Solitary Pulmonary Nodule

Definition: a single, <3 cm discrete, well-marginated, rounded opacity, surrounded by normal lung, with no lymphadenopathy or pleural effusion.
It is often an incidental finding, especially with increased use of CT scan but still it could be an be early, curable malignancy.

Etiology:
1. Benign (70%): Granuloma, Hemartoma, Bronchogenic cyst, AV malformation, Rheumatoid nodule
2. Malignant (39%): Bronchogenic carcinoma, Metastases from breast, heard, neck , colon.

Initial evaluation
• History: h/o cancer, smoking, age (<30 years = 2% malignant)
• CT: size/shape, calcium deposits, Lymphadenopathy, effusions, bony destruction, compare with old studies.

• High-risk features for malignancy: 

• ≥2.3 cm diameter, 
• spiculated,
•  >60 years old, 
• >1 ppd current smoker, 
• no prior smoking cessation

Approach To A Patient With Chronic Obstructive Pulmonary Disease (COPD)

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation due to impedance to expiratory airflow, mucosal edema, infection, bronchospasm and bronchoconstriction due to decreased lung elasticity.

Smoking is the main cause, but others are chronic asthma, α-1 antitrypsin deficiency and chronic infection (eg bronchiectasis).

History
Exertional dyspnoea, cough, and sputum are usual complaints.
Ask about:
• Present treatment including inhalers, steroids, antibiotics, theophyllines, nebulizers, opiate analgesia, and home O 2 treatment.
• Past history: inquire about previous admissions and co-morbidity.
• Exercise tolerance: how far can they walk on the flat without stopping? How many stairs can they climb? Do they get out of the house?
• Recent history: ask about wheeze and dyspnoea, sputum volume and color. Chest injuries, abdominal problems and other infections may cause respiratory decompensation.
• Read the hospital notes: have there been prior ICU assessments? Has the respiratory consultant advised whether ICU would be appropriate?

Examination

• Examine for dyspnoea, tachypnoea, accessory muscle use, and lip-pursing.
• Look for hyperinflation (‘barrel chest’) and listen for wheeze or coarse crackles (large airway secretions). 
• Cyanosis, plethora (due to secondary polycythaemia) and right heart failure (cor pulmonale) suggest advanced disease. 
• Look for evidence of hypercarbia: tremor, bounding pulses, peripheral vasodilatation, drowsiness, or confusion.
• Check for evidence of other causes of acute dyspnoea, particularly: asthma, pulmonary edema, pneumothorax , Pulmonary embolism. Remember that these conditions may co-exist with COPD.

Hemoptysis - Causes. Workup And Management

Definition and Pathophysiology
• Expectoration of blood or blood-streaked sputum
• Massive hemoptysis: ~>600 mL/24–48 h; gas exchange more important than blood loss
• Massive hemoptysis usually results from tortuous or invaded bronchial arteries

Etiology

1. Infections/Inflammation:

• Bronchitis - the most common cause of trivial hemoptysis
• Bronchiectasis 
• Cystic fibrosis
• Tuberculosis
• Aspergilloma
• Pneumonia
• Lung abscess

2. Neoplasms:

• Usually primary lung cancer
• sometimes metastases

3. Cardiovascular causes:

• Pulmonary embolism - can cause massive hemoptysis
• Pulmonary arterial rupture
• Congestive heart failure
• Mitral stenosis
• Trauma
• Foreign body
• Broncovascualr fistula

Acute Asthma - Management

Acute severe asthma (also referred to in Latin as status asthmaticus, or asthmatic status) is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and steroids.
Initial treatment
Follow the steps as summarized below:

