CASE REPORT |
https://doi.org/10.5005/jp-journals-11006-0151 |
Cadmium Toxicity Presenting as Multiorgan Dysfunction of Uncertain Etiology—A Diagnostic Dilemma: Case Report
1,3Department of Critical Care, SPS Hospitals, Ludhiana, Punjab, India
2Department of Critical Care Medicine and Emergency Services, SPS Hospitals, Ludhiana, Punjab, India
4Department of Medicine, SPS Hospitals, Ludhiana, Punjab, India
Corresponding Author: Puneet Chopra, Department of Critical Care, SPS Hospitals, Ludhiana, Punjab, India, Phone: +91 9888891543, e-mail: PUNEET9832@GMAIL.COM
Received: 14 August 2024; Accepted: 12 December 2024; Published on: 25 February 2025
ABSTRACT
Aim and background: Heavy metal poisoning, including cadmium, can occur with occupational exposure or intake of contaminated food products. The exposed patients may present in the critical care unit with nonspecific symptoms involving multiple organs. The diagnosis may be easily missed in the absence of clinical suspicion, as the presentation may mimic commonly encountered diseases.
Case description: We present an unusual case of a 32-year-old woman presenting with a history of intermittent vomiting, loss of appetite, anemia, jaundice, respiratory distress, and decreased urine output. Her sepsis workup, vasculitis profile, antinuclear antibodies (ANA)-18, and investigations for tropical fever were negative. The patient had a tobacco factory at home and was taking weight loss herbal supplements. In view of the clinical history and multiorgan dysfunction of uncertain etiology, heavy metal screening was sent, which revealed high levels of urinary cadmium. The patient was managed in the intensive care unit with supportive treatment, including sustained low-efficiency dialysis (SLED), vasopressors, and mechanical ventilation. However, the patient expired on hospital day 10 due to multiorgan dysfunction.
Conclusion: Cadmium toxicity usually occurs with occupational exposure; however, the use of tobacco and ingestion of contaminated food products can be important sources of cadmium exposure. Cadmium toxicity can result in multiorgan dysfunction and shock, which may be difficult to differentiate from other common causes, including sepsis. The management is mainly supportive and involves avoidance of further exposure.
Clinical significance: Our case highlights the importance of maintaining a low threshold for suspicion of heavy metal toxicity in patients with unusual presentations and multiorgan dysfunction of uncertain etiology.
Keywords: Cadmium, Case report, Heavy metal toxicity, Multiorgan dysfunction
How to cite this article: Chopra P, Singhal V, Nirmal J, et al. Cadmium Toxicity Presenting as Multiorgan Dysfunction of Uncertain Etiology—A Diagnostic Dilemma: Case Report. Indian J Crit Care Case Rep 2025;4(2):38–40.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
INTRODUCTION
Heavy metal poisoning in humans is usually associated with lead, mercury, arsenic, and cadmium. Cadmium toxicity can occur with exposure to tobacco, working in high-risk industries, or ingestion of contaminated food products. High-dose acute cadmium exposure usually presents as gastrointestinal or respiratory symptoms, depending on the route of exposure. On the contrary, low-dose chronic exposure to cadmium may present as painful degenerative bone disease or renal failure and may eventually progress to multiorgan dysfunction. In critically ill patients presenting with multiorgan dysfunction of uncertain etiology, it is easy to overlook heavy metal intoxication. With this background, we present a case of cadmium toxicity in a patient who presented with multisystem involvement. Although treatment of cadmium toxicity is supportive and involves avoidance of further exposure, detailed clinical history, exclusion of other common etiologies of multiorgan dysfunction, a high index of suspicion, and the use of heavy metal toxicological screening can help in early diagnosis.
