Electrophysiologic Study in Acute Lead Poisoning Virginia C.N. Wong, MBBS, MRCP*, T h o m a s H.K. Ng, M B B S , M R C Path, F R C P A + , a n d C.Y. Y e u n g , M B , F R C P *
A 2-month-old girl with acute lead poisoning demonstrated electrophysiologic evidence of neurotoxicity. Motor nerve conduction studies of the median, ulnar, peroneal, and posterior tibial nerves revealed both axonal and demyelinating neuropathy. Somatosensory evoked potential studies of median and posterior tibial nerves demonstrated evidence of cortical involvement. Brainstem auditory evoked potential study disclosed the possibility of acoustic nerve involvement but no evidence of a brainstem lesion. Postmortem examination revealed cerebral edema and focal segmental demyelination of the median nerve. Wong VCN, Ng THK, Yeung CY. Electrophysiologic study in acute lead poisoning. Pediatr Neurol 1991;7: 133-6.
Introduction Lead poisoning often results in neurotoxicity. Both the central and peripheral nervous systems can be affected. Encephalopathy is more common in children, whereas peripheral neuropathy, such as wrist drop or foot drop, is more common in adults [1,2]. The basal ganglia, spinal cord, optic nerve, or acoustic nerve may also be affected [3,4]. The clinical manifestations have included motor neuron dysfunction, extrapyramidal disorder, spasticity, dementia, headache, dizziness, irritability, and mood changes [5]. In children, an increased risk of mental retardation, learning problems, and hyperactivity has also been reported [6]. Lead neurotoxicity in young infants is less well documented. We report a 2-month-old female with clinical and electrophysiologic features of acute lead encephalopathy and neuropathy.
Case Report This 2-month-old girl was admitted into the University Paediatric Unit, Queen Mary Hospital, for repeated episodes of generalized tonic-
From the Departments of *Paediatrics and tPathology; University of Hong Kong; Queen Mary Hospital; Pokfulam, Hong Kong.
clonic seizures and loss of consciousness. She was the second child of nonconsanguineous parents. The family fished for a living and lived on a boat. The family went out to sea for several months with a supply of water stored in tanks. The infant was born after an uneventful delivery and was fed formula. She was thriving until 2 days before admission when she vomited, had tarry stools, and had a decrease in appetite and urine volume. There was no history of head trauma, drug ingestion, or topical medication, including herbs and related products. Physical examination revealed a conscious, afebrile, pale but very irritable girl. The tension of the anterior fontanel was greater than normal, although there was no separation of the cranial sutures. Muscle tone was increased and deep tendon reflexes were brisk. The pupils were equal and reactive. Funduscopic examination did not reveal any evidence of papilledema or optic atrophy. The blood pressure was 90/80 torr. The enlarged liver was extended to 3 cm below the right costal margin. The respiratory and cardiovascular systems were normal. Investigations demonstrated normochromic, normocytic anemia (hemoglobin: 7.5 gm/dl) with normal leukocyte and platelet counts. Basophilic stippling of erythrocytes was observed on the peripheral smear. Renal and liver function tests, blood glucose, blood gases, and coagulation profile all were normal. Lumbar puncture revealed normal cerebrospinal fluid pressure with a markedly increased protein content (5.38 gm/dl; normal: 0.45 gm/dl), normal glucose, and slight mononuclear leukocytosis (leukocytes: 22/ul; 53% lymphocytes, 47% monocytes). Cranial computed tomography revealed cerebral edema. Electroencephalogram disclosed diffuse slow-wave activities. Skeletal survey revealed dense white lines at the proximal ends of the humerus and the head of the ribs. Blood lead level was markedly elevated (6.9 lamol/L; normal: 0.2-(/.7 ~tmol/L). Blood fi-ALA dehydratase was decreased (12.2 ~mol/min, 1 erythrocyte; normal: 19-27 ramol/min, 1 erythrocyte). Urinalysis demonstrated proteinuria and glycosuria. Acute lead encephalopathy was diagnosed.
Nerve Conduction Velocity Study Motor nerve conduction velocity (NCV) study revealed absent motor action potential of the left median nerve; demyelinating neuropathy of both posterior tibial nerves and possible axonal neuropathy of both ulnar and peroneal nerves. Blood lead concentration was 6.9 lamol/L (normal: 0.2-0.7 ~tmol/L) at the time the study was performed.
