2. GENERAL APPROACH
Ensure
patient
is
stable
A – Trachea patent?
Trachea central?
Stridor?
B – Equal chest rise?
Tachypnoeic? Accessory
respiratory muscle use?
C – Pink? Pulse volume?
CRT? Hydration status?
D – GCS? Pupils?
Initiate resuscitation if
patient is not stable
Give
oxygen
therapy
Nasal prong
Venturi mask
High flow mask
Intubation & mechanical
ventilation
Keep SpO2 > 95%
Give
analgaesia
Insert 2 large bore IV
branulla (18G, green
branula) and give:
Paracetamol
Fentanyl
Tramadol
Morphine
3. FOCUSED HISTORY
• Age, gender
• Chest pain - SOCRATES
• Associated Sx
• Past medical / surgical Hx
• Family Hx
• Social Hx, risk factors
• Allergies
PHYSICAL EXAMINATION
• General appearance, vital signs
• Chest exam:
• Inspection (deformity, scars,
heaves, tachypnea, work of
breathing)
• Palpation (tenderness, apex beat,
crepitus)
• Percussion (dullness, resonance)
• Auscultation (murmurs, gallops,
breath sounds, air entry,
crepitation)
• Extremities: swelling / edema,
pulses
5. ACUTE CORONARY SYNDROME
• Heart disease is number 1 killer in
Malaysia
• Can be divided into:
• Unstable Angina
• Non-ST elevated MI
• ST- elevated MI
• STEMI mortality in Malaysia:
• In-hospital mortality: 10.6%
• 30-daymortality:12.3%
• 1-year mortality: 17.9%
11. General Treatment for ACS:
• Give analgaesia & oxygen support as required
• Medication:
• Sublingual GTN 1/1 STAT, then PRN
• T Aspirin 300mg STAT, then 150mg OD
• T Clopidogrel 300mg STAT, then 75mg OD
• S/C Fondaparinux 2.5mg STAT, then 2.5mg OD
Thrombolytic therapy for STEMI:
• IV Streptokinase 1.5 million units in 100cc NS over 1 hour
• IV Alteplase (rtPA) 15mg bolus, followed by 50mg over 30 minutes, then
35mg over 60 minutes
• IV Tenecteplase 30-50mg over 5 seconds
• Contraindicated in patients with risk of bleeding / intra-cranial haemorrhage
12. Primary PCI for STEMI:
• In Kuala Lumpur, MYSTEMI Network
(previously HISNET) provides spoke-
hub connection for pPCI
• Indication:
• Chest pain or ischeamia < 12 hours onset
• Persistent ST-elevation in > 2 contiguous
leads
• Rescue PCI in patients that failed /
contraindicated for thrombolytic therapy
• Contraindications:
• Previous intra-cranial haemorrhage
• Intra-cranial vascular or malignant lesion
• Ischaemic stroke < 3 months
• Sustained hypertension; SBP > 180, DBP >
110
• Active bleeding, bleeding diathesis
• Major trauma < 3 months Aim: Door-To-Balloon time < 90 minutes
13. Ref: Impact of Regional STEMI Network on Patient Outcomes in Malaysia; presentation, NHAM Congress 2019
14. Ref: Impact of Regional STEMI Network on Patient Outcomes in Malaysia; presentation, NHAM Congress 2019
15. CARDIAC TAMPONADE
• Excessive fluid accumulation in the
pericardium causing compression of
all cardiac chambers leading to:
• Impaired cardiac filling and compromised
cardiac output
• Resultant myocardial ischaemia from
epicardial coronary artery compression
• Risk factors:
• Malignancy, infective pericarditis,
cardiothoracic surgery, post-coronary
intervention, post-MI, connective tissue
disorders, iatrogenic
16. Symptoms and Signs
• Left sided chest pain
• Palpitations, SOB
• Tachycardia
• Narrow pulse pressure
• Cyanosis
• Beck’s Triad
• Hypotension, distended
jugular vein, muffled heart
sounds
Factors Leading To
Cardiac Tamponade
• Rate of pericardial fluid
accumulation
• Amount of fluid in pericardium
• Pericardial compliance
17. ECG changes in
Cardiac Tamponade:
• Sinus tachycardia
• Electrical alterans
• Low QRS voltage
CXR in Cardiac Tamponade:
CXR: globular heart
19. Pericardiocentesis for Cardiac Tamponade:
• Subxiphoid approach:
• A long 18-22 G needle attached to syringe is inserted between
xiphisternum and left costal margin
• Direct needle towards the left shoulder at 40° angle, with
continual aspiration as needle approaches RV
• Once pericardial fluid aspirated, insert cannula into pericardial
space
• Attach a 3 way tap and remove fluid as required
• Complications:
• Myocardial perforation
• Pleeding
• Pneumothorax, pneumopericardium
• Arrhythmia
• Acute pulmonary edema (due to rapid drainage of pericardial
fluid leading to excessive LV preload)
• Acute ventricular dilatation
20. TENSION PNEUMOTHORAX
• Air is forced into the pleural space with no means of
escape, eventually collapsing the affected lung
• Mediastinum is displaced to the opposite side,
decreasing venous return and compressing the
contralateral lung.
