Transcript OSCE Feb 2012

OSCE Feb 2012
Dr. Wong Kim Chiu
Associate Consultant
North District Hospital
Case 1
 2/3/2011
 M/67
 Chronic smoker
 GERD
Case 1
 c/o: found collapsed at home at 10:15 a.m.
 Last seen well at 10 a.m
 Arrived A&E at 10:51 a.m.
 ? Preceded by headache and neck pain
Case 1
 On arrival :
 P/E: GCS E3, V2, M6
 PERL, 3mm
 Left hemiparesis
 (Rt. side power 4/5, Lt. side power 2/5)
Case 1
 ECG : SR, no acute ischemic changes
Case 1
 CT brain :
Evidence of right MCA infarct with dense MCA
sign and effacement of sulci.
Case 1
 rt PA was given at 11:55 a.m.
 Transferred to ICU for close monitoring
Case 1
 Developed hypotension at 3:30 p.m.
 PR  no tarry stool
 H’cue 11.2
 No evidence of acute hemorrhage
Case 1
 ECG : new onset ST depression over
inferior leads
 Bedside Echo:
no free fluid in abdomen
no pericardial effusion / pleural effusion
RWMA +ve
RV no dilated
 Dx: NSTEMI
Case 1
 Neurologist consulted:
Not for aspirin in view of recent adminstration of
rt PA
Case 1
 Rapid deterioration with shock and bradycardia
 Intubation
 Adrenaline and noradrenaline were given
 BP on low side despite inotropes support
Case 1
 Succumbed at 6:44 p.m. on the same day.
Case 2
 M/59
 Good past health
 c/o: constricting chest pain after running on
the day of attention
 P/E: unremarkable
 1st ECG showed SR with V.E. x 1
Case 2
 Proceed chest pain protocol in O Ward.
 Smart M.O. dug out history of right calf pain
for 20 days.
 ? Right calf swelling
 Feeling SOB just after jogging
 Still pending 1st TnI
Case 2
 USG doppler was booked.
 It showed right superficial femoral vein and
popliteal vein thrombosis.
 1st TnI came back 0.26
 ECG repeated : sinus tachy 139/min.,
No RAD or RBBB
No S1Q3T3
Case 2
 CT thorax showed:
Extensive intra-arterial tubular filling defects
suggestive of bilateral pulmonary
thromboembolism involving the main pulmonary
trunk and all of its branches, the right pulmonary
lobar arteries and their branches.
Both lungs are clear, no pleural effusion
Dx: acute massive pulmonary
thromboembolism
Diagnosis of PE
 The decision to do medical imaging is
usually based on clinical grounds, i.e. the
medical history, symptoms and findings on
physical examination, followed by an
assessment of clinical probability.
Diagnosis of PE
 The most commonly used method to predict
clinical probability, the Wells score, is a
clinical prediction rule.
Diagnosis of PE
 The Wells score:
 clinically suspected DVT - 3.0 points
 alternative diagnosis is less likely than PE - 3.0 points
 tachycardia - 1.5 points
 immobilization/surgery in previous four weeks - 1.5 points
 history of DVT or PE - 1.5 points
 hemoptysis - 1.0 points
 malignancy (treatment for within 6 months, palliative) - 1.0 points
Diagnosis of PE
 Traditional interpretation
Score >6.0 - High (probability 59% based on
pooled data)
Score 2.0 to 6.0 - Moderate (probability 29%
based on pooled data)
Score <2.0 - Low (probability 15% based on
pooled data)
Diagnosis of PE
 Alternate interpretation
Score > 4 - PE likely. Consider diagnostic
imaging.
Score 4 or less - PE unlikely. Consider D-dimer
to rule out PE.
Diagnosis of PE
 The gold standard for diagnosing pulmonary
embolism (PE) is pulmonary angiography.
Pulmonary angiography is used less often
due to wider acceptance of CT scans, which
are non-invasive.
Treatment of PE
 Anticoagulation
In most cases, anticoagulant therapy is the
mainstay of treatment. Acutely, supportive
treatments, such as oxygen or analgesia, are
often required.
