Unilateral vocal fold paralysis post-thyroidectomy: does early intervention allow for better voice recovery?

OBJECTIVE: Thyroidectomy is the primary cause of unilateral vocal fold paralysis (UVFP). A delay in rehabilitation may cause dysfunctional phenomena and worsen dysphonia. The main aim is to investigate the impact of early Speech Therapy (ST) on voice recovery in UVFP post-thyroidectomy and propose an appropriate treatment schedule. PATIENTS AND METHODS: 93 patients with UVFP were analysed. 72 presented transient paralysis and 21 permanent ones. Individuals with permanent paralysis were retrospectively divided in two groups. Group A was composed of 11 patients (8 F, 3 M; mean age: 50.5 ± 8.6) who received ST within 8 weeks; Group B comprised 10 patients (7 F, 3 M; mean age: 57 ± 11.5) treated after more than 8 weeks. Videolaryngostroboscopy (VLS) was assessed and both objective and subjective voice parameters were collected. The non-parametric Wilcoxon test was applied to the sample. RESULTS: The resolution of supraglottic compensations was observed in 91% of cases in Group A, whereas in only 40% of cases in Group B. A functional glottal closure occurred in 73% of patients in group A, while it was completely absent in group B. Group A showed a statistically significant difference between the values of Jitter, NHR, TMF and VHI collected pre-ST compared to that collected after 1 year. Conversely, a statistically significant difference was found only for VHI values in group B. CONCLUSIONS: Early ST brings benefits to patients with permanent UVFP, both on voice recovery and on quality of life. A ST protocol should be applied both before and after thyroidectomy. The ST treatment should start early after surgery.

Acute liver and renal failure during treatment with buprenorphine at therapeutic dose.

Buprenorphine is a semi-synthetic opioid derivative commonly used in the treatment of heroin addiction. Life-threatening complications have been described following overdoses while few cases of hepatotoxicity due to drug use at therapeutic doses have been recently described in hepatitis C virus carriers. In these cases, however, histological assessment was not exhaustive and no extra-hepatic organ failure was observed. We describe herein a case of acute liver and kidney failure in a patient with previously latent hepatitis C virus chronic infection following recommended doses of buprenorphine. Histology did not demonstrate any feature compatible with hepatitis C virus reactivation or liver cirrhosis and suspension of the treatment led to the resolution of both liver and kidney failure. Causality criteria fulfillment indicates a high probability of buprenorphine-induced liver toxicity. No signs of pre-existant kidney impairment or of pre- or post-renal causes were observed. Since buprenorphine is metabolized through cytochrome P450 3A4, we genotyped six genetic polymorphisms previously described in poor metabolizers but could not confirm these pharmacogenetic bases in this case. In conclusion, we surmise that buprenorphine at suggested doses can induce liver and kidney failure in susceptible individuals, possibly through direct mitochondrial toxicity.

[Middle lobe syndrome in children. Critical review]. / La sindrome del lobo medio nel bambino. Rivisitazione critica.

The clinical, radiological and anatomo-evolutive pictures of this syndrome are typical. It is suggested that cases are more frequent than is generally thought and that their recognition is delayed on account of the considerable time that often elapses before repeated infection of the respiratory system, particularly the middle lobe, results in the onset of the syndrome.