Medicine - cardiorespiratory emergencies Flashcards
Acute coronary syndrome: UA and NSTEMI
- Presentation
- Investigations
- Management
PRESENTATION:
- Typical angina like chest pain but this time present at rest, and increasing in frequency, duration and severity
INVESTIGATIONS:
- ECG to show ST segment changes
- Troponins for ischaemia
MANAGEMENT:
- ABCDE
- Oxygenate and monitor spO2 with aim to maintain at 90-94%
- Attach cardiac monitoring/ECG to identify ST segment changes
- IV morphine; SL GTN for pain
- PO aspirin 300mg
- PO clopidogrel 300mg or PO prasugrel 60mg, or PO ticagrelor 180mg according to local guidelines
- SC fondaparinux 2.5mg daily should be commenced unless there is a risk of bleeding and renal impairment or there is a plan to go to cath lab (in which IV UFH is preferred)
- IV GTN infusion at 0.6mg/hour can be commenced if pain is uncontrolled, provided that SBP > 90mmHg
- Admit to cardiology
FURTHER DISCUSSION AND MANAGEMENT:
- If high GRACE score and low bleeding risk, consider glycoprotein IIb/IIIa inhibitors with IV heparin
- If high risk of NSTEMI, haemodynamically stable and no contraindications, consider IV atenolol 5mg slowly over 5 minutes (contraindicated in hypotension, bradycardia, 2nd/3rd degree heart-block, heart failure)
- Maintain CBG < 11mmol/L
STEMI:
- Presentation
- Investigations
- Management
- What are the indications for PCI or thrombolysis?
- What are the contraindications for PCI or thrombolysis?
- What are some drugs used for thrombolysis?
- Complications of MI?
PRESENTATION:
- Classic = sudden-onset, severe, constant, central chest pain radiating to the arms, neck or jaw; might be similar to previous angina episodes but much more severe and not relieved by GTN; often a/w N+V and SOB
- Atypical = non-specific chest pain which is sometimes attributed to indigestion; often a/w frailty, DM, or HF
INVESTIGATIONS:
- ECG shows ST segment elevation in the affected artery; watch for associated ST segment in the “opposite” lead
- Troponins raised
MANAGEMENT:
- ABCDE
- Oxygenate to aim for 90-94%
- IV access; send bloods for U&E, FBC, glucose, and troponins
- IV morphine +/- antiemetics
- PO aspirin 300mg stat
- PO ticagrelor 180mg; or prasugrel, or clopidogrel (avoid ticagrelor if PMH of intracranial bleeding, active bleeding or hepatic impairment)
- Arrange transfer to cath lab for PCI if < 12 hours from symptom onset
- If PCI cannot be delivered within 90 minutes, offer thrombolysis with tenecteplase, alteplase or reteplase
- If pain continues, give IV GTN infusion at 0.6mg/hour and increasing it as necessary, provided SBP > 90mmHg
- Consider atenolol 5mg IV slowly over 5 minutes and repeated after 15 minutes, or metoprolol unless contraindicated (HF, hypotension, bradyarrhythmias, COPD)
INDICATIONS FOR PCI OR THROMBOLYSIS:
- ST elevation > 1mm in two limb leads, or
- ST elevation 2mm or more in two contiguous limb leads, or
- LBBB
[NB: PCI is favoured over thrombolysis; PCI must be given < 12 hours from symptom onset and within 90 minutes of diagnosis]
CONTRAINDICATIONS TO THROMBOLYSIS:
a) Absolute
- Stroke < 3 months
- Neurosurgery < 6 months
- Intracranial bleed < 12 months
- Cerebral tumours or mets
- Coagulopathy
- Anticoagulation
- Platelet count < 50x10^9
- Severe hypertension SBP > 200mmHg
- Major surgery < 14 days
- GI/GU/retroperitoneal bleeding
