POSTSCRIPT
Hypophosphataemic neuropathy in a patient who received intravenous hyperalimentation
1 Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
2 Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
3 Department of Neurology, Japanese Red Cross Nagoya First Hospital, Nagoya, Japan
4 Department of Gastroenterology, Japanese Red Cross Nagoya First Hospital, Nagoya, Japan
5 Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
Correspondence to:
Professor Gen Sobue, 65 Tsurumaicho, Showaku, Nagoya 466-8550, Japan; sobueg@med.nagoya-u.ac.jp
| The first 150 words of the full text of this article appear below. |
A malnourished patient that received intravenous hyperalimentation (IVH) without inorganic phosphate (IP) developed hypophosphataemia and acute sensorimotor neuropathy. F waves in the peripheral nerve trunk were absent or diminished, while nerve conduction velocities were nearly normal. The sural nerve biopsy revealed the presence of some subperineurial oedema and mild axonal atrophy. Prompt IP administration reversed the patients’ neurological symptoms and normalised F waves. Our data suggest that hypophosphataemia plays a role in the pathogenesis of neuropathy that develops in patients following IVH without IP.
Intravenous glucose administration is the most common cause of hypophosphataemia in hospitalised patients.1 While most of these cases are asymptomatic, severe hypophosphataemia, when combined with phosphorus depletion, can cause acute neuropathy that mimics Guillain–Barré syndrome. However, prompt IP administration can reverse this clinical condition. While there have been several reports of acute neuropathies caused by hypophosphataemia, most are anecdotal and no report has described an associated
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