effusions explored
TRANSCRIPT
M1 UNITDR.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 , tachypnicpallor+B/L pitting pedal edema+JVP elevatedPulse-102/minBP-180/110 mmhgCVS-S1S2 heardRS-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/dlTC -8200DC -P60,L37,E3ESR -5/11PLC -2.0 LacksURINE albumin-+ sugar -nil dep-4-6 epi cells
CONTD………….RBS-146 mg/dlUREA-22CREATININE-0.9Na-130 meq/lK-3.1 meq/lSERUM bil-1.0 mg (D)-0.3AST -45 UALT-37 USAP-92 USERUM 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:
DYSPNEAHYPERTENSIONNORMAL ECHOB/L PLEURAL EFFUSIONANEMIAHYPONATREMIAHYPOKALEMIA
PLEURAL FLUID ANALYSIS:
PROTEIN-1.3SUGAR-113CELLS-Few lymphocytesCYTOLOGY-reactive effusionAFB-negativeGRAM STAIN-negativeADA-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 RESPIRATORYBradycardiaHypertensionPericardial effusionPulmonary
hypertensionQT prolongation Ventricular
arrhythmiasCardiomyopathyCardiac failure
Pleural effusionImpaired
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 , afebrileThin & ill-nourishedSparse hairDry scaly skinHyper pigmented rash around both elbowsPallor+Pedal edema+
Contd………..
Pulse-80/minBP -100/70 mmhgCVS-S1S2 heardRS - B/L basal crepitations+P/A- palpable liverCNS- 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 effusionSystemic symptomsAlopeciaSkin rashArthalgiaSeizures
IMPRESSION:
SLETO R/O TUBERCULOSIS
INVESTIGATIONS:Hb-8 gm/dlTC-7100DC-P60 , L40ESR-8/15PLC-1.82 lacksRBS-124UREA-29CREATININE-0.7Na-138K-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-reactiveMANTOUX-negativeFT4-0.96 ng/dlTSH-13.7324 hr URINARY PROTEIN-170 mg/dayANA-++++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 tamponadePERICARDIAL 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 SLEMost common cardiac abnormality- pericardial
involvementClinically evident pericarditis 20 – 40 %PE is an infrequent presenting manifestationDiagnosis rests on other signs and positive ANAPericardial fluid is typically an exudateSymptomatic PE often accompanied by pleural effusionPericardial tamponade is rareTreatment ; NSAID for pericarditisCorticosteroids for large effusionsImmunosuppressant for resistant effusions
PHT ASSOCIATED WITH SLERare but potentially life threatening complication of
SLEIncidence 0.5 – 14 %Mortality 25 – 50 % in two years after diagnosisECHO may show RVH even before onset of symptomsVasoconstriction, vasculitis and thrombosis are
implicatedEndothelial dysfunction is evident with high
endothelin levelsRt 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
VitiligoPernicious anemiaAddissons disease Alopecia areataType1 DM
Celiac diseaseDermatitis
herpetiformisChronic active
hepatitisRheumatoid arthritisSLESjogren’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:ConsciousOrientedAfebrilePallor+I0 C0 E0 LN0PULSE-90/minBP-110/70 mmhgCVS-S1S2 heardRS-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/dlTC -9500DC -P50L45E5ESR -10/22PCV -28RBC -3.1PLC -3.7G/T -B+veP/S -normocytic normochromic
CONTD……….RBS -126mg/dlUREA -26CREATININE-0.9Na -134K -4.2Cl -98.8LFT Bilirubin(T)-0.8 AST -25 ALT -37 SAP -69 Proteins(T)-6.2 Albumin -3.9
CONTD……….CHEST X-RAY:NADECG:WNLUSG 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- haemaorrhagicProtein-3.3Albumin-2.9Sugar-83ADA-15U/LCells-50 cells mostly lymphocytesCytology-reactive effusionAFB-negativeGram stain-negativeC/S-no growthSAAG-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 exam2)Laboratory and radiographic studies3)Detailed histological evaluation
STANDARD WORKUP FOR CUP:
HaemogramChest x-rayRFTLFTCT abdomen & pelvisMammographyPSA
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
LymphomaMelanomaHCCBreast cancer
Germ cell tumourNeuroendocrine
tumour
Leucocyte common antigen
S-100,HMB-45Alphafeto proteinEstrogen & progesterone
receptors,BRST-1,gross cystic disease fibrous protein.
Beta-HCGChromogranin,synaptophy
sin,neuron specific enolase
CONTD……….
TUMOUR IHC STAIN
Lung & thyroid ca
MesotheliomaBladder caGastrointestinal caProstate ca
Thyroid transcription factor-1,thyroglobulin
Calretinin,mesothelinURO-III,
thrombomodulinCDX-2PSA
IMMUNOHISTOCHEMISTRY: CK phenotype
CK7-/CK20-
CK7+/CK20-
CK7-/CK20+
CK7+/CK20+
TumorsHCC, 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 MARKERSCommonly 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 adenopathyWomen with peritoneal carcinomatosisSquamous cell carcinoma of cervical lymph
nodesMen with bone metastasis ,elevated PSAPoorly differentiated carcinoma with
midline adenopathyNeuroendocrine carcinomaSolitary 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/RTNeoadjuvant 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 cancerLow stage (N1) – Surgery RT or RT aloneHigh 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
TREATMENTUNFAVORABLE 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
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