Evoked Potential Study Somatosensory evoked potential (SSEP) study demonstrated markedly increased latencies of cortical SSEP of both median nerves and absent cortical SSEP of the left posterior tibial nerve. Brainstem auditory evoked potential (BAEP) study revealed absent wave I of the right ear at 80 dB nHL stimulation but normal I-V interpeak latency and normal BAEP of the left ear. Both evoked potential (EP) studies were performed at blood lead levels of 10.5 lamol/L after beginning chelation therapy. The patient was treated with edetate calcium disodium and dimercaprol. Her blood lead level decreased gradually. Phenobarbital was administered to control her seizures and dexamethasone and mannitol to control cerebral edema. Her clinical condition did not improve and she developed high spiking fever and subsequently died of fulminant septicemia, disseminated intravascular coagulation, and hepatic failure 2 weeks after admission. Her last blood lead level before death was 4.1 ~tmol/L. Postmortem examination disclosed brain edema with subarachnoid hemorrhage, acute tubular necrosis of the kidneys, and massive liver necrosis. The brain was swollen with flattened gyri and compressed
Communications should be addressed to: Dr. Wong; Department of Paediatrics; Queen Mary Hospital; Pokfulam, Hong Kong. Received July 2, 1990; accepted August 20, 1990.
Wong et al: Acute Lead Poisoning
133
Figure 1. Photomicrograph revealing perivascular and periceUular space due to fluid accumulation indicative of marked cerebral edema: hemato,rvlin and eosin stain, original magnifi~'a tion x 100. ventricles. Microscopically, there was dilatation of perivascular spaces with PAS-positive exudate and local capillary proliferation. Focal necrosis of neurons with reactive astrocytosis and microgliosis were observed in the cerebral cortex (Figs 1,21. Section of the median nerve revealed mild perineurial edema and local segmental demyelination. Lead screening was performed on other family members who shared the same water tank, the main suspicious source for lead contamination in the infant. All had elevated blood lead levels: father ((I.9 lamol/L), mother (1.2 ~tmol/L), aunt (1.0 ~tmol/L), and elder brother (3.3 ~amol/L); however, lead was not detected in the water tank. They all were treated accordingly and the possible source of lead poisoning was removed from the family.
Discussion
Neurotoxicity due to lead affects both the brain and peripheral nerves. In brain, acute lead encephalopathy in children manifests as cerebral edema, as illustrated in our patient. Pathologic changes of peripheral nerves in human lead neuropathy include both axonal degeneration and segmental demyelination which rarely are reported [7]. Lead neuropathy in children was described initially by Turner in a series of children with lead poisoning 181. Children with lead neuropathy presented with generalized weakness, diaphragmatic paralysis and respiratory failure, footdrop, or wrist drop. Postmortem examination of a 3year-old girl presenting with a 3-week history of ascending paralysis and diaphragmatic paralysis revealed extensive myelin degeneration of the peripheral nerves [9]. Segmental demyelination and axonal degeneration were demonstrated in experimental lead neuropathy of guinea pigs and rats [10]. Chronic lead poisoning in chickens led to a decrease in motor response amplitude of motor NCV and
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histologic evidence of spinal motor neuron degeneration, motor axonal loss, and atrophy of muscle similar to human motor neuronal disease 1111. Both nerve conduction studies and electromyography (EMG) of patients with lead neuropathy had demonstrated demyelination neuropathy and denervation changes [I]. Schwartz et al. reported a negative correlation between blood lead level and NCV in 202 asymptomatic children, 5-9 years of age, and indicated that, although the threshold for lead-induced peripheral neuropathy was 20-30 gm/dl, measurement of the maximal motor NCV was an insensitive screening for low levels of lead toxicity [12]. Ehle reviewed the literature on NCV and EMG studies in lead-exposed populations [ 13]; 7% demonstrated mild slowing of motor and sensory NCV in the median and posterior tibial nerves but the ulnar and peroneal NCVs were not slowed at blood levels of 60 gm/dl. The majority of studies did not demonstrate a correlation between NCV and blood lead levels of 70 gm/dl or the length of lead exposure. Most studies found EMG abnormalities only in patients with blood lead levels 60-70 gm/dl, and lead colic or other systemic symptoms of lead intoxication. Slowing of NCV in low lead level exposure is apparently clinically insignificant. Seppalainen reported an EP study that revealed evidence of neurotoxicity in a lead-exposed population [14]. In the same report, an SSEP study revealed significant amplitude changes in relation to lead values and the increased amplitude of cortical SSEP may be caused by a "release from inhibition" in the thalamic reticular nuclei. An increase in
Figure 2. Area of cortical necrosis with reactive astrocytosis, reactive microgliosis, and neuronal loss: hematoxylin and eosin stain, original magnification xlO0.
