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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 (< 60mmHg(8.0kPa))
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
?

APO .

? Other drug(s) to be
considered
? Underlying cause
CCU was consulted

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 1
Day 2

Day 3

Day 4

Day 20

PatientwasdischargeonD8andSOPDFU
OnDay20
GoodRecovery,ClassIII,ET3-4FOS

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%)

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

embolization
Pulmonary (R)
PE
Pul infarction
Pul HT

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


interleukin-6 overporduction

Physical
JVP
Loud S1 ( delay mitral valve closure)
Early diastolic sound (Tumor plop)

tumor hit

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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