Group members:

Sathon, Pitipong
Pathak, Upendra
Meema, Pawarisa
Sinha, Milankumar
John, Alan
Rajendran Nair Bindu, Sreelekshmi
Gunturu, Rishitha Reddy
Petchto, Pantila
Mehra, Disha
Anilkumar Menon, Athulya
Felix Devapriam, Angela Karen
General Data

Patient X is a 71-year-old female, retired corporate

attorney, currently residing alone in city, came to Emergency
Department due to fever and productive cough
Chief complaint

Fever and productive cough

 History Of Present Illnesses

➤ 4 days PTA patient noted the onset of cough. Initially nonproductive, then
became productive with yellowish sputum and was associated with left sided chest
pain.

► 2 days PTA she noted feeling chills and had a temperature of 38.9°C. The fever,
cough and chest pain continued over the next 48 hrs. which prompt her to seek
consult to Yale Emergency Department.

➤ She denied hemoptysis, weight loss, sore throat, sinusitis, back pain, diarrhea,
rash, joint pain or headaches.
 Past Medical History

She has a history of congestive heart failure related to ischemic

heart disease that has been controlled with Lasix, an ACE-inhibitor, and
Lopressor
 Personal Social History

Patient X is a retired corporate attorney and lives alone. She is a

former smoker but quit 3 months ago when her husband died of lung
cancer. She denies alcohol use, recent travel, domestic pets or any risk
factors for HIV exposure
 Medical History Findings

● 39.4 C° Fever
● Productive cough
● Yellow sputum
● Chills
● Left sided chest pain
● History of congestive heart failure related to ischemic heart disease that
has been controlled with Lasix
● Former smoker
● Husband died of lung cancer
 Physical Examination
● General Survey :
○ Patient is thin
○ In Mild respiratory distress
● Vital Signs :
○ Temperature: 39.4°C
○ RR: 28 cycles per min
○ PR: 120beats per min
○ BP: 128/84 mmHg
○ 02 saturation: is 89% on room air
● Skin :
○ Decrease turgor
● HEENT :
○ TMs mildly red
○ Oropharyngeal is mildly red
○ Sinuses nontender
 Physical Examination

● Chest and Lungs :

○ Remarkable for splinting to the left side on deep inspiration
○ Dullness to percussion= 1/4 way up on left side
○ Decreased breath sounds at left base
○ Egophony and bronchial breath sounds are evident as one
listens more superiorly on the left side. The right chest is clear.
COR-RRR without murmurs or rubs.
○ Right chest is clear
 Laboratory Findings
Abnormal Findings
● HCO3: 29 (NV: 22 to 28 mEq/L)
● Glu: 150 (NV:70 to 99 mg/dL)
● WBC 18.0 (NV (4.5 to 11.0 x 10/L)
● 41 lymphs (NV: 20-40%)
● Sputum Gram's stain: a few PMN, many epithelial
cells, and scattered Gram positive and Gram
negative cocci and rods are seen
● Size/left lower lobe infiltrate is present that
obscures the left heart border
Normal Findings
● Na: 143(NV:135-145 mEq/L)
● K: 4.2 (NV:3.6-5.2 mmol/L)
● CI: 100 (NV: 96-106 mEq/L)
● Cr: 1.0 (NV: 0.59 to 1.04 mg/dL)
● Hb: 13.8(NV:12.1 to 15.1 g/dL)
● Hct:39.8(NV:36% to 48%)
● 54 segmenters (NV:40-60%)
● 5 bands (NV:0-5%)
● Platelets 255K (NV:150,000 to 450,000)
● EKG NSR/normal rate, intervals and no ischemic
changes
● CXR: Normal heart size
● UA: clear/1.020/1+ protein/no cells or casts
Differential Diagnosis
● Pulmonary Tuberculosis
● Acute Rheumatic heart
fever
● COPD
 Pulmonary Tuberculosis
Etiology
● Mycobacterium tuberculosis
● Droplet nuclei(coughing, sneezing, laughing)
● Exposure to TB
 Pulmonary Tuberculosis

Symptoms
Constitutional symptoms Pulmonary symptoms
● Dyspnea
● Anorexia ● Non resolving
● Low grade fever bronchopneumonia
● Night sweats ● Chest tightness
● Fatique ● Non productive cough
● Weight loss ● Mucopurulent sputum with
hemoptpysis
● Chest pain
 Pulmonary Tuberculosis

Symptoms
Extra Pulmonary symptoms
● Pain
● Inflammation
 Pulmonary Tuberculosis

Pathophysiology
● (Initial infection or primary infection)

● Entry of micro organism through droplet nuclei

● Bacteria is transmitted to alveoli through airways

● Deposition and multiplication of bacteria

 Pulmonary Tuberculosis
Pathophysiology
● Bacilli are also transported to other parts of the body through blood
stream and phagocytosis by neutrophils and macrophages