CASE DESCRIPTION
A 32-year-old female presented to the hospital with complaints of episodes of vomiting, loss of appetite for 2 weeks, yellowish discoloration of skin and eyes for 1 week, photosensitivity for 1 week, blurring of vision, especially at night, altered color perception for 1 week, decreased urine output, and pain in both legs for 4 days. The patient had a history of mini gastric bypass surgery 3 years ago. On examination, the patient was thin with dehydrated oral mucosa and decreased skin turgor. Vitals on arrival were heart rate: 100/minute, BP: 70/50 mm Hg, SpO2: 92% on room air. On auscultation, decreased air entry was noted in the right basal lung fields. The abdomen was distended and tender, and hepatosplenomegaly was noted. After emergency fluid resuscitation and blood pressure stabilization, the patient was shifted to the intensive care unit for further management.
Laboratory investigations on day 1 revealed hemoglobin: 4.9 gm/dL (11.5–15 gm/dL), total leukocyte count: 3.6 × 103 cells/μL (4–10 × 103 cells/μL), platelets: 115 × 106 cells/μL (150–450 × 106 cells/μL), and INR: 1.90. Liver function tests revealed SGOT 52 U/L, SGPT 18 U/L, alkaline phosphatase 115 U/L, bilirubin (total) 6.9 mg/dL, and direct bilirubin level of 6.1 mg/dL. Urine routine examination showed protein ++, 5–6 RBC, 8–10 pus cells, and serum creatinine level of 2.29 mg/dL. Peripheral blood smear showed the presence of normocytic normochromic red blood cells and some schistocytes. Chest X-ray was suggestive of haziness in bilateral lower zones and ill-defined opacities in perihilar locations. The patient was managed with supplemental oxygen and started on broad-spectrum empirical antibiotics after sending tropical fever work-up, blood, and urine cultures.
The patient started to have respiratory distress and decreased urine output on day 2 of admission. The patient was intubated, put on mechanical ventilation, vasopressor support, and sustained low-efficiency dialysis (SLED) was initiated in view of severe metabolic acidosis. Serum haptoglobin was <40 (normal range 40–280 mg/dL), and the iron profile revealed TIBC <36 μg/dL (250–450 μg/dL), serum iron 42 μg/dL (28–170 μg/dL), and serum ferritin 948.5 ng/mL (10–291 ng/mL). Bone marrow examination showed normocellular to mildly hypercellular hematopoietic marrow comprising erythroid precursors, maturing cells of the myeloid series, and adequate megakaryocytes. Rapid malaria card, widal test, leptospira serology, scrub typhus serology, ELISA anti-HAV IgM, ELISA anti-HEV IgM, vasculitis, and antinuclear antibodies (ANA)-18 profile were negative.
On further inquiry, it was found that the patient had a tobacco factory at home for the past 8–10 years. There was a history of tobacco intake for the last 3 years (quantity not specified), along with the intake of weight loss herbal supplements. Considering the high risk of exposure to tobacco and herbal supplements, it was decided to send a panel of heavy metals in the body. Blood levels of lead, and urinary levels of arsenic, cadmium, chromium, and mercury were sent. On the 6th day of ICU stay, the patient had episodes of seizures, which were controlled with levetiracetam.
On day 8, the reports of heavy metal screening showed high levels of urine cadmium (inductively coupled plasma mass spectrometry—ICPMS method): 15.80 μg/L (normal: <2.60 μg/L) with normal levels of mercury, arsenic, chromium, and lead. The patient received multiple sessions of SLED, vasopressor infusion, blood products, and multiorgan supportive care during her stay in the ICU. The patient continued to deteriorate due to persistent shock, multiorgan dysfunction, metabolic acidosis, poor sensorium, coagulopathy, and expired on day 10 of hospitalization.