amplitude of the pattern-reversal visual evoked potential and upper limb SSEP cortical components together with an increase in central conduction time of the lower limb SSEP were reported in 13 adults occupationally exposed to lead [15]. An event-related potentials study in asymptomatic children exposed to lead demonstrated amplitude changes in relation to lead levels [16]. Studies of lead exposure demonstrated elevation of the hearing threshold [5]. In the National Health and Nutrition Examination Survey (1976 to 1980) of 4,519 children with audiometric testing and monitoring of blood lead level, the hearing thresholds were elevated significantly with increasing lead levels for both ears [15]. In a study o f B A E P in 75 l e a d - e x p o s e d children, Robinson et al. reported a biphasic effect of lead on B A E P [4]. There was a curvilinear relationship of waves III and V latencies, I-III, and I-V interpeak latencies with blood lead level. The hearing threshold was linearly increased with a maximal lead level. In a study of the residual effects of lead exposure on 49 children 5 years after initial assessment, Otto et al. reported an increase in waves III and V latencies as a function of the original lead levels, but no threshold for the effect of lead on auditory function was demonstrated [18]. The authors suggested that subclinical pathology of the auditory pathway rostral to the cochlear nucleus was probable, although end organ impairment could not be excluded. Other cognitive problems related to lead exposure in children, such as reduced mentality, learning disability, and hyperactivity have also been reported [6].
The children of fishermen in the Aberdeen fishing area of Hong Kong are at increased risk of lead toxicity due to chronic exposure from weights and fishing equipment made of lead and from nutritional factors that enhance lead absorption [ 13]. The possible source of lead poisoning in this infant was the water stored in a tank used for months while fishing at sea. Unfortunately, we were unable to prove this theory because the family had changed the water in the tank before our investigative process. The other possibility was lead exposure through clothes contaminated with lead or inhaled vapor from high-lead diesel used for running the engine. Our patient illustrated electrophysiologic and pathologic evidence of lead neurotoxicity, both central and peripheral. She was one of the two youngest patients to present recently with acute lead encephalopathy in our hospital. The other infant was only 6 weeks of age and was also from a fisherman's family [20]. The possibility of monitoring for subclinical involvement in this group of high-risk children with chronic lead exposure is worthwhile. Currently, we are screening this population's blood lead levels.
References
[1] Feldman RG, Hayes MK, Younes R, Aldrieh FD. Lead neuropathy in adults and children. Arch Neurol 1977;34:481-8. [2] Seto DSY, Freeman JM. Lead neuropathy in childhood. Am J Dis Child 1964;107:337-42. [3] Baghdassarian SA. Optic neuropathy due to lead poisoning: Report of a case. Arch Ophthalmol 1968;80:721.
Wong et al: Acute Lead Poisoning 135
[4] Robinson G, Baumann S, Kleinbaum D. et al. Neurobehavioural methods in occupational and environmental health. Abstracts from the Secnnd Intematinal Symposium, Copenhagen, World Health Organization 1985:177-82. [51 Livesley B. Sission CE. Chronic lead intoxication mimicking motor neuron disease. Br Med J 1968;4:387. [6] LaPorte RE, Talbott EE. Effects of low levels of lead exposure on cognitive function: A review. Arch Environ Health 1978;33:236. [71 Jacobs JM, Le Quesne PM. Toxic disorders of the nervous system. In: Arnold E, Adams JH, Corsellis JAN, Duchen LW, eds. Greenfield's neuropathology, 4th ed. London: Edward Arnold, 1984: 62%36. [8] "litrner AJ. Lead poisoning among Queensland children. Aust Med Gaz 1987; 16:475. [9] Goodwin TC. Lead poisoning: Report of a case m a child with extensive peripheral neuritis. Bull Hopkins Hosp 1934;55:347. [10] Fullerton R. Chronic peripheral neuropathy produced by lead poisoning in guinea pigs. J Neuropathol Exp Neurol 1966:25:214-36. [11] Mazliah J, Barton S, Bental E, Rogowski Z, Coleman R. Silbermann M. The effects of long-term lead intoxication nn the nervous system of the chicken. Neurosci Lett 1989; 101:253-7. [12] Schwartz J, Landrigan PJ, Feldman RG, Silbergeld EK, Baker EL Jr. yon Lindem IH. Threshold effect in lead-induced peripheral neuropathy. J Pediatr 1988;112:12-7.
