Many types of heavy metal cadmium directly injure people. It frequently coexists with other heavy metals, including lead, copper, & zinc. Concentrations rise as a result of industrial operations, disturbed soil, & volcanic activity. In the industrial world, electroplating and the creation of nickel-cadmium cells are where it is most commonly used.
Epidemiology
Workers who weld, solder, & make jewelry run the risk of breathing in cadmium oxide vapors. The most common outcome of metalworking in a cramped location with inadequate ventilation is significant toxicity.
Anatomy
Pathophysiology
Cadmium is not very accessible when consumed orally, however, it is readily bioavailable when breathed. Cadmium enters the bloodstream, adheres to albumin & alpha-2-macroglobulin, and is transported to the liver & kidneys. Cadmium concentrates in the spleen, pancreas, lung, & testes in addition to these two primary organs.
Cadmium attaches to metallothionein in the liver, where it forms a complex that is slowly released. It is biological half-life can be at least ten years due to the delayed release. After that, cadmium moves to the glomerulus, where it concentrates in significant concentrations in the proximal tubule, causing kidney toxicity.
Etiology
Cadmium toxicity typically develops after exposure through employment, the environment, or recreational activities. Environmental exposures may result from metal pollution of the nearby soil and subsequent consumption of the food produced there. Areas, where ores are mined or refined are susceptible to this kind of pollution.
When a mine released a significant amount of cadmium into the environment in the Jinzu River in Japan in the 1950s, something similar occurred. The majority of the postmenopausal multiparous women who experienced this excruciating osteomalacia epidemic were rice farmers in the area.
Itai-Itai sickness, which translates to “ouch-ouch” in Japanese, was the name given to this condition since persons who had it would utter it every time they moved.
Genetics
Prognostic Factors
Restrictive lung disease may last a lifetime in cases of acute exposure. Kidney damage from persistent exposure might worsen and be permanent.
Clinical History
Clinical History
Clinical history of cadmium toxicity:
Acute exposure: Acute exposure to high levels of cadmium can lead to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and headache. In severe cases, there may be respiratory distress, shock, and even death.
Chronic exposure: Chronic exposure to lower levels of cadmium can result in a wide range of symptoms, including kidney damage, lung damage, anemia, bone damage, and hypertension. In some cases, there may be no symptoms until the damage is advanced.
Kidney damage: Cadmium is toxic to the kidneys, and chronic exposure can result in progressive kidney damage that may lead to kidney failure. Symptoms of kidney damage may include fatigue, loss of appetite, nausea, and swelling in the legs and feet.
Lung damage: Cadmium exposure can also lead to lung damage, including chronic bronchitis, emphysema, and lung cancer. Symptoms of lung damage may include coughing, wheezing, shortness of breath, and chest pain.
Anemia: Cadmium can interfere with the production of red blood cells, leading to anemia. Symptoms of anemia may include fatigue, weakness, pale skin, and shortness of breath.
Bone damage: Cadmium can accumulate in bones and lead to a condition called osteomalacia, which is a softening of the bones that can lead to fractures. Symptoms of bone damage may include bone pain, muscle weakness, and difficulty walking.
Hypertension: Chronic cadmium exposure has also been linked to the development of hypertension or high blood pressure.
Overall, the clinical history of cadmium toxicity can vary depending on the extent and duration of exposure and can involve a wide range of symptoms and complications affecting different organ systems. Early identification and management of cadmium exposure are important in preventing long-term health effects.
Physical Examination
Physical examination
The physical examination findings in cadmium toxicity can vary depending on the extent and duration of exposure, as well as the affected organ systems. Here are some of the possible physical examination findings in cadmium toxicity:
Gastrointestinal system: The abdomen may be tender or distended, and there may be evidence of gastrointestinal irritation, such as vomiting or diarrhea. There may also be signs of dehydration, such as dry mucous membranes and decreased skin turgor.
Respiratory system: The patient may have wheezing, coughing, and decreased breath sounds, indicating bronchoconstriction or pulmonary edema. There may also be cyanosis (bluish discoloration) of the lips or nail beds.
Renal system: There may be signs of renal damage, such as edema in the legs and ankles, hypertension (high blood pressure), and proteinuria (excessive protein in the urine).
Skeletal system: The patient may have decreased bone density, leading to skeletal deformities, tenderness, and fractures.
