Acute Care & Trauma Flashcards
Define acute kidney injury (AKI).
An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.
Spectrum - mild to severe
Explain the aetiology / risk factors of acute kidney injury (AKI).
Impaired clearance and regulation of metabolic homeostasis, altered acid / base and electrolyte regulation and impaired volume regulation.
Caused by:
- Impaired kidney perfusion
- Exposure to nephrotoxins - e.g. aminoglycosides, vancomycin + piperacilliin-tazobactam, cancer therapies, NSAIDs, ACE inhibitors
- Outflow obstruction
- Intrinsic kidney disease
Risk Factors:
- Advanced age
- Underlying kidney disease
- DM
- Sepsis
- Iodinated contrast
- Exposure to nephrotoxins
- Excessive fluid loss
- Sugrery
- Haemorrhage
- Recent vascular intervention
- Cardiac arrest
- Pancreatitis
- Trauma
- Malignant hypertension
- Myeloproliferative disorders - e.g. multiple myeloma
- Connective tissue disease
- Sodium-retaining states - e.g. congestive heart failure, cirrhosis, nephrotic syndrome
- Drug overdose
- Nephrolithiasis
Staging on the basis of Creatinine:
Stage 1 - rise of>26micromol/L within 48 hours or 1.5-1.9x baseline
Stage 2 - rise to 2-2.9x baseline
Stage 3 - rise to >3x baseline or >354 micromol/L or initiated on RRT (irrespective of staging)
Summarise the epidemiology of acute kidney injury (AKI).
10,400 per million
Seen in 10-20% of people admitted to hospital as emergencies
Inpatient mortality >20%
ICU incidence - 20-50%, mortality >50%
Recognize the presenting symptoms of acute kidney injury (AKI).
- Hypotension
- Risk factors
- Kidney insults
- Reduced urine production
- Lower urinary tract symptoms - e.g. urgency, frequency, hesitancy
- Symptoms of volume overload or pulmonary oedema - e.g. orthopnoea, swollen ankles, crackles on auscultation of lungs, tachypnoea
- N&V
- Fever
- Rash
- Arthralgia
- Haematuria - visible or non-visible
- Palpable bladder and/or enlarged prostate and/or abdominal distension
Recognise the signs of acute kidney injury (AKI) on physical examination.
- Hypotension
- Risk factors
- Kidney insults
- Reduced urine production
- Lower urinary tract symptoms - e.g. urgency, frequency, hesitancy
- Symptoms of volume overload or pulmonary oedema - e.g. orthopnoea, swollen ankles, crackles on auscultation of lungs, tachypnoea
- N&V
- Fever
- Rash
- Arthralgia
- Haematuria - visible or non-visible
- Palpable bladder and/or enlarged prostate and/or abdominal distension
Identify appropriate investigations for acute kidney injury (AKI) and interpret the results.
- Basic metabolic profile - includes urea, creatinine (HIGH), LFTs (hepatorenal syndrome)
- K+ serum - HIGH - >6mmol/L or ECG changes = urgent treatment
- FBC - leukocytosis (sepsis), low platelets (haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, cryoglobulinaemia), anaemia (haemolytic uraemic syndrome, myeloma, vasculitis)
- Bicarbonate - LOW = acidosis
- CRP - HIGH (sepsis, infection, vasculitis)
- Blood culture - bacterial pathogen causing sepsis
- Urinalysis - RBCs, WBCs, celllular casts, proteinuria, positive nitrile, leukocyte esterase
- Urine culture - bacterial growth with antibiotic sensitivity
- Urine output monitoring - hourly if catheterised, 4-hourly if not - <0.5ml/kg/hour for 6 hours at least
- Fluid challenge - kidney function improves rapidly
- Venous blood gases (metabolic acidosis) - anion gap acidosis
- CXR - infection, pulmonary oedema, haemorrhage, cardiomegaly
- ECG - peaked T waves, increased PR interval, widened QRS, atrial arrest, deterioration to a sine wave pattern = hyperkalaemia
Measure serum creatinine to check for AKI if - compare to baseline over 3 months (if none, repeat within 12 hours):
- > 65 years
- History - CKD, heart failure, liver disease, diabetes, dementia
- Previous AKI
- Exposure to iodinated contrast agent, nephrotoxins, RAS modifying agent, diuretic
- History of urological obstruction
- Sepsis
- Hypovolaemia (with/without hypotension)
- Hypotenison (SBP <90mmHg or a fall of >40mmHg from baseline BP)
- Oliguria - urine output <0.5ml/kg/hour
- Acute rise in NEWS >5
CKD Features (doesn’t exclude):
- Rise in serum creatinine over a long period of time
- Hypocalcaemia
- Hyperphosphataemia
- Anaemia
- Small kidneys on ultrasound, sometimes scarred
NB: CKD is a risk factor for AKI.