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[13] Ehle AL. Lead neuropathy and electrophysiological studies in low level lead exposure: A critical review. Neuromxicoh)gy 1986;3: 203-16. [14] Seppalainen AM. Etectrophysiological cwtluation of central and peripheral neural efi-i2cts of lead exposure. Neuroloxicology IO84: 5:43 52. [15] Lille F, itazemann P, Gamier R, Dally S. Ellecl~, or lead and mercury intoxications on evoked potentials. J Toxicol Clin "loxicol 1988;26: 103-16. [16] Otto DA, Benignus VA, Muller KE, Barton CN. Eft;eels of age and body lead burden on CNS fi.mction in young children, 1. SIm~ cor tical potentials. Electroencephalogr Clin Neurophysiol 1981;52:229-39. [17] Schwartz J, Otto D. Blood lead, hearing thresholds, and neurobehavioral development in children and youth. Arch Environ l teahh 1987;42: 153-60. [18] (lttn D, Robinson G, Baunlann S, el al. 5 year li)llow tlp ~,ltldy of children with low-to-moderate lead absnrptinn: Eleclrophysiological evaluation. Environ Res 1985:38:168-86. 119] Yeung CY. Yu CL, Lau V, Fung KW. Lead poisoning in fisherman's children. World Paediatr Child Care, in press. [2(11 Yu CL, Yeung CY. Lead encephalopathy due to Chinese herbal modicine. Chin Med J 1989;100:915-7.
A 2-month-old girl with acute lead poisoning demonstrated electrophysiologic evidence of neurotoxicity. Motor nerve conduction studies of the median, ulnar, peroneal, and posterior tibial nerves revealed both axonal and demyelinating neuropathy. Somatosensory evoked potential studies of median and posterior tibial nerves demonstrated evidence of cortical involvement. Brainstem auditory evoked potential study disclosed the possibility of acoustic nerve involvement but no evidence of a brainstem lesion. Postmortem examination revealed cerebral edema and focal segmental demyelination of the median nerve. Wong VCN, Ng THK, Yeung CY. Electrophysiologic study in acute lead poisoning. Pediatr Neurol 1991;7: 133-6.
Introduction Lead poisoning often results in neurotoxicity. Both the central and peripheral nervous systems can be affected. Encephalopathy is more common in children, whereas peripheral neuropathy, such as wrist drop or foot drop, is more common in adults [1,2]. The basal ganglia, spinal cord, optic nerve, or acoustic nerve may also be affected [3,4]. The clinical manifestations have included motor neuron dysfunction, extrapyramidal disorder, spasticity, dementia, headache, dizziness, irritability, and mood changes [5]. In children, an increased risk of mental retardation, learning problems, and hyperactivity has also been reported [6]. Lead neurotoxicity in young infants is less well documented. We report a 2-month-old female with clinical and electrophysiologic features of acute lead encephalopathy and neuropathy.
