ED - Lectures Flashcards
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Give differentials for abdominal pain.
- 5 RUQ?
- 4 LUQ?
- 7 LLQ?
- 7 RLQ?
- 4 Epigastric?
- 4 Periumbilical?
- NSAIDs given = increased risk of perforation.
- Free air under the diaphragm
- Next Steps = ABCDE approach
- Call the surgical reg = emergency
- Nil by mouth
- IV fluids
- Pain relief = IV fentanyl/morphine
- Ixs = G+H, FBC
- Abx - eTg = Triple therapy for intra-abdominal sepsis
- Large bore IV cannulas = Orange (14) or Grey (16)
- Disposition = Surgical team & anaesthetist & maybe contact ICU
Differentials?
Ixs?
Case 2 – 55M diabetic fever, upper abdominal pain
- Peptic ulcer disease
- MI
- DKA
- Pancreatitis
What is Charcot’s Triad?
What is Reynold’s Pentad?
What is Murphy’s sign?
Charcot’s Triad = Acute Cholangitis
1. Fever
2. RUQ pain
3. Jaundice
Reynold’s Pentad = Charcot’s Triad + Confusion + Hypotension
Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.
- 2 Causes of Upper GIT Bleeding?
- 4 Causes of Lower GIT Bleeding?
- Specific Management for this patient?
Hx
- Alcoholic? = Portal hypertension, liver doesn’t make clotting factors, marrow suppressed (platelets), gastritis
- Collapsing after opening bowels = really low volume status
- Bilirubin UP
Causes of Upper GIT Bleeding
1. Gastric ulcer
2. Duodenal ulcer
Causes of Lower GIT Bleeding
1. Diverticulitis = LLQ
2. Haemorrhoids
3. Polyps/Adenocarcinoma
4. Angiodysplasia
Specific Management
* 80mg Esomeprazole daily
* TXA? = Tranexamic acid – benefit for upper GI bleed??
What are the 6 colour codes of cannulas - their gauge and their max flow rates?
Case 4 – Upper abdo pain (extra-abdominal cause)
Inferior STEMI - ST elevation in leads II, III, aVf & Reciprocal changes in leads ….= Right coronary but also could be circumflex
- Consider AV node may be affected with inferior MIs = complete heart block
- ST elevation in avR could be severe triple vessel disease or left main occlusion.
Tx = MONA & Revascularisation: PCI or thrombolysis, clexane vs. heparin, & dual-antiplatelet therapy
- 300mg loading aspirin
Case 5 – 33 Female presents with 3 hours of severe flank pain.
- 5 Ddx?
- Immediate tx approach?
- Which ixs?
- Which 4 patients with ureteric colic should you not send home?
- Meds & follow-up?
Ddx
1. Pyelonephritis
2. Nephrolithiasis
3. Ruptured ectopic
4. Adnexal torsion
5. Appendix
Immediate tx = ABCDE approach - Give analgesic (NSAIDs, opioids) & anti-emetic (IV or rectal)
Ixs = Imaging - Ultrasound or CT abdo/pelvis
Don’t send home if ureteric colic AND:
1. Pregnant
2. Only 1 kidney
3. Poor kidney function
4. Infected & obstructed
What are the 3 common sites of kidney stone impaction/obstruction?
- The ureteropelvic junction (UPJ)
- The pelvic brim = where the iliac arteries cross the ureters.
- The ureterovesical junction (UVJ)
- What features on history would make you concerned?
- What are your treatment priorities with confirmed bowel obstruction?
Case 6 – 62M 4 days of Constipation
What features on history would make you concerned?
- Bilious
- Copremesis = fecal matter = Bowel obstruction
- Small bowel obstruction features vs. large bowel on abdo xray – 3, 6, 9 rule
What are your treatment priorities with confirmed bowel obstruction?
Check your magnesium too
Diagnosis?
(ECG shows irregular rhythm)
- When pain is out of keeping with the clinical exam what 2 dx should you consider?
Irregular rhythm on ECG - AF throwing off clots
Hypoperfusion/Ischaemia – Lactate >2 abnormal
Ddx = Mesenteric ischaemia? Aortic syndrome? Dissection?
Causes of mesenteric ischaemia
1. Embolism (40-50%)
2. Thrombosis (25-30%)
3. Non-occlusive = low-flow (10-15%)
Pain out of keeping with the clinical exam?
1. Cellulitis & Necrotising fasciitis
2. Fractures & Compartment syndrome
= Functional abdominal pain
Spot Diagnosis?
= DKA (Severe if pH<7) & remember K+ (When K+<5.5 give it!)
If someone presents with chest pain and neurological symptoms, what is the diagnosis until proven otherwise?
Anyone with chest pain + neurological sxs = dissection until proven otherwise!
- If you dissect up – carotids = stroke
- Dissect down – numbness & loss of pulses in lower limbs
- Be mindful you can dissect in to the coronary arteries which will show a STEMI on the ECG
Interpret the ECG.
- Complications?
- Treatment?
= Big anterolateral STEMI – LAD – Left Ventricle
- Anterior = V4,5
- Leads I & aVL = lateral
- Q waves in V2 + V3 = suggests MI in the past
- Complications = progression to VF & Arrest/Death, Cardiogenic shock – HR goes up because you panic & vicious cycle
Tx – PCI or thrombolysis – CATH LAB ASAP!
- MONA = Morphine, Oxygen, Nitrates, Anti-platelet
- Nitrates = veins & arteries dilate = decrease preload & afterload
- De-fib pads on!
What is the diagnosis? Which vessel? Complications? Would you give nitrates?