Check for:
- Recent use of trimethoprim - false positive rise
- Creatinine falls during pregnancy, so a rise in creatinine after recent delivery - false positive rise
Serum K+
5.5 to 5.9 mmol/L indicates mild hyperkalaemia
6.0 to 6.4 mmol/L indicates moderate hyperkalaemia
≥6.5 mmol/L indicates severe hyperkalaemia
To catheterise or not to catheterise?
- Benefits - sustained fall in urine output suggests AKI, difficult to measure without, diagnostic and therapeutic for bladder neck obstruction, assessment of response to treatment, urinalysis performed on samples
- Risks - infection, trauma, falls risk
Generate a management plan for acute kidney injury (AKI).
Treat sepsis, optimization of volume status, correction of acidaemia or electrolyte complications, avoidance of nephrotoxins and relief of any obstruction.
STOP AKI
S = Sepsis - implement Sepsis Six within 1 hour, source and treat infection
T = Toxins - stop nephrotoxins
O = Optimise volume status /BP - assess and give IV fluids, hold antihypertensives and diuretics, consider vasopressors if not responding
P = Prevent harm - treat complications and cause
If HYPOVOLAEMIC - e.g. sepsis, fluid loss, reduced fluid intake(pre-kidney):
- Mild hyperkalaemia (5.5-5.9) - fluid resus (500mL bolus over 15mins, wide bore cannula, crystalloid, reassess) , review meds, stop nephrotoxins (e.g. aminoglycoside antibiotics, NSAIDs, iodinated contrast agents, ACEi, ARB, diuretics), treat cause, vasoactive drug (e.g. noradrenaline, vasopressin, dobutamine), blood transfusion, specialist referral, cation-exchange resin (e.g. calcium polystyrene sulfonate to remove K+ from body)
- Moderate hyperkalaemia (6.0-6.4) and no ECG changes - fluid resus, review meds, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, insulin / glucose (to push potassium intracellularly, give over 15 mins, acts within 10-20 mins, lasts 4-6 hours) , salbutamol (to push potassium intracellularly)
- Moderate (6.0-6.4) or Severe hyperkalaemia (>6.5) and associated ECG changes - fluid resus, review meds, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, calcium chloride or gluconate (IV over 5-10 mins for cardiac protection vs arrhythmias), insulin/glucose, salbutamol
- Metabolic acidosis - fluid resus, review medications, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, sodium bicarbonate (if pH <7.2, refer to ICU possibly?, venous bicarb <16mmol/L with no volume overload)
- Uraemia, refractory severe hyperkalaemia etc - fluid resus, review meds, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, renal replacement therapy (if end-organ complications of uraemia, severe hyperkalaemia, refractory acidosis that is not responding - give intermittent haemodialysis [4hrs, fast removal of toxins] or continuous RRT [24-72hours, slower blood flow] or peritoneal dialysis)
If HYPERVOLAEMIC - e.g. obstruction to urinary flow (post-renal):
- Pulmoary oedema - loop diuretic (furosemide), sodium restriction, treat cause, renal replacement therapy (on basis of condition, not urea or creatinine value - intermittent haemodialysis, CRRT, peritoneal dialysis), upright positioning, high-flow oxygen (15L/min via resevoir mask, CPAP), glyceryl trinitrate IV (aim for SBP >95mmHg)
