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    Effusions Explored Effusions Explored Presentation Transcript

    • M1 UNIT DR.G.KANNAN PROF.RUKMANI REDDY EFFUSIONS EXPLORED
    • CASE 1
    • HISTORY:
      • Hemavathy 65/F not a known HT/DM/CAD/COPD.
      • H/O Breathlessness 3 days, insidious onset, progressive in nature , worsened over past 4 hrs.
      • Preceded by NSAID intake for flu –like symptoms.
      • Associated with decreased urine output , swelling of face & legs.
      • Patient was treated in a private hospital with inj.lasix & Tab.nifedipine and referred to SGH.
      • No other significant positive history.
    • EXAMINATION:
      • Conscious , Oriented , afebrile.
      • Dyspnic , tachypnic
      • pallor +
      • B/L pitting pedal edema +
      • JVP elevated
      • Pulse-102/min
      • BP-180/110 mmhg
      • CVS-S1S2 heard
      • RS-B/L crepitations +,BS↓ both bases.
      • P/A-soft.
    • CONTD…………..
      • ECG-T inversion L II,L III,AVF
      • CHEST XRAY-Cardiomegaly , b/l pleural effusion , congestive lung fields
    • IMPRESSION
      • HT
      • ACUTE LVF
      • TO R/O ACUTE ON CHRONIC KIDNEY DISEASE.
    • TREATMENT:
      • Backrest
      • Nasal O2
      • I.V.Dieuretics
      • Antihypertensives
    • INVESTIGATIONS:
      • Hb -10.5 g/dl
      • TC -8200
      • DC -P60,L37,E3
      • ESR -5/11
      • PLC -2.0 Lacks
      • URINE albumin- +
      • sugar -nil
      • dep-4-6 epi cells
    • CONTD………….
      • RBS-146 mg/dl
      • UREA-22
      • CREATININE-0.9
      • Na-130 meq /l
      • K-3.1 meq/l
      • SERUM bil-1.0 mg
      • (D)-0.3
      • AST -45 U
      • ALT-37 U
      • SAP-92 U
      • SERUM PROTEINS -5.6
      • ALBUMIN-3.6
    • CONTD………
      • USG ABDOMEN-post –menopausal status of uterus.
      • ECHO -NO RWMA
      • normal LV systolic function
    • REVIEW:
      • Patient improved marginally but continued to be dyspnic.
      • CT CHEST (P)-B/L PLEURAL EFFUSION CAUSING COLLAPSE OF UNDERLYING LUNG PARENCHYMA
    • CT-CHEST:
    • PROBLEMS:
      • DYSPNEA
      • HYPERTENSION
      • NORMAL ECHO
      • B/L PLEURAL EFFUSION
      • ANEMIA
      • HYPONATREMIA
      • HYPOKALEMIA
    • PLEURAL FLUID ANALYSIS:
      • PROTEIN-1.3
      • SUGAR-113
      • CELLS-Few lymphocytes
      • CYTOLOGY-reactive effusion
      • AFB-negative
      • GRAM STAIN-negative
      • ADA-5.52 U/L
    • CONTD………..
      • 24 HRS URINARY PROTEIN-110 mg/day
      • F T3-1.99 pg/ml(2.30-4.2)
      • FT4-0.83 ng/ml(0.8-2.0)
      • TSH-29.4 MIU/ml(0.35-5.5)
      • RF,CRP, ANA-negative
    • DIAGNOSIS:
      • SYSTEMIC HYPERTENSION
      • HYPOTHYROIDISM
    • TREATMENT:
      • Thyroxin replacement
      • Antihypertensives
    • FOLLOW UP
      • BEFORE TREATMENT
      • AFTER TREATMENT
    • PATIENT
      • BEFORE
      • AFTER
    • TFT
      • BEFORE
      • AFTER
      • -F T3-1.99 pg/ml(2.30-4.2)
      • -FT4-0.83 ng/ml(0.8-2.0)
      • -TSH-29.4 MIU/ml(0.35-5.5)
      • -FT3-2.6 pg/ml
      • -FT4-1.8 ng/ml
      • -TSH-4.6 MIU/ml
    • MANIFESTATIONS OF HYPOTHYROIDISM
      • CARDIAC
      • RESPIRATORY
      • Bradycardia
      • Hypertension
      • Pericardial effusion
      • Pulmonary hypertension
      • QT prolongation
      • Ventricular arrhythmias
      • Cardiomyopathy
      • Cardiac failure
      • Pleural effusion
      • Impaired respiratory muscle function
      • Decreased ventilatory drive
      • Sleep apnea
    • CASE 2
    • HISTORY:
      • Shanthi 20/F admitted with C/O breathlessness since 1 month.