- ST elevation in II, III & aVF = Inferior MI – Right Coronary or Circumflex & risk of AV/SA node pacemakers cells
- Complications = heart block - Look at HR & PR interval on ECG to check for block
- Reliant on venous return when contractility of RHS fails therefore need to be very mindful of giving nitrates!
o You will see the BP drop
Diagnosis?
- What type of arrythmia is it?
6 ECG features?
Atrial flutter = type of SVT
Diagnosis?
- Possible cause?
- Mobitz Type II Heart block = A form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR interval
- Not complete heart block
- Often candidate for pacemaker
- Amiodarone can be a cause
Diagnosis?
- 5 ECG features?
- Hyperkalaemia = big tall T waves (repolarisation)
- Abnormalities in Na+ = QRS changes
ECG features of hyperkalaemia
1. Peaked T waves
2. P wave widening/flattening, PR prolongation
3. Bradyarrhythmias: sinus bradycardia, high-grade AV block with slow junctional and ventricular escape rhythms, slow AF
4. Conduction blocks (bundle branch block, fascicular blocks)
5. QRS widening with bizarre QRS morphology
Diagnosis?
Severe Hyperkalaemia: Sine wave appearance with severe hyperkalaemia (K+ 9.9 mEq/L).
Diagnosis?
- 9 Causes?
- QT Prolongation: Apparent QTc 500ms
- There are prominent U waves in precordial leads
- Cause: Hypokalaemia (K of 1.9)
- Hypokalaemia causes apparent QTc prolongation in the limb leads (due to T-U fusion) with prominent U waves in the precordial leads.
Diagnosis?
Give magnesium!
Diagnosis?
Supraventricular tachycardia (SVT): Rhythm strip demonstrating a regular, narrow-complex tachycardia
Diagnosis?
- VT usually goes into VF
- Tx = Cardioversion = pacing chemical cardioversion w/amiodarone & mechanical
Diagnosis?
Causes?
Sodium channel blockage
- Sinus tachy (HR100bpm), normal QRS (maybe slightly long),
- aVR points down – normal that it points the wrong way
- aVR is pointing up in this ECG = very normal = check lead placement first!!
- Causes = TCAs – usually OD’d – cause tachycardia & slurring of QRS & dominant R wave
Cardiac Physiology
- What is the equation for Arterial blood pressure/MAP?
- What is the equation for Cardiac Output?
- What is the equation for SV?
- What determines LV size?
Heart Failure
- Definition?
- 2 Types?
- Pathophysiology of the 2 types?
Left Ventricular Failure
- List 10 Causes
- 9 Symptoms?
- 10 Signs?
LVF - Why is it important?
- 480,000 Australians have heart failure
- 10% of >75 years old
- 80% hospitalized when presenting to ED
- 1 yr mortality rate (NYHA III and IV) still 45%
- Quality of life
Outline the general components of treatment for Left Ventricular Failure.
- 3 Complications?
- List 11 Precipitants of Acute LVF?
LVF - Treatment
1. Investigate (ECHO, ECG, CXR)
2. Treat failure (reduced or preserved EF) – ACE, diuretics, b-blockade, spironolactone etc..
3. Treat cause
4. Treat complications = Acute decompensation (LVF), Pulmonary oedema, Arrythmias (AF / flutter / VT)
Acute left ventricular failure
(acute decompensated heart failure)
- 5 Symptoms?
- 7 Signs?
Acute Pulmonary Oedema
- What is it?
- 10 S&S?
- Pathophysiology?
Acute pulmonary oedema = Left ventricular failure in its most extreme form = A Life threatening emergency.
1. Anxious
2. Diaphoretic
3. Pale and cold peripherally
4. Tachypnoea (often >35)
5. Tachycardia (often >130)
6. Hypoxia
7. Hypertensive (can be >200 systolic)
8. Crackles throughout chest
9. ?rasied JVP
10. ?peripheral oedema
6 Goals of Therapy?
List 6 investigations would you order.
Goals of therapy
1. Resuscitation if required
2. Investigate underlying cause and severity of failure
3. Treat heart failure
4. Treat cause of deterioration
5. Treat complications of illness
6. Determine appropriate and safe disposition
Ixs
1. VBG - looking at lactate & respiratory faiilure (hypoxia)
2. ECG - looking for infarct & arrhythmias
3. CXR - looking for fluid & heart size
4. FBC - Hb?
5. U&Es - renal function
6. Troponin
APO - Case 1
75 F, BIBA, 2 day history of worsening SOB, intermittent palpitations and markedly decreased exercise tolerance, Background of previous NSTEMI, diabetes, hypertension. Takes Ramipril 5mg, Aspirin 100mg, Metoprolol 25mg BD, statin, frusemide 20mg.
O/E: Speaking in short sentences, Normal colour, RR 20, sats 94%, HR95, BP 167/100, Afebrile, Warm peripherally, JVP slightly elevated, Chest - few crackles at the bases bilaterally, No peripheral oedema.
Interpret her CXR? - 8 features of APO on CXR?
- NO air bronchograms or pleural effusions in this case
APO - Case 1
75 F, BIBA, 2 day history of worsening SOB, intermittent palpitations and markedly decreased exercise tolerance, Background of previous NSTEMI, diabetes, hypertension. Takes Ramipril 5mg, Aspirin 100mg, Metoprolol 25mg BD, statin, frusemide 20mg.
O/E: Speaking in short sentences, Normal colour, RR 20, sats 94%, HR95, BP 167/100, Afebrile, Warm peripherally, JVP slightly elevated, Chest - few crackles at the bases bilaterally, No peripheral oedema.
Interpret her ECG? How would you manage this patient?