● Accumulation of exudate in Alveoli Broncho pnemonia

● New tissue masses of live and dead bacilli are surrounded by

macrophages which form a protective mass around granulamas

● Granulomas then transforms to fibrous tissue mass and central portion of

which is called ghon tubercle
 Pulmonary Tuberculosis

Pathophysiology
● The material (Bacteria and Macrophages) becomes necrotic
forming cheesy mass

● Mass becomes calcified and becomes colagenous scar

● Bacteria become dormant and no further progression of

active disease

● (Active disease or re infection)

 Pulmonary Tuberculosis

Pathophysiology
● Inadequate immune response

● Activation of dormant bacteria

● Ghon tubercle ulcerates and releasing cheesy material into

bronchi

● Bacteria then become airborne resulting in further spread of

infection
 Pulmonary Tuberculosis

Pathophysiology
● Ulcerated tubercle heals and becomes scar tissue

● Infected lung become inflamed

● Further development of pneumonia and tubercle formation

● Unless the process is arrested it spreads downwards to the hilum of

lungs and later extends to adjascent lobes
 Pulmonary Tuberculosis

Diagnosis
● Sputum examination and cultures (ZN STAIN)
● Chest X-ray
● Chest CT scan
● Bronchoscopy
● tuberculin skin test
 Pulmonary Tuberculosis

Medical management
● Pulmonary TB is treated primarily with antituberculosis agents
for 6 to 12 month
● Pharmacological management
● First line antitubercular medications
- Streptomycin 15mg/kg
- Isoniazid or INH(Nygrazid) 5mg/kg(300mg max perday)
- Rifampin 10mg/kg
- Pyrazinamide 15-30mg/kg
- Ethambutol(Myambutol) 15-25mg/kg daily for 8 weeks and continuing
for up to 4 to 7 months
 Pulmonary Tuberculosis

Medical management
● Second line medications
- Capreomycin 12-15 mg/kg
- Ethionamide 15mg/kg
- Paraaminosalycilate sodium 200-300 mg/kg
- Cycloserine 15mg/kg
- Vitamin B(pyridoxine) usually adminstered with INH
 Pulmonary Tuberculosis

Medical management
● Third line drugs
- Other drugs that may be useful, but are not on the
WHO list of SLDs:
- Rifabutin
- Macrolides: e.g.Clarithromycin(CLR)
- Linezolid(LZD)
- Thioacetazone(T)
- Thioridazine
- Arginine
 Acute Rheumatic heart fever

Etiology
● The etiology of rheumatic fever is not clear.
● Group A beta hemolytic streptococcal infection
● Delayed non- suppurative Squeal URTI with GAB STREPTOCOCCI
● Diffuse inflammatory disease of connective tissue.
● Primalily involving heart, blood vessels, joints, subcutaneous tissue
and CNS
 Acute Rheumatic heart fever

Symptoms
● Multisystem disorder that usually presents with
– Fever
– Anorexia
– Lethargy
– Joint pain
● Latent period: 2–3 weeks after an episode of streptococcal pharyngitis.
● Diagnosis is made using the revised Duckett Jones criteria
– 2 or more major manifestations,
– Or 1 major and 2 or more minor manifestations,
– along with evidence of preceding streptococcal infection
 Acute Rheumatic heart fever
Pathophysiology
● The exact etiopathogenesis or ARF is not well understood.
● Preceding streptococcal infection may not always critically manifest. It is considered as a sort of
hypersensitivity reaction.
● There is an antigen antibody reaction usually following streptococcal sore throat
● Ant streptococcal antibody titer elevated in majority of the patients ,although the streptococci have
never been isolated from rheumatic lesions in joints, heart or in the bloodstream.
● The auto antibodies attack the myocardium, pericardium and cardiac valves.
● Asch offs bodies develop on the valve, especially on the mitral valve and leading t permanent valve
dysfunction.
● Severe myocarditis may result dilation of the heart and heart failure.
● The antibodies may react with striated muscle, vascular smooth muscle and nervous tissue resulting
joint inflammation,involuntary movements as chorea and lesions in blood vessels and other connective
tissue
 Acute Rheumatic heart fever

Management
• Treatment strategies can be divided into management
– acute attack,
– management of the current infection
– prevention of further infection and attacks.
• Management of the acute attack
– Single dose of benzyl penicillin 1.2 million U i.m.
– Oral phenoxymethylpenicillin 250 mg 6-hourly for 10 days
– Penicillin-allergic: erythromycin or a cephalosporin
– Analgesia: optimally achieved with high doses of salicylates
• Treatment is then directed towards limiting cardiac damage and relieving symptoms.
 Acute Rheumatic heart fever