      • -insidious onset
      • -slowly progressive
      • -grade III/IV
      • -no orthopnea/PND
      • -no chest pain/syncope/palpitations
      • -cough with minimal expectoration +
      • -associated with systemic symptoms like low grade fever , myalgia , arthalgia ,loss of appetite & weight×3 months.
      • -one episode of GTCS.
    • O/E:
      • Conscious , oriented , afebrile
      • Thin & ill-nourished
      • Sparse hair
      • Dry scaly skin
      • Hyper pigmented rash around both elbows
      • Pallor +
      • Pedal edema +
    • Contd………..
      • Pulse-80/min
      • BP -100/70 mmhg
      • CVS-S1S2 heard
      • RS - B/L basal crepitations +
      • P/A- palpable liver
      • CNS- generalized muscle tenderness+
    • Contd……..
      • ECG-low voltage complexes
      • CHEST X-RAY-cardiomegaly.
      • USG ABDOMEN- hepatomegaly , minimal free fluid in the abdomen , significant pericardial effusion.
      • CT BRAIN-normal study
    • PROBLEMS:
      • Pericardial effusion
      • Systemic symptoms
      • Alopecia
      • Skin rash
      • Arthalgia
      • Seizures
    • IMPRESSION:
      • SLE
      • TO R/O TUBERCULOSIS
    • INVESTIGATIONS:
      • Hb-8 gm/dl
      • TC-7100
      • DC-P60 , L40
      • ESR-8/15
      • PLC-1.82 lacks
      • RBS-124
      • UREA-29
      • CREATININE-0.7
      • Na-138
      • K-4.3
    • CONTD……..
      • LFT:
      • -serum bilirubin-0.8
      • - (D)-O.3
      • -AST -24
      • -ALT -36
      • -SAP -84
      • -SERUM PROTEINS-5.6
      • - ALBUMIN-3.2
    • CONTD…..
      • HIV- non-reactive
      • MANTOUX-negative
      • FT4-0.96 ng/dl
      • TSH-13.73
      • 24 hr URINARY PROTEIN-170 mg/day
      • ANA- ++++
      • ds DNA+
      • APTT-31.2 sec(T),30.2 sec(C)
    • Contd………
      • ECHO-RA/RV dilated
      • LA/LV normal
      • mild TR
      • TRPG-52
      • PHT-moderate
      • large pericardial effusion
      • no tamponade
      • PERICARDIAL FLUID:
      • -protein:2.9
      • -sugar :124
      • -cells :30(90% lymphocytes)
      • -ADA :15 U/L
    • DIAGNOSIS:
      • SYSTEMIC LUPUS ERYTHEMATOSES
      • SUB CLINICAL HYPOTHYROIDISM
      • ASSOCIATED PULMONARY ARTERIAL HYPERTENSION
    •  
    • TREATMENT:
      • -Steroids
      • -Antibiotics
      • -Low dose diuretics
      • - Thyroxin replacement
      • Patient was taken over by rheumatology GH.
    • PERICARDIAL EFFUSION IN SLE
      • Most common cardiac abnormality- pericardial involvement
      • Clinically evident pericarditis 20 – 40 %
      • PE is an infrequent presenting manifestation
      • Diagnosis rests on other signs and positive ANA
      • Pericardial fluid is typically an exudate
      • Symptomatic PE often accompanied by pleural effusion
      • Pericardial tamponade is rare
      • Treatment ; NSAID for pericarditis
      • Corticosteroids for large effusions
      • Immunosuppressant for resistant effusions
    • PHT ASSOCIATED WITH SLE
      • Rare but potentially life threatening complication of SLE
      • Incidence 0.5 – 14 %
      • Mortality 25 – 50 % in two years after diagnosis
      • ECHO may show RVH even before onset of symptoms
      • Vasoconstriction, vasculitis and thrombosis are implicated
      • Endothelial dysfunction is evident with high endothelin levels
      • Rt heart cath with assessment of vascular reactivity should be done.
      • Treatment – Ca channel blockers, Prostacyclin ,endothelin receptor antagonists.