• Provide high flow O 2 .
• Put the trolley back and side rails up so the patient is sitting up and holding on to the side rails (to use pectoral muscles as accessory muscles of respiration).
• If the patient cannot talk, start treatment, but get senior Emergency department and ICU help in case intubation and ventilation are required.
• Check trachea and chest signs for pneumothorax.
• Ask about previous admissions to ICU.
• Administer high dose nebulized B 2 agonist (eg salbutamol 5mg or terbutaline 10mg), or 10 puffs of salbutamol into spacer device and face mask.
For severe asthma or asthma that rseponds poorly to the initial nebulizer, consider continuous nebulization.
• Give a corticosteroid: either prednisolone 40–50mg PO or hydrocortisone (preferably as sodium succinate) 100mg IV.
• Add nebulized ipratropium bromide (500mcg) to B 2 agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to B 2 agonist therapy.
• Consider a single dose of IV magnesium sulphate (1.2–2g IVI over 20min) after consultation with senior medical staff, for patients with acute severe asthma without a good initial response to inhaled bronchodilator therapy or for those with life-threatening or near-fatal asthma.
• Use IV aminophylline only after consultation with senior medical staff.
Some individual patients with near-fatal or life-threatening asthma with a poor response to initial therapy may gain additional benefit. The loading dose of IVI aminophylline is 5mg/kg over 20min unless on maintenance therapy, in which case check blood theophylline level and start IVI of aminophylline at 0.5–0.7mg/kg/hr.
• IV salbutamol is an alternative in severe asthma, after consultation with senior staff. Draw up 5mg salbutamol into 500mL 5 % dextrose and run at a rate of 30–60mL/hr.
• A patient who cannot talk will be unable to drink fluids and may be dehydrated.
• Avoid ‘routine’ antibiotics.
• Repeat ABG within an hour.
• Hypokalaemia may be caused or exacerbated by B 2 agonist and/or steroid therapy.

Acute Asthma - Assessment

Make an initial assessment of the severity of acute asthma based upon a combination of

• clinical features, 
• peak flow measurement and 
• pulse oximetry 

This is as outlined as below.

Moderate exacerbation of asthma
• Increasing symptoms.
• Peak fl ow 50–75 % best or predicted.
• No features of acute severe asthma (below).

Acute severe asthma
Any one of the following:
• Inability to complete sentences in 1 breath.
• Respiratory rate ≥25/min.
• Heart rate ≥110/min.
• Peak flow 33–50 % best or predicted.

Approach to A Patient Presenting With Difficulty In Breathing ( Dyspnea)

The normal adult respiratory rate is 11–18/min, with a tidal volume of 400–800mL. Acute dyspnoea That is difficult or labored breathing is a common presenting symptom.

Common causes of Acute Dyspnoea
Cardiac
• Cardiogenic pulmonary oedema.
• MI .
• Pulmonary embolism.
• Arrhythmias .
Respiratory
• Asthma  or exacerbation of COPD
• Pneumonia .
• Pleural effusion .
• Pneumothorax
Trauma
• Aspiration of foreign body or vomit .
• Pneumothorax/haemothorax .
• Flail chest .
• Drowning incident .
Others
• Hypovolaemia or fever from any cause.
• Hyperventilation syndrome .
• Respiratory compensation for metabolic acidosis (DKA, salicylate overdose).
Psychological
• Anxiety
• Panic attack

Croup or Viral Laryngotracheobronchitis in Children

Definition 
Croup or viral laryngotracheobronchitis is an acute inflammation of the entire airway, mainly in the glottis and subglottic area, resulting in airway narrowing, obstruction, and voice loss. 

Therefore, it has generally been described as a triad of 

1. hoarse voice, 
2. harsh barking cough, and 
3. inspiratory stridor.

Epidemiology

Typically, the condition affects younger children (6–36 months), with a peak incidence at 2 years of age. It is the most common cause of acute upper airway obstruction in young children; a reported 3% of children experience it before 6 years of age.
Seasonal outbreaks have been described in the fall and winter, although it may occur year round in some areas.
Males are more often affected than females.

Etiology and Pathophysiology
Viral infection is the predominant etiology; parainfluenza (types 1, 2, and 3) is the most common agent. Other common viral agents are respiratory syncytial virus (RSV) and influenza. Less commonly encountered viruses include adenovirus, rhinovirus, enterovirus, and measles virus.
Mycoplasma pneumoniae is one of the few bacterial microorganisms that has been reported as an etiologic agent.

In children, the larynx is very narrow and is comprised by the rigid ring of the cricoid cartilage; therefore, a viral infection causing inflammation of this area leads to airway edema and subsequent obstruction. This obstruction results in the classic symptoms of stridor and cough.