Management
• Bed rest and supportive therapy
– Lessens joint pain and reduces cardiac workload.
– Duration should be guided by symptoms along with temperature, leucocyte count and ESR
– Should be continued until these have settled.
– Return to normal physical activity but strenuous exercise should be avoided in those who have had carditis
• Cardiac failure
- Mild heart failure usually responds to rest and corticosteroid therapy.
- Severe carditis: Digoxin, but its use should be monitored closely - AV block
- Vasodilators and diuretics also may be used
- If heart failure in these cases does not respond to medical treatment, valve replacement may be necessary
 Acute Rheumatic heart fever
Management
• Protracted Sydenham chorea has responded to haloperidol
• It requires long-term antimicrobial prophylaxis, even if no other manifestations of rheumatic fever evolve.
• Complete physical and mental rest is essential because the manifestations of chorea may be exaggerated by
emotional trauma.
• Aspirin
– relieve the symptoms of arthritis rapidly and a response within 24 hours helps to confirm the diagnosis.
– Reasonable starting dose is 60 mg/kg body weight/day, divided into six doses.
– In adults, 100 mg/kg per day may be needed up to the limits of tolerance or a maximum of 8 g per day.
– should be continued until the ESR has fallen and then gradually tailed off.
• Corticosteroids
– more rapid symptomatic relief than aspirin and are indicated in cases with carditis or severe arthritis.
– Prednisolone, 1.0–2.0 mg/kg per day in divided doses, should be continued until the ESR is normal then tailed
off.
 Chronic Obstructive Pulmonary Disease
(COPD)

Etiology
COPD is caused by prolonged exposure to harmful particles or gases.

● Cigarette smoking is the most common cause of COPD worldwide.

● Other causes may include second-hand smoke, environmental and
occupational exposures, and alpha-1 antitrypsin deficiency (AATD)
 Chronic Obstructive Pulmonary Disease
(COPD)

Symptoms
The characteristic symptoms of COPD are chronic and progressive
dyspnea, cough, and sputum production that can be variable from day- to-day.
Dyspnea: Progressive, persistent and characteristically worse with exercise.
Chronic cough: May be intermittent and may be unproductive.
Chronic sputum production: COPD patients commonly cough up sputum.
 Chronic Obstructive Pulmonary Disease
(COPD)

Pathophysiology
● Airflow limitation and gas trapping
● Gas exchange abnormalities
● Mucus hypersecretion
● Pulmonary hypertension
 Chronic Obstructive Pulmonary Disease
(COPD)
Diagnosis
-The presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of
persistent airflow limitation and thus of COPD,

Symptoms Exposure to risk factors

Shortness of breath Tobacco
chronic cough Occupation
sputum indoor/outdoor pollution

SPIROMETRY: Required to establish diagnosis

 Chronic Obstructive Pulmonary Disease
(COPD)

Management
Based on the principles of

● Prevention of further progress of disease

● J Preservation and enhancement of pulmonary functional
capacity
● Avoidance of exacerbations in order to improve the quality of
life.
Primary Diagnosis
Pneumonia

● Patient present to hospital cause of fever

cough and productive yellowish sputum with
left side chest pain and admitted for
pneumonia
● Patient has a history of congestive heart
failure which increased risk of pneumonia
 Definition
Community-acquired pneumonia (CAP) refers to an acute infection of the
pulmonary parenchyma acquired outside of the hospital.

Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma

acquired in hospital settings and encompasses both hospital-acquired pneumonia

(HAP) and ventilator-associated pneumonia (VAP).

 Epidemiology

● 150.7 million new cases worldwide in 2020

● 2ndleading cause of hospitalization worldwide
● ~20% of patients with pneumonia require hospitalization
● 6thleading cause of death in the world~10% of patients with pneumonia die
Variations in rates of disease:
● More common in men
● More common in African Americans compared to Caucasians and Asians
● More common in children and older adults (overall rate for 18
● -49 yois ~5 per 1000overall rate for >65 yois 75 per 1000 )
● Immunosuppression, smoking, chronic obstructive pulmonary disease,
congestive heart failure, diabetes mellitus, lung cancer, serious nonpulmonary
malignancy and previous hospitalizations for pneumonia were all
independently associated with risk of CAP patients aged 65 years and over.
 Regions with the highest incidence of
Community acquired pneumonia

We can see that the death rate from

pneumonia is highest in Sub-Saharan Africa
and Southeast-Asia. The difference between
richer and poorer countries is large:
European populations suffer a rate of
around 10 deaths per 100,000 while poorer
countries see rate of more than 100 deaths
per 100,000 is

In Southeast-Asia, the population of

the Philippines suffer from particularly high
pneumonia mortality rates; pneumonia is
the second leading cause of death in both
under-5-year-old and older than 70-year-old
populations in this country.
 Risk factor