Case Report This 2-month-old girl was admitted into the University Paediatric Unit, Queen Mary Hospital, for repeated episodes of generalized tonic-
From the Departments of *Paediatrics and tPathology; University of Hong Kong; Queen Mary Hospital; Pokfulam, Hong Kong.
clonic seizures and loss of consciousness. She was the second child of nonconsanguineous parents. The family fished for a living and lived on a boat. The family went out to sea for several months with a supply of water stored in tanks. The infant was born after an uneventful delivery and was fed formula. She was thriving until 2 days before admission when she vomited, had tarry stools, and had a decrease in appetite and urine volume. There was no history of head trauma, drug ingestion, or topical medication, including herbs and related products. Physical examination revealed a conscious, afebrile, pale but very irritable girl. The tension of the anterior fontanel was greater than normal, although there was no separation of the cranial sutures. Muscle tone was increased and deep tendon reflexes were brisk. The pupils were equal and reactive. Funduscopic examination did not reveal any evidence of papilledema or optic atrophy. The blood pressure was 90/80 torr. The enlarged liver was extended to 3 cm below the right costal margin. The respiratory and cardiovascular systems were normal. Investigations demonstrated normochromic, normocytic anemia (hemoglobin: 7.5 gm/dl) with normal leukocyte and platelet counts. Basophilic stippling of erythrocytes was observed on the peripheral smear. Renal and liver function tests, blood glucose, blood gases, and coagulation profile all were normal. Lumbar puncture revealed normal cerebrospinal fluid pressure with a markedly increased protein content (5.38 gm/dl; normal: 0.45 gm/dl), normal glucose, and slight mononuclear leukocytosis (leukocytes: 22/ul; 53% lymphocytes, 47% monocytes). Cranial computed tomography revealed cerebral edema. Electroencephalogram disclosed diffuse slow-wave activities. Skeletal survey revealed dense white lines at the proximal ends of the humerus and the head of the ribs. Blood lead level was markedly elevated (6.9 lamol/L; normal: 0.2-(/.7 ~tmol/L). Blood fi-ALA dehydratase was decreased (12.2 ~mol/min, 1 erythrocyte; normal: 19-27 ramol/min, 1 erythrocyte). Urinalysis demonstrated proteinuria and glycosuria. Acute lead encephalopathy was diagnosed.
Nerve Conduction Velocity Study Motor nerve conduction velocity (NCV) study revealed absent motor action potential of the left median nerve; demyelinating neuropathy of both posterior tibial nerves and possible axonal neuropathy of both ulnar and peroneal nerves. Blood lead concentration was 6.9 lamol/L (normal: 0.2-0.7 ~tmol/L) at the time the study was performed.
Evoked Potential Study Somatosensory evoked potential (SSEP) study demonstrated markedly increased latencies of cortical SSEP of both median nerves and absent cortical SSEP of the left posterior tibial nerve. Brainstem auditory evoked potential (BAEP) study revealed absent wave I of the right ear at 80 dB nHL stimulation but normal I-V interpeak latency and normal BAEP of the left ear. Both evoked potential (EP) studies were performed at blood lead levels of 10.5 lamol/L after beginning chelation therapy. The patient was treated with edetate calcium disodium and dimercaprol. Her blood lead level decreased gradually. Phenobarbital was administered to control her seizures and dexamethasone and mannitol to control cerebral edema. Her clinical condition did not improve and she developed high spiking fever and subsequently died of fulminant septicemia, disseminated intravascular coagulation, and hepatic failure 2 weeks after admission. Her last blood lead level before death was 4.1 ~tmol/L. Postmortem examination disclosed brain edema with subarachnoid hemorrhage, acute tubular necrosis of the kidneys, and massive liver necrosis. The brain was swollen with flattened gyri and compressed
Communications should be addressed to: Dr. Wong; Department of Paediatrics; Queen Mary Hospital; Pokfulam, Hong Kong. Received July 2, 1990; accepted August 20, 1990.
Wong et al: Acute Lead Poisoning
133
Figure 1. Photomicrograph revealing perivascular and periceUular space due to fluid accumulation indicative of marked cerebral edema: hemato,rvlin and eosin stain, original magnifi~'a tion x 100. ventricles. Microscopically, there was dilatation of perivascular spaces with PAS-positive exudate and local capillary proliferation. Focal necrosis of neurons with reactive astrocytosis and microgliosis were observed in the cerebral cortex (Figs 1,21. Section of the median nerve revealed mild perineurial edema and local segmental demyelination. Lead screening was performed on other family members who shared the same water tank, the main suspicious source for lead contamination in the infant. All had elevated blood lead levels: father ((I.9 lamol/L), mother (1.2 ~tmol/L), aunt (1.0 ~tmol/L), and elder brother (3.3 ~amol/L); however, lead was not detected in the water tank. They all were treated accordingly and the possible source of lead poisoning was removed from the family.