ECG
- Rate: 102
- Rhymth: irregularly irregular
- Axis; normal
- DX: AF
Mx
- O2 Aim for sats over 94%
- GTN 400mcg sublingual
- IV Frusemide - 40mg (usually give double what they’re on)
- Ixs & Treat AF: CHADS-VAS & anticoagulant
- Admit - needs O2 & cause of deterioration
APO Case 2
80 M, BIBA as a priority, Sudden onset severe dyspnoea which woke him from his sleep. Background diabetes and hypertension. Takes Ramipril 10mg, Aspirin 100mg, metformin 500mg BD, statin. Lives at home, otherwise fit/healthy
O/E: Unable to speak, Pale, clammy, cold. RR 34, sats 86% on 10L NRBM, HR145, BP 207/100, Afebrile, JVP not seen, Coarse crackles throughout his chest. No peripheral oedema, No murmurs.
- 7 Goals of Therapy?
- Interpret the CXR?
- Management?
Goals of therapy
1. Resuscitate
2. Investigate underlying cause
3. Treat pulmonary oedema
4. Treat cause of deterioration
5. Treat complications of illness
6. Determine appropriate and safe disposition
7. Determine goals of care
CXR
- Cardiomegaly
- Increased cardiothoracic ratio
- Widespread pulmonary oedema - revise features
Ventilation
- What is CPAP - What 3 things does it do? When is it indicated? Contraindications?
- What is Bi-level positive airway pressure? Is it better than CPAP in APO from acute LVF?
APO Case 3
60 M, BIBA as a priority, Sudden onset severe chest pain and subsequent dyspnoea. Background hypertension. Takes Ramipril 5mg. Lives at home, otherwise fit/healthy.
O/E: Speaking short sentences, Clammy and cold peripherally. RR 28, sats 92% on 15L NRBM, HR 130, BP 89/56, Afebrile, JVP raised, Coarse crackles throughout his chest, No peripheral oedema. No murmurs.
- 7 Goals of Therapy?
- Interpret his ECG?
- Management?
Goals of therapy
1. Resuscitate
2. Investigate underlying cause
3. Treat pulmonary oedema
4. Treat hypotension
5. Treat cause of deterioration
6. Treat complications of illness
7. Determine appropriate and safe disposition
ECG
- Tachycardia
- Regular
- P waves present = sinus
- ST depression anterolateral leads - widespread
- Dx: LAD disease
Outline the different types of diabetic emergencies?
Hypoglycaemia
- Definition?
- Signs & symptoms?
- Whipple triad?
- Hypoglycemia in patients with diabetes generally described as ≤ 70 mg/dL (≤ 3.9 mmol/L).
- Hypoglycemia in patients without diabetes: blood glucose level < 55 mg/dL with symptoms of hypoglycemia.
- Whipple triad: helps to confirm the diagnosis of hypoglycemia:
1. Low blood glucose levels
2. Signs or symptoms consistent with hypoglycemia
3. Relief of symptoms when blood glucose increases after treatment
Causes of Hypoglycaemia
- In the diabetic patient?
- In the non-diabetic patient?
- (Relative) overdose of insulin or a noninsulin drug is by far the most common cause of hypoglycemia.
- Consider factitious disorder in patients with access to insulin and other diabetes medications (e.g., healthcare professionals), for whom there is no other obvious explanation for hypoglycemia.
Signs & Symptoms of Hypoglycaemia
- Threshold?
- Which medication can mask it?
- Neurogenic?
- Neuroglycopenic?
Signs and symptoms
Neurogenic/autonomic
1. Increased sympathetic activity: tremor, pallor, anxiety, tachycardia, sweating, and palpitations
2. Increased parasympathetic activity: hunger, paresthesias, nausea, and vomiting
Neuroglycopenic
1. Agitation, confusion, behavioral changes
2. Fatigue
3. Seizure, focal neurological signs
4. Somnolence → obtundation → stupor → coma → death
Outline how excess Insulin & Oral hypoglycaemic agents can cause hypoglycaemia.
- Management?
- MOA of Octreotide?
Hypoglycaemia – Excess Insulin
- Deliberate or accidental
- Relative to need (food intake, exercise)
- Treatment
1. Glucose – IV or oral
2. Glucagon – release endogenous glucose. Can’t repeat endlessly as glycogen stores deplete
3. Determine cause and prevent recurrence
- NOTE: Patients on acarbose won’t respond to sucrose (fruit juice or milk)
- Usually wears off relatively quickly
- Unless long acting or deliberate (massive OD)
- Can usually go home once eaten and returned to normal
What are the 4 effects of Insulin in the body?
- Deficiency?
- Decrease glycogenolysis
- Decrease gluconeogenesis
- Increase glucose utilisation
- Inhibits lipolysis and ketone formation
Hyperglycemic crises - Diabetic Ketoacidosis
- Definition?
- Most important findings?
The most important findings of diabetic ketoacidosis (DKA) are: Delirium/psychosis, Dehydration, Kussmaul respirations, Abdominal pain/nausea/vomiting, fruity (Acetone) breath odor.
Hyperglycemic crises - Diabetic Ketoacidosis
- Pathophysiology?
Hyperglycemic crises - DKA
- Clinical Features?
Specific findings in DKA
1. Rapid onset (< 24 h) in contrast to HHS
2. Abdominal pain
3. Fruity odor on the breath (from exhaled acetone)
4. Hyperventilation: long, deep breaths (Kussmaul respirations)
Hyperglycemic crises - Diagnosis
- Approach?
- Electrolytes & Renal function? (5)
- Additional diagnostic workup?
Electrolytes and renal function
1. Sodium: Hyponatremia is common in both DKA and HHS, due to hypovolemic hyponatremia and hypertonic hyponatremia. Always check corrected sodium for hyperglycemia.
