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APPROACH TO
CHEST PAIN
• HO Nazim
• HO Hakimi
• HO Muhaimin
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
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
Investigations
ECG:
• Arrhythmia
• Ischaemic changes
Bloods:
• FBC
• RP, electrolytes
• TropT, CK, CK-MB
• ABG
CXR:
• Pneumothorax
• Widened mediastinum
POCUS
LIFE THREATENING
CAUSES OF CHEST PAIN
• Acute Coronary Syndrome
• Cardiac Tamonade
• Pulmonary Embolism
• Tension Pneumothorax
• Aortic Dissection
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%
Symptoms
• Left sided chest pain (heavy
/ crushing)
• Left sided neck / UL
numbness
• Palpitations, SOB
• Nausea / vomiting,
diaphoresis
• Worse on exertion
• Relieved with rest
Signs
• General: diaphoretic, pale, cool
• CVS: tachycardia, arrhythmia,
murmur, 4th heart sound,
jugular vein distension
• Lungs: crepitation
(acute pulmonary oedema)
• Extremities: LL pitting oedema
• Levine’s sign
ECG changes for ACS:
• ST-segment changes
(elevation / depression) >
0.05 mV
• T-wave inversion > 0.2 mV
• New LBBB
• Pathologic Q-wave
(previous MI)
• Posterior MI: tall R-waves
in V1 with ST-depression
Cardiac Biomarkers In ACS: POCUS in ACS:
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
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
Ref: Impact of Regional STEMI Network on Patient Outcomes in Malaysia; presentation, NHAM Congress 2019
Ref: Impact of Regional STEMI Network on Patient Outcomes in Malaysia; presentation, NHAM Congress 2019
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
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
ECG changes in
Cardiac Tamponade:
• Sinus tachycardia
• Electrical alterans
• Low QRS voltage
CXR in Cardiac Tamponade:
CXR: globular heart
POCUS in Cardiac Tamponade:
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
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
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
Radiographic Evidence of Tension Pneumothorax:
Treatment
Supportive:
• Oxygen
• Analgaesia
Definitive:
• Needle thoracostomy
• Finger thoracostomy
• Chest tube insertion (22F)
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
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
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.
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
• 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
• 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
• 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
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%)
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
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)
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
POCUS in Aortic Dissection
CT Angiogram in Aortic Dissection
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
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
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
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
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
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)
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
• 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
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
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
Peripancreatic Necrosis
Acute Necrosis Collection (ANC)
• First 4 weeks
• Fluid, pancreatic necrotic tissue
Walled-Off Necrosis (WON)
• After 4 weeks
• Matured
• Well-defined, enhancing
inflammatory wall
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
THANK YOU

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Approach to chest pain

  • 1. APPROACH TO CHEST PAIN • HO Nazim • HO Hakimi • HO Muhaimin
  • 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
  • 4. Investigations ECG: • Arrhythmia • Ischaemic changes Bloods: • FBC • RP, electrolytes • TropT, CK, CK-MB • ABG CXR: • Pneumothorax • Widened mediastinum POCUS LIFE THREATENING CAUSES OF CHEST PAIN • Acute Coronary Syndrome • Cardiac Tamonade • Pulmonary Embolism • Tension Pneumothorax • Aortic Dissection
  • 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%
  • 6. Symptoms • Left sided chest pain (heavy / crushing) • Left sided neck / UL numbness • Palpitations, SOB • Nausea / vomiting, diaphoresis • Worse on exertion • Relieved with rest Signs • General: diaphoretic, pale, cool • CVS: tachycardia, arrhythmia, murmur, 4th heart sound, jugular vein distension • Lungs: crepitation (acute pulmonary oedema) • Extremities: LL pitting oedema • Levine’s sign
  • 7.
  • 8. ECG changes for ACS: • ST-segment changes (elevation / depression) > 0.05 mV • T-wave inversion > 0.2 mV • New LBBB • Pathologic Q-wave (previous MI) • Posterior MI: tall R-waves in V1 with ST-depression
  • 9. Cardiac Biomarkers In ACS: POCUS in ACS:
  • 10.
  • 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
  • 18. POCUS in Cardiac Tamponade:
  • 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
  • 22. Radiographic Evidence of Tension Pneumothorax:
  • 23. Treatment Supportive: • Oxygen • Analgaesia Definitive: • Needle thoracostomy • Finger thoracostomy • Chest tube insertion (22F)
  • 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
  • 36. POCUS in Aortic Dissection
  • 37. CT Angiogram in Aortic Dissection
  • 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
  • 48. Peripancreatic Necrosis Acute Necrosis Collection (ANC) • First 4 weeks • Fluid, pancreatic necrotic tissue Walled-Off Necrosis (WON) • After 4 weeks • Matured • Well-defined, enhancing inflammatory wall
  • 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