Discussion
Neurotoxicity due to lead affects both the brain and peripheral nerves. In brain, acute lead encephalopathy in children manifests as cerebral edema, as illustrated in our patient. Pathologic changes of peripheral nerves in human lead neuropathy include both axonal degeneration and segmental demyelination which rarely are reported [7]. Lead neuropathy in children was described initially by Turner in a series of children with lead poisoning 181. Children with lead neuropathy presented with generalized weakness, diaphragmatic paralysis and respiratory failure, footdrop, or wrist drop. Postmortem examination of a 3year-old girl presenting with a 3-week history of ascending paralysis and diaphragmatic paralysis revealed extensive myelin degeneration of the peripheral nerves [9]. Segmental demyelination and axonal degeneration were demonstrated in experimental lead neuropathy of guinea pigs and rats [10]. Chronic lead poisoning in chickens led to a decrease in motor response amplitude of motor NCV and
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histologic evidence of spinal motor neuron degeneration, motor axonal loss, and atrophy of muscle similar to human motor neuronal disease 1111. Both nerve conduction studies and electromyography (EMG) of patients with lead neuropathy had demonstrated demyelination neuropathy and denervation changes [I]. Schwartz et al. reported a negative correlation between blood lead level and NCV in 202 asymptomatic children, 5-9 years of age, and indicated that, although the threshold for lead-induced peripheral neuropathy was 20-30 gm/dl, measurement of the maximal motor NCV was an insensitive screening for low levels of lead toxicity [12]. Ehle reviewed the literature on NCV and EMG studies in lead-exposed populations [ 13]; 7% demonstrated mild slowing of motor and sensory NCV in the median and posterior tibial nerves but the ulnar and peroneal NCVs were not slowed at blood levels of 60 gm/dl. The majority of studies did not demonstrate a correlation between NCV and blood lead levels of 70 gm/dl or the length of lead exposure. Most studies found EMG abnormalities only in patients with blood lead levels 60-70 gm/dl, and lead colic or other systemic symptoms of lead intoxication. Slowing of NCV in low lead level exposure is apparently clinically insignificant. Seppalainen reported an EP study that revealed evidence of neurotoxicity in a lead-exposed population [14]. In the same report, an SSEP study revealed significant amplitude changes in relation to lead values and the increased amplitude of cortical SSEP may be caused by a "release from inhibition" in the thalamic reticular nuclei. An increase in
Figure 2. Area of cortical necrosis with reactive astrocytosis, reactive microgliosis, and neuronal loss: hematoxylin and eosin stain, original magnification xlO0.
amplitude of the pattern-reversal visual evoked potential and upper limb SSEP cortical components together with an increase in central conduction time of the lower limb SSEP were reported in 13 adults occupationally exposed to lead [15]. An event-related potentials study in asymptomatic children exposed to lead demonstrated amplitude changes in relation to lead levels [16]. Studies of lead exposure demonstrated elevation of the hearing threshold [5]. In the National Health and Nutrition Examination Survey (1976 to 1980) of 4,519 children with audiometric testing and monitoring of blood lead level, the hearing thresholds were elevated significantly with increasing lead levels for both ears [15]. In a study o f B A E P in 75 l e a d - e x p o s e d children, Robinson et al. reported a biphasic effect of lead on B A E P [4]. There was a curvilinear relationship of waves III and V latencies, I-III, and I-V interpeak latencies with blood lead level. The hearing threshold was linearly increased with a maximal lead level. In a study of the residual effects of lead exposure on 49 children 5 years after initial assessment, Otto et al. reported an increase in waves III and V latencies as a function of the original lead levels, but no threshold for the effect of lead on auditory function was demonstrated [18]. The authors suggested that subclinical pathology of the auditory pathway rostral to the cochlear nucleus was probable, although end organ impairment could not be excluded. Other cognitive problems related to lead exposure in children, such as reduced mentality, learning disability, and hyperactivity have also been reported [6].