2. Potassium in DKA: normal or elevated (despite a total body deficit)
3. Magnesium levels are typically low.
4. Phosphorus levels may be elevated despite a total body deficit.
5. BUN and creatinine are often elevated.
Severity of DKA?
Hyperglycemic crises - Management
- 4 Principle Interventions?
Principal interventions
1. Fluid resuscitation: initially with isotonic saline (0.9% NaCl)
2. Potassium repletion: for potassium level < 5.3 mEq/L
3. Insulin therapy: initiate short-acting insulin once potassium level is > 3.3 mEq/L
4. Identify and treat precipitating causes (e.g., sepsis).
DKA Management
- Fluids?
- Potassium?
- Insulin - rate? when to cease?
Insulin for DKA
- Check K=>3.5mmol/L
- Infusion of short acting insulin
- 0.1units/kg/hr
- Adjust rate so glucose falls 5mmol/L per hour
- When glucose <15, change fluids to dextrose
- KEEP insulin infusion going until acidosis and ketosis resolves (unless hypoglycaemia occurs)
Hyperglycemic crises - Management
- Fluid resuscitation?
- Acid-base status?
- Electrolyte resuscitation?
Acid-base status
- Acidosis usually resolves with fluids and insulin therapy and the use of IV bicarbonate is usually not necessary.
- If pH < 6.9 despite adequate IV fluid resuscitation, administer IV sodium bicarbonate.
What are the criteria for resolution of:
- DKA?
- HHS?
Compare DKA & HHS?
HHS = Hyperosmolar Hyperglycaemic State
- Older & Sicker (higher mortality)
- Usually altered mental state
- Occurs more slowly
- Usually precipitated by another illness
- Often new diagnosis of diabetes
- Hyperglycaemia is often extreme: Serum osmolarity >320mmol/L, profound dehydration, NOT ketotic, NOT acidotic
- Treatment is similar to DKA but SLOWER!
How does the pathophysiology of HHS compare to that of DKA?
Hyperosmolar hyperglycemic state (HHS)
- Primarily affects patients with type 2 diabetes.
- The pathophysiology of HHS is similar to that of DKA.
- However, in HHS, there are still small amounts of insulin being secreted by the pancreas, and this is sufficient to prevent DKA by suppressing lipolysis and, in turn, ketogenesis.
- HHS is characterized by symptoms of marked dehydration (and loss of electrolytes) due to the predominating hyperglycemia and osmotic diuresis.
HHS Management
- Fluids?
- Potassium?
- Insulin?
- Other?
Insulin
- Usually not required as glucose falls with fluid administration
- Commence once glucose levels plateau
- Insulin infusion 0.05units/kg/hr
- Rate of fall <5mmol/Hr, remain >15mmol/L first 24hrs
- Risk of rapid drop in osmolarity = cerebral oedema
List 7 Differentials for a Cervicofacial/neck swelling in the ED.
- Dental abscess
- Peritonsillar abscess/quincy
- Cutaneous infections
- Sialadenitis: parotid, submandibular gland
- Orbital cellulitis: pre- vs. post- septal
- Infected cysts; epidermoid, branchial
- Don’t forget neoplastic/aggressive pathology
Outline the managment for an Odontogenic ‘dental’ abscess (4).
- 7 Possible complications?
Potentially serious complications
1. Airway compromise
2. Necrotising fasciitis
3. Cavernous sinus thrombosis, jugular vein thrombosis
4. Sepsis, endocarditis
5. Mediastinitis
6. Maxillary sinusitis, orbital abscess
7. Osteomyelitis
Cervicofacial/neck swelling - Dental abscess
- Clinical exam in ED: 7 important signs?
- When to contact OMS service? (7)
Complications of the Maxillary vs. Mandibular abscess?
The Maxillary Abscess
- Usually less urgent than mandibular abscess
- Can still cause significant issues including spread to orbits and intracranially
Maxillofacial Trauma
- What is it?
- Why is facial trauma important? (4)
- Initial management?
- Frequency of fractures?
Maxillofacial Trauma
- Trauma to the face, jaws and mouth.
- Soft issue, dentoalveolar injury/fractures
- Often impressive, rarely lifethreatening
Why is facial trauma important?
1. Potentially life-threatening; airway obstruction or severe haemorrhage
2. May cause permanent disability to vision, taste, smell, mastication
3. Injury to the facial and trigeminal nerves
4. Facial cosmesis is important
Most common facial fracture?
- 2 immediate concerns?
- Imaging?
- 5 Signs?
Nasal Fracture
- Most prominent facial bone, most common fracture
- Distinguish external nasal bones and septum
- Immediate concerns: epistaxis, septal haematoma
- Long-term concerns: Functional & cosmetic
- Imaging: Is it always necessary? Plain films pointless. CT if concern of other midfacial trauma or septal involvement.
Septal Haematoma
- Treatment?
- Complications?
Mandibular Fractures
- 2 Immediate concerns?
- 6 Delayed concerns?
Mandibular Fractures
- Largest and one of strongest facial bones
- 2nd most frequently involved
- Typically bilateral fractures, so look for a 2nd
- Manage within 24hrs as open fracture
Mandibular Fractures
- 7 Signs & Symptoms?
- 3 Special Circumstances?
- Imaging?
Mandibular Fractures
Special circumstances include:
1. Mandibular condyles; ORIF vs. closed
2. Paediatric: unerupted teeth
3. Geriatric/edentulous: atrophic bone
Zygomatic Complex Fractures
- Main concern?
- When to take to theatre?
- 7 Signs/Symptoms/Evidence?
