DR Awadhesh kr sharma,SRDR Awadhesh kr sharma,SR

DEPTT OF MEDICINEDEPTT OF MEDICINE

MLB MEDICAL COLLEGE MLB MEDICAL COLLEGE JHANSI(UP)JHANSI(UP)

Two Case studiesTwo Case studies

TWO CASE STUDIES

CASE - I

Mr. Durga Prasad 70 years ,Male, farmer by occupation presented with chief complaints of –

Productive cough for 8 months. Loss of appetite for 8 months. Loss of weight upto 25% for 8 months.

Negative History – No history of…..High grade fever HaemoptysisFoul smelling sputum Exertional dyspnoeaChest painOrthopnoea PNDPedal edemaEngorgement of neck veinsAscitisRt hypochondriac tendernessOligurea Burning micturation

Past history – no h/o DM, HTN & TB.Personnel history –

Patient is chronic bidi smoker for 48 years, he used to smoke 30 bidi per day.Smoking index = 48 x 30 = 1440

i.e. > 300

General examination –Built – AveragePR – 82/min BP- 110/80 mm of Hg RR – 16 / min Temp – afebrile Pallar--- ++ Cyanosis – absentClubbing – absentIcterus – absentLymph node enlargement – absent JVP – not raised

On respiratory system examination -----

Trachea is central. In right inframammary, lower axillary, inter and infra scapular region –o diminished chest movemento increased tactile vocal fremitus, vocal rasonaceo impaired percussion noteo bronchial breath sound

Examination of other systems is with in normal limit.

INVESTIGATIONS

On the basis of above history, examination and investigations the presumptive diagnosis is------ Right middle and lower lobe consolidation with cavitation

Cause?

Pulmonary Kochs Lung carcinoma Lung abbcess

Points against pulmonary Kochs –

1. No h/o fever with evening rise of temperature.2. Right lower lobe involvement – an unsual site3. Sputum microscopy negative for AFB.4. No response to ATT.

Points against lung abcess –

1. No h/o high grade fever.2. No h/o copious amount of foul smelling sputum.3. No tachycardia & tachypnea.4. Total leucocytes count are normal.

So we think in terms of lung malignancy, & go for HRCT which shows –

Then we done USG guided FNAC of the lesion which confirms it to be squamous cell carcinoma involving rt middle & lower lobe of lung.

DiscussionPrimary carcinoma of the lung is the leading cause of death in both men and women, accounting for 1.18 million deaths from lung cancer worldwide in 2007.The relative risk of developing lung cancer is increased about thirteen fold by active smoking and about 1.5 fold by long term passive exposure to cigarette smoke.About 15% of lung cancers occur in individuals who have never smoked. The majority of these are found in women.Radiation is another enviromental cause of lung cancer.Four major cell types make up 80% of all primary lung neoplasms according to WHO there are –

o Squamous or epidermoid CAo Small cell (oat cell) CAo Adenocarcinoma (including bronchioloalveolar)o Large cell CA

Most frequent histologic subtype is adenocarcinoma.

Major treatment discussion are made on the basis of wheather they are classified as a small cell lung CA or non small cell lung cencer.

At presentation, SCLCs usually have already spread such that surgery is unlikely to be curative and are managed primarily by chemotherapy with or without radiotherapy.

NSCLC that are clinically localized at the time of presentation may be cured with either surgery or radiotherapy.

Squamous and small cell cancers usually present as central masses with endobronchial growth, while adenocarcinomas present as peripheral masses.

Squamous cell CA cavitate in 10-20% of cases.

Although 5-15% of patients with lung cancer are identified while they are asymptomatic usually as a result of routine CXR or through the use of screening CT scan, most patients presents with some sign or symptom.

Central/endobronchial growth- causes cough, hemoptysis, wheeze, stridor, dyspnoea and post obstructive pneumonitis.Peripheral growth- Pancoast or superior sulcus syndromesSVC syndromeExtrathoraccic metastatic diseaseParaneoplastic syndromesSkeletal connective tissue syndromeThe role of screening high risk patients (for example current or former smokers >50yrs of age) for early stage lung cancers is debated.Low dose, non-contrast, thin slice, helical or spiral CT has emerged as a possible new tool for lung cancer screening.

Once sign, symptoms or screening studies suggest lung cancer, a tissue diagnosis must be established . Tumour tissue can be obtained by a bronchial or trans bronchial biopsy during fiberoptic bronchoscopy, by fine- needle aspiration of thoracic or extrathoracic tumour masses using CT guidance or by percutanecus biopsy of enlarged lymph node, soft tissue mass. According to TNM staging, our patient belongs to T3 NoMo i.e. stage IB. Stage IB, IIA and IIB who can tolerate operation, the treatment of choice is pulmonary resection. The role of adjuvant chemotherapy for stage IB disease is undefined, subset analysis of all the randomized studies showed no benefit in patient with stage IB.

CASE – II

Mrs. Leelawati 75 years, Female, Housewife, resident of Oraiya, admitted with chief complaints of –

1. Cough with progressively increasing breathlessness for 5 months.

2. Acute exaggravation of breathlessness with bilateral pedal edema for 10 days.

Negative history –No history of – chest pain, perspiration PND Fever Drugs intake Intermittent claudication DVT

Past history – no h/o DM, HTN, TBPersonnel history – Non bidi smokerFamily history – not significant

On ExaminationPR – 100/min, regular, normovolumic, normal in character without any radiofemoral and radioradial delay.BP – 90/60 mmHg in right arm in supine position.RR – 22/min, regular, thoracoabdominal Temp – NSpO2 – 86% without O2Pallar-absentCyanosis-absentClubbing-absentIcterus-absentLymphadenopathy-absentJVP – raised, cv wave present Pedal edema--- +

Cardiovascular system examination

apical impulse is in 5th ICS at MCL palpable & loud second sound (P2) Left PSH of grade II/III Pansystolic murmur of grade III/VI in tricuspid area which increases in intensity on inspiration.

Respiratory system ---- Bilateral coarse basal crepts present on auscultation.

Abdominal system examination---- Tender hepatomegaly 2 cm below costal margin.

So, Clinical diagnosis –Severe pulmonary artery hypertension with severe TR

with congestive heart failure stage C cause ? Cor pulmonale Pulmonary thromboembolism Primary pulmonary artery HTN

On investigation Routine investigations ECG CXR PA view USG abdomen D- dimmer assay PFT

So, final diagnosis is pulmonary hypertension associated with lung disease and or hypoxemia cause COAD.