• Shock (often classified as obstructive shock) results from
marked decrease in venous return, causing a reduction in
cardiac output.
• Tension pneumothorax is a clinical diagnosis, don’t wait
for CXR to start treatment.
• Risk factors:
• Spontaneous (tall, thin, male, marfanoid)
• Secondary to underlying respiratory condition
• Penetrating trauma
21. Symptoms and Signs
• Chest pain
• Tachypnea
• Respiratory distress
• Tachycardia
• Hypotension
• Tracheal deviation away from
the side of the injury
• Unilateral absence of breath
sounds
• Neck vein distention
• Hyperresonant on percussion
Risk Factors
• Spontaneous (tall, thin, male,
marfanoid)
• Secondary to underlying
respiratory condition
• Penetrating trauma
24. PULMONARY EMBOLISM
• Usually arise from venous thrombosis in the pelvis or legs
• Other causes:
Ø Right ventricular thrombus (post MI)
Ø Septic emboli (right sided endocarditis)
• Risk factors:
Ø Recent surgery; especially abdominal/pelvic or hip/knee
replacement
Ø Leg fracture
Ø Prolonged bed rest/reduced mobility
Ø Malignancy
Ø Pregnancy/postpartum
Ø Previous PE
25. Symptoms and Signs
• Dyspnoea of sudden onset
• Chest pain (pleuritic or substernal)
• Haemoptysis
• Syncope
• Tachypnoea
• Tachycardia
• Hypotension
• Raised JVP
Pulmonary Embolism History Vascular Obstruction Presentation
Acute minor Short, sudden onset <50% Dyspnoea with or without
pleuritic chest pain and
haemoptysis
Acute massive Short, sudden onset >50% Right heart strain with or
without haemodynamic
instability and syncope
Subacute massive Several weeks >50% Dyspnoea with right heart
strain
26. Wells Criteria for Pulmonary Embolism
Criteria Points
Clinical evidemce of DVT +3
PE is #1 diagnosis or equally likely +3
Heart rate >100 +1.5
Immobilization at least 3 days OR
surgery in the previous 4 weeks
+1.5
Previous, objectively diagnosed PE
or DVT
+1.5
Haemoptysis +1
Cancer +1
• Low risk (< 2 points:1.3% incidence PE):
Ø consider d-dimer testing to rule out Pulmonary
embolism.
Ø If the d-dimer is negative consider stopping workup.
Ø If the d-dimer is positive consider CTA.
• Moderate risk (2 - 6 points, 16.2% incidence of PE):
Øconsider high sensitivity d-dimer testing or CTA.
Ø If the d-dimer is negative consider stopping workup.
Ø If the d-dimer is positive consider CTA.
• High risk (score > 6 points: 37.5% incidence of PE):
consider CTA. D-dimer testing is not recommended.
27. Investigations
• ECG:
Ø In minor PE: sinus tachycardia
Ø In acute or subacute massive PE evidence of right
heart strain may be seen:
vRightward shift of the QRS axis
vTransient right bundle branch block
vT-wave inversion in leads V1-V3
vP pulmonale
Ø S1Q3T3 changes
• Arterial Blood Gas:
Ø Reduced PaO2 and a PaCO2 that is normal or
reduced
• D-Dimer; can be raised but non-specific
28. • Chest X-Ray (CXR):
ØTo rule out other conditions mimicking PE (e.g. pneumothorax, pneumonia, left heart failure,
tumour, rib fracture, massive pleural effusion and lobar collapse)
ØMay show the following:
vNormal CXR (~40%) – a normal film in a patient with severe acute dyspnoea without
wheezing is very suspicious of PE
vFleischner sign (distended central pulmonary artery due to the presence of a large clot)
vHampton’s hump (pulmonary infarction)
vWestermark sign (focal pulmonary oligaemia)
vFleischner lines (long bands of focal atelectasis)
• Computed Tomography Pulmonary Angiogram (CTPA):
ØGold standard
ØFilling defects
29.