Zygomatic Complex Fractures
- Urgent issues relate to risk of retrobulbar haemorrhage
- Often wait for swelling to resolve before theatre (10-14 days)
- Concerns are cosmetic and functional (inc. ocular motility)
- Arch vs. Malar vs. Zygomaticoorbital
Midfacial Fractures
- 3 Types?
- Immediate concerns?
- When to take to theatre?
- 8 Signs?
Signs of Midfacial Fractures
1. ION paraesthesia
2. Potential injury of maxillary artery, epistaxis
3. Ecchymosis, facial oedema
4. Mobile maxilla/face
5. Flattened midface
6. Altered bite; pull of pterygoid muscles when bone dettached
7. CSF rhinorrhoea
8. Associated naso-orbital-ethmoidal injury; telecanthus
Midfacial Fractures
- Imaging?
Orbital Fractures
- 7 Signs & Symptoms of an orbital floor fracture?
- Immediate risks?
- Imaging?
- 2 Unique patterns?
- Surgical risks?
Orbital Fractures
- Isolated orbital floors (blowouts) or part of zygomatico-maxillary fracture
- Orbital floor the thinnest wall of orbit, thus most frequently involved
- Isolated orbital floor = blowout fracture
- Imaging: CT
- Immediate risks: retrobulbar haemorrhage & oculovagal haemodynamic instability
- Typically observe 1-2 weeks prior to decision
- Risks surgery include: blindness, infection, migration of implants, worsening of diplopia, surgical access issues such as entropian & ectropian with epiphora.
What is the main complication we are worried about with orbital fracture?
- Signs?
- Mx in ED?
Avulsed Tooth
- Management?
ED Aspects of Management of Maxillofacial injuries? (5)
List the top 10 ocular emergencies that require same day referral?
What are the 2 types of chemical ocular injuries? Which is worse? What type of necrosis do they each cause?
Alkali injuries cause liquefactive necrosis – can continue to penetrate over time – most household cleaning products and workplace chemicals = alkali = Plaster & cement
Acid injuries cause a coagulative necrosis.
Should you attempt to neutralise chemical ocular injuries? How should you manage these?
= NO
- DO NOT attempt to neutralise chemicals. The products of the neutralising reaction can be more toxic than the original chemical.
- If you want to know whether the chemical was acid or alkaline, litmus and urine dipstix can give a reasonable idea. Wash the eye out first as to avoid delay. Alkaline injuries remain alkaline for hours!
List 4 sequelae of chemical ocular injuries.
Sequelae of chemical ocular injuries:
- Conjunctivalisation
- Symblepharon
How do we classify ocular traumas?
Penetrating – one point of entry
Peforating – one point of entry and one point of exit at the other side
IOFB – object has entered eye and stayed there
What is a Hyphema?
Eight ball hyphema = entire anterior chamber filled with blood = poor prognosis as usually significant internal structure damage
How does an anteriorly dislocated lens present? Management?
What test can be performed to determine if an ocular trauma is lamellar or penetrating?
Seidel test positive when fluorescein dye gets washed away by aqueous fluid as the injury is full thickness require surgery
How does a Uveal prolapse present?
Uveal prolapse
- Peaked pupil
- Corneal haze around laceration
Describe the FAST acronym for management ocular trauma?
Abx = Ciprofloxacin – penetrates the eye quite well
Antiemetics – needed as vomiting can increase intraocular pressure further and cause more damage
What does this indicate? How should this patient be managed?
Central Retinal Artery Occlusion
List 6 features of Giant Cell Arteritis (Temporal Arteritis)? Which 2 symptoms should you always enquire about? 3 complications?
CRAO – Central Renal Artery occlusion
How should you manage Giant Cell Arteritis?
= pus in the anterior chamber = Endophthalmitis
Features of Endophthalmitis? 2 Hx? 2 Exam?
Management of Endophthalmitis?
What are the Features of Acute angle-closure glaucoma?
- 4 Hx?
- 5 Exam?
Acute angle-closure glaucoma (AACG): sudden obstruction of the iridocorneal angle causing a rapid, acutely symptomatic, and vision-threatening elevation of IOP, often > 30 mm Hg.
Treatment of Acute angle-closure glaucoma? (5)
What is the single most important risk factor for corneal abscess?
- Describe the pneumonic PEDAL for distinguishing between infective and non-infective keratitis?
**Corneal Abscess **
- Contact lens wear is the single most important risk factor.
- Any contact lens wearer who presents with an acute red eye has an infection until proven otherwise.
Treatment for a corneal abscess? (7)
What is this?
= Orbital Cellulitis
How can you differentiate orbital from preseptal cellulitis?
RAPD = Relative Afferent Pupillary Defect
How is an orbital cellulitis managed?
What is this? Work-up?
Third Nerve Palsy
- pupil-involving right third nerve palsy.
- The lid is ptotic and the eye position is “down and out”.
How does the assessment framework for emergency scenarios compare to routine patient interactions?
- Outline the assesment for a soft tissue injury in ED: Hx? Exam? Ixs?
What 7 things must you consider when a patient presents to ED with facial lacerations?
Facial Lacerations – Consider…
1. Airway
2. Eyes – retrobulbar haemorrhage?
3. Nasal – septal haematoma?
4. Teeth
5. Lower lip avulsion
6. Intra-oral/ mucosal injury
7. Facial nerve (CN VII) – 5 Branches of the facial nerve – need to know & locations
What things must you consider when a patient presents to ED with a bite? Management - Assessment? Treatment?
Bites
* Human
* Animals
* “Fight bite” – fist vs. mouth – teeth hit knuckle joint – can develop to osteomyelitis
* Main concern = infection – staph & strep = skin commensals (cat bite – Pasteurella) – Augmentin
What are the managment principles for Pre-tibial injuries in the ED?
