Obstructive sleep apnea- a short review

 

Introduction1

• ·         Obstructive sleep apnea is defined as recurrent episodes of partial or complete upper airway obstruction during sleep resulting in repetitive apneas and/or hypopneas1.

• ·         This is the most common type of sleep-disordered breathing, characterized by oxygen desaturations and arousals from sleep.

• ·         If sleep-related obstruction in breathing is associated with excessive daytime sleepiness, it is termed as obstructive sleep apnea syndrome (OSAS) or obstructive sleep apnea-hypopnea syndrome (OSAHS).

Epidemiology2

• ·         The prevalence of OSA varies according to the geographical location.

• ·         It ranges from 9-37% in men and 4-50% in women2.  

• ·         Obstructive sleep apnea syndrome occurs in 6% of men and 4% of women2.

Risk factors

• Male sex: Male to female ratio is 3:1.13. More among elderly males and postmenopausal women.

• Obesity and increased neck circumference: Obesity is considered as a major risk factor for the development and progression of OSA3.  Neck circumference of more than 17 inches in males and 15 inches in female increases the risk of OSA.

• Craniofacial abnormalities such as micrognathia, retrognathia, and tonsillar hypertrophy are risk factors for OSA.

Risk factors in children5

• Most cases of OSA in children are caused by either obesity or adenotonsillar hypertrophy.

• Facial, oral, and throat asymmetry seen in numerous congenital syndromes like Pierre Robin anomaly and Treacher Collins syndrome leads to OSA.

• Certain storage diseases, hypothyroidism, and Down syndrome result in upper airway crowding due to a relative increase in tongue mass causing OSA.

•  Neuromuscular diseases contribute to obstructive sleep apnea because of abnormal muscle tone in the pharyngeal constrictors.

Clinical features

• Nocturnal symptoms of OSA include loud snoring, witnessed apneas, choking, nocturnal restlessness, nocturia and diaphoresis.

• Daytime symptoms related with OSA are daytime hypersomnolence, non-restorative sleep, lack of concentration, cognitive deficits, mood changes, morning headache, dry mouth and decreased libido.

• Symptoms in children include excessive daytime sleepiness, difficult arousing from sleep, aggressive behavior, poor school performance, attention deficit,  hyperactivity, mouth breathing, nasal congestion and nasal speech.

• Physical findings in OSA are obesity, increased neck circumference, large tongue, tonsillar hypertrophy, increased Mallampati score, craniofacial abnormalities such as micrognathia, features of hypothyroidism, systemic hypertension and pulmonary hypertension.

Classification

• Obstructive sleep apnea is classified based on apnea-hypopnea index (AHI) measured by polysomnography.

•  If AHI is <5 it is normal, AHI of 5-15 is mild OSA, AHI of 15-30 is moderate OSA and AHI >30 is severe OSA.

Complications

• Systemic inflammation in OSA results in many serious complications and comorbidities.

• Major complications include systemic hypertension, Type-2 diabetes mellitus, metabolic syndrome, pulmonary hypertension, myocardial infarction, stroke and congestive cardiac failure.

• Drivers with OSA are involved in motor vehicle accidents due to increased daytime sleepiness.

Work up4

• Gold standard diagnostic test for OSA is polysomnography4. This is done either as a full night study or as a split night study.

•  Polysomnography assesses sleep stages, apnea, hypopnea, oxygen saturation, breathing effort, limb movements, heart rate and body positions.

•  Based on these apnea-hypopnea index (AHI) and respiratory disturbance index (RDI) are calculated.

• Limited studies with portable monitors are used with less number of parameters to avoid hospitalization.

 Management

• Mild OSA is treated with lifestyle modification. This includes weight reduction, regular exercise, and sleep hygiene.

•  Moderate to severe OSA is treated with continuous positive airway pressure (CPAP) device.

• Oral appliances for mandibular advancement is the option for mild to moderate OSA who do not tolerate CPAP or fails with CPAP

• Surgical treatment such as correction of craniofacial abnormalities, uvulopalatopharyngoplasty are also considered for those who fail to respond to CPAP.

• The accepted first-line treatment in children is tonsillectomy and adenoidectomy.

References

1. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999; 22:667-89. [PubMed] [Google Scholar]

2. Franklin KA, Sahlin C, Stenlund H, et al. Sleep apnoea is a common occurrence in females. Eur Respir J 2013; 41:610-5. [PubMed] [Google Scholar]

3. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep 2008; 31(8):1071–78.

4. Iber C, Ancoli-Israel S, Chesson AL, Quan SF. The AASM Manual for the Scoring of Sleep and Associated Events. Westchester,IL: American Academy of Sleep Medicine. 2007.