30. • Bedside ECHO in PE:
ØRight ventricle can be dilated and have
reduced function or contractility
ØRight atrium can be dilated
ØLeft ventricle can be underfilled and
hyperdynamic
ØMc Conell’s Sign: right ventricular free
wall akinesia with sparing of the apex.
ØD-shaped left ventricle: right ventricle
strain
31. • Give Thrombolytic (alteplase)
• Suspected PE: give IV heparin
• In cases of massive PE with signs of haemodynamic instability
ØGive oxygen via non rebreather mask or intubate if unable to maintain
oxygenation
ØCan start inotropes if BP is still low despite fluid resuscitations
ØGive pain relief medications
Management
32. AORTIC DISSECTION
• Due to intimal tear, intramural
hematoma or separation of tunica
media à forming a false lumen
• Risk factors: hypertension,
atherosclerosis, smoking, pregnant,
connective tissue diseases (Marfan
syndrome, giant cell arthritis)
• Locations:
• Ascending aorta (65%)
• Aortic arch (10%)
• Descending aorta (20%)
33. Clinical Presentation
• Sudden onset excruciating
chest pain
• Tearing in nature, radiating to
the back
• Migratory pain from chest to
lower limbs
• Ischemia Lower Extremities
from Aortic Dissection, ILEAD)
• DDx: MI, Lower limb ischemia,
stroke, pnuemonia
General Approach
• A – secure airway, patient might present
unconscious due to spontaneous
bleeding
• B – For oxygen therapy if not saturating
well
• C – to optimize BP or resuscitate, might
be discrepancy of BP on both side,
check for radio-radial delay, look for
heart murmur (aortic regurg), check for
pulse pressure, look for Beck’s Triad,
insert CBD ensure UO >0.5
• D – GCS, pupil
• E – ECG, mimic MI, might complicate
with MI (but not true MI – CI for DAPT
and anticoag therapy), adequate
analgesia
34. Blood Investigations
• FBC – look for Hb drop
• RP – AKI, if dissection
involving renal arteries
• Coag – bleeding tendency,
pre-op bloods
• GXM 4 pint – pre-op bloods
• Cardiac enzymes
• VBG – might be complicated
with abdominal ischemia
Radiographic Investigations
• CXR
• POCUS
• CT Angiogram (gold standard)
35. CXR Findings in
Aortic Dissection
• Widened mediastinum > 8cm at
aortic knob level on AP film
• Extension of aortic shadow >
5mm from its calcified wall
• eggshell/calcium sign, most specific
• Double à obscure à loss of
aortic knob
• Deviation Esophagus and trachea
to right side
• Depression of Left main bronchus
140*
• Increased thicness of left and
right paratracheal stripe
38. Management Goal
If patient is relatively stable (not
in hypovolemic shock)
• to reach lowest BP/HR possible while
maintaining organ perfusion
• IVI Labetolol
• For pain management
If patient is in shock, for
resuscitation
• To keep MAP > 70
• To expedite surgical intervention if
possible
Specific Managements
Stanford A
• no role for endovascular repair
• urgent referral to cardiothoracic surgery
Standford B
• possible for endovascular repair if
• Complicated with rupture,
ischemia, pain, uncontrolled
hypertension
• Progression of dissection
• Otherwise, medically managed
39. PERFORATED PEPTIC ULCER DISEASE
• Acid peptic damage to
gastro-duodenal mucosa à
erosion à exposure of
underlying tissue to gastric
secretions
• Bleeding
• Perforated
• Risk factor: NSAID, H Pylori
infection, alcoholism
• >2cm : giant peptic ulcer
40. Clinical Presentation
• Upper abdominal pain or lower
chest pain
• Burning sensation
• assoc with nausea and vomitting
• Poor oral intake, tiredness,
giddiness
• Might preset with coffee ground
vomit and melena
• Peritonitis, but may not be in
contained leak
• Unable to differentiate gastric
and duodenal ulcers from hx
General Approach
• Oxygen theraphy
• KNBM with IVD NS / 24H
• Decompression with NGT
• IV broad spectrum antibiotics