Pre-Tibial Injuries
- More fragile, compromised skin than other areas
- Worsened by pre-existing arterial or venous disease & oedema
- Not much tissue over the tibia
- Often a degloving mechanism of injury
- Need to exclude underlying fracture
- Flap orientation – distal = poor blood supply vs. proximal to the flap = higher success
Approach to Hand Lacerations in the ED?
- Flexor tendon injuries – cannot be missed!
Devascularised Extremity
- Dx & Management?
Devascularised Extremity
- Index of suspicion from mechanism & location
- Level of injury dictates degree of urgency
- Only occasionally needs a tourniquet for control
- Time critical for muscle ischeamia
- Refer early
- White ‘empty’ finger with no CRT & numb!!
Amputatation - Management? What to do with ‘the amputate’?
What to do with ‘the amputate’?
- Moistened saline gauze around amputate
- Into sterile jar or sealed specimen bag
- Into another specimen bag containing ice water slurry
- Call plastics for advice
Soft Tissue Injuries in ED - Case 1
A 45 year old had a heavy palate fall on their leg 3 hours ago.
You are the ED intern assessing the patient.
Your seniors are busy in resus so ask you to look after the case.
How do you proceed?
Diagnosis?
- Primary Survey: A to E
Issues with crush injuries
- Compartment syndrome = Fasciotomy: diagnostic & therapeutic procedure
- Fractures
- Rhabdomyolysis = Bloods: Creatinine kinase, U&Es
Compartment Syndrome
Raised pressure within fascial compartment = Swelling & venous outflow obstruction = Worsens pressure & venous outflow = Arterial insufficiency – ischemia = Worsens all the above causing irreversible damage.
Soft Tissue Injuries in ED - Case 1
- 75 year old BIBA with forearm pain following a skin tear 10 days prior
- PMH: DM & IHD
- Lives alone, neighbour found them confused
- Assessment & Mx?
- Diagnosis?
= Subcutaneous emphysema & Necrotising Fasciitis = potentially limb or life threatening infection of subcutaneous tissue/ fascia. Classically rapidly progressive with clinical deterioration.
Aetiology/Risk Factors
- Initial infective source OR wound (minor/major)
- Systemic risk factors: Immunosupression, DM, Obesity, Transplant, Steroids & Medications, Malignancy, Malnutrition
- Local Risk Factors: Arterial & venous disease, smoking, oedema, trauma or surgery.
Outline the 3 types of necrotising fasciitis?
Necrotizing fasciitis (most common NSTI): a rapidly progressive infection resulting in extensive necrosis of superficial and deep fascia and overlying subcutaneous fat that can develop into a life-threatening condition within hours.
Define:
- Dyspnoea?
- Respiratory Distress?
- Respiratory Failure?
- Respiratory Arrest?
- Dyspnoea = Subjective feeling of difficult, laboured or uncomfortable breathing.
- Respiratory Distress = Work of breathing is increased to the point where there are clinical signs visible to others.
What are the 4 ED Evaluation Goals when assessing a patient with Acute dyspnoea/Acute Severe Asthma?
- General Management Principles?
ED Evaluation Goals
1. Detect life threatening hypoxia or hypercarbia
2. Differential diagnosis (or/and plan)
3. Treatment
4. Escalation (assisted ventilation)
NOTE: Respiratory rate most important vital sign – first response to shock = tachypnoeic
Acute Dyspnoea - Case I
- 24yo female with Chest tightness, wheezing & SOB
- Asymptotic earlier in the day
- She is visiting from out of town, is staying with a friend who owns 3 cats
- By evening she had begun feeling progressively worse with chest tightness and difficulty breathing with chest tightness & difficulty breathing that did not improve with several puffs of her ventolin inhaler.
Questions
1. List of differentials?
2. Questions you want to ask?
3. Severity of Asthma by Clinical findings: Mild/Moderate (3), Severe (4), Life-threatening (5)?
3. Tx - Mild/Moderate? Severe? Life-threatening?
- DDx: Asthma, Pneumonia/Pneumonitis, Allergic reaction, pneumothorax, PE
- Qs: Onset – sudden (10-15mins)? Associated sxs? PMH?
- Tx of Severe Asthma: Spacer 1st as can give a higher dose in one go but if too sick to use then need a nebuliser
Managing acute asthma in adults - What should be done:
- Immediately?
- Within minutes?
Managing acute asthma in adults - What should be done:
- Within the first hour?
- At 1 hour after starting bronchodilator treatment?
- After 1 hour check?
Acute Dyspnoea - Case 2
- List 3 Differentials?
- Ddx: pulmonary edema, IECOPD, pneumonia
CXR Interpretation for 76yo male with SOB & Fatigue?
- Diagnosis?
- 8 features of this on CXR?
- 6 Goals of therapy for this patient?
- CXR Interpretation:
- Diffuse fluffy opacifications in bilaterally, more of a perihilar distribution
- Mild cardiomegaly
- Curly B lines
- Peribranchial cuffing
- Bilateral pulmonary effusions
- Dx = Pulmonary oedema
- Alveolar oedema vs. interstitial oedema
Features of APO on CXR
1. upper lobe pulmonary venous diversion
2. increased cardiothoracic ratio
3. peribronchial cuffing
4. Kerley B lines
5. Thickening of interlobar fissures
6. Air space opacification (batwing distribution)
7. Air bronchograms = bronchi is open but is surrounded by fluid
8. Pleural effusions
2 Types of Non-Invasive Ventilation?
Non-Invasive Ventilation
1. CPAP = Continuous PEEP pressure – don’t collapse alveoli – very beneficial in pulmonary oedema
2. BIPAP = Bilevel = Varied PEEP depending on inspiratory pressures – triggered by own respiratory pattern – removes use of accessory muscles – Type II respiratory failure to blow off CO2
Differentials?