    • Prevalence of thyroid dysfunction in SLE
      • Appenzeller, Simone MD, PhD; Pallone, Ana T. MD; Natalin, Ricardo A. MD; Costallat, Lilian T. L. MD, PhD
      • Our patients with SLE had a high prevalence of symptomatic (6.1%) and significantly more subclinical hypothyroidism(11.5%) and positive thyroid auto antibodies (17%). Thyroid auto antibodies may precede the appearance of clinical autoimmune disease. Sjögren syndrome and positive rheumatoid factors were more frequently observed in SLE patients with autoimmune thyroid disease. We believe that, since symptoms of SLE and thyroid disease can be similar, that SLE patients should routinely been investigated for autoimmune thyroid disease.
      • COMMON
      • LESS COMMON
      • Vitiligo
      • Pernicious anemia
      • Addissons disease
      • Alopecia areata
      • Type1 DM
      • Celiac disease
      • Dermatitis herpetiformis
      • Chronic active hepatitis
      • Rheumatoid arthritis
      • SLE
      • Sjogren’s syndrome
      HYPOTHYROIDISM AND AUTO IMMUNE DISORDERS
    • CASE 3
    • HISTORY:
      • Fathima 45/F not a known DM , HT ,CAD , PULM KOCHS.
      • H/O abdominal distension ×2 weaks
      • -insidious onset
      • -progressive
      • -no associated symptoms
      • -No other significant history.
    • EXAMINATION:
      • Conscious
      • Oriented
      • Afebrile
      • Pallor +
      • I0 C0 E0 LN0
      • PULSE-90/min
      • BP-110/70 mmhg
      • CVS-S1S2 heard
      • RS-NVBS heard
    • Contd………
      • P/A
      • -distended
      • -umbilicus flushed with surface
      • - no dilated veins
      • - no organomegaly
      • - free fluid ++
    • IMPRESSION:
      • ASCITES FOR EVALUATION
      • ?MALIGNANCY
    • INVESTIGATIONS:
      • Hb -9.2gm/dl
      • TC -9500
      • DC -P50L45E5
      • ESR -10/22
      • PCV -28
      • RBC -3.1
      • PLC -3.7
      • G/T -B +ve
      • P/S -normocytic normochromic
    • CONTD……….
      • RBS -126mg/dl
      • UREA -26
      • CREATININE-0.9
      • Na -134
      • K -4.2
      • Cl -98.8
      • LFT
      • Bilirubin(T)-0.8
      • AST -25
      • ALT -37
      • SAP -69
      • Proteins(T)-6.2
      • Albumin -3.9
    • CONTD……….
      • CHEST X-RAY:NAD
      • ECG:WNL
      • USG abdomen :
      • -massive ascites
      • no significant abnormality in solid abdominal& pelvic organs
      • ECHO:
      • MVP,AML
      • Mild MR
      • No RWMA
      • Normal LV systolic function
    • Ascitic fluid analysis:
      • Gross- haemaorrhagic
      • Protein-3.3
      • Albumin-2.9
      • Sugar-83
      • ADA-15U/L
      • Cells-50 cells mostly lymphocytes
      • Cytology-reactive effusion
      • AFB-negative
      • Gram stain-negative
      • C/S-no growth
      • SAAG-1.0
    • CONTD…….
      • CA 125-1902 U/ml (N <35 U/ml)
      • CEA -0.393 ng/ml(N up to 5 ng/ml)
      • CECT ABDOMEN &PELVIS: massive ascites
      • OGD SCOPY: normal
      • COLONOSCOPY: normal
    • CECT ABDOMEN& PELVIS:
    • PROBLEMS:
      • Low gradient ascites
      • Elevated CA-125
      • Imaging studies not contributory.
    • OPINION:
      • MGE-peritoneal carcinomatosis , advised lap. Biopsy.
      • ONCOLOGY-HPE evidence for malignancy ,advised cell block.
      • SGE-P/R deposits , suggested USG guided peritoneal biopsy.
      • GYN-P/V :uterus anteverted , cervix normal , POD free.
    • Contd………
      • USG –GUIDED PERITONEAL BIOPSY :no e/o malignancy
      • LAPROSCOPY & BIOPSY:
      • -serosanguinous ,turbid ascitic fluid of more than 5 L
      • -multiple peritoneal deposits
      • -omentum walled -up like a mass
      • -uterus & ovaries appears normal.
      • -liver appears normal
    • Contd……….
      • HPE REPORT(2998/09 ) of peritoneal biopsy :
      • -sections show fibrocollagenous tissue with an adjacent neoplasm composed of neoplastic cells arranged in papillary pattern & sheets.
