosable disorder. It appears to be nonprogressive, with no deterioration of functioning—or, in some cases, improvement—occurring after diagnosis, presumably because of cessation of exposure. If such a syndrome of chronic painters’ encephalopathy exists, it may have been caused by toluene, as most subjects were exposed to solvent mixtures, often of unknown composition, and toluene is a common constituent of such mixtures.
Chronic abuse of toluene in large doses taken for recreational purposes may cause dementia, ataxia, dysarthria, nystagmus, tremor, and spasticity. Magnetic resonance imaging (MRI) shows diffuse cerebral and cerebellar atrophy and widespread periventricular white matter lesions. Brainstem auditory evoked potentials (BAEPs) may be abnormal, even in the absence of clinical or neuroimaging abnormalities, suggesting that the BAEP may be useful for screening at-risk workers. A similar syndrome has not been seen with occupational exposure, perhaps because of the prolonged exposure to very large doses during abuse, but contamination of the solvents with other toxins or the concomitant use of other chemicals and drugs may also be relevant.
A more persuasive example of toxic encephalopathy with chronic exposure to organic solvents is the chronic encephalopathy that follows long-term exposure to carbon disulfide, used to manufacture cellophane and rayon.
Peripheral Neuropathy
Relatively few organic solvents or solvent mixtures used industrially are known to be toxic to peripheral nerves. Discussion here focuses on n -hexane and methyl n- butyl ketone (MnBK) because the use of these hexacarbons has led to several outbreaks of neuropathy. Their metabolite, 2,5-hexanedione, is primarily responsible for the distal axonopathy that occurs with repeated and prolonged exposure to n -hexane. Methyl ethyl ketone, a common constituent of organic solvent mixtures, potentiates the neurotoxic properties of n -hexane and MnBK.
Onset is typically insidious and progression occurs slowly. Numbness begins distally in the feet, spreading proximally with continuing exposure and then coming to involve the hands. Motor disturbances are less conspicuous but, in severe cases, mild footdrop and weakness of the intrinsic hand muscles develop. With recreational exposure, which is typically heavier than occupational exposure, more rapid progression occurs and symptoms may be more extensive and severe. Examination shows significant cutaneous sensory deficits, and loss or attenuation of muscle stretch reflexes, especially distally. Gradual improvement (by axonal regeneration) eventually follows cessation of exposure, but coasting may occur for a period of several weeks.
Electrodiagnostic screening is useful in the detection of subclinical hexacarbon neuropathy. In a major outbreak of MnBK neuropathy in Ohio, 43 percent of cases had characteristic electrophysiologic abnormalities in the absence of symptoms and signs of neuropathy. Needle electromyography usually showed signs of active denervation in distal leg muscles, and motor conduction velocity was slowed. Pathologically, the neuropathy is characterized by defective axonal transport, axonal degeneration, and secondary demyelination. Such changes may be seen on sural nerve biopsy and are also present at autopsy in the distal (i.e., most rostral) portion of the sensory axons in the posterior columns of the spinal cord.
A distal axonopathy can also result from exposure to trichloroethylene, which has been used as a degreaser. It is confined to the cranial nerves, initially the trigeminal nerve, with early onset of facial numbness, analgesia, or dysesthesias and later weakness of the masticatory muscles. The lower cranial nerves are involved in some patients; optic neuropathy (with an enlarged blind spot, paracentral scotoma, or constricted fields) has also been described. Recovery occurs with time after discontinuation of exposure, but patchy facial sensory loss may persist indefinitely. The neuropathy has been attributed to dichloroacetylene, which is formed by decomposition when trichloroethylene is exposed to alkalis.
Heavy Metals
Heavy metals accumulate, especially in bone, during lengthy periods of low-level exposure, as in the workplace, and it may take years to eliminate them from the body. Heavy metals are neurotoxic but also have other effects, particularly on the hematopoietic and gastrointestinal systems. The present discussion focuses on lead and arsenic, as exposure to these is most likely to occur, on mercury because of the large outbreaks that have occurred in the past (to environmental rather than occupational exposure), and on manganese because of suggestions that it may be a cause of classic Parkinson disease.