- Ddx = infective (covid, etc), aspiration pneumonia, IE of COPD
Results
- ABG (on 15L O2): pH 7.12 (7.35-7.45), pCO2 91 (35-45), pO2 271 (90-100), HCO3 30 (24-26)
- CXR Interpretation?
- ABG Interpretation?
- Treatment - Would you intubate this patient?
- List 11 Non-infective Causes of COPD Exacerbation?
CXR = Hyperinflated (flattened hemidiaphragms)
- Uncompensated Respiratory Acidosis
- Acute COPD (uncompensated) - For every 10 increase in CO2, there should be a 1 increase in HCO3
- Chronic COPD - For every 10 increase in CO2, there should be a 4 increase in HCO3
- Type II RF because the CO2 is up a lot
Treatment
* NIV – BIPAP, Bronchodilators, Steroids, Antibiotics
* You wouldn’t intubate this patient because they couldn’t recover once you’ve taken over their breathing for them.
* Discussion about Goals of Care
Acute Dyspnoea
- Diagnosis?
- Red flags indicating severe: 4 Clinical & 4 Investigations?
- Treatment stratification?
= Pneumonia
Ddx: PE, Infective (pneumonia)
Urea = crude estimate of hydration
Treatment Stratification
- SMART COP vs. CORB vs. CURB 65
- Predictors of the requirement for intensive respiratory or vasopressor support in addition to predictors of mortality
- Severity score must be interpreted in the clinical and social context of the patient
- Sensitivity ~80%, Specificity ~60%
- High NPV (>95%), Low PPV (15-25%)
The Patient with an Altered Mental State
- How might they present?
- 5 Tools for Assessing?
- Causes?
- What investigation must every patient with an altered AMS have?
Every patient with an altered AMS MUST have a Blood Sugar Level measured!!
Outline the 4 Components of the 4AT for Delirium Screening?
- Score interpretation?
- Hallmark feature of Delirium?
Delirium
- An important cause of AMS
- Subtypes: Hypoactive, Hyperactive, Mixed
- High mortality + hard to spot (esp. hypoactive)
- Alteration of the sleep-wake cycle (“sundowning”) = hallmark feature
- Think of it as a BRAIN FAILURE underpinned by a cause (eg. Sepsis)
- Delirium is a disorder of: Consciousness, Cognition, Perception, Attention, Sleep cycle
- Visual hallucinations are much more common in delirium vs. psychosis (psychiatric conditions)
- Mental health diagnoses are persistent vs. organic problems fluctuate.
Causes of Altered Mental State?
- Cerebral vs. Non-cerebral?
Aetiology of AMS
- Single factor vs. Multi-factorial
- Cerebral vs. Extra-dural
- Vulnerable brains require less of an insult to produce an AMS, ie.:
1. An old lady with a simple UTI can be badly confused and drowsy
2. A young man who is delirious with a fever has a serious illness
Patients with an Altered Mental State
- What is Useful Information to know?
- Where will you source your history from?
- What are you looking for on examination?
- What investigations might you order?
- In a patient presenting with AMS and headache, what must you rule out? How will you do this?
- In a patient presenting with AMS + Headache + Fever, what is the diagnosis until proven otherwise?
Non-contrast CT brain – contrast shows as blood on a CT so if you suspect a bleed must do a non-contrast CT!
AMS Case 1: 80yo lady in NH, complained of a headache last night – Given Panadol and put to bed. Could not be woken by the NH carer this morning. Brought to ED by ambulance. You’re the ED intern.
- What assessment will you perform?
- What are your differentials?
- What investigations might you consider?
- Diagnosis based on CT?
Non-contrast CT – small blob in ventricle and larger irregular shape is within the basal ganglia = intraparenchymal with extension into the ventricle = spontaneous hypertensive bleed.
- What are her goals of care?
- What meds is she on – blood thinners? Reversals?
AMS Case 2 – 66yo man living at home with his wife. Worsening, intermittent confusion over last 3-4 weeks. Very unusual ‘out of character’ behaviour. Normally healthy except for a “bad back” for the last 6 months – attributed to too much gardening. Wife: “Is it Alzheimer’s doctor?”
- What are the possible causes?
- Do you think it could be Alzheimers?
- How would you assess the patient - History, Examination, Investigations?
- Diagnosis?
AMS Case 3 – 16yo female brought in by her Mum, found excessively drowsy this morning, unable to get out of bed and slurring her words. Recent issues with online bullying at school.
- History?
- Examination?
- Investigations?
- Diagnosis?
- Management?
Investigations
* ECG: Sinus tachycardia
* Bedside bladder scan: >500mls
* Blood sugar: 5.8mmol
* Paracetamol level: <10
* WCC/CRP: Normal
* Urine drug screen: negative
Diagnosis = Anticholinergic delirium
- Drugs – benzos
- Stimulants – eg. Amphetamine, dexamphetamine/vybance overdose
- TCA overdose – anticholinergics = QT elongation & QRS widening in TCA overdose OR antihistamines, antinausea, antipsychotics
- What drugs can cause an anticholinergic toxidrome? (9)
- Clinical Features of an Anticholinergic Toxidrome? (5)
List 6 Applications of ultrasound in an emergency setting?
Applications of ultrasound in an emergency setting
1. Assessment for abdominal aortic aneurysm
2. Assessment of trauma
3. Vascular access
4. Assessment of the shocked patient
5. Assessment of the patient with dyspnoea
6. Procedural – line placement, draining fluid, nerve blockade
What is Nutcracker Syndrome?