b) Relative contraindications
- Pregnancy
- Traumatic CPR
- Previous intracranial bleed
- Major bleeding < 3 months
- Stroke < 12 months
CHOICE OF THROMBOLYTIC AGENTS:
- Alteplase, give LMWH or heparin separetely via separate IV line
- Tenecteplase; give LMWH or heparin as above
- Retelase; give LMWH or heparin as above
- Streptokinase
POST-MI COMPLICATIONS:
- Arrhythmias (eg: ventricular ectopics, AF, VT/VF)
- Hypokalaemia
- Pulmonary oedema
- Cardiogenic shock
Myocardial infarction: ECG changes
- Hyperacute changes (within minutes)
- Evolving acute changes
- Chronic changes (months)
HYPERACUTE CHANGES (~MINUTES):
- Increased ventricular activation time; since the infarcting myocardium is slower to conduct electrical impulses, the interval between the start of the QRS and the apex of the R wave may be prolonged > 0.045s
- Increased height of R waves in inferior leads for inferior MI (Lead II, III, avF)
- Upward sloping ST segments
- Tall and widened T waves
EVOLVING ACUTE CHANGES:
- ST elevation: >1mm in two limb leads, or >2mm in to adjacent chest leads
- Reciprocal ST depression on the “opposite” side of the heart
- Pathological Q waves
- T wave inversion
- Conduction problems such as LBBB
CHRONIC CHANGES (~MONTHS):
- ST segments become isoelectric
- T waves become positive again
- Q waves remain which indicates previous MI
Acute pericarditis:
- Causes
- Presentation
- Investigations
- Management
CAUSES:
- Viruses (eg: coxsackie, mumps, EBV, CMV, rubella, HIV, parvovirus B19)
- Bacterial (eg: pneumococcus, meningococcus, chlamydia, gonorrhoea, TB)
- Rheumatic fever
- Uraemia
- Post cardiac surgery/radiotherapy
- Iatrogenic (eg: hydralazine, methyldopa, procainamide)
PRESENTATION:
- Chest pain = central, sharp, retrosternal, worse on inspiration and postural changes and swallowing etc
- Fever and viral prodrome
- PMH of infection
O/E:
- Pericardial friction rub tends to be louder with inspiration and is elusive
INVESTIGATIONS:
a) Bedside
- ECG changes of pericarditis = widespread saddle-shaped ST elevation, PR depression (reflecting atrial inflammation); T waves are initially upright and prominent but become flattened over days
b) Bloods
- Troponins may actually be raised; therefore consider repeat troponins or comparison with previous results
- FBC for signs of infection
- CRP for evidence of inflammation
MANAGEMENT:
- Idiopathic or viral pericarditis is self-limiting over days, advise rest, take simple NSAIDs, avoid of exercise, then discharge to GP; if symptoms don’t resolve despite NSAIDs consider GP to prescribe colchicine
- Admit those with high-risk features (eg: temperature > 38, raised WCC, large pericardial effusion causing tamponade, trauma, immunocompromise)
- Be alert to Dressler’s syndrome (autoimmune pericarditis +/- effusion occurring 2-14 weeks following MI)
- If suspicious of pericardial effusion and tamponade, call for help; pericardiocentesis under USS guidance is definitive treatment
Acute Bradyarrhythmia:
- Definition
- Causes
- Management
DEFINITION:
- < 60 bpm in the adult
- Often reflects diseases of the SAN or AVN
CAUSES:
a) Sick sinus syndrome
- Due to ischaemia or degeneration of SAN
- Characterised by sinus pauses > 2 seconds or sinus arrest
b) AV block
- 1st degree HB: conduction occurs from atria to ventricles everytime but is delayed, therefore PR interval > 0.2 seconds (5 small squares)