The children of fishermen in the Aberdeen fishing area of Hong Kong are at increased risk of lead toxicity due to chronic exposure from weights and fishing equipment made of lead and from nutritional factors that enhance lead absorption [ 13]. The possible source of lead poisoning in this infant was the water stored in a tank used for months while fishing at sea. Unfortunately, we were unable to prove this theory because the family had changed the water in the tank before our investigative process. The other possibility was lead exposure through clothes contaminated with lead or inhaled vapor from high-lead diesel used for running the engine. Our patient illustrated electrophysiologic and pathologic evidence of lead neurotoxicity, both central and peripheral. She was one of the two youngest patients to present recently with acute lead encephalopathy in our hospital. The other infant was only 6 weeks of age and was also from a fisherman's family [20]. The possibility of monitoring for subclinical involvement in this group of high-risk children with chronic lead exposure is worthwhile. Currently, we are screening this population's blood lead levels.
References
[1] Feldman RG, Hayes MK, Younes R, Aldrieh FD. Lead neuropathy in adults and children. Arch Neurol 1977;34:481-8. [2] Seto DSY, Freeman JM. Lead neuropathy in childhood. Am J Dis Child 1964;107:337-42. [3] Baghdassarian SA. Optic neuropathy due to lead poisoning: Report of a case. Arch Ophthalmol 1968;80:721.
Wong et al: Acute Lead Poisoning 135
[4] Robinson G, Baumann S, Kleinbaum D. et al. Neurobehavioural methods in occupational and environmental health. Abstracts from the Secnnd Intematinal Symposium, Copenhagen, World Health Organization 1985:177-82. [51 Livesley B. Sission CE. Chronic lead intoxication mimicking motor neuron disease. Br Med J 1968;4:387. [6] LaPorte RE, Talbott EE. Effects of low levels of lead exposure on cognitive function: A review. Arch Environ Health 1978;33:236. [71 Jacobs JM, Le Quesne PM. Toxic disorders of the nervous system. In: Arnold E, Adams JH, Corsellis JAN, Duchen LW, eds. Greenfield's neuropathology, 4th ed. London: Edward Arnold, 1984: 62%36. [8] "litrner AJ. Lead poisoning among Queensland children. Aust Med Gaz 1987; 16:475. [9] Goodwin TC. Lead poisoning: Report of a case m a child with extensive peripheral neuritis. Bull Hopkins Hosp 1934;55:347. [10] Fullerton R. Chronic peripheral neuropathy produced by lead poisoning in guinea pigs. J Neuropathol Exp Neurol 1966:25:214-36. [11] Mazliah J, Barton S, Bental E, Rogowski Z, Coleman R. Silbermann M. The effects of long-term lead intoxication nn the nervous system of the chicken. Neurosci Lett 1989; 101:253-7. [12] Schwartz J, Landrigan PJ, Feldman RG, Silbergeld EK, Baker EL Jr. yon Lindem IH. Threshold effect in lead-induced peripheral neuropathy. J Pediatr 1988;112:12-7.
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[13] Ehle AL. Lead neuropathy and electrophysiological studies in low level lead exposure: A critical review. Neuromxicoh)gy 1986;3: 203-16. [14] Seppalainen AM. Etectrophysiological cwtluation of central and peripheral neural efi-i2cts of lead exposure. Neuroloxicology IO84: 5:43 52. [15] Lille F, itazemann P, Gamier R, Dally S. Ellecl~, or lead and mercury intoxications on evoked potentials. J Toxicol Clin "loxicol 1988;26: 103-16. [16] Otto DA, Benignus VA, Muller KE, Barton CN. Eft;eels of age and body lead burden on CNS fi.mction in young children, 1. SIm~ cor tical potentials. Electroencephalogr Clin Neurophysiol 1981;52:229-39. [17] Schwartz J, Otto D. Blood lead, hearing thresholds, and neurobehavioral development in children and youth. Arch Environ l teahh 1987;42: 153-60. [18] (lttn D, Robinson G, Baunlann S, el al. 5 year li)llow tlp ~,ltldy of children with low-to-moderate lead absnrptinn: Eleclrophysiological evaluation. Environ Res 1985:38:168-86. 119] Yeung CY. Yu CL, Lau V, Fung KW. Lead poisoning in fisherman's children. World Paediatr Child Care, in press. [2(11 Yu CL, Yeung CY. Lead encephalopathy due to Chinese herbal modicine. Chin Med J 1989;100:915-7.
![[Acute lead poisoning].](/assets/img/hold.png)