Clinical Presentation

• Croup usually presents initially with a coryzal prodrome (1–4 days).
• Common symptoms include clear rhinorrhea, low-grade temperature, and mild tachypnea followed by barking cough, hoarseness, and stridor.
• Obstructive symptoms occur most commonly at night.
• Severity of airway narrowing may be determined by the presence of stridor at rest, tachypnea, retractions, tracheal tug, cyanosis, and pallor, as well as decreased breath sounds, which indicate critical narrowing.

Lung Abscess - A Brief Discussion

A lung abscess is an infection accompanied by pus accumulation and tissue destruction. The abscess may be putrid (due to anaerobic bacteria) or non putrid (due to anaerobes or aerobes), and it commonly has a well-defined border. The availability of effective antibiotics has made lung abscesses much less common than they were in the past.

Causes
A lung abscess is a manifestation of necrotizing pneumonia, commonly the result of aspiration of oropharyngeal contents. Poor oral hygiene with dental or gingival (gum) disease is strongly associated with a putrid lung abscess. Septic pulmonary emboli commonly produce cavitary lesions. Infected cystic lung lesions and cavitating bronchial carcinoma must be distinguished from lung abscesses.

Signs and symptoms
Signs and symptoms of lung abscess include a cough that may produce bloody, purulent, or foul-smelling sputum; pleuritic chest pain; dyspnea; excessive sweating; chills; fever; headache; malaise; diaphoresis; and weight loss.

Brief Summary of Acute Pulmonary Embolism

Definition:
A pulmonary embolism results from the migration of venous thrombi from the systemic veins to pulmonary arterial system, resulting in varying degrees of obstruction of pulmonary arterial blood flow.
The incidence of pulmonary emboli in the United States exceeds 500,000 per year, with a mortality approaching 10%. If not diagnosed or if improperly treated, the mortality rate can reach 30%.

Common Sources:
Up to 90% of pulmonary emboli originate from the deep venous system of the legs. The upper extremities can also be a source of venous thrombi. Usually related to trauma, congenital fibromuscular bands, or the use of central venous catheters, 12% of all upper extremity thrombi result in pulmonary emboli. In addition, blood clot formation in the pelvic veins may cause either septic or bland pulmonary emboli, especially in the setting of complicated obstetric procedures or gynecologic surgery.
Other causes of pulmonary arterial obstructive emboli include air introduced during intravenous injections, hemodialysis, or the placement of central venous catheters; amniotic fluid secondary to vigorous uterine contractions; fat as a result of multiple long bone fractures; parasites; tumor cells; or injected foreign material (talc, mercury).

Risk Factors:
Three basic risk factors, known collectively as Virchow’s triad, are associated with thrombus formation and subsequent pulmonary emboli:

1. stasis,
2. hypercoagulability, and 
3. endothelial injury.

Management Of Acute Pulmonary Embolism

The goal of therapy is to prevent further embolic episodes, and heparin is the initial drug of choice for accomplishing this. First, a large intravenous loading bolus should be given, followed by continuous-drip infusion, maintained for at least 5 and often 7 to 10 days. Anticoagulation should not be withheld pending the results of further studies unless the patient’s risk of bleeding complications is greater than the clinical suspicion of pulmonary emboli. The partial thromboplastin time should be monitored and the heparin dosage adjusted to keep the time between 1.5 to 2.0 times the control.

Warfarin is started 24 to 48 hours after heparin therapy has been initiated. During the first 3 days of warfarin therapy, the prothrombin time or INR is increased before the onset of true anticoagulation. Therefore, before discontinuing the heparin, the prothrombin time or INR should be therapeutic (1.5 to 2 times normal) for approximately 2 to 3 days.

Low-molecular-weight heparins are indicated for prophylaxis in postoperative patients and probably have a role in the management of acute pulmonary embolism and deep venous thrombosis because they do not require monitoring of the anticoagulation effects.

Continuing the Treatment:
Long-term anticoagulation is usually achieved with warfarin, although low-molecular-weight heparins can also be used. Patients with reversible risk factors that are subsequently eliminated should undergo anticoagulation for a total of 3 months.