- Mild hyperkalaemia (5.5-5.9) - loop diuretic (furosemide), sodium restriction, treat cause (review meds, restrict dietary intake, monitor K+ and glucose), renal replacement, cation-exchange resin (calcium polystyrene sulfonate - remove K+ from the body)
- Moderate hyperkalaemia (6.0-6.4) and no ECG changes - loop diuretic (furosemide), sodium restriction, RRT, treat cause, insulin & glucose (push potassium intracellularly, give over 15 mins, acts within 10-20 mins, lasts 4-6 hours) , salbutamol (drive potassium intracellularly)
- Severe hyperkalaemia (>6.5) or moderate hyperkalaemia (6.0-6.4) and associated ECG changes - loop diuretic (furosemide), sodium restriction, RRT, treat cause, calcium (for cardiac protection vs arrhythmias- can be calcium chloride or calcium gluconate), insulin & glucose, salbutamol
- Metabolic acidosis - loop diuretic, sodium restriction, treat cause, RRT, specialist advice (once obstruction relieved, diuresis progressing, renal team decides whether to use sodium bicarbonate)
Identify the possible complications of acute kidney injury (AKI) and its management.
- Renal replacement therapy if do not respond to medical management
- Hyperkalaemia
- Acidaemia
- Uraemic encephalopathy
- Pericarditis
- Pulmonary oedema
- Volume overload
- Electrolyte and acid-base disturbances
- Hyponatraemia
- Metabolic acidosis
- Nutritional and gastrointestinal disturbances
- Anaemia
- Bleeding diathesis
- Infection
- Sepsis
- Death
- Multi-organ failure
- Arrythmias
- Muscle weakness
Summarise the prognosis for patients with acute kidney injury (AKI).
Prompt recognition and treatment is important.
AKI occurs in 10% to 20% of emergency admissions and has an inpatient mortality >20%.
Important to monitor:
- Review haemodynamic status, including postural BP
- Weight monitroing
- Fluid input / out put chart
- Urea and electrolytes
- ECG changes
- Dietary intake - avoid K+ rich foods
What is Resuscitation, Replacement or Routine Maintenance, when you’re prescribing IV fluid therapy?
Resuscitation fluid therapy is aimed at re-establishing haemodynamic stability by restoring intravascular volume.
Replacement fluid therapy provides daily maintenance water and electrolyte requirements and replaces any ongoing abnormal fluid losses.
Maintenance fluid therapy must provide daily ongoing water and electrolyte requirements (i.e., sodium 1 mmol/kg, potassium 1 mmol/kg, and water 25-35 mL/kg)
Never give maintenance fluids at a rate of >100 mL/hour.
Define adrenal insufficiency.
Deficiency of adrenal cortical hormones - e.g. mineralcorticoids, glucocorticoids and androgens.
Explain the aetiology / risk factors of adrenal insufficiency.
- Primary (Addison’s Disease) - autoimmune >70%
- Infections - TB, meningococcal septicaemia (Waterhouse-Friderichsen Syndrome), CMV (HIV patients), histoplasmosis
- Infiltration - metastasis (e.g. lung, breast, melanoma), lymphomas, amyloidosis
- Infarction - secondary to thrombophilia
- Inherited - adrenoleukodystrophy, ACTH receptor mutation
NB: Adrenoleukodystrophy - X-linked inherited disease characterized by adrenal atrophy and demyelination.
- Surgical - after bilateral adrenalectomy
- Secondary - pituitary or hypothalamic disease
- Iatrogenic - sudden cessation of long-term steroid therapy
Summarise the epidemiology of adrenal insufficiency.
