Combined system disease after nitrous oxide anesthesia

Abstract

presentation suggested a bilateral C-5 radiculopathy. EMG studies revealed that this clinical picture was, in fact, produced by injury at the level of the brachial plexus, with a C-5, C-6, and C-7 denervation, and the authors proposed an ischemic mechanism that could involve the subclavian and axillary arteries.Typical pathologic findings of GCA occur in these vessel^.^ In our patient, however, only C-5 abnormalities were present in electrodiagnostic studies.Even if the ischemic mechanism remains unclear, the ipsilat-era1 vertebral artery was grossly abnormal in this patient, and the clinical response to corticosteroid therapy with concomitant improvement of the lumen of the vertebral artery on MRI angiography supports a local vascular mechanism caused by GCA.In conclusion, C-5 radiculopathy is a rare manifestation of GCA. After exclusion of radicular compression, the presence of other typical manifestations of GCA and, probably, angiographic abnormalities of the ipsilateral vertebral artery would be necessary for the diagnosis. The prognosis appears excellent with corticosteroid therapy.

Reversible nitrous oxide–induced myeloneuropathy with pernicious anemia: Case report and literature review

“…Abuse of nitrous oxide can precipitate vitamin B 12 deficiency in otherwise normal individuals 3, 13, 18, 20. More recently, the occurrence of cobalamin deficiency in previously asymptomatic vitamin B 12 –deficient individuals has been observed following only limited exposure to nitrous oxide during surgery 1, 2, 5, 6, 10–12, 14–16, 21–23, 25. We report such a case of cobalamin deficiency arising after dental procedures in a previously healthy young woman subsequently found to have pernicious anemia.…”

“Whippets”-Induced Cobalamin Deficiency Manifesting as Cervical Myelopathy

“…With normal Cbl levels, patients may develop deficiency after prolonged and repeated N 2 O exposure, while with preexisting Cbl deficiency, a single exposure to N 2 O may suffice. 9 N 2 O exposure may be recreational, iatrogenic, or occupational (in dental or anesthesia professionals 8,9,11,14,15 ). Of note, abuse via whipped cream dispensers may expose not only to N 2 O but also to other neurotoxic agents such as phenol, toluene, and trichloroethylene.…”

“…While existing reports of the neurological features of N 2 Oinduced Cbl deficiency may not reflect the complete spectrum of symptoms and signs, it is noteworthy that spinal cord and peripheral nerve complications appear to predominate over cerebral manifestations. [1][2][3][9][10][11][12][13][14][15]18,19 One might speculate whether this seeming predilection could be related to the more acute mode of onset. Several reports have described megaloblastic anemia, 7,[9][10][11][12][13][14]18 but in countries such as the United States that supplement cereals with folate, this has become unlikely, as exemplified by the present case.…”

“…An immediate goal when treating N 2 O-associated Cbl deficiency is to stop the exposure, which, together with supplementation, may lead to partial or complete resolution of the clinical manifestations within weeks to months. 3,10,11,13,18,19 Standard protocols rely on parenteral Cbl. 10,[12][13][14]18 Numerous regimens have been proposed, including Cbl 1000 mcg intramuscularly/ subcutaneously daily for 5 days followed by 1000 mcg/wk for 5 weeks, then 100 to 1000 mcg/mo.…”

“…6 Thus, it may be surprising that N 2 O-induced B12 deficiency is rarely reported. 1,3,[7][8][9][10][11][12][13][14][15] We present a case of N 2 O abuse in the form of whippets leading to Cbl deficiency and cervical myelopathy.…”