Nitrous Oxide-induced Polyneuropathy, Pancytopenia and PE

In This Article

Abstract and Introduction

Abstract

Background: Nitrous oxide is a medical and household gas that has seen its use drift to recreational purpose among the young population in recent years. Significant neurological, hematological and psychiatric side effects, generally related to an induced functional vitamin B12 deficiency, have been described separately in the literature.

Case Report: A 22-year-old woman of North African origin experienced an exceptional combination of polyneuropathy, bilateral pulmonary embolism and severe pancytopenia related to vitamin B12 deficiency and hyperhomocysteinemia induced by recreational nitrous oxide use. After treatment with vitamin B12 supplementation and intensive rehabilitative management, the patient progressively regained the ability to walk and her biological parameters gradually returned to normal. The pathophysiological mechanisms related to a decrease in vitamin B12 activity are the reduction of products needed for synthesis of deoxyribonucleic acid, carbohydrate or fatty acids, and the increase of hyperhomocysteinemia. Other mechanisms involving a direct action of N2O are also suspected.

Conclusion: This case report brings elements to support our knowledge about pathological pathway, recovery and prognosis of recreational N2O abuse complications. The general and medical population should be aware to the serious consequences of this type of consumption.

Introduction

Nitrogen peroxide (N2O) is a colourless and odourless inhaled substance that has been classically used in anaesthesia for over 150 years for its analgesic and anxiolytic properties.^[1] Unfortunately, its use has been derived for recreational purposes in recent decades among the young population wishing to exploit its euphoric effect. Young people ingest N2O from bottles intended for domestic use, which are easily available on the market.^[2] Many side effects related to chronic intake have been reported with some dramatic consequences in this population. Among the reported side effects, we note psychiatric disorders, damage to the central and peripheral nervous systems, hematological disorders, thromboembolic phenomena, and others.^[2,3] These side effects generally result from an induced vitamin B12 deficiency.

Here we describe the case of a young patient who exceptionally presented a simultaneous combination of several side effects, namely polyneuropathy, pulmonary embolism, and pancytopenia.

Table 1. Evolution of biological data
Time after presentation (days)	1	2	7	18	74
Hemoglobin [g/dl] (nl: 11.5–15)	7.5	7.7	7 .6	8.9	12.4
Hematocrit [%] (nl: 34.4–44.6)	21.7	21.8	22.6	27.4	37.8
MCV [fl] (nl: 75–96)	83.5	82.6	86.6	94.5	92.2
Leucocytes [10^3/μL] (nl: 3.8–11.4)	2.12	2.01	6.27	4.81	5.81
Neutrophils [10^3/μL] (nl: 1.4–7.7)	0.17	0.28		2.14	2.71
Thrombocytes [10^3/μL] (nl: 150–445)	133	88	83	425	326
Reticulocytes [10^9/l] (nl: 20–100)	10.2	–	–	210.8	–
Haptoglobin [g/l] (nl: 0.35–2.5)	2.69	–	–	3.19	–
Schizocytes	Absents	–	–		–
Iron [μg/dl] (nl: 50–170)	18	–	–	40	38
Ferritin [μg/l] (nl: 4.63–204)	1240.14	–	–	256.98	31.69
Transferrin [g/l] (nl: 1.8–3.82)	1.54	–	–	2.34	2.67
Transferrin saturation [%] (nl: 15–50)	8	–	–	12	10
CRP [mg/l] (nl: 0–5)	316.6	297.1	63	12.1	–
Folic acid [μg/l] (nl: 3.1–20.5)	13,39	–	–	15.49	19.78
Vitamin B12 [ng/l] (nl: 187–883)	< 148	–	> 2000	> 2000	374
Homocysteine [μmol/L] (nl: < 10)	207.1	–	–	–	–
Methylmalonic acid [μg/l] (nl: < 47)	919	–	–	–	–

MCV: mean corpuscular volume
CRP: C-reactive protein
Nl: normal

Table 2. Electroneuromyography parameters
2a Motor conduction study
	Latency (ms)	Amplitude (mV)	MNCV (m/s)	F wave latency (ms)
Tibial nerve (right)
Ankle—AHB	4.89	2.1	–	NR
Popliteal fossa—Ankle	18.0	0.3	32.0	–
Tibial nerve (left)
Ankle—AHB	5.12	0.9	–	NR
Popliteal fossa—Ankle	17.5	0.55	32.3	–
Peroneal nerve (right)
Ankle—EDB	6.08	0.33	–	NR
Fibula head—Ankle	18.8	0.21	28.3	–
Median nerve (right)
Wrist—APB	3.58	9.7	–	26.3
Elbow—Wrist	7.38	9.6	51.3	–
Ulnar nerve (right)
Wrist—ADM	2.75	8.9	–	27.9
Elbow (below)—Wrist	6.69	7.0	54.6	–
2b Sensitive conduction study
	Latency (ms)	Amplitude (μV)		SNCV (m/s)
Sural nerve (right)	2.88	8.4		48.6
Median nerve (right)	3.04	25.9		59.2

ADM: abductor digiti minimi; AHB: Abductor hallucis brevis; APB: abductor pollicis brevis; EDB: Extensor digitorum brevis; MNCV: Motor nerve conduction velocity; NR: No response; SNCV: Sensitive nerve conduction velocity

Table 3. Functional evolution
3a Lower limbs muscle testing (MRC scale)
Time after presentation (weeks)	1	4	6	8	10	12	33
Psoas
Right	3	3	3	4	5	5	5
Left	3	3	3	4	5	5	5
Quadriceps
Right	2	2	2	4	5	5	5
Left	1	1	1	3	5	5	5
Tibialis anterior
Right	1	1	2	2	2	2	2
Left	0	0	1	1	1	1	2
Tibialis posterior
Right	1	1			3	3	3
Left	0	0			2	2	5
Peroneus longus
Right	1	1			1	1	5
Left	0	0			1	1	5
Triceps surae
Right	4	4	4	4	4	4	5
Left	1	1	1	2	2	4	5
Extensor hallucis longus
Right	2	2	2	2
Left	0	0	1	1
3b Evolution of walking ability (FAC)
Time after presentation (weeks)	1	4	6	8	10	12	33
FAC	0	0	1	3	4	5	5