5. American Thoracic Society. Standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med 1996; 153:866–78.

Pneumothorax-a short review

 

Definition1

Pneumothorax is accumulation of air within the pleural space leading to passive atelectasis of the lung.

Classification

Pneumothorax is classified into 2 major types

• Spontaneous

• Traumatic.

Spontaneous pneumothorax is of 2 types2

• Primary spontaneous pneumothorax (PSP) which develops without any obvious cause. Unrecognized subpleural bleb may be the cause2.

• Secondary spontaneous pneumothorax develops in diseased lungs and causes are asthma, COPD, lung cavity, lung abscess, and cysts.

Traumatic pneumothorax is of two types

• Accidental: due to penetrating or blunt trauma and air enters the pleural cavity through the chest wall or visceral pleura through alveolar rupture from sudden compression of the chest.

• Iatrogenic: develops during diagnostic or therapeutic interventions. Common situations are endoscopic procedures, insertion of jugular/subclavian vein cannula, transthoracic needle biopsy, and aspiration of pleural fluid.

Clinical types

• Closed: air leak stops as the defect gets closed and will not progress further.

• Open: there is a fistulous communication and air moves to and fro during respiration. This type of pneumothorax does not cause increased intrapleural pressure.

• Tension: This is a medical emergency as air enters the pleural space, but will not escape.   This creates high intrapleural pressure and exerts a pressure effect on the heart and opposite lung. If not interfered immediately, it may lead to cardio-respiratory distress.

Clinical features

• Main symptoms are chest pain and shortness of breath. Chest pain is sharp and sudden in onset Cough and fatigue are other symptoms of pneumothorax.

• Physical signs include tachycardia, tachypnoea and hypotension. There will be reduced expansion and reduced breath sound on the affected side. Percussion shows hyper-resonant notes and added sounds are absent.

Investigations

• X-Ray chest shows increased translucency without lung markings on the affected side. Lung is collapsed towards the midline and is seen as a dense lesion close to the hilum. Radiographic manifestations of tension pneumothorax are mediastinal shift, depression of diaphragm and rib cage expansion.

• In a supine film taken in ICU, pneumothorax is often missed as the collapsed lung overlaps the air shadow. The presence of a deep costophrenic angle (deep sulcus sign) may be the only sign.

• CT may be necessary to diagnose pneumothorax in critically ill patients in whom upright or decubitus films are not possible3. CT demonstrates focal areas of emphysema or bleb in spontaneous pneumothorax.

Treatment4

• Based on five principles which are, removal of air, reducing air leakage, healing the pleural fistula, promoting re-expansion and preventing recurrences.

• Treating underlying diseases, preventing, and dealing complications are also important.

Treatment of pneumothorax is depended on:

• Size of the pneumothorax

• Symptoms

• Underlying lung disease

According to the British Thoracic Society (BTS) guidelines5, pneumothorax is measured from the inner chest wall to the lung edge at the level of the hilum.

• <2 cm- small pneumothorax.

• ≥2 cm- large pneumothorax.

• If asymptomatic no treatment is recommended for small pneumothorax. Follow-up radiology is advised to confirm resolution.

• Pneumothorax with mild symptoms without any underlying lung condition, needle aspiration is advised. Needle aspiration is as effective as large-bore chest drains. 

• But if failed, needle aspiration should not be repeated and a small-bore (<14 F) chest drains is inserted. Cannula connected to one-way Heimlich valve devices or small-bore pigtail catheters are also used.

• Pneumothorax in a patient with underlying chronic lung disease or large pneumothorax with significant symptoms should be treated with intercostal drain. The distal drainage device includes a water seal bottle and negative pressure suction device.

• Pleurodesis is considered in patients with recurrence pneumothorax. Pleurodesis is indicated in second ipsilateral recurrence or first contralateral recurrence. Chemical pleurodesis with talc under medical thoracoscopic guidance is preferred.

 References

1. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med. 2000; 342(12):868-74. [Medline].

2. Mitlehner W, Friedrich M, Dissmann W. Value of computer tomography in the detection of bullae and blebs in patients with primary spontaneous pneumothorax. Respiration. 1992; 59(4):221-27. [Medline].

3. Lesur O, Delorme N, Fromaget JM, et al. Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax. Chest. 1990; (2):341-47. [Medline].

4. Tschopp JM, Rami-Porta R, Noppen M, Astoul P. Management of spontaneous pneumothorax: state of the art. Eur Respir J. 2006; (3):637-50. [Medline].