Neurological system: In severe cases of cadmium toxicity, there may be neurological symptoms such as confusion, seizures, and coma.
In addition to the physical examination, laboratory tests such as blood and urine tests may be used to assess the extent of cadmium exposure and the degree of organ damage. Imaging studies, such as X-rays or bone scans, may also be used to evaluate skeletal damage. Overall, early identification and management of cadmium toxicity is important in preventing long-term health effects.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential diagnosis
One must consider the other common metal toxins, such as arsenic, lead, iron, mercury, & thallium, for any environmental or workplace occupational exposure. Metal fume fever is an exclusion diagnosis in acute toxicities; other causes of ARDS & pneumonitis are on the differential.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Acute Poisoning
The lungs are significantly at risk from cadmium fumes. It’s crucial to regulate the airways while using supplemental oxygen. Since their benefit has not yet been established, steroids are frequently the choice of treatment. Concerns for cadmium ingestion are a little different. Gastric lavage & activated charcoal are choices.
Monitoring of the patient’s liver and kidney damage as well as gastrointestinal harm, is necessary. Chelators have yet to be conclusively demonstrated to be helpful in cadmium toxicity, despite their promise. Yet, succimer has promising effects if it is administered early in the course.
Chronic Poisoning
These patients’ exposure will be known, and their dysfunction is often identified during standard screening. The patient must always be taken out of the exposure as the initial action. Despite the fact that the effects could be long-lasting & progressive, chelation is not currently advised for these patients.
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References
https://www.ncbi.nlm.nih.gov/books/NBK536966/
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Many types of heavy metal cadmium directly injure people. It frequently coexists with other heavy metals, including lead, copper, & zinc. Concentrations rise as a result of industrial operations, disturbed soil, & volcanic activity. In the industrial world, electroplating and the creation of nickel-cadmium cells are where it is most commonly used.
Workers who weld, solder, & make jewelry run the risk of breathing in cadmium oxide vapors. The most common outcome of metalworking in a cramped location with inadequate ventilation is significant toxicity.
Cadmium is not very accessible when consumed orally, however, it is readily bioavailable when breathed. Cadmium enters the bloodstream, adheres to albumin & alpha-2-macroglobulin, and is transported to the liver & kidneys. Cadmium concentrates in the spleen, pancreas, lung, & testes in addition to these two primary organs.
Cadmium attaches to metallothionein in the liver, where it forms a complex that is slowly released. It is biological half-life can be at least ten years due to the delayed release. After that, cadmium moves to the glomerulus, where it concentrates in significant concentrations in the proximal tubule, causing kidney toxicity.
Cadmium toxicity typically develops after exposure through employment, the environment, or recreational activities. Environmental exposures may result from metal pollution of the nearby soil and subsequent consumption of the food produced there. Areas, where ores are mined or refined are susceptible to this kind of pollution.
When a mine released a significant amount of cadmium into the environment in the Jinzu River in Japan in the 1950s, something similar occurred. The majority of the postmenopausal multiparous women who experienced this excruciating osteomalacia epidemic were rice farmers in the area.
Itai-Itai sickness, which translates to “ouch-ouch” in Japanese, was the name given to this condition since persons who had it would utter it every time they moved.
Restrictive lung disease may last a lifetime in cases of acute exposure. Kidney damage from persistent exposure might worsen and be permanent.
Clinical History
Clinical history of cadmium toxicity:
Acute exposure: Acute exposure to high levels of cadmium can lead to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and headache. In severe cases, there may be respiratory distress, shock, and even death.
Chronic exposure: Chronic exposure to lower levels of cadmium can result in a wide range of symptoms, including kidney damage, lung damage, anemia, bone damage, and hypertension. In some cases, there may be no symptoms until the damage is advanced.
Kidney damage: Cadmium is toxic to the kidneys, and chronic exposure can result in progressive kidney damage that may lead to kidney failure. Symptoms of kidney damage may include fatigue, loss of appetite, nausea, and swelling in the legs and feet.
Lung damage: Cadmium exposure can also lead to lung damage, including chronic bronchitis, emphysema, and lung cancer. Symptoms of lung damage may include coughing, wheezing, shortness of breath, and chest pain.
Anemia: Cadmium can interfere with the production of red blood cells, leading to anemia. Symptoms of anemia may include fatigue, weakness, pale skin, and shortness of breath.