Nutcracker syndrome is a vascular compression disorder that refers to the compression of the left renal vein, most commonly between the superior mesenteric artery (SMA) and aorta, although other variations can exist. This can lead to renal venous hypertension, resulting in the rupture of thin-walled veins into the collecting system with resultant haematuria.
What is the diagnosis?
- How might this patient present?
- When would you treat this?
Abdominal Aortic Aneurysm
- Normal <3cm
- 3-5cm = Aneurysmal
- >5cm = intervene - endovascular stent
- Presentation: Abdominal/flank pain, usually acute onset, triad of pain/hypotension/ palpable pulsatile mass is seen in around 50%
- 95% are infrarenal
- AAAs cause 1-3% of all deaths among men aged 65-85yrs in developed countries.
- These are typically asymptomatic until the catastrophic event of rupture.
- Don’t forget 1st presentation of renal colic in an elderly person should raise suspicion for AAA as it can press on the ureters!!
How useful is ultrasound for detecting AAA?
US in AAA
- In the patient with a detected AAA, want to check if the aorta has leaked
- US unreliable to answer this Q - need a CT
How useful is ultrasound in ED for trauma assessment?
- 7 Benefits of Bedside US in trauma?
- What is eFAST?
Ultrasound in trauma – the changes over 20 years
* Smaller
* More affordable machines
* Increased features and resolution of images
* Increased physician use
Benefits of Bedside ultrasound in trauma:
1. Accurate
2. Rapid
3. Non-invasive
4. Portable
5. Repeatable
6. No contrast
7. No radiation
eFAST
- What is the idea?
- 4 Views?
- An algorithm?
- What does it tell me?
- What is the right/wrong questions to answer US with in trauma?
What are the 4 different views for the eFAST scan and how are they done?
What are we looking for in each?
+ Pelvic view
What are the cons of ultrasound in ED trauma patients?
- 4 Limitations?
- 3 Pitfalls?
How can ultrasound be used to assess fluid resuscitation in trauma?
Assessing fluid resuscitation in trauma
- Estimation of RA filling from IVC diameter
- Measuring the IVC
- Dimension of the IVC <10mm
- Inspiratory change >50%
= Likely to represent hypovolaemia in the traumatised patient
Role of Lung Ultrasound in the ED?
- How useful?
- Other roles?
Lung Ultrasound
- High specificity for pneumothorax
- High sensitivity (but variable)
- Better than supine CXR
- Not as good as CT
Trauma
- What is the primary survey and what does it involve?
- Airway?
Algorithm for C-Spine Clearance?
Trauma - The Primary Survey: Breathing
- Assessment?
- 5 Breathing life-threats in trauma?
- Investigations?
5 Breathing life threats in trauma:
1. Haemothorax
2. Pneumothorax
3. Flail chest
4. Open pneumothorax
5. Diaphragm rupture
What is the diagnosis?
Left side abnormal = increased opacification - signifies fluid
Tracheal & mediastinal structure deviation - tension pneumothorax
Cardiac
What is the diagnosis?
Midline deviation – several rib fractures
1. Look for subcut emphysema first of all!
2. Tension pneumothorax
Diagnosis? Which side has the abnormality?
Which side has the abnormality
- Lack of lung markings on the RHS
- Subcut emphysema on RHS
- Visible rib fractures on RHS
- Cannot see heart border on RHS – can on the left
Diagnosis?
= Diaphragmatic rupture – common with seatbelt injuries - CALL A SURGEON!
- Intubate
- Possible left deviation of mediastinum
RHS –
LHS – No lung markings = stomach
Name 2 Interventions you might consider when breathing is threatened in trauma?
- What is the Triangle of Safety?
Intercostal Catheters (ICC) may be used to drain a pneumothorax or pleural effusion or may be placed post thoracic surgery.
Trauma - The Primary Survey: Circulation
- Assessment?
- Interventions?
Basic principles of management for an external exsanguinating haemorrhage?
- Call for Help!
- Primary Survey - A to E protocol
- Secondary Survey
Trauma - The Primary Survey: Disability
- Assessment?
Trauma
- Primary survey: Environment/Exposure?
- Secondary Survey?
Environment/Exposure
- Expose patient fully
- Check EVERYWHERE for injuries
- Logroll
- Once this is done, cover them
- Avoid hypothermia!
ED Phone call re: MVA
- What do you want to know?
- How are you going to prepare?
Provide an algorithm for an approach to the trauma patient
- Cardiac arrest/periarrest situation?
ATLS – primary survey
- ATOM FC?
- Management for a Tension
- Pneumothroax?
- Management for a Flail Chest?
- Remember not just to identify but also treat! - ATOM FC
- Airway Obstruction
- Tension Pneumothorax
- Open Pneumothroax
- Massive Haemothorax
- Flail Chest
- Cardiac Tamponade
Tension Pneumothroax - management
* Large bore cannula 2nd IC space midclavicular line
* Thoracostomy
* ICC
Management of:
- Tension Pneumothorax?
- FLAIL Chest?
- Massive Haemothorax?
- Open Pneumothorax?
NEXUS v Canadian c-spine precautions guidelines? Which are more sensitive?
What is a Thoracotomy?
- Indications? (2)
-
A thoracotomy is a surgical procedure in which a cut is made between the ribs to see and reach the lungs or other organs in the chest or thorax. Typically, a thoracotomy is performed on the right or left side of the chest. An incision on the front of the chest through the breast bone can also be used, but is rare.
Only widely accepted indication:
- Penetrating injury with previously witnessed cardiac output
- Rapid exsanguination from chest tube (>1500ml immediately)