Approach To A Patient Presenting With Haemoptysis (Blood In Sputum)

Haemoptysis (Blood In Sputum) may be the chief or sole complaint of patients presenting to the emergency department or their family doctors. . It always warrants investigation.

Causes of haemoptysis:

Respiratory causes;
• Infection (URTI, pneumonia, TB, lung abscess)
• Carcinoma (bronchial or laryngeal)
• Bronchiectasis

Cardiovascular causes:
• Pulmonary oedema
• PE
• Ruptured aortic aneurysm (aorto-bronchial fistula)

Coagulation disorder:
• Drugs (eg warfarin, heparin)
• Inherited (eg Haemophilia, Christmas disease)

Trauma:
• Penetrating or blunt

Others:
• Goodpasture’s, Wegener’s granulomatosis

Introduction To Influenza

Also called commonly as the flu, influenza is an acute, highly contagious infection of the respiratory tract that results from three types of Myxovirus influenzae. It occurs sporadically or in epidemics (usually during the colder months). Epidemics tend to peak within 2 to 3 weeks after initial cases and subside within 1 month.
Although influenza affects all age-groups, its incidence is highest in schoolchildren. Its severity is greatest in the very young, the elderly, and those with chronic disease. In these groups, influenza may even lead to death.

Causes
Transmission of influenza occurs through inhalation of a respiratory droplet from an infected person or by indirect contact such as using a contaminated drinking glass. The virus then invades the epithelium of the respiratory tract, causing inflammation and desquamation.
One remarkable feature of the influenza virus is its capacity for antigenic variation. Such variation leads to infection by strains of the virus to which little or no immunologic resistance is present in the population at risk. Antigenic variation is characterized as antigenic drift (minor changes that occur yearly or every few years) and antigenic shift (major changes that lead to pandemics).

Influenza viruses are classified into three groups:
Type A, the most prevalent, strikes every year, with new serotypes causing epidemics every 3 years.
Type B also strikes annually, but only causes epidemics every 4 to 6 years.
Type C is endemic and causes only sporadic cases.

Signs and symptoms
After an incubation period of 24 to 48 hours, signs and symptoms appear: the sudden onset of chills, a temperature of 101° to 104° F (38.3° to 40° C), headache, malaise, myalgia (particularly in the back and limbs), a nonproductive cough and, occasionally, laryngitis, hoarseness, conjunctivitis, rhinitis, and rhinorrhea.
These signs and symptoms usually subside in 3 to 5 days, but cough and weakness may persist. Fever is usually higher in children than in adults. Also, cervical adenopathy and croup are likely to be associated with influenza in children. In some patients (especially elderly ones), lack of energy and easy fatigability may persist for several weeks.

Legionnaires’ disease

Introduction

An acute bronchopneumonia, legionnaires’ disease is produced by a fastidious, gram-negative bacillus. This disease may occur epidemically or sporadically, usually in late summer or early fall. Its severity ranges from a mild illness, with or without pneumonitis, to multilobar pneumonia, with a mortality as high as 15%. A milder, self-limiting form (Pontiac fever) subsides within a few days, but leaves the patient fatigued for several weeks; this form mimics legionnaires’ disease, but produces few or no respiratory symptoms, no pneumonia, and no fatalities.

Causes

The cause of legionnaires’ disease, Legionella pneumophila, is an aerobic, gram-negative bacillus that’s probably transmitted by an airborne route. With past epidemics, it has spread through cooling towers or evaporation condensers in air-conditioning systems. However, Legionella bacilli also flourish in soil and excavation sites. The disease doesn’t spread from person to person.

Predisposing Factors:

Legionnaires’ disease is more common in men than in women and is most likely to affect:

• middle-aged to elderly people
• immunocompromised people (particularly those receiving a corticosteroid, for example, after a transplant) or those with lymphoma or other disorders ssociated with delayed hypersensitivity
• patients with a chronic underlying disease, such as diabetes, chronic renal failure, or chronic obstructive pulmonary disease
• alcoholics
• cigarette smokers (three to four times more likely to develop legionnaires’ disease than nonsmokers).

