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

Shock - A Brief Discussion

Shock is a condition of severe impairment of tissue perfusion leading to cellular injury and dysfunction. Rapid recognition and treatment are essential to prevent irreversible organ damage and death.

Different Causes And Categories Of Shock:

Hypovolemic shock

• Hemorrhage
• Intravascular volume depletion (e.g., vomiting, diarrhea, ketoacidosis)
• Internal sequestration (ascites, pancreatitis, intestinal obstruction)

Cardiogenic shock

• Myopathic (acute MI, fulminant myocarditis)
• Mechanical (e.g., acute mitral regurgitation, ventricular septal defect, severe aortic stenosis, aortic dissection with aortic insufficiency)
• Arrhythmic

Extracardiac obstructive shock

• Pericardial tamponade
• Massive pulmonary embolism
• Tension pneumothorax

Distributive shock (profound decrease in systemic vascular tone)

• Sepsis
• Toxic overdoses
• Anaphylaxis
• Neurogenic (e.g., spinal cord injury)
• Endocrinologic (Addison’s disease, myxedema)

Clinical Manifestations:

• Hypotension (mean arterial BP <60 mmHg), tachycardia, tachypnea, pallor, restlessness, and altered sensorium.

• Signs of intense peripheral vasoconstriction, with weak pulses and cold clammy extremities. In distributive (e.g., septic) shock, vasodilation predominates and extremities are warm.

• Oliguria (<20 mL/h) and metabolic acidosis common.

• Acute lung injury and acute respiratory distress syndrome with noncardiogenic pulmonary edema, hypoxemia, and diffuse pulmonary infiltrates.

Approach To The Patient: 

Obtain history for underlying causes, including 

• cardiac disease (coronary disease, heart failure, pericardial disease), 
• recent fever or infection leading to sepsis, 
• drug effects (e.g., excess diuretics or ), 
• conditions leading to pulmonary embolism and 
• potential sources of bleeding.

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.

How Should Doctors Recognize and Treat their Own Metal Illness

Introduction
Doctors have a higher than average incidence of suicide and alcoholism, and so all doctors must be prepared to face (and try to prevent) these and other health risks in their professional and private lives. A doctor's  skill at looking after himself/herself has never been as good as their skill at looking after others, but when the healer is wounded, is it clear that his ability to help others will be correspondingly reduced.

Indicators of Affected Mental State
If the time comes when a doctor's mental state seriously reduces the ability to work, the doctor must be able to recognize this and take appropriate action. The following may indicate that this point is approaching:
• Drinking alcohol before ward rounds or surgeries.
• The minimizing of every contact with patients, so that the doctor does the bare minimum which will suffice.
• Inability to concentrate on the matter in hand. The thoughts are entirely taken up with the workload ahead.
• Irritability (defined as disagreeing with >1 nurse in 24 hours time period).
• Inability to take time off without feeling guilty.
• Feelings of excessive shame or anger when reviewing past mistakes.
• Emotional exhaustion—for example knowing that you should be feeling pleased or cross with yourself or others, but on consulting your heart you draw a blank.
• Prospective studies suggest that introversion, masochism, and isolation are important risk factors for doctors’ impairment.

Hypersensitivity - Different Types

Type I Anaphylactic

• antigen reacts with IgE bound to mast cells
• anaphylaxis, atopy (e.g. asthma, eczema and hayfever)

Type II Cell bound

• IgG or IgM binds to antigen on cell surface
• autoimmune haemolytic anaemia, ITP, Goodpasture's, pernicious anemia, acute hemolytic transfusion reactions, rheumatic fever, bullous pemphigoid, pemphigus vulgaris.

Type III Immune complex

• free antigen and antibody (IgG, IgA) combine
• serum sickness, systemic lupus erythematosus, poststreptococcal glomerulonephritis, extrinsic allergic alveolitis (especially acute phase)

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

Endocarditis Prophylaxis - A Quick Review

Endocarditis Prophylaxis
The only cardiac defects that need prophylaxis are the following:
·· Prosthetic valves
·· Unrepaired cyanotic heart disease
·· Previous endocarditis
·· Transplant recipients who develop valve disease

The only procedures that need prophylaxis are the following:
·· Dental procedures that cause bleeding: The prophylactic antibiotic to use for dental procedures is amoxicillin. For penicillin-allergic patients, clindamycin is the drug of choice.
·· Respiratory tract surgery
·· Surgery of infected skin

The following procedures do not need prophylaxis:
·· Dental fillings
·· All flexible scopes
·· All OB/GYN procedures
·· All urinary procedures, including cystoscopy

The following cardiac defects do not need prophylaxis:
·· Aortic stenosis or regurgitation
·· Mitral stenosis or regurgitation
·· Atrial or ventricular septal defects
·· Pacemakers and implantable defibrillators
·· Mitral valve prolapse, even if there is a murmur
·· HOCM (IHSS)

Introduction To Malnutrition

Malnutrition results from inadequate intake or abnormal GI assimilation of dietary calories, excessive energy expenditure, or altered metabolism of energy supplies by an intrinsic disease process.