5. MacDuff A, Arnold A, Harvey J, et al. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax 2010; 65 (Suppl 2):ii18-31. [PubMed]

Pulmonary tuberculosis-Overview

 

Introduction1

• Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (tubercle bacilli).

• The lungs are the most common site of involvement in tuberculosis and are a major source of spread of the disease.

• Pulmonary manifestations of tuberculosis are varied and depend on whether the infection is primary or post-primary.

Classification2

• Pulmonary: involves lung parenchyma and airways.

• Primary tuberculosis: infection following first time entry of the bacilli into the body; common sites being upper airways and lungs.Usually seen in children and young adults. Maybe self limiting or progress to progressive primary tuberculosis.

• Post primary tuberculosis: adult type of tuberculosis in an otherwise sensitized individual by reactivation of primary focus or by reinfection.

• Extra pulmonary: Involvement of pleura, lymph nodes, bone, kidney, brain and genital tract.

Etiology

• TB is spread from person to person through air by droplet nuclei. M. tuberculosis may be expelled when an infectious person coughs, sneezes, speaks or sings. Transmission occurs when another person inhales these droplet nuclei.

Pathogenesis

• The primary focus (Ghon’s focus) in the lung parenchyma consists of bacteria surrounded by lymphocytes, macrophages, epithelioid cells, giant cells and fibroblasts. Ghon’s focus along with lymphangitis and regional lymphadenopathy is called primary complex (Ghon’s complex). The primary infection is usually asymptomatic. Progression occurs in 5% of patients, usually in those with impaired immunity, and is called progressive primary tuberculosis.

• Post-primary pulmonary tuberculosis develops later in adult life as pneumonia involving the upper lobes or superior segment of lower lobes. Pneumonia undergoes caseous necrosis and fibrosis subsequently.

Clinical features

• Children with primary complex are mostly asymptomatic. However it can present as fever, loss of appetite and failure to thrive3.

• Post primary tuberculosis presents with chronic cough, fever, malaise and weight loss. They may also have hemoptysis. Sometimes massive hemoptysis develops due to erosion of a bronchial artery (Rasmussen’s aneurysm).

• Patients with acquired immunodeficiency syndrome have features similar to primary tuberculosis or disseminated tuberculosis.

Workup2

• Sputum smear examination for acid fast bacilli (AFB). All patients with cough of more than 2 weeks should undergo sputum smear on 2 consecutive days. It is difficult to obtain sputum in young children and hence gastric aspirate is subjected to AFB smear.

• Chest X-ray: All pulmonary TB suspects should undergo X-ray chest examination. X-ray is highly sensitive but not specific. Subcentimeter nodules or hilar lymphadenopathy may be seen3. In post primary TB, X-ray shows cavitating consolidation, fibrosis, miliary shadows and pleural effusion4.

• Molecular methods such as TB-PCR, CBNAAT and true NAAT are widely used and are considered highly sensitive.

• Sputum for mycobacterial culture is also done to confirm infection and to rule out drug resistance.

Management5

• The major goals of treatment include cure the individual patient; minimize risk of death and disability and to prevent airborne transmission.

• Tuberculosis must be treated for at least 6 months and in some cases even longer. Most of the bacteria are killed during the first 8 weeks of treatment; however, there are persistent organisms that require longer treatment. If treatment is inadequate, the surviving bacteria may cause relapse, potentially drug-resistant tuberculosis.

• Treatment includes;

• Intensive phase:8 weeks with 4 drugs- rifampicin, INH, ethambutol, pyrazinamide.

• Continuation phase: f 16 weeks with 3 drugs- rifampicin, INH, ethambutol.

• Directly Observed Therapy (DOT) is a component of case management that helps ensure patients adhere to therapy. It is the method whereby a trained health-care worker or another trained designated person observes drug intake to ensure compliance.

Prophylaxis

• Treatment of latent TB infection by INH monotherapy for 6 months

References

1.       Dye C. Global epidemiology of tuberculosis. Lancet 2006; 367: 938-40. [PubMed]

2.       National Institute for Health and Clinical Excellence. Tuberculosis: clinical diagnosis and management of tuberculosis, and measures for its prevention and control. London: NICE, 2006. Available at: www.nice.org.uk/page.aspx?o=CG033.

3.       Schaaf HS, Beyers N, Gie RB, Schaaf HS, Beyers N, Gie RP, et al. Respiratory tuberculosis in children: the diagnostic value of clinical features and special investigations. Pediatr Infect Dis J 1995; 14: 189-94. [PubMed]

4.       Van Dyck P, Vanhoenacker FM, Van den Brande P, De Schepper AM. Imaging of pulmonary tuberculosis. Eur Radiol. 2003; 13:1771–85. [PubMed] [Google Scholar]

5.       World Health Organization Stop TB Department. Treatment of tuberculosis: guidelines for national programmes. 3rd ed. Geneva: WHO, 2003.