Most common cause is iatrogenic - sudden cessation of long-term steroid therapy.
Primary cause is rare - 8 in 1 million
Recognise the presenting symptoms of adrenal insufficiency.
Chronic
- Non-specific vague symptoms
- Dizziness
- Anorexia
- Weight loss
- Diarrhoea
- Vomiting
- Abdominal pain
- Lethargy
- Weakness
- Depression
Acute
- Acute adrenal insufficiency with major haemodynamic collapse often precipitated by stress - e.g. infection or surgery
Recognise the signs of adrenal insufficiency on physical examination.
- Postural hypotension
- Increased pigmentation - generalized but more on buccal mucosa, scars, skin creases, nails, pressure points (due to melanocytes being stimulated by increased ACTH levels)
- Loss of body hair in women - androgen deficiency
- Associated autoimmune conditions - e.g. vitiligo
- Addisonian Crisis - hypotensive shock, tachycardia, pale, cold, clammy, oliguria
Identify appropriate investigations for adrenal insufficiency and interpret the results.
- Confirm Diagnosis
- Identify level of defect ACTH.
- Identify cause.
- Investigations in Addisonian Crisis.
Confirm Diagnosis:
- 9am serum cortisol <100nmol/L = adrenal insufficiency
- > 550nmol/L - unlikely adrenal insufficiency
- between 100-500nmol/L - conduct short ACTH stimulation test (Synacthen test)
- Synacthen test - IM 250ug tetracosactrin given, cortisol at 30 min <550nmol/L = adrenal failure
Identify Level of ACTH Defect
- High in primary disease
- Low in secondary disease
- Long Synacthen test - 1mg tetracosactrin given, measure cortisol at 0, 30, 60, 90 and 120 mins, then at 4,6,8,12,24h
- No increase after 6 = primary adrenal insufficiency
Identfiy the Cause:
- Autoantibodies - against 21-hydroxylase
- Abdominal CT / MRI
- Adrenal biopsy for microscopy, culture PCR depending on suspected cause
- Check TFTs
Investigations in Addisonian Crisis:
- FBC - neutrophilia
- U&E - increase urea, low Na, high K
- ESR or CRP - acute infection increased
- Ca2+ - increase
- Glucose - low
- Blood cultures
- Urinalysis
- Culture and sensitivity - UTI may be trigger
- CXR - identify cause (e.g. TB, carcinoma) or precipitant of crisis (e.g. infection)
Generate a management plan for adrenal insufficiency.
Addisonian Crisis:
- Rapid IV fluid rehydration - 0.9% saline, 1L over 30-60min, 2-4L in 12-24h
- 50ml of 50% dextrose to correct hypoglycaemia
- IV 200mg hydrocortisone bolus followed by 100mg 6 hourly until BP stable
- Treat precipitating cause - e.g. antibiotics for infection
- Monitor temperature, pulse, respiratory rate, BP, sat O2, urine output
Chronic
- Replacement of glucocorticoids with hydrocortisone - TDS
- Replacement of mineralocorticoids with fludrocortisone
- Hydrocortisone dose needs to be increased during acute illness or stress
- If associated with hypothyroidism, give hydrocortisone before thyroxine to avoid precipitating an Addisonian crisis
Advice
- Steroid warning card
- Medic alert bracelet
- Emergency hydrocortisone ampoule
- Patient education
Identify the possible complications of adrenal insufficiency and its management.
- Hyperkalaemia
- Death during Addisonian crisis
Summarise the prognosis for patients with adrenal insufficiency.
- Adrenal function rarely recovers, but normal life expectancy can be expected if treated
- Type I (autosomal recessive disorder caused by mutations in AIRE gene which encodes of nuclear transcription factor) - Addison’s disease, chronic mucocutaneous candidiasis, hypoparathyroidism
- Type II (Schmidt’s Syndrome) - Addison’s disease, T1DM, hypothyroidism, hypogonadism
Define cardiac arrest.