      • -The cells are round to cuboidal with the presence of nuclear pleomorphism,vescicular nuclei & prominent nucleoli.
      • -Stroma shows inflammatory cell infiltrate
      • IMPRESSION :
      • METASTATIC CARCINOMATOUS DEPOSITS
    • QUES:
      • DIAGNOSIS ?
      • PROGNOSIS?
      • TREATMENT?
    • ANS:
      • CARCINOMA OF UNKNOWN PRIMARY(CUP) -WOMEN WITH PERITONEAL CARCINOMATOSIS
      • MEDIAN SURVIVAL -18 months.
      • TREAT AS STAGE 3 OVARIAN CANCER
      • -debulking surgery followed by taxane & platinum based chemotherapy.
    • CARCINOMA OF UNKNOWN PRIMARY (CUP)
    • DEFINITION:
      • Carcinoma of unknown primary (CUP) is a biopsy-proven metastatic malignant tumour whose primary site can not be identified during pre treatment evaluation including
      • 1)Thorough history and physical exam
      • 2)Laboratory and radiographic studies
      • 3)Detailed histological evaluation
    • STANDARD WORKUP FOR CUP:
      • Haemogram
      • Chest x-ray
      • RFT
      • LFT
      • CT abdomen & pelvis
      • Mammography
      • PSA
    • EPIDEMIOLOGY:
      • CUP constitutes 2.3% of all cancers in US (SEER 1973-87)
      • Annual age-adjusted incidence in US is 7-12 cases per 100,000 population
      • Median age at presentation is 60 years
      • Slightly more prevalent in males
    • BIOLOGY:
      • CUP represents a heterogeneous group of malignancies characterized by:
      • -Early dissemination in the absence of a detectable primary
      • -Unpredictable metastatic pattern
      • -Aggressive biological and clinical behaviour
      • The hypothesis is that the primary tumour either remains microscopic and escapes clinical detection or disappears after seeding the metastasis
    • CLINICAL MANIFESTATIONS:
      • Patients usually present with a short history of local findings related to the metastatic sites and constitutional symptoms
      • Physical exam is often abnormal with effusions, adenopathy, hepatomegaly and other abnormalities related to the involved sites
      • The majority of patients have multiple metastatic sites.
    • PATHOLOGY – LIGHT MICROSCOPY
      • Light microscopy with hematoxylin and eosin stain can identify four main histologic subtypes of CUP
      • Adenocarcinoma (50%-60%)
      • Poorly differentiated carcinomas (30%)
      • Squamous cell carcinomas (5%-15%)
      • Undifferentiated malignant neoplasm
    • IMMUNOHISTOCHEMISTRY:
      • Tumour type
      • Immunohistochemistry
      • Lymphoma
      • Melanoma
      • HCC
      • Breast cancer
      • Germ cell tumour
      • Neuroendocrine tumour
      • Leucocyte common antigen
      • S-100,HMB-45
      • Alphafeto protein
      • Estrogen & progesterone receptors,BRST-1,gross cystic disease fibrous protein.
      • Beta-HCG
      • Chromogranin,synaptophysin,neuron specific enolase
    • CONTD……….