Lead
Industrial exposure is mainly to inorganic lead and occurs by inhalation of fine particulate matter; lead may also be absorbed after ingestion, as occurs in children. Occupational exposure occurs in the construction industry as well as in various other industrial settings (such as lead production or smelting; scrap metal handling; battery manufacturing; lead and other metal foundries; lead soldering; metal radiator repair; firing ranges; and ceramics or plastics manufacturing). Lead is taken up into bone and then slowly released into the blood over many years and excreted primarily through the urine, with smaller amounts in feces, hair, nails, and sweat. There is increasing concern about the health effects of lead at blood levels once thought to be harmless. For example, a causal relationship of lead exposure to hypertension has been suggested, with implications for stroke prevention, as has an association of blood lead levels with declining cognitive function. Recent studies have led to a reappraisal of the levels of lead exposure that may be safely tolerated in the workplace. It is important that workers are in well-ventilated premises; wear appropriate personal protective equipment such as goggles, boots, special clothing, and proper respiratory protection; shower after work; and undergo routine determination of blood lead level.
Lead Encephalopathy
Acute occupational exposure to lead results mainly in systemic effects involving the hematopoietic, gastrointestinal, and renal systems, rather than the nervous system. An acute lead encephalopathy, resulting from increasing cerebral edema, tends to occur in children rather than exposed workers and is therefore not considered further here. A chronic encephalopathy may follow long-term exposure to low levels of lead, and progressive cerebral atrophy can occur long after further exposure is prevented. Symptoms may include apathy, fatigue, insomnia, reduced libido, headache, irritability, memory loss, and difficulty in concentration; testing reveals neuropsychologic and neurophysiologic abnormalities.
Lead Neuropathy
Chronic exposure (i.e., for several years) to lead causes neuropathy. In one study, the average duration of exposure in subjects with lead neuropathy was almost 22 years. Nerve conduction slowing may occur earlier, increasing with duration of exposure and blood lead levels, but whether these neurophysiologic changes progress to overt neuropathy is unclear.
Lead neuropathy, when it develops subacutely, is unusual in that it is predominantly motor, often asymmetric, and affects the arms more than the legs, and the wrist and finger extensors more than other muscles. Wrist drop is characteristic. This form of neuropathy typically develops after a relatively short period of intense exposure. A more typical toxic neuropathy, with distal sensory impairment and weakness, may also occur, however, especially after prolonged exposure. Individuals with lead neuropathy generally have a microcytic, hypochromic anemia; basophilic stippling of red blood cells is not always present and is not specific for lead poisoning. In patients with continuing exposure to lead, neuropathy is unlikely if the urinary δ-aminolevulinic acid (δALA) is normal. Lead interferes with hemoglobin synthesis by inhibiting the enzyme δALA dehydrase, and the enzyme substrate begins to appear in the urine when the blood lead level reaches 40 to 50 µg/dl, which is less than the level at which neuropathy usually results. An increased blood lead level or increased 24-hour urinary excretion should also be present in patients with suspected lead neuropathy, provided that exposure to lead is ongoing. A 24-hour urinary excretion of lead exceeding 2 mg after an intravenous dose of the chelator ethylenediamine tetra-acetic acid (EDTA) helps to confirm the diagnosis and distinguish it from porphyria. Past excessive exposure to lead can be measured through its accumulation in teeth or bones, but this is seldom practical.
The pathophysiologic basis of lead neuropathy in humans is unknown. There are species differences in the effects of lead on the nervous system. The early development of slowed conduction velocity suggests that the primary pathologic process is demyelination, but in established neuropathy the predominant abnormality is axonal degeneration.