Signs and symptoms
Although signs and symptoms of legionnaires’ disease emerge in a predictable sequence, onset of the disease may be gradual or sudden.

After a 2- to 10-day incubation period, nonspecific, prodromal signs and symptoms appear, including diarrhea, anorexia, malaise, diffuse myalgia and generalized weakness, headache, recurrent chills, and an unremitting fever, which develops within 12 to 48 hours with a temperature as high as 105° F (40.6° C). A cough then develops that is initially nonproductive but eventually may produce grayish, nonpurulent and, occasionally, blood-streaked sputum.

Acute Respiratory Distress Syndrome

Introduction

A form of pulmonary edema that causes acute respiratory failure, acute respiratory distress syndrome (ARDS, shock lung, stiff lung) results from increased permeability of the alveolocapillary membrane. Fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lung to stiffen. Effective ventilation is thus impaired, prohibiting adequate oxygenation of pulmonary capillary blood. Severe ARDS can cause intractable and fatal hypoxemia; however, patients who recover may have little or no permanent lung damage.

Causes
ARDS can result from any one of several respiratory and non respiratory causes:

• aspiration of gastric contents
• sepsis (primarily gram-negative), trauma (lung contusion, head injury, long bone fracture with fat emboli), or oxygen toxicity
• viral, bacterial, or fungal pneumonia or microemboli (fat or air emboli or disseminated intravascular coagulation)
• drug overdose (barbiturates, glutethimide, narcotics) or blood transfusion
• smoke or chemical inhalation (nitrous oxide, chlorine, ammonia)
• pancreatitis, hypertransfusion, cardiopulmonary bypass
• near drowning.

Pathophysiology

Altered permeability of the alveolocapillary membranes causes fluid to accumulate in the interstitial space. If the pulmonary lymphatics can’t remove this fluid, interstitial edema develops. The fluid collects in the peribronchial and peribronchiolar spaces, producing bronchiolar narrowing.
Hypoxemia occurs as a result of fluid accumulation in alveoli and subsequent alveolar collapse, causing the shunting of blood through nonventilated lung regions. In addition, regional differences in compliance and airway narrowing cause regions of low ventilation and inadequate perfusion, which also contribute to hypoxemia.

Treatment For Cystic Fibrosis

Cystic fibrosis is a genetic disorder that is inherited in an autosomal recessive pattern and is characterized by a defective transport of chloride and sodium across the epithelium that causes thick, sticky mucus to build up in the lungs, digestive tract, and other areas of the body. It is one of the most common chronic lung diseases in children and young adults.

Some of the treatment options are discussed briefly here:

1. Physiotherapy
Daily chest percussion and physiotherapy with postural drainage reduces respiratory exacerbations

3. Antibiotics
Early high dose , broad spectrum , long duration (minimum 2-3 weeks) antibiotics helps minimize lung damage in infective exacerbations. Oral or intravenous fluroquinolones combined with nebulized antibiotic is often the initial choice; resistance and chronic carriage needs intravenous combinations. Prophylactic antibiotics are also increasingly used.

3. Bronchodilators
These are helpful for symptomatic relief.

4. DNase- alpha mucolytics
These are administered as areosol spray. Mechanism of action is that it interferes with sputum neutrophil DNA, helping to liquefy sputum and encourage expectoration, thus helps in reducing cough.

Causes Of Pleural Effusion

Pleural effusion is a condition in which there is abnormal fluid accumulation in the layers of tissues that line the lung and the chest cavity. 

There are a number of causes that may lead to pleural effusion. Some of them are briefly described as follows:

1. Congestive Heart failure: It is one of the most common causes in which because of deficient pumping by the heart the body cannot handle fluids properly leading to collection in the pleural spaces.

2. Pneumonia: In which later the fluid may get infected leading to empyma or abscess.

3. Liver disease Or Cirrhosis

5. Nephrotic Syndrome: due to low blood protein counts

6. End stage renal disease

7. Cancer

8. Pulmonary embolism

9. Blockage in the blood vessels or the lympahtic flow.