The Effect of Extension of the Head and Neck upon the Infrahyoid Respiratory Passage and the Supraclavicular Portion of the Human Trachea

ABSTRACT Tracheostomy plays a vital role in respiratory distress caused by different conditions, like respiratory passage of obstruction, head and neck tumor, surgeries, trauma patients and inflammatory conditions. Timing of the operation and postoperative care deserves more emphasis. Delay in the performance of this operation defeats the purpose of tracheostomy and if managed properly, it is a life saving procedure. The aim of the study was not only to give immediate relief to the patients of respiratory distress. But also to study age and sex distribution indication and evaluate factors associated with morbidity and mortality, intraoperative and postoperative complications associated with this procedure. This study was done on 50 cases of respiratory distress admitted in different department of Rajindra Hospital, Patiala, who underwent tracheostomy as an emergency or elective procedure. Most of the patients (24%) were of 50 to 60 years of age of which 60% were males. Emergency tracheostomy was done in most of the cases (64%). Most common complication was wound infection and granuloma formation (16%). Mortality due to primary disease (tumors of head and neck) was 34%. Followed by head injury (29%). Only one patient died of tracheostomy due to excessive bleeding. How to cite this article Sahni D. Role of Tracheostomy in Respiratory Distress: A Study of 50 Cases. Clin Rhinol An Int J 2015;8(1):20-23.

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Implications for clinical staging of metastatic cutaneous squamous carcinoma of the head and neck based on a multicenter study of treatment outcomes

The Journal of Laryngology & Otology ◽

10.1017/s0022215106002891 ◽

2005 ◽

pp. 1

Keyword(s):

Head And Neck ◽

Treatment Outcomes ◽

Multicenter Study ◽

Squamous Carcinoma ◽

Clinical Staging

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[Triple-combined therapy of malignant cancer of the head and neck-maxillary cancer]

Journal of Dental Education ◽

10.1002/j.0022-0337.1969.33.4.tb00237.x ◽

1969 ◽

Vol 33 (4) ◽

pp. 596-598

Author(s):

Y Sato

Keyword(s):

Head And Neck ◽

Combined Therapy ◽

Maxillary Cancer

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Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

Biochemical Journal ◽

10.1042/bcj20190591 ◽

2019 ◽

Vol 476 (24) ◽

pp. 3705-3719 ◽

Cited By ~ 2

Author(s):

Avani Vyas ◽

Umamaheswar Duvvuri ◽

Kirill Kiselyov

Keyword(s):

Oxidative Stress ◽

Head And Neck ◽

Transcriptional Activation ◽

Platinum Resistance ◽

Mrna Levels ◽

Strong Positive Correlation ◽

Platinum Compounds ◽

Copper Chelation ◽

Novel Approach ◽

Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

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