Treatment of PE
 Thrombolysis
Massive PE causing hemodynamic instability
(shock and/or hypotension, defined as a systolic
blood pressure <90 mmHg or a pressure drop
of 40 mmHg for>15 min if not caused by newonset arrhythmia, hypovolemia or sepsis) is an
indication for thrombolysis.
Treatment of PE
 Surgery
Surgical management of acute pulmonary
embolism (pulmonary thrombectomy) is
uncommon and has largely been abandoned
because of poor long-term outcomes.
Treatment of PE
 Inferior vena cava filter
 If anticoagulant therapy is contraindicated and/or
ineffective, or to prevent new emboli from entering the
pulmonary artery.
Case 3
 M/33
 Chronic smoker
 Good past health
 c/o: sudden onset of chest pain after
repeated vomiting because of drunk
Case 3
 GCS 15/15
 BP 167/67, P 67/min
 Temp 36.9 C
 SaO2 100%
 Surgical emphysema +ve
Case 3
 CXR showed pneumomediastinum & diffuse
subcutaneous emphysema
Case 3
 ECG showed normal sinus rhythm
Case 3
 CT thorax:
Pneumomediastinum & surgical emphysema.
Diffuse increase in mediastinal fat density and
patch of oral contrast of irregular outline over
the lower thoracic region (at level of T10),
suspicious of acute mediastinitis due to leaking
from the lower oesophagus.
Case 3
 EOT was done:
1.5 cm x 0.5 cm perforation at left side of lower
oesophagus at T10 level
Loculation of ~ 6 ml pus surrounding the
perforation
Case 3
 Esophageal rupture (also known as
Boerhaave's syndrome) is rupture of the
esophageal wall due to vomiting.
Case 3
 56% of esophageal perforations are
iatrogenic, usually due to medical
instrumentation such as an endoscopy.
 Boerhaave's syndrome is reserved for the
10% of esophageal perforations which occur
due to vomiting.
Case 3
 Boerhaave's syndrome is the result of a
sudden rise in internal esophageal pressure
produced during vomiting, as a result of
neuromuscular incoordination causing
failure of the cricopharyngeus muscle to
relax.
Case 3
 In most cases of Boerhaave's syndrome, the
tear occurs at the left postero-lateral aspect
of the distal esophagus and extends for
several centimeters.
 It is associated with high morbidity and
mortality.
 The mortality of untreated Boerhaave
syndrome is nearly 100%.
Case 3
 The diagnosis of Boerhaave's syndrome is
suggested on the plain chest radiography
and confirmed by chest CT scan.
Case 3
 Its treatment includes immediate antibiotics
therapy to prevent mediatinits and sepsis,
surgical repair of the perforation.
Case 4
 M/79
 PMHx: DM, HT, Gout
Case 4
 c/o: persistent right shoulder pain after
sprain while putting on clothes 1 month ago.
 Progressively increase in pain
 No systemic symptoms
 Treated by bone settor
Case 4
 P/E:
 No swelling or bruises
 non-specific tenderness over the right
shoulder.
 ROM:
Flexion 30
Ext 0
Abd 30
Case 4
Case 4
Case 4
Case 4
 PSA 329
 CT right shoulder:
Bony sclerosis with irregularity at the bony
outline is seen at the right scapula, involving its
body, glenoid process, acromion and coracoid
process.
Case 4
Case 4
 TRUS Bx:
Adenocarcinoma
Gleason score 9 (4+5)
Extensive involvement
Case 4
 Dx: Ca prostate with extensive bone mets
 Rx:
Pt. refused orchidectomy
For palliative RT and hormonal therapy
Sclerotic lesions of bone
 Mnemonic = VINDICATE
Sclerotic lesions of bone


Generic Differential Diagnosis of Sclerotic Bone Lesions
Vascular
 hemangiomas
 infarct

Infection
 chronic osteomyelitis

Neoplasm
 primary
 osteoma
 osteosarcoma
 metastatic
 prostate
 breast
 other
Sclerotic lesions of bone
 Drugs
 Vitamin D
 fluoride
 Inflammatory/Idiopathic
 Congenital
 bone islands
 osteopoikilosis
 osteopetrosis
 pyknodysostosis
Sclerotic lesions of bone
 Autoimmune
 Trauma
fracture (stress)
 Endocrine/Metabolic
hyperparathyroidism
Paget's disease
Case 5
 M/22
 Good past health
 Renovation worker
 Chronic smoker, chronic drinker
Case 5
 c/o: NPU x 1/7
Both LL numbness x 2/7
Unsteady gait
URTI x 4/7
Myalgia +
Constipation +
LBP –
Trauma –
Recreational drug -
Case 5
 P/E: GC sat.