- Smoking
- Weak immune system, such as from drug treatment or a
health problem like diabetes, cancer, or HIV
- Other lung problems such as chronic obstructive pulmonary
disease
- Other health problems such as kidney failure
- Use of certain medicines, including proton-pump inhibitors
Heavy alcohol use
Diagnosis
 Clinical Diagnosis

Chest radiography is often necessary to differentiate CAP from

other conditions. Radiographic findings may include risk factors for
increased severity
For outpatients, the clinical and radiologic assessments are
usually all that is done before treatment for CAP is started since
most laboratory results are not available soon enough to influence
initial management significantly.
 Etiologic Diagnosis

● Without culture and susceptibility data, trends in resistance cannot

be followed accurately, and appropriate empirical therapeutic
regimens are harder to devise.
 Laboratory Identification
Diagnostic Testing Methods for Determining Pneumonia Etiology

Testing Method Specimen Types

Blood, sputum, pleural fluid, lung aspirates, bronchoscopic

Bacterial culture
specimens

Blood, sputum, pleural fluid, lung aspirates, bronchoscopic

Mycobacterial culture
specimens, gastric aspirates

Nasopharyngeal specimens, oropharyngeal specimens,

Viral culture
sputum, lung aspirates, bronchoscopic specimens

Nasopharyngeal specimens, oropharyngeal specimens,

Antigen detection
urine, pleural fluid

Antibody detection Serum

Nasopharyngeal specimens, oropharyngeal specimens,

Nucleic acid detection (eg, polymerase chain reaction) sputum, lung aspirates, pleural fluid, bronchoscopic
specimens, blood
 ROUTINE LABORATORY TEST

The following laboratory tests may not be useful for diagnostic purposes but
are useful for classifying illness severity and site-of-care/admission decisions:
● Serum electrolyte panel (sodium, potassium, bicarbonate,blood urea
nitrogen [BUN], creatinine, glucose)
● Arterial blood gas (ABG)determination (serum pH, arterial oxygen
saturation, arterial partial pressure of oxygen and carbon dioxide) –
Hypoxia and respiratory acidosis may be present.
● Venous blood gas determination (central venous oxygen saturation)
● Complete blood cell (CBC) count with differential
● Serum free cortisol value
● Serum lactate level
 BLOOD CULTURE

● Blood cultures should be obtained

before the administration of
antibiotics. These cultures require 24
hours (minimum) to incubate. When
blood cultures are positive, they
correlate well with the microbiologic
agent causing the pneumonia
 SPUTUM EVALUATION
Sputum Gram stain and culture
should be performed before initiating
antibiotic therapy (if a good quality,
contaminant-sparse specimen containing
< 10 squamous epithelial cells per low
power field can be obtained). The white
blood cell (WBC) count should be more
than 25 per low power field in non-
immunosuppressed patients
 CHEST RADIOGRAPH

Chest radiography is considered

the standard method for diagnosing the
presence of pneumonia, that is, the
presence of an infiltrate is required for
the diagnosis. However, it must be noted
that the accuracy of plain chest
radiography for detecting pneumonia
decreases depending on the setting of
infection
 CHEST ULTRASONOGRAPHY

Ultrasonography (US) is useful in

evaluating suspected parapneumoniceffusions.
US can identify septations within the fluid
collection that may not be visible on CT scans.
US also has great utility for directing needle
placement for pleural fluid aspiration
(throacentesis) at the patient's bedside.
Management
 Treatment

● Oxygen therapy
● Fluids and antibiotics through your veins :
Empiric
antimicrobial regimens should cover S. pneumoniae with β-lactam medications or
new respiratory fluoroquinolones, and atypical pathogens should be treated with
macrolides or respiratory fluoroquinolones.
● Breathing treatments (possibly)
 Prevention
● Get vaccinated. Vaccines are available to prevent some types of pneumonia and the flu.
Talk with your doctor about getting these shots. The vaccination guidelines have changed
over time so make sure to review your vaccination status with your doctor even if you
recall previously receiving a pneumonia vaccine.
● Make sure children get vaccinated. Doctors recommend a different pneumonia vaccine
for children younger than age 2 and for children ages 2 to 5 years who are at particular
risk of pneumococcal disease. Children who attend a group child care center should also
get the vaccine. Doctors also recommend flu shots for children older than 6 months.
● Practice good hygiene. To protect yourself against respiratory infections that sometimes
lead to pneumonia, wash your hands regularly or use an alcohol-based hand sanitizer.
● Don't smoke. Smoking damages your lungs' natural defenses against respiratory
infections.
● Keep your immune system strong. Get enough sleep, exercise regularly and eat a healthy
diet.
CONCEPTUAL
FRAMEWORK