Both outpatients and inpatients are at risk for malnutrition if they meet one or more of the following criteria:
• Unintentional loss of >10% of usual body weight in the preceding 3 months
• Body weight <90% of ideal for height.
• Body mass index (BMI: weight/height2 in kg/m2) <18.5

Two forms of severe malnutrition can be seen:

1. marasmus, which refers to generalized starvation that occurs in the setting of chronically decreased energy intake without systemic inflammation, and 
2. kwashiorkor, which refers to selective protein malnutrition due to decreased protein intake and catabolism in the setting of acute, life-threatening illnesses or chronic inflammatory disorders. Aggressive nutritional support is indicated in kwashiorkor to prevent infectious complications and poor wound healing.

Etiology

The major etiologies of malnutrition are 

• starvation,
• stress from surgery or severe illness, and 
• mixed mechanisms. 

Starvation results from decreased dietary intake (from poverty, chronic alcoholism, anorexia nervosa, fad diets, severe depression, neurodegenerative disorders, dementia, or strict vegetarianism; abdominal pain from intestinal ischemia or pancreatitis; or anorexia associated with AIDS, disseminated cancer, heart failure, or renal failure) or decreased assimilation of the diet (from

pancreatic insufficiency; short bowel syndrome; celiac disease; or esophageal, gastric,or intestinal obstruction). 

Contributors to physical stress include fever, acute trauma, major surgery, burns, acute sepsis, hyperthyroidism, and inflammation as occurs in pancreatitis, collagen vascular diseases, and chronic infectious diseases such as tuberculosis or AIDS opportunistic infections. 

Mixed mechanisms occur in AIDS, disseminated cancer, chronic obstructive pulmonary disease, chronic liver disease, Crohn’s disease, ulcerative colitis, and renal failure.

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.

The Mental State Examination

This assesses state of mind at the time of interview with the patient. A true description of mental states entails valid knowledge about current emotions plus their reactions to those emotions.

Take notes under the following headings.

• Appearance and behavior: see for signs of self-neglect; slowness, anxiety, or suspiciousness.

• Mode of speech: Speech rate, eg gabbling (pressure of speech), or slow/retarded. Note content.

• Mood: Note thoughts about harming self or others. Gauge your own response to the patient. The
laughter and grand ideas of manic patients are contagious, as to a lesser extent is the expression of thoughts from a depressed person.

• Beliefs: Eg about himself, his own body, about other people and the future. Note abnormal beliefs
(delusions) eg that thoughts are overheard, and ideas (eg persecutory, grandiose).

• Unusual experiences or hallucinations: “Sometimes when people are low they have unusual
experiences; have you heard anything unusual recently?” Note modality, eg visual.

• Orientation: In time, place, and person. What year? What season? What month/day of week? Is
it morning or afternoon? What is your name?

• Short-term memory: Recall a name & address 5 minutes after learning it. Ensure he really has learned it before waiting for the 5 minutes to elapse.

• Concentration: Months of the year backwards.

• Patient’s insight and degree of your rapport.

• Long-term memory: Current affairs recall. Who is the monarch/head of state? This tests other functions, not just memory

Down’s Syndrome Screening- A Brief Introduction

Down’s syndrome screening
The screening procedures offered currently in most of the countries are listed here. Each consists of a risk assessment based on maternal age and a scan performed in the first trimester or a blood test in the first or second trimester or a combination of scans and blood test.

Triple test
Done in early second trimester (14–20 completed weeks). This test is based on the measurement of

1. α-fetoprotein,
2. unconjugated oestriol (uE3) and 
3. hCG (either total hCG or free β-hCG)

together considering the maternal age.

Nuchal translucency scan
A first trimester (11–13 weeks) test is based on the measurement of the fold of skin on the back of the fetal neck.

Quadruple test
Early second trimester (14–21 weeks) test is based on the measurement of

1. α-fetoprotein, 
2. uE3, 
3. free β-hCG (or total hCG) and 
4. inhibin-A 

together considering the maternal age.

Combined test
Late first trimester (10–13 weeks) test is based on combining NT measurement with free β-hCG, pregnancy associated plasma protein-A (PAPP-A) and maternal age.

Integrated test
This is the integration of different screening markers measured at different stages of pregnancy into a single test result. Unless otherwise qualified, ’Integrated test’ refers to the integration of NT measurement and PAPP-A in the first trimester with serum α-fetoprotein, β-hCG and uE3 in the second.