Acute cessation of cardiac function.
Explain the aetiology / risk factors of cardiac arrest.
4 H’s:
- Hypoxia
- Hypothermia
- Hypovolaemia
- Hypo or hyperkalaemia
4 T’s:
- Tamponade
- Tension pneumothorax
- Thromboembolism (TBE)
- Toxins (drugs, therapeutic agents, sepsis)
Recognise the presenting symptoms of cardiac arrest.
Management precedes or is concurrent to history (e.g. from witnesses)
Recognise the signs of cardiac arrest on physical examination.
- Unconscious
- Not breathing
- Absent carotid pulses
Identify appropriate investigations for cardiac arrest and interpret the results.
1) Cardiac monitor - classifcation of rhythm directs management
2) Bloods - ABG, U&E, FBC, cross-match,clotting, toxicology screen, glucose
Generate a management plan for cardiac arrest.
Safety
- Approprach with caution
- Cause of arrest may still pose a threat
- Defibrillators and oxygen = hazards
- Help summoned as soon as possible
BLS
- If arrest is witnessed and monitored, consider giving a precordial thump if no defibrillators avaliable
- Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift
- Assess breathing by look, listen and feel
- If not breathing, give 2 effective breaths immediately
- Assess circulation at carotid pulse for 10s
- If absent, give 30 chest compressions at a rate of 100/min
- Continue cycles of 30 compressions for every two breaths
- Proceed to advanced life support as soon as possible
ALS
- Attach cardiac monitor and defibrillator
- Assess rhthym
A) If pulseless ventricular tachycardia or ventricularfibrillation (SHOCKABLE)
- Defibrillate once - 150-360J biphasic, 360J monophasic
- Resume CPR immediately for 2 mins and then return to 2
- Administer adrenaline (1mg IV) after 2nd defibrillation and again every 3-5 mins
- If SHOCKABLE persists, administer amiodarone 300mg IV bolus or lidocaine
B) If pulseless electrical activity (PEA) or asystole:
- CPR for 2 minutes then return to 2
- Administer adrenaline 1mg IV every 3-5 minutes
- Atropine (3mg IV) if asystole or PEA with rate <60/min
C) During CPR
- Check electrodes, paddle positions and contacts
- Secure the airway - e.g. attempt ET intubation, high-flow oxygen
- Once airway secure, give continuous compresisons and breaths
- Consider Mg, HCO3, external pacing
- Stop CPR and check pulse only if change in rhythm or signs of life
Treatment of Reversible Causes:
- Hypothermia - warm slowly
- Hypo/hyperkalaemia - correction of electrolytes
- Hypovolaemia - IV colloids, crystalloids or blood products
- Tamponade - pericardiocentesis under xiphisterum up and leftwards
- Tension pneumothorax - needle into second intercostal space, mid-clavicular line
Identify the possible complications of cardiac arrest and its management.
- Irreversible hypoxic brain damage
- Death
Summarise the prognosis for patients with cardiac arrest.
- Less successful outside hospital
- Duration of inadequate effective cardiac output is associated with poor prognosis
Define cardiac failure (acute and chronic).
Inability of the cardiac output to meet the body’s demands despite normal venous pressures.
Explain the aetiology / risk factors of cardiac failure (acute and chronic).
LOW CARDIAC OUTPUT
- Left heart failure - ischaemic heart disease, hypertension, cardiomyopathy aortic valve disease, mitral regurgitation
- Right heart failure - secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade
- Biventricular failure - arrhythmia, cardiomyopathy (dilated or restirctive), myocarditis, drug toxicity
HIGH DEMAND
- Anaemia
- Berberi
- Pregnancy
- Paget’s disease
- Hyperthyroidism
- Arteriovenous malformation
Summarise the epidemiology of