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A lady with acute SOB

Sammi Pe

Case Presentation
54/F Cat II BP 129/69mmHg P 128 Temp 36.9 SpO2 78% ( 100% O2) Triage : SOB since afternoon, cough with sputum, mild chest discomfort

What will you do ?


What further history need?

What further Hx
Good Past Health Domestic helper SOB since ~2 hrs ago Mild cough with yellowish sputum xdays become blood stained on AED No fever Chest discomfort today ( tightness) Palpitation +ve

More hx from employer


Mild exertional SOB x several days Need resting after her work No fever all along No Travel hx Work in HK x ~17yrs No GI upset/ abd pain Not on regular medication Non-smoker, non-drinker

P/E
Alert GCS 15/15 BP 139/78 P 120 RR 48 Sit up for breathing SpO2 80% on 100% O2 Recheck Temp 37.2 Hstix 13.2

P/E
Chest: AE fair with bilateral basal crep, occ wheeze Abd soft HS dual, no murmur No ankle edema

What will you do next ?

ABC 100% O2 mask HB set Blood x CBC, L/RFT, Trop I , Clotting ECG i stat ( arterial) CXR

ECG x 2

i stat (arterial, on 100%O2)


pH 7.398 pCO2 5.39 kPa pO2 5.8 kPa BE 0 HCO3 24.9 mmol/L SO2 79% Na 141 K 3.5 i Ca 1.21

Hb 14.6

Our Patient
Problem: Sudden onset SOB Desaturation even on 100% O2 Type I Resp Failure What is yr DDx?

Type I Resp Failure


Typically due to V/Q mismatch
PaO2 low (< 60 mmHg(8.0 kPa)) PaCO2 normal or low PA-aO2 increased

Parenchymal disease (V/Q mismatch) Diseases of vasculature and shunts: right-to-left shunt, pulmonary embolism interstitial lung diseases: ARDS, pneumonia, emphysema.

Patient was still in distress even on 100% O2


What will you do then?

Patient was put on CPAP Lasix 40mg iv BP 110/70 Clinically improved

CXR film A/V.

CXR
What is yr Diagnosis?

? Other drug(s) to be considered ? Underlying cause


CCU was consulted

APO .

Medications
Nitrates
Vasodilation Reduced preload and afterload Improved CO Rapid effect Not prescribed likely due to BP on low side

Diuretics
Reduced plasma volume / preload Pulmonary vasodilatation

ACEI
Reduced afterload Improved CO

Underlying Causes
ACS HT Aortic/mitral valve disease Arrhythmias VSD Cardiomyopathy Acute myocarditis Pericardial disease Atrial myxoma

Echo was performed

Our case

What is show in the Echocardiogram?

CCU input
ECHO: LA mass ~4cm Likely atrial myxoma Trivial MR/AR Normal LV size and EF

Our Patient
APO secondary to large atrial myxoma
Transfer to CCU then CTSU for further Mx.

Progress
Emergency excision of atrial myxoma
6x5cm encapsulated LA tumour attached to inter-atrial septum. Causing obstruction & pul edema Bi-atrial exploration + excision of tumour

Extubated on D1 Post-op echo: EF 70% no PE

Day 0

Day 2

Day 1

Day 3

Day 4

Day 20

Patient was discharge on D8 and SOPD FU On Day 20 Good Recovery, Class I II , ET 3-4 FOS

Atrial Myxoma

Background
Most common 1 Heart tumour (40-50%) 90% solitarty and pedunculated
Multiple tumours occur in 50% of familial case

10% familial ( autosomal dominant) 75-85% occur in LA ~25% RA Attach to fossa ovalis Symptomatic ~ 70g 140g

Myxoma polypoid, round, oval in shape Smooth / lobulated surface White/ yellow/ brown Produce numberus growth factors and cytokines e.g. interleukin-6

Histology
lipidic cells embedded in a vascular myxoid stroma In a series of 37 cases, 74% of tumors showed immunohistochemical expression of interleukin-6 while 17% had abnormal DNA content

Epidemiology
US ~ 75 case / million autopsies 75% sporadic Female Mean age 56 15% present as sudden death
tumour embolism, HF, mechanical obstruction

History
Asymptomatic (20%) symptomatic sudden death (15%)
embolization
Pulmonary (R)
PE Pul infarction Pul HT

Mechanical interference with cardiac fx


LHF
Exertional SOB Orthopnea PND Pul edema Postural dizziness

RHF
fatigue peripheral edema ascites

systematic (L)
infarct / haemorrhage of viscera e.g. CVA visual loss

Constitutional symptoms : fever, Wt loss, arthralgias, Raynaud ~ 50% of patient due to


interleukin-6 overporduction

Physical
JVP
Loud S1
( delay mitral valve closure)
tumor hit

Early diastolic sound (Tumor plop)


against the endocardial wall

Diastolic atrial rumble ( obstruction in MV) MR/ TR ( valvar damage/ prolapse)

DDX
Mitral Regurgitation Mitral Stenosis Pul Embolism Pul HT , primary Tricuspid Regurgitation Tricuspid Stenosis

Ix
Lab: ESR, CRP, CBC, serum interleukin-6 CXR ECHO
need to differentiate thrombus from myxoma
Thrombus ( in posterior portion, in layers) Myxoma ( presence of stalk and mobility)

MRI (point of attachment ) CT scan

Treatment
Medical treatment for CHF and arrhythmia Surgical excision is the definitive tx Safe and curative Recurrence is possible if incomplete excision

Thank you

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