Manganese toxicity in critical care: Case report, literature review and recommendations for practice

Abstract

We present the case of a 62-year-old man on the intensive care unit with pancreatitis. Since early in his admission, and for the remainder of his prolonged stay in intensive care, he has received parenteral nutrition for intestinal failure. The whole blood manganese concentration was significantly increased after 2½ months of parenteral nutrition (PN). Three months into his stay, he developed a resting tremor and extra-pyramidal dyskinesia. In the absence of other neurological symptoms, and with no history of essential tremor, Parkinsonism or cerebral signs, hypermanganesaemia was presumed to be the cause. We review manganese metabolism and toxicity in patients who are fed with parenteral nutrition and review the current recommendations and guidelines.

Manganese Provision in Parenteral Nutrition: An Update

“…However, critically ill patients may be susceptible to neurotoxicity at lower doses. A recent report described a 62 year old man, chronically critically ill with acute pancreatitis, who developed parkinsonian‐like symptoms after 10 weeks of PN containing Mn doses of 270 μg/d . Most case reports of Mn toxicity in PN have been for patients treated for >3 months, suggesting that the cumulative dose is important .…”

“…Whole blood Mn is the preferred test and should be considered the mainstay of monitoring. A practical point to note is that use of MRI is precluded when ferrous equipment is being used and for patients who are bedbound …”

“…A practical point to note is that use of MRI is precluded when ferrous equipment is being used and for patients who are bedbound. 74…”

Iron and manganese-related CNS toxicity: mechanisms, diagnosis and treatment

“…Lack of treatment for manganism has been the major barrier in clinical management of Mn intoxication. The foremost therapeutic strategy is removal of the source of Mn exposure [242,243]. Levodopa is considered ineffective in manganism [142,244], presumably because the nigrostriatal pathway remains intact.…”

“…Chelation therapy has been suggested in order to reduce the body burden of Mn in severe cases of Mn intoxication [242]. Chelating therapy with intravenous ethylene-diamine-tetra-acetic acid (EDTA) has been shown to successfully increase Mn elimination in urine and decrease Mn concentrations in blood [242,245]; however, its efficacy to ameliorate clinical symptoms is questionable [243,246]. Chelation therapy has been found to alleviate parkinsonian symptoms in patients with inherited hypermanganesemia [117,247].…”