DISCUSSION
Our patient presented with multisystem involvement, including the hematological, hepatic, renal, and respiratory systems. Tropical fever workup, vasculitis profile, microbiological cultures, and ANA-18 profile were negative. Given the history of tobacco exposure, use of herbal products, and multiorgan dysfunction of uncertain etiology, the possibility of heavy metal intoxication was considered. Heavy metal screening revealed significantly high levels of urinary cadmium. Urinary cadmium levels correlate strongly with total cadmium intake and are a useful indicator of cadmium exposure in an individual.1
Cadmium is primarily used in nickel–cadmium batteries, paint pigments, cosmetics, electroplating, and galvanizing steel. Cadmium can also be found in soil and water, particularly those contaminated with sewage sludge or phosphate fertilizers. Crops such as rice can accumulate high concentrations of cadmium if grown on polluted soil. The tobacco plant contains significantly high concentrations of cadmium (1–2 µg/gm dry weight), and smoking cigarettes is an important source of cadmium exposure.2 Workers involved in tobacco leaf processing may be exposed to cadmium through inhalation of tobacco dust and by oral route from contaminated hands/food from the environment. Blood cadmium levels in workers involved in tobacco processing were found to be significantly higher than in the general population. There was also significant elevation of urinary enzymes and proteins in workers exposed to tobacco leaves, suggesting early nephrotoxicity, even though none of the workers had cadmium levels >10 µg/L, which is the limit of toxicity.3 Cadmium levels were assessed by Nath et al. in 54 Indian herbal medicines, and they found that all marketed varieties of studied herbal medicines had cadmium levels exceeding the World Health Organization (WHO) limit.4 The exact cause of the high cadmium level in our patient remains speculative; however, the use of tobacco and unsupervised ingestion of herbal medicines could have led to cadmium toxicity.
Acute cadmium toxicity occurs with inhalation of toxic fumes or large ingestion of contaminated food/water, while chronic toxicity can occur with occupational exposures or tobacco smoke. Ingestion of cadmium-containing food products can produce gastrointestinal symptoms, including nausea, vomiting, and abdominal cramps. Severe cadmium poisoning can lead to renal dysfunction, hepatic impairment, pneumonitis, anemia, and coagulopathy, as was present in our case.5 Ocular symptoms seen in our patient can be due to retinal accumulation of cadmium, though no fundus examination could be done. The patient, on presentation, had low hemoglobin (4.9 gm/dL), low serum haptoglobin, and the presence of schistocytes on peripheral smear. Cadmium exposure can lead to oxidative stress in red blood cells, direct hemolysis, inhibition of protein synthesis, and has been associated with anemia.6 The kidneys are the main target organs with chronic exposure to cadmium and present with renal tubular dysfunction, proteinuria, or overt nephropathy. Itai-Itai disease occurs due to chronic cadmium exposure and is characterized by osteomalacia, osteoporosis, and painful bone fractures. Long-term exposure to cadmium is carcinogenic to humans.7 Cadmium poisoning induces tissue injury in multiple organs through various mechanisms, including oxidative stress, changes in DNA expression, inhibition or upregulation of transport proteins, and induction of apoptosis. There is limited literature regarding the management of acute cadmium toxicity, with most evidence coming from animal studies and case reports.5,6 Although there are no controlled studies on the role of extracorporeal therapies, including hemodialysis and plasmapheresis, in removing cadmium, these are unlikely to be effective, as cadmium gets fixed to cells.8 Chelation therapy with ethylenediaminetetraacetic acid (EDTA) may reduce the total cadmium burden in some cases after acute exposure; however, there is concern that chelation therapy may aggravate renal tubular damage. The management is mainly supportive and avoidance of further cadmium exposure.9
CONCLUSION
Cadmium toxicity may involve multiple organ systems and can be lethal. It is not a common toxin but can pose a risk to the health of people exposed to tobacco, cadmium-contaminated food products, or various industries. This case highlights the importance of detailed clinical history, early suspicion, and the use of heavy metal toxicological screening, including cadmium levels, in patients who present with multiorgan failure of unexplained etiology.
Clinical Significance
Our case highlights the importance of maintaining a low threshold for suspicion of heavy metal toxicity in patients with unusual presentations and multiorgan dysfunction of uncertain etiology. In the absence of a specific antidote or management, it is important to have an early diagnosis, supportive treatment, and avoidance of further exposure to the toxin.
ORCID
Puneet Chopra https://orcid.org/0000-0002-8651-5333
Vinay Singhal https://orcid.org/0000-0003-0297-5058
Jasmine Nirmal https://orcid.org/0009-0004-1625-1995
Parambir Singh https://orcid.org/0009-0009-8489-7794
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