- 2nd degree HB Mobitz I: only a proportion of P waves are conducted from the atria to the ventricles; PR interval becomes increasingly lengthened until one P wave fails to conduct
- 2nd degree HB Mobitz II: only a proportion of P waves are conducted from the atria to the ventricles; failure to conduct P waves may occur regularly or irregularly, but the PR interval remains constant
- 3rd degree/complete HB: atrial activity is not conducted to the ventricles; there are regular P waves but no association between P waves and QRS complexes, and QRS complexes are broad at a ventricular rate of ~30bpm
c) Intraventricular conduction disturbances
- RBBB pattern on ECG
MANAGEMENT:
- ABCDE
- Vitals monitoring
- Oxygenation
- IV access
- If no life-threatening signs AND no risk of asystole, observe only
- If no life-threatening signs BUT risk of asystole, for interim measures (IV atropine 500mcg IV repeated to maximum of 3 mg, or IV adrenaline 2–10mcg/min, or IV isoprenaline 5mcg/min, or transcutaneous pacing)
- For all cases with life-threatening signs, give IV atropine 500mcg stat, then assess if response is satisfactory; if not, for interim measures; if satisfactory, then assess risk of asystole and if present for interim measures
- Trans-venous pacing is definitive treatment
- Always seek expert help
Tachyarrhythmias: principles of management for unstable patients
INITIAL STEPS:
- ABCDE
- Oxygenate
- Cardiac monitoring
- Identify reversible causes and treat
FOR UNSTABLE PATIENTS:
1) Attempt synchronised cardioversion first
- One doctor to attempt cardioversion
- One doctor to provide sedation/anaesthesia
- Synchronise electrical cardioversion with the R wave to minimise the risk of VF
- Suitable for patients with evidence of instability and an underlying rhythm of SVT, AF, atrial flutter and VT
- For broad-complex tachycardia or AF, start at 120-150J, then increase
- For atrial flutter or paroxysmal SVT, start at 70-120J, then increase
2) Amiodarone
- If cardioversion is unsuccessful after 3 attempts
- Give IV amiodarone 300mg over 10-20 minutes and repeat the shock
- Use a central vein due to risk of thrombophlebitis in peripheral veins
FOR CLINICALLY STABLE PATIENTS:
- Tailor treatment according to underlying likely rhythm
- Establish QRS complex if it is broad or narrow complex, and the rhythm if regular or not
Tachyarrhythmias: principles of management
- Broad complex tachycardia
- Narrow complex tachycardia
BROAD COMPLEX TACHYARRHYTHMIAS:
- Likely to be VT; less likely to be SVT with aberrant conduction
- Oxygenate, gain IV access, then shock if pulseless VT
FOR TORSADES DE POINTES:
- a/w hypomagnesaemia, hypokalaemia, prolonged QT interval
- Stop amiodarone and drugs that prolong QT
- Treatment is with IV magnesium sulfate; consider synchronised cardioversion
NARROW COMPLEX TACHYARRHYTHMIAS:
a) Regular rhythm
- Likely to be SVT if it is not sinus tachycardia
- Attempt vagal stimulation first by asking patient to blow into 20ml syringe for 15 seconds, then lie supine and raise legs for 15 seconds
- Carotid sinus massage can be considered but caution in risk of stroke/TIA
- IV adenosine 6mg stat as a bolus, if unsuccessful increase to 12mg and repeat; warn patient about impending doom and discomfort; it is contraindicated in 2/3 degree heart blocks, severe hypotension and asthma