Bone damage: Cadmium can accumulate in bones and lead to a condition called osteomalacia, which is a softening of the bones that can lead to fractures. Symptoms of bone damage may include bone pain, muscle weakness, and difficulty walking.
Hypertension: Chronic cadmium exposure has also been linked to the development of hypertension or high blood pressure.
Overall, the clinical history of cadmium toxicity can vary depending on the extent and duration of exposure and can involve a wide range of symptoms and complications affecting different organ systems. Early identification and management of cadmium exposure are important in preventing long-term health effects.
Physical examination
The physical examination findings in cadmium toxicity can vary depending on the extent and duration of exposure, as well as the affected organ systems. Here are some of the possible physical examination findings in cadmium toxicity:
Gastrointestinal system: The abdomen may be tender or distended, and there may be evidence of gastrointestinal irritation, such as vomiting or diarrhea. There may also be signs of dehydration, such as dry mucous membranes and decreased skin turgor.
Respiratory system: The patient may have wheezing, coughing, and decreased breath sounds, indicating bronchoconstriction or pulmonary edema. There may also be cyanosis (bluish discoloration) of the lips or nail beds.
Renal system: There may be signs of renal damage, such as edema in the legs and ankles, hypertension (high blood pressure), and proteinuria (excessive protein in the urine).
Skeletal system: The patient may have decreased bone density, leading to skeletal deformities, tenderness, and fractures.
Neurological system: In severe cases of cadmium toxicity, there may be neurological symptoms such as confusion, seizures, and coma.
In addition to the physical examination, laboratory tests such as blood and urine tests may be used to assess the extent of cadmium exposure and the degree of organ damage. Imaging studies, such as X-rays or bone scans, may also be used to evaluate skeletal damage. Overall, early identification and management of cadmium toxicity is important in preventing long-term health effects.
Differential diagnosis
One must consider the other common metal toxins, such as arsenic, lead, iron, mercury, & thallium, for any environmental or workplace occupational exposure. Metal fume fever is an exclusion diagnosis in acute toxicities; other causes of ARDS & pneumonitis are on the differential.
Acute Poisoning
The lungs are significantly at risk from cadmium fumes. It’s crucial to regulate the airways while using supplemental oxygen. Since their benefit has not yet been established, steroids are frequently the choice of treatment. Concerns for cadmium ingestion are a little different. Gastric lavage & activated charcoal are choices.
Monitoring of the patient’s liver and kidney damage as well as gastrointestinal harm, is necessary. Chelators have yet to be conclusively demonstrated to be helpful in cadmium toxicity, despite their promise. Yet, succimer has promising effects if it is administered early in the course.
Chronic Poisoning
These patients’ exposure will be known, and their dysfunction is often identified during standard screening. The patient must always be taken out of the exposure as the initial action. Despite the fact that the effects could be long-lasting & progressive, chelation is not currently advised for these patients.
https://www.ncbi.nlm.nih.gov/books/NBK536966/
medtigo
Cadmium Toxicity
Updated :
February 22, 2023
Many types of heavy metal cadmium directly injure people. It frequently coexists with other heavy metals, including lead, copper, & zinc. Concentrations rise as a result of industrial operations, disturbed soil, & volcanic activity. In the industrial world, electroplating and the creation of nickel-cadmium cells are where it is most commonly used.
Workers who weld, solder, & make jewelry run the risk of breathing in cadmium oxide vapors. The most common outcome of metalworking in a cramped location with inadequate ventilation is significant toxicity.
Cadmium is not very accessible when consumed orally, however, it is readily bioavailable when breathed. Cadmium enters the bloodstream, adheres to albumin & alpha-2-macroglobulin, and is transported to the liver & kidneys. Cadmium concentrates in the spleen, pancreas, lung, & testes in addition to these two primary organs.
Cadmium attaches to metallothionein in the liver, where it forms a complex that is slowly released. It is biological half-life can be at least ten years due to the delayed release. After that, cadmium moves to the glomerulus, where it concentrates in significant concentrations in the proximal tubule, causing kidney toxicity.
Cadmium toxicity typically develops after exposure through employment, the environment, or recreational activities. Environmental exposures may result from metal pollution of the nearby soil and subsequent consumption of the food produced there. Areas, where ores are mined or refined are susceptible to this kind of pollution.