Revised National TB Control Program (RNTCP)

 

Introduction

·         India is the highest TB burden country in the world, accounting for nearly 27% of the global incidence¹.

·         The revised national TB Control program (RNTCP), based on the internationally recommended Directly Observed Treatment Short-course (DOTS) strategy, was launched in 1997 and expanded across the country in a phased manner.

·         RNTCP is the largest and the fastest expanding TB control program in the world.

·         In 2020, Govt. of India has renamed RNTCP as National Tuberculosis Elimination Program (NTEP). This is to achieve the sustainable development goal of ending TB in India by 2025².

 

Objectives

·         To achieve and maintain a TB treatment success rate of at least 85% among new sputum positive (NSP) patients. New sputum positive patients are those people who have never received TB treatment before, or who have taken TB drugs for less than a month with a positive result to a sputum test³.

·         To achieve and maintain detection of at least 70% of the estimated new sputum positive people in the community.

Secondary objectives

·         To reduce the incidence of, and mortality due to TB

·         To prevent further emergence of drug resistance and effectively manage drug-resistant TB cases

·         To improve outcomes among HIV-infected TB patients

·         To involve private sector recognizing their dominant presence in health care services.

Program implementation²

·         NTEP is implemented by the central TB division through the state TB cell (STDC).

·         Each district has a district TB center (DTC) to co-ordinate the activities.

·         Under the DTC the functioning unit is a tuberculosis unit (TU) which caters to 1.5 -2.5 lakh population.

·         The peripheral health institution (PHI) is a health unit manned by at least one medical officer and is called tuberculosis diagnostic center (formerly designated microscopy center).

Strategic component of NTEP²

·         Active case detection through laboratory methods including highly sensitive molecular methods.

·         Treatment of drug susceptible tuberculosis.

·         Treatment of latent TB infection.

·         Treatment of drug resistant TB.

·         Implementation of air borne infection control.

TB notification

·         To ensure proper TB diagnosis and case management, to reduce TB transmission and to address emergence and spread of drug resistant TB, it is essential to have complete information of all TB cases.

·         Healthcare providers should notify every TB case diagnosed or treated to local authorities.

·         This can be easily done through Nikshay, a case based web based platform.

Treatment guidelines

·         New TB cases are treated with daily regimen.

·         Intensive phase consists of 8 weeks of isoniazid, rifampicin, pyrazinamide and ethambutol as per 4 weight bands.

·         There is no need for extension of intensive phase.

·         Continuation phase consists of 16 weeks with 3 drugs. Pyrazinamide is stopped in this phase.

·         Regimen is (2) HRZE + (4) HRE in fixed dose combination where each tablet contain 75 mg of INH, 150 mg of Rifampicin, 400 mg of pyrazinamide and 275 mg of ethambutol.

·         Dose is 25-39 Kg -2 tablets, 40-54kg-3 tablets, 55-70 kg-4 tablets and more than 70 kg-5 tablets

Treatment of latent TB infection⁴

The treatment options are:

·         Isoniazid monotherapy for 6 months at a dose of 5 mg/kg in adults, and 10 mg/kg in children up to a maximum of 300 mg.

·         Rifampicin and isoniazid combination daily for 3 months (in children <15 years). Rifampicin is given at a dose of 10 mg/kg in adults and 15 mg/kg in children up to a maximum of 600 mg.

·         Rifapentine and isoniazid weekly for 3 months.  

Treatment of drug resistant TB

·         The standardized treatment for MDR TB is a 6-drug regimen, with an intensive phase of 6–9 months and a continuation phase of 18 months (Total duration is 24–27 months)

·         The six drugs used are kanamycin, levofloxacin, cycloserine, ethionamide, pyrazinamide, and ethambutol.

 

References

1.       GLOBAL TUBERCULOSIS REPORT 2019 downloaded from www.who.int/tb/data

2.       RNTCP gets name change, now called National Tuberculosis Elimination Program (NTEP)", 2020,  https://medicaldialogues.in/rntcp-gets-a-name-change-now-called-national-tuberculosis-elimination-program-ntep

3.       Mukherjee, A “Outcomes of different subgroups of smear-positive retreatment patients under RNTCP in rural West Bengal, India”, Rural and Remote Health www.ncbi.nlm.nih.gov/pubmed/19260766

4.       Latent Tuberculosis Infection: Updated and Consolidated Guidelines for Programmatic Management, Licence: CC BY-NC-SA 3.0 IGO. Geneva: World Health Organization; 2018.