- IV verapamil 2-5mg over 2 minutes if adenosine contraindicated
b) Irregular rhythm
- Likely to be AF
- Underlying cardiac causes include IHD, HF, hypertension and valvular disease; non-cardiac causes include sepsis, PE, thyrotoxicosis, electrocution, hypokalaemia and hypothermia
- Rate control = for older patients or for those with symptoms > 48 hours due to risk of stroke; give IV metoprolol 5mg and diltiazem; for CCF patients give IV digoxin 500mcg
- Rhythm control = for younger, stable patients give flecainide or IV amiodarone 300mg; if signs of shock/syncope/ischaemia/acute HF consider electrical cardioversion under sedation
CHADS2VA2SC SCORE FOR AF:
- Determines the risk of stroke secondary to underlying AF
- Any patient scoring > 1 should be considered for anticoagulation to prevent the risk of stroke secondary to AF
Hypertensive emergency:
- Presentation
- Investigations
- Management
PRESENTATION:
- Increased BP with rapid-onset neurological signs or retinopathy or myocardial ischaemia or renal failure
- BP often > 230mmHg
- Other features include: headaches, N+V, confusion, visual changes, seizures, decreased GCS
INVESTIGATIONS:
- Bloods = U&Es, creatinine and glucose
- Bedside = ECG, urinalysis
- Imaging = CXR for aortic dissection; CT head if suspicious of stroke
MANAGEMENT:
- Aim to reduce BP by no more than 25% per hour
- IV sodium nitroprusside or IV labetalol or GTN are all suitable drugs; sodium nitroprusside has short half-life and vasodilates both arteries and veins; labetalol is preferred for aortic dissection or phaeochromocytoma
- Commence continuous BP monitoring via arterial line
- Admit to HDU/ICU for monitoring
General approach to the following:
- Haemoptysis
- Oxygen
- Dyspnoea
- Hyperventilation
HAEMOPTYSIS:
- Respiratory causes = carcinoma, infection (TB), bronchiectasis, PE, pulmonary oedema
- Cardiac causes = ruptured aortic aneurysm with aorto-bronchial fistula
- Haematological = warfarin, DOACs, haemophilia
- Management = ABCDE, suction airway, consider ETT, give oxygen and maintain at 94%, gain IV access with large bore (14G) cannulae in case of transfusion
OXYGEN:
- Patients with high oxygen requirements include: CO poisoning, cluster headaches, sickle-cell crisis and pneumothorax
- Aims of oxygen treatment is to maximise O2 delivery to tissues; aim for 96% in most cases, except COPD or T2RF in which it is 88-92% (take ABG in these patients)
DYSPNOEA:
- ABCDE and resuscitate as necessary; use pulse oximetry
- Limitations of pulse oximetry: poor peripheral perfusion (eg: shock), hypothermia, CO poisoning, nail varnish, excess movement
HYPERVENTILATION:
- Occurs in attempt to blow off CO2
- Primary hyperventilation is often psychogenic; typically the patient is distressed and might complain of dizziness, paraesthesia, spasms
- Secondary hyperventilation causes = metabolic acidosis (eg: DKA, uraemia, sepsis, hepatic failure), poisoning, pain, hypoxia, hypovolaemia, respiratory pathology (eg: PE, asthma, pneumothorax)
- Management = do not sedate, exclude serious diagnoses, then reassure and consider discharge with simple breathing exercises
ABGs:
- How to differentiate between T1RF and T2RF?
- How to differentiate between acute and chronic T2RF?
- What are the causes of metabolic acidosis?
- What does HAGMA suggest and what are the its causes?
- What are the causes of NAGMA?