Management involves removal of the individual from the toxic environment to prevent further exposure. Workers exposed to lead occupationally should undergo regular determination of the blood lead level, and exposure terminated in those with an increased level before neuropathy develops. The blood lead level reflects the amount of lead in the blood and soft tissues but does not indicate either previous or current exposure, or total body burden . National and state guidelines indicate surveillance requirements (including blood level monitoring requirements) for at-risk workers, such as those of the California Department of Public Health Occupational Lead Poisoning Prevention Program. Based on a literature review and their own experience in evaluating lead-exposed adults, Kosnett and colleagues recommended in 2007 that subjects should be removed from occupational lead exposure if a single blood lead level exceeds 30 µg/dl or two successive blood lead levels measured over a 4-week interval exceed 19 µg/dl. Removal of individuals from lead exposure should be considered to avoid long-term risk to health if exposure control measures over an extended period do not decrease blood lead concentrations to less than 10 µg/dl or if selected medical conditions exist that would increase the risk of continued exposure. They recommended that medical surveillance for all lead-exposed workers should include quarterly blood lead measurements for individuals with blood lead concentrations between 10 and 19 µg/dl and semiannual blood lead measurements when sustained blood lead concentrations are less than 10 µg/dl.
It is unclear whether chelation therapy, which accelerates removal of lead from the blood and soft tissues (but less so from bone), benefits the clinical neuropathy. Clinical trials are lacking. Guidelines are controversial and liable to change. One therapeutic approach has been with EDTA (with or without dimercaprol) followed by oral penicillamine; another oral agent, 2,3-dimercaptosuccinic acid (DMSA; succimer), seems equally effective and can be used alone or after EDTA. Regardless of the treatment chosen, it should be continued until a steady-state level of lead excretion has been achieved. In patients with large lead stores in bone, chelation may be followed by movement of lead from bone back into the blood and soft tissues, leading to a rebound increase in blood lead level after an initial drop. Chelation therapy is not appropriate for workers with continuing lead exposure as prophylaxis against rising blood lead levels.
Arsenic
Arsenic intoxication may occur occupationally but more commonly by ingestion of contaminated food or water. It may relate to attempted homicide. Occupational exposures may occur in the manufacture of paints, fungicides, wood preservatives, and semiconductors; in certain mining and smelting operations; from combustion of arsenic-containing coal or incineration of certain preserved wood products; and in pesticide spraying. A hemorrhagic encephalopathy and various systemic effects (including QTc prolongation on the electrocardiogram and subsequent ventricular tachycardias) occur with acute intoxication; the role of arsenic in the development of a chronic encephalopathy is controversial. Arsenic leads to a peripheral neuropathy that is a predominantly sensory, distal axonopathy and occurs after exposure to high levels of arsenic, usually by ingestion with suicidal or homicidal intent, or after long-duration low-level exposure. Chronic exposure is associated also with an increased risk of skin and various other cancers. Acute intoxication leads to prominent gastrointestinal symptoms followed, after 1 to 3 weeks, by the onset of neuropathy. Numbness, burning, and paresthesias begin in the feet and spread to the legs, hands, and arms. Pain is sometimes prominent. Sensory ataxia occurs in severe cases. Weakness is usually mild and overshadowed by the sensory disturbances, but marked weakness and respiratory insufficiency may occur with severe intoxication. Autonomic instability is usually a minor feature. Examination confirms that there is symmetrical, distally conspicuous sensory loss and weakness.
Other toxic effects of arsenic accompany the neuropathy and include hyperkeratosis and desquamation of the skin, particularly in the palms ( Fig. 35-1 ) and soles; redness and swelling of the hands and feet; patchy areas of skin discoloration with chronic intoxication; and, particularly with acute poisoning, transverse gray lines in the nails (Mees lines; Fig. 35-2 ). Kidney failure may occur. Anemia is common, and red blood cells may show basophilic stippling.
Related posts:
Neurologic Complications of Cardiac Surgery
Neurologic Manifestations of Nutritional Disorders
Neurologic Complications of Chemotherapy and Radiation Therapy
Neurologic Complications of Thermal and Electric Burns
HIV and other Retroviral Infections of the Nervous System
Neuromuscular Complications of General Medical Disorders
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