(polymicrobial)
• High dose IV PPI – to stabilize clot
• IV Esomeprazole 80mg stat
• IVI Esomeprazole 8mg/H for next 72
hours
• For urgent OGDS
41. Radiographic Findings
• Xray sensitivity in literature ranging
30-85%
• Due to high variability, negative CXR
cannot rule out PGU
• If clear evidence of peritonitis or high
suspicion, proceed wit CT Abdomen
• CXR Sitting or Lying may not reveal air
under diaphragm à false negative
• USG Abdomen may reveal
intraperitoneal collection
42. Definitive management
If stable, and no radiological sign of leak
• for conservative management
If evidence of leak, patient stable
• for endoscopic repair
• Insufflaxation causes hypercapnia and increased intraab pressure
• Increased SVR, reduced venous return, reduced stroke volume, reduced pH
If patient unstable, for op
43. PANCREATITIS
• Acute inflammation of pancreas
with histologically acinar cell
destruction
• Common causes (I GET SMASHED):
• Idiopathic
• Gallstones
• Ethanol
• Trauma
• Steroids
• Mumps/Malignancy
• Autoimmune
• Scorpion sting
• Hypertriglyceride,
Hypercalcemia
• ERCP
• Drugs (HCTZ,
Bactrim,
Azathioprine)
44. Clinical Presentation
• Abdominal pain (epigastrium)
or lower chest pain
• Excruciating, deep,
penetrating to back
• Exacerbated with oral intake,
esp alcohol
• Patient restless
• Nausea, vomitting
General Approach
• Oxygen therapy if required
• KNBM with IVD NS / 24H
• NGT insertion if ileus / persistent vomiting
• IV Analgesia
• IV antibiotics - controversial
• FBC, RP, Ca, LFT, Coag, Amylase/Lipase,
Triglyceride, GXM
• ECG, CXR Erect
• USG – assess GB, Billiary tree, look for
stones, sludge
• CT Abdomen if Dx uncertain
• All severe acute pancreatitis will require CT
Abdomen 72H after symptoms to assess
peripancreatic necrosis
45. • HCT > 44: risk for pancreatic necrosis
• Urea > 20: increased increased mortality
• CRP >150 at 72H: severe acute pancreatitis
• Amylase: isoenzymes found in pancreas and salivary glands, rises in 6
– 24H, peaks at 48H, normalizes 3 – 7 days later
• Lipase: more specific to pancreas, rises in 4 – 8 hours, peaks at 24H,
normalizes 8 – 14 days later
• In the absence of Gallstone, and no history of alcohol use, Triglyceride
level > 11.3 mmol/L can be considered as the cause of pancreatitis
46. Ranson Criteria
(admission)
• G – Gluc > 10mmol/L
• A – Age > 55
• L – LDH > 350
• A – AST > 250
• W – WBC > 16k
Ranson Criteria
(48 hours)
• C – Ca <2mmol
• H – HCT drop > 10%
• O – PO2 < 60
• B – BE > 4
• B – BUN inc > 5
• S – Fluid needed > 6L
47. Atlanta Criteria
(diagnosis)
Requires two of of the following:
• Abdominal pain suggestive of
acute pancreatitis
• Serum lipase/amylase 3x normal
upper limit
• Radiological findings (CT or TAS)
• Evidence of bilestones
• Pancreatic inflammation
• Peripancreatic fat
• Peripancreatic fluid collection
• Retroperitoneal air
• Non-enhancement of pancreas
(necrosis)
Atlanta Classification
Mild Acute Pancreatitis
• Interstitial edematous pancreas
• No organ failure, no other complication
• Resolves within 1 week
Moderately Severe AP
• Transient organ failure <48H
Severe AP
• Persistent organ failure >48H
• May be infected with peripancreatic
necrosis
49. REFERRENCES
• Sarawak Handbook of Medical Emergencies, 4th Edition, 2019
• Malaysian STEMI CPG, 2019
• Shirley Ooi, Guide to The Essentials in Emergency Medicine
• 2010 ACCF/AHA Guidelines for the Diagnosis and Management of Patients
with Thoracic Aortic Disease
• Tarasconi et al, Perforated and bleeding peptic ulcer: WSES guidelines,
World Journal of Emergency Surgery (2020) 15:3
• Leppaniemi et al, 2019 WSES guidelines for the management of severe
acute pancreatitis, World Journal of Emergency Surgery (2019) 14:27
• Radiopaedia.org