DIFFERENTIATING BETWEEN T1RF AND T2RF:
- T1RF = hypoxia with normal or reduced pCO2
- T2RF = hypoxia with raised pCO2 and frequently raised HCO3- indicating metabolic compensation
[NB: exercise caution with administering high amounts of oxygen in T2RF due to risk of life-threatening respiratory failure, aim to keep spO2 at 88-92% in COPD and recheck ABGs every 30 minutes]
DIFFERENTIATING BETWEEN ACUTE AND CHRONIC T2RF:
- Check HCO3- levels as the kidneys will normally adapt to retain HCO3- to buffer H+ levels, but this takes a period of days
- T2RF always presents with raised pCO2
CAUSES OF METABOLIC ACIDOSIS (low pH, low HCO3-, BE < -2):
- Raised acid load = lactate acidosis, ketoacidosis, salicylate poisoning, methanol, metformin
- Poor acid clearance = renal failure, renal tubular acidosis type 1 or 4
- Loss of HCO3- from the body = diarrhoea, pancreatic/intestinal fistulae, renal tubular acidosis type 2, acetazolamide
CAUSES OF HAGMA (NORMAL IS 12-16):
“MUDPILES”
- Methanol/Metformin
- Uraemia
- Diabetic ketoacidosis (or any form of ketoacidosis)
- Prophylene glycol
- Isoniazid
- Lactic acidosis (eg: strenous exercise)
- Ethylene glycol
- Salicylate poisoning (eg: aspirin)
[NB: indicates excess H+ secondary to lactate acidosis (normal < 2)]
CAUSES OF NAGMA:
- Chronic diarrhoea
- Pancreatic or intestinal fistulae
- Acetazolamide
- Renal tubular acidosis
Cardiogenic pulmonary oedema:
- Causes
- Presentation
- Investigations
- Management
CAUSES:
- Arrhythmias
- Post-MI
- Prosthetic valve failure
- Cardiomyopathy
- B-blockers (or any negative inotropic drug)
- Myocarditis
- Pericardial disease
[IE: anything that induces L-sided heart failure, which leads to raised LV EDP, causing raised capillary pulmonary hydrostatic pressure, leading to fluid collecting in the extravascular space secondary to transudative forces]
PRESENTATION:
- SOB and distress of dramatic nature
- Chest pain possible
O/E:
- Tachycardia, tachypnoea, reduced sats
- Cyanosis with frothy sputum if severe
- S3/4 may be heard
- JVP might be raised in PE and tamponade
- Bilateral crepitations starting from bases and spreading generally
INVESTIGATIONS:
a) Bedside
- ABG to diagnose RF, esp if sats low
- ECG to pick up arrhythmias, LVH, LBBB, or MI
b) Bloods
- U&Es, glucose, FBC
- Troponins to exclude MI
- NT-pro-BNP to diagnose HF
c) Imaging
- CXR may reveal ABCDE features = Alveolar oedema, kerley B lines, Cardiomegaly, Dilated upper lobe vessels and Effusions (pleural)
- Transthoracic echo for patients with prosthetic valves to exclude valve failure; if diagnosed, emergency surgery is necessary
MANAGEMENT:
- ABCDE
- Oxygenate with high-flow O2
- IV access
- IV furosemide 40mg
- IV nitrates (eg: GTN IVI) should only be reserved for specific circumstances (eg: MI, AR, mitral valve pathology)
- Consider IV opioids with antiemetics if chest pain
- Consider CPAP if very breathless
Non-cardiogenic pulmonary oedema:
- Pathophysiology
- Causes
- Management
PATHOPHYSIOLOGY:
- Pulmonary oedema in the absence of raised pulmonary venous pressure
- Raised capillary permeability causing exudative forces
- Decreased plasma oncotic pressure
- Raised lymphatic pressure
CAUSES:
- ARDS secondary to pancreatitis/COVID/sepsis/trauma etc
- Intracranial haemorrhage (esp SAH)
- IV fluid overload
- Hypoalbuminemia (eg: liver failure, nephrotic syndrome)
- Drugs and poisons
- Smoke inhalation
- High-altitude sickness
MANAGEMENT:
- Supportive
- Admit to HCU/IDU if need be
- Consider positive end-expiratory pressure (PEEP); additional pressure in the airways at the end of exhalation stops the airways from collapsing, therefore forms of respiratory support that add PEEP helps keep the airways from collapsing and improves ventilation
Pleural effusion:
- Causes of exudates
- Causes of transudates
- How to differentiate between exudate vs transudate?