      • TUMOUR
      • IHC STAIN
      • Lung & thyroid ca
      • Mesothelioma
      • Bladder ca
      • Gastrointestinal ca
      • Prostate ca
      • Thyroid transcription factor-1,thyroglobulin
      • Calretinin,mesothelin
      • URO-III, thrombomodulin
      • CDX-2
      • PSA
    • IMMUNOHISTOCHEMISTRY:
      • CK phenotype
      • CK7-/CK20-
      • CK7+/CK20-
      • CK7-/CK20+
      • CK7+/CK20+
      • Tumors
      • HCC, liver, lung (Squamous, small cell), prostate, renal
      • Biliary and pancreas, breast, cervical, endometrial, lung (Adenocarcinoma), ovarian (non- mucinous), thyroid
      • Colon, gastric, Merckel cell carcinoma
      • Biliary and pancreas, ovarian (mucinous), urothelial
      CK7+/CK20+
    • TUMOR MARKERS
      • Commonly used tumour markers (CEA, CA 19-9, CA 125) are nonspecific and have limited value in the diagnosis of patients with CUP
      • They may have a role as a prognostic marker and to evaluate response to therapy
      • Serum HCG and AFP may be used to exclude testicular cancer
      • Serum PSA can identify cases of prostate cancer
      • Elevated thyroglobulin in patients with bone metastases suggests occult thyroid primary
    • Imaging Studies and Endoscopy:
      • Initial evaluation includes chest radiograph and CT scan of the abdomen/pelvis
      • The role of chest CT has not been established
      • Mammogram is indicated in all women with CUP Adenocarcinoma
      • The experience with PET is limited
      • Endoscopy is not recommended as a routine work up for asymptomatic patients and should be used according to the clinical presentation
    • TREATMENT:
      • Once the diagnosis of carcinoma is established, the main objective is determine whether the patient belong to one of the favourable subsets, for which there is a specific treatment
    • Favorable subsets:
      • Women with isolated axillary adenopathy
      • Women with peritoneal carcinomatosis
      • Squamous cell carcinoma of cervical lymph nodes
      • Men with bone metastasis ,elevated PSA
      • Poorly differentiated carcinoma with midline adenopathy
      • Neuroendocrine carcinoma
      • Solitary metastatic site
    • Women with isolated axillary adenopathy:
      • Lymph nodes should be tested for ER, PR, and HER-2/neu
      • In cases of negative mammogram, the primary may be seen on MRI or after mastectomy
      • Prognosis is similar to lymph node positive breast cancer
      • Mobile lymph nodes (N1) - Treat as stage IIA breast cancer
      • Fixed lymph nodes (N2) - Treated as stage IIIA breast cancer
      • MRM + AND chemotherapy ± hormonal therapy/RT
      • Neoadjuvant chemotheray for N2 disease
    • WOMEN WITH PERITONEAL CARCINOMATOSIS:
      • The germinal epithelium of the ovary and peritoneal mesothelium share the same embryological origin (mullerian)
      • Pathologic & lab (elevated CA-125)characteristics of ovarian CA but no primary tumor identified on TVS/ laparotomy.
      • More common in women with BRCA-1 mutation and may also be seen after prophylactic oophorectomy
      • Outcomes are similar to ovarian cancer at equivalent stage
      • Median survival of 18 months.
      • Patients should be treated as stage III ovarian carcinoma
      • Surgical debulking followed by chemotherapy
    • Squamous cell carcinoma of the cervical lymph nodes:
      • Despite aggressive diagnostic approach, the primary site is not found in the majority of patients
      • Ipsilateral tonsillectomy is often performed since the primary can be found in 10 to 25% of cases - Small tumours may originate in the deep crypts and not be detected by superficial biopsy
      • Treat as locally advanced head and neck cancer
      • Low stage (N1) – Surgery  RT or RT alone
      • High stage (N2-N3) - Chemoradiotherapy
    • . . Men with bone metastasis , elevated PSA:
      • Prostate cancer is the most likely diagnosis
      • - Elderly men with Adenocarcinoma of unknown primary and predominantly blastic bone metastases
      • - Patients with increased PSA or positive PSA staining on the biopsy specimen despite atypical presentation
      • Hormonal therapy
    • Poorly differentiated carcinoma with midline adenopathy
      • Young males with tumours of predominant midline distribution (mediastinum and retro peritoneum) should be treated as extragonadal germ cell tumours
      • Cisplatin-based chemotherapy (BEP)
    • Neuroendocrine carcinoma
      • IHC usually stains positive for chromogranin or NSE
      • Patients frequently present with diffuse metastases to the liver or bones
      • Platinum-based chemotherapy (platinum + etoposide)
    • Single metastatic site:
      • Although other metastatic sites may become evident within a short period, some patients may achieve a prolonged disease-free interval with local therapies such as surgery or radiotherapy
      • Adjuvant chemotherapy may also be considered
      • Surgery or RT
    • TREATMENT UNFAVORABLE SUBSETS
      • With the exception of the favourable subsets, most patients with CUP have a tumour that is resistant to chemotherapy
      • The prognosis is very poor, with median survival of 2 to 3 months in unselected patients and 6 to 10 months in those enrolled into clinical trials
      • Patients with good performance status may benefit from systemic chemotherapy
    • CONCLUSIONS:
      • CUP represents a group of heterogeneous tumours sharing the unique characteristic of metastatic disease without identifiable origin at the time of initial therapy
      • Although identification of the primary tumour may provide valuable information regarding both treatment and prognosis, aggressive diagnostic workup is usually of little value and not cost effective
      • The recommended approach is to pursue a limited diagnostic approach to identify favourable subsets
    • THANK YOU