When a mine released a significant amount of cadmium into the environment in the Jinzu River in Japan in the 1950s, something similar occurred. The majority of the postmenopausal multiparous women who experienced this excruciating osteomalacia epidemic were rice farmers in the area.
Itai-Itai sickness, which translates to “ouch-ouch” in Japanese, was the name given to this condition since persons who had it would utter it every time they moved.
Restrictive lung disease may last a lifetime in cases of acute exposure. Kidney damage from persistent exposure might worsen and be permanent.
Clinical History
Clinical history of cadmium toxicity:
Acute exposure: Acute exposure to high levels of cadmium can lead to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and headache. In severe cases, there may be respiratory distress, shock, and even death.
Chronic exposure: Chronic exposure to lower levels of cadmium can result in a wide range of symptoms, including kidney damage, lung damage, anemia, bone damage, and hypertension. In some cases, there may be no symptoms until the damage is advanced.
Kidney damage: Cadmium is toxic to the kidneys, and chronic exposure can result in progressive kidney damage that may lead to kidney failure. Symptoms of kidney damage may include fatigue, loss of appetite, nausea, and swelling in the legs and feet.
Lung damage: Cadmium exposure can also lead to lung damage, including chronic bronchitis, emphysema, and lung cancer. Symptoms of lung damage may include coughing, wheezing, shortness of breath, and chest pain.
Anemia: Cadmium can interfere with the production of red blood cells, leading to anemia. Symptoms of anemia may include fatigue, weakness, pale skin, and shortness of breath.
Bone damage: Cadmium can accumulate in bones and lead to a condition called osteomalacia, which is a softening of the bones that can lead to fractures. Symptoms of bone damage may include bone pain, muscle weakness, and difficulty walking.
Hypertension: Chronic cadmium exposure has also been linked to the development of hypertension or high blood pressure.
Overall, the clinical history of cadmium toxicity can vary depending on the extent and duration of exposure and can involve a wide range of symptoms and complications affecting different organ systems. Early identification and management of cadmium exposure are important in preventing long-term health effects.
Physical examination
The physical examination findings in cadmium toxicity can vary depending on the extent and duration of exposure, as well as the affected organ systems. Here are some of the possible physical examination findings in cadmium toxicity:
Gastrointestinal system: The abdomen may be tender or distended, and there may be evidence of gastrointestinal irritation, such as vomiting or diarrhea. There may also be signs of dehydration, such as dry mucous membranes and decreased skin turgor.
Respiratory system: The patient may have wheezing, coughing, and decreased breath sounds, indicating bronchoconstriction or pulmonary edema. There may also be cyanosis (bluish discoloration) of the lips or nail beds.
Renal system: There may be signs of renal damage, such as edema in the legs and ankles, hypertension (high blood pressure), and proteinuria (excessive protein in the urine).
Skeletal system: The patient may have decreased bone density, leading to skeletal deformities, tenderness, and fractures.
Neurological system: In severe cases of cadmium toxicity, there may be neurological symptoms such as confusion, seizures, and coma.
In addition to the physical examination, laboratory tests such as blood and urine tests may be used to assess the extent of cadmium exposure and the degree of organ damage. Imaging studies, such as X-rays or bone scans, may also be used to evaluate skeletal damage. Overall, early identification and management of cadmium toxicity is important in preventing long-term health effects.
Differential diagnosis
One must consider the other common metal toxins, such as arsenic, lead, iron, mercury, & thallium, for any environmental or workplace occupational exposure. Metal fume fever is an exclusion diagnosis in acute toxicities; other causes of ARDS & pneumonitis are on the differential.
Acute Poisoning
The lungs are significantly at risk from cadmium fumes. It’s crucial to regulate the airways while using supplemental oxygen. Since their benefit has not yet been established, steroids are frequently the choice of treatment. Concerns for cadmium ingestion are a little different. Gastric lavage & activated charcoal are choices.
Monitoring of the patient’s liver and kidney damage as well as gastrointestinal harm, is necessary. Chelators have yet to be conclusively demonstrated to be helpful in cadmium toxicity, despite their promise. Yet, succimer has promising effects if it is administered early in the course.
Chronic Poisoning
These patients’ exposure will be known, and their dysfunction is often identified during standard screening. The patient must always be taken out of the exposure as the initial action. Despite the fact that the effects could be long-lasting & progressive, chelation is not currently advised for these patients.
https://www.ncbi.nlm.nih.gov/books/NBK536966/
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