- Presentation
- Investigations
- Management
CAUSES OF EXUDATES:
- Pneumonia
- Malignancy
- TB
- PE with pulmonary infarction
- Pancreatitis
- Abscess
- Chylothorax
CAUSES OF TRANSUDATES:
- Cardiac failure
- Nephrotic syndrome
- Hepatic failure
- Ovarian hyperstimulation
- Peritoneal dialysis
EXUDATE VS TRANSUDATE:
- Diagnose an exudate if the pleural fluid : serum fluid ratio is > 0.5; or if the fluid LDH : serum LDH ratio is > 0.6; or if the fluid LDH is more than 2/3 the upper limit of the laboratory normal value for serum LDH
PRESENTATION:
- Mild dull ache
- SOB initially on exercise and later on rest
O/E:
- Stony dullness to percussion
- Absent breath sounds
- Reduced chest expansion
- Tracheal deviation if large
[NB: signs may not be apparent until > 500mL are present]
INVESTIAGTIONS:
- CXR is diagnostic showing blurring of costophrenic angle
- Pleural paracentesis for pH, LDH, protein count, MCS and cytology as basic; other investigations include gram staining, glucose testing, amylase etc
MANAGEMENT:
- Treat underlying causes
- Small effusions actually don’t need treatment
- Large and symptomatic effusions may warrant pleural aspiration via therapeutic paracentesis (use a special drainage kit) or chest drain insertion (insert a 10-14 Fr tube into the pleural space allowing drainage over hours or days)
- Recurrent or malignant pleural effusions can consider referral to thoracic surgery for pleurodesis or VATS
COMPLICATIONS OF PLEURAL ASPIRATION:
- Re-expansion pulmonary oedema if done too quickly, therefore limit drainage to 1-1.5L each time
- Pneumothorax
- Infection
- Bleeding
- Damage to the thoracic viscera
Acute asthma:
- Presentation
- Classification
- Investigations
- Management
- Admission criteria
- Discharge criteria
- ICU referral criteria
PRESENTATION:
- Cough, SOB, chest tightness, unable to speak
O/E:
- Tachycardia, tachypnoea, reduced sats, reduced air entry, generalised wheeze, cyanosis and pallor
CLASSIFICATION OF ASTHMA:
- Moderate = PEFR 50-70%, spO2 92% or more, vitals unremarkable
- Severe = PEFR 33-50%, spO2 92% or more, HR > 110, RR > 25, can’t complete sentences
- Life-threatening = PEFR < 33%, spO2 < 92%, paO2 < 8kPa
- Near-fatal = raised pCO2
INVESTIGATIONS:
a) In the ED
- Peak flow
- SpO2 to guide oxygen therapy and aim for 94-98%
- ABG if spO2 < 92% to diagnose RF
- U&Es may diagnose hypokalaemia secondary to B2-agonist/steroid use
- CXR to exclude other pathologies (should not delay treatment)
b) After discharge/in out-patient settings
- Spirometry to show obstructive pattern where FVC is reduced, FEV1:FVC < 70%
- PEFR diaries may show characteristic variability
- Fractional exhaled nitric oxide (FeNO) >25 ppb at 50 ml/sec is seen in 70-80% of patients with untreated asthma
MANAGEMENT:
- ABCDE
- Oxygenate aiming for 94-98%
- Sit patient up and raise the handlebars of the trolley so the patient can grasp onto them for support (eg: using pectoralis muscles)
- NEB salbutamol 5.0mg driven with O2; or 10x puffs of salbutamol into a spacer and mask; reserve IV salbutamol for those who can’t inhale well
- PO prednisolone 40-50mg or IV hydrocortisone 100mg
- NEB ipratropium bromide 500mcg 4-6 hourly for those with severe or life-threatening asthma (acts as a SAMA)
- IV magnesium sulfate 1.2-2g infusion over 20 minutes (there is some evidence of it having bronchodilator effects)
- IV aminophylline use is controversial
- Repeat ABG within 1 hour to monitor treatment
- Repeat U&E to exclude hypokalaemia secondary to B2-agonist/steroid use
ADMISSION CRITERIA:
- Life-threatening asthma
- Severe asthma persisting despite treatment
DISCHARGE CRITERIA:
- PEFR > 75% of best 1 hour after initial treatment
- If PEFT < 50% but haemodynamically stable, consider discharge with PO prednisolone 40-50mg OD for 5 days
- Arrange review with asthma liaison nurse before discharge
- Review inhaler technique and PEFR monitoring at minimum
- Discharge with GP follow-up within 2 days
- Safety-net to return to A&E if symptoms worsen
ICU REFERRAL CRITERIA:
- PEFR deteriorating
- Worsening hypoxia
- Hypercapnia (T2RF)
- ABG showing respiratory acidosis
- Exhaustion, reduced GCS, confusion, drowsiness
Acute COPD exacerbation:
- Pathophysiology
- Presentation
- Investigations
- Management
PATHOPHYSIOLOGY:
- Chronic airflow limitation due to impedance to expiratory airflow, mucosal oedema, infection, bronchospasm and bronchoconstriction due to reduced lung elasticity
- Causes include smoking, a-1 antitrypsin deficiency and chronic infection
PRESENTATION:
- SOB, cough, sputum are usual complaints
- Exercise intolerance possible
- Ask about treatment including inhalers, steroids, abx and theophyllines
O/E:
- Tachypnoea, tachycardia, accessory muscle use, lip-pursing, barrel chest, hyper-resonance to percussion etc
- Cyanosis if late sign
- Plethora due to compensatory polycythaemia
- Right heart failure causing cor-pulmonale suggests advanced disease
- Look for evidence of hypercarbia such as tremor, bounding pulses, drowsiness and confusion
INVESTIGATIONS:
a) Bedside
- Sputum to identify pathogens if infective
- ECG to identify RV strain or MI
b) Bloods
- ABG should identify RF and document FiO2, using pCO2 to guide therapy
- FBC for infection and CRP for inflammation
- Blood cultures if infective
c) Imaging
- CXR for hyperinflation, pneumonia, and pneumothorax etc
MANAGEMENT:
- ABCDE
- Oxygenate aiming for 88-92%, bearing in mind possibility of hypercapnia and T2RF
- If known COPD and drowsy or previous T2RF, consider Fio2 of 28% via venturi mask
- NEB salbutamol 5.0mg or terbutaline 5-10mg, consider adding NEB ipratropium bromide 0.5mg/500mcg
- PO prednisolone 30mg stat then OD for 7 days; use IV hydrocortisone 100mg if patient cannot take oral drugs
- Give antibiotics (eg: doxycycline, amoxicillin, clarithromycin) if patient reports purulent sputum or CXR demonstrates evidence of pneumonia
- Only consider IV aminophylline if there is poor response to NEB bronchodilators
DEFINITIVE TREATMENT:
- Non-invasive ventilation (NIV) is standard early therapy for hypercapnia respiratory failure due to COPD exacerbations; NIV takes the form of either CPAP or BiPAP
- Coma and vomiting are contraindications to NIV as it doesn’t protect the airway; apnoea and cardiac arrest are also absolute contraindications (use ETT intubation instead)
- Check CXR before commencing NIV as pneumothoraxes can be converted to a tension pneumothorax with NIV
DVT:
- Subtypes
- Risk factors
- Presentation
- Differential diagnoses
- Investigations
- Management
SUBTYPES:
- Provoked = caused by an identifiable, transient, major risk factor
- Unprovoked = no obvious, transient risk factor identified
RISK FACTORS:
- Immobility (eg: long-haul flights, hospital admission, bedbound)
- Recent surgery
- Malignancy
- Sepsis
- IVDU into femoral vein
- Pregnancy
- Pelvic masses
- Previous DVT/PE
- Thrombophilia
PRESENTATION:
- Unilateral leg pain, swelling, warmth, tenderness, dilated superficial veins
DIFFERENTIAL DIAGNOSES:
- Cellulitis
- Ruptured baker’s cyst
- Traumatic muscular tear
INVESTIGATIONS:
- Measure both legs 10cm distal to tibial tuberosity; a difference of > 3cm increases the probability of DVT
- DVT Wells score = 1 or less suggests DVT is unlikely, if 2 or more DVT is likely
- If DVT Wells score is 1 or less, take D-dimer; if normal, DVT is excluded but if raised, then do whole leg USS
- If DVT Wells score is 2 or more, or if D-dimer is raised, then do whole leg USS
INTERIM MANAGEMENT:
- Offer apixaban or rivaroxaban first line for those waiting outpatient USS evaluation or D-dimer test; if apixaban or rivaroxaban unavailable then offer LMWH for at least 5 days followed by dabigatran or edoxaban, or LMWH concurrently with a vitamin K antagonist for at least 5 days
- For those on anticoagulation, send bloods for PT/APTT, FBC, U&E and LFTs
DEFINITIVE MANAGEMENT:
- Anticoagulation is required as maintenance treatment; use warfarin, apixaban, dabigatran, edoxaban, or rivaroxaban
- Warfarin needs INR monitoring to ensure INR remains within 2.0-3.0
- DOACs don’t need monitoring
- Treatment should continue for 3 months in provoked DVT but may be longer for unprovoked DVT
FOR UPPER LIMB DVT:
- Often seen with chemotherapy central or long lines
- Request USS of axillary, subclavian and jugular veins
- Treatment is the same
FOR SUPERFICIAL THROMBOPHLEBITIS:
- Presents as a firm tender superficial vein with overlying erythema
- Offer NSAIDs or a 6-week course of anticoagulation
- Discharge with follow-up in GP or ED
PE:
- Presentation
- Investigations
- Management (routine PE vs massive PE)
PRESENTATION:
- SOB is often the most common presenting complaint
- Sometimes there is pleuritic chest pain +/- haemoptysis
- If cyanosed, unconscious or angina think massive PE
O/E:
- Tachycardia and tachypnoea are common
- Fever following lung infarction is common
- SpO2 reduced (but note that 30% of patients might be normal still)
- BP if hypotensive suggests massive PE
- Check for evidence of DVT
INVESTIGATIONS:
a) Bedside
- Calculate Wells PE score: 4.0 or less suggests PE is unlikely, but 4.5 or more suggests PE likely
- ECG may reveal sinus tachycardia; S1Q3T3 is uncommon; other less common signs are RBBB, RV strain (inverted T waves in V1-4 and lead III/avF)
b) Bloods
- Bloods for FBC and U&E
- D-dimer = if Wells PE score is 4.0 or less perform D-dimer to exclude PE
[NB: D-dimer is sensitive but not specific as other pathologies can cause a raised D-dimer (eg: recent surgery or trauma, ongoing infection or inflammation, liver disease, or pregnancy)]
c) Imaging
- CXR can exclude other causes of chest pain and is often normal; wedge-shaped pleural infiltrate is uncommon
- CTPA gives definitive diagnosis but is not good for younger patients due to high dose of radiation
- V/Q scanning use lower radiation but therefore aren’t as definitive
MANAGEMENT:
- Aim to treat as outpatient after senior review if vital signs are normal
- Admit those with tachycardia, tachypnoea or if unable to cope at home
- Anticoagulation should be commenced if waiting for D-dimer results, or as soon as PE is diagnosed; choices include DOACs and UFH
- Treatment should continue for 3 months in provoked DVT but may be longer for unprovoked DVT
MANAGEMENT OF SUSPECTED MASSIVE PE:
- Call for senior and ICU help
- Arrange bedside POCUS/echo which will show RV strain; do NOT do CTPA or V/Q scanning as this will waste time
- Thrombolysis should be commenced empirically without delay; use IV alteplase 10mg slow infusion over 1-2 minutes followed by 90mg IVI over 2 hours
- Consider surgical embolectomy or catheter-directed thrombolysis if pharmacological thrombolysis is not available
- After thrombolysis, commence UFH IVI with the dose based on weight