Back no tender spot
Power
Hip
Knee
Ankle
R
L
5
4+
3+
5
43-
Case 5
Bil. LL increase muscle tone
Hyper-reflexia +
Bil. ankle clonus
Bil. LL mild impaired light touch sensation up to
L1
PR  weak anal tone
Unsteady gait
Chest, CVS, Abdo . Unremarkable.
Case 5
 Bladder scan 675ml
 Foley to BSB
 CXR  NAD
 AXR  faecal loaded bowel
 Admitted Medical x ? Multiple sclerosis
Case 5
 After admission:
? Cord compression,
DDx: transverse myelitis
Case 5
 LP:
Normal cell count
Mild raised TP 0.53
Glucose 3.4
Case 5
 Orthopaedics consulted:
MRI spine with contrast :
 T11 enhancing intramedullary nodule ~ 0.4 cm
associated with extensive cord oedema and
evidence of previous hemorrhage. Overall features
favour an intramedullary tumour such as
ependymoma.
Case 5
 Dexamethasone was started
 Neurosurgery was consulted and took over
 Gradual improvement in symptoms and
signs.
 Started walking exercise 2 days after dexa.
 Dexa was tailed down on day 5.
 Planned MRI and MRA/V study for T-L spine 6 weeks later.
 On 26-10-2011
Causes of Spinal Cord Compression
 1. Vertebral
 2. Outside the dura
 3. Within the dura but extramedullary
 4. Intramedullary
Causes of Spinal Cord Compression
 1. Vertebral
Spondylosis
Trauma
Prolapse of a disc
Tumour
Infection
Causes of Spinal Cord Compression
 2. Outside the dura
Lymphoma, metastases
Infection – e.g. abscess
Causes of Spinal Cord Compression
 3. Within the dura but extramedullary
Tumour – e.g. meningioma, neurofibroma
Causes of Spinal Cord Compression
 4. Intramedullary
Tumour – e.g. glioma, ependymoma
Syringomyelia
Haematomyelia
Transverse myelitis
 a neurological disorder caused by an
inflammatory process of the spinal cord, and
can cause axonal demyelination.
Transverse myelitis
 arises idiopathically following infections or
vaccination, or due to multiple sclerosis.
One major theory posits that immunemediated inflammation is present as the
result of exposure to a viral antigen.
Transverse myelitis
 involve the spinal cord typically on both
sides
 onset is sudden and progresses rapidly in
hours and days
 can be present anywhere in the spinal cord,
though it is usually restricted to only a small
portion.
Transverse myelitis
 DDx:
compression of the spinal cord in the spinal
canal
dissection of the Aorta, extending into one or
more of the spinal arteries
 An urgent MRI is thus indicated.
Transverse myelitis
 Symptoms & signs
weakness and numbness of the limbs as well
as motor, sensory, and sphincter deficits
Severe back pain may occur in some patients at
the onset of the disease
depend upon the level of the spinal cord
involved and the extent of the involvement of
the various long tracts
Transverse myelitis
 Prognosis:
Recovery from transverse myelitis usually
begins between weeks 2 and 12 following onset
may continue for up to 2 years in some patients
Some patients may never show signs of
recovery
significant recovery from acute transverse
myelitis is poor in approximately 80% of the
cases
Transverse myelitis
 Treatment:
symptomatic only
corticosteroids being used with limited success
Transverse myelitis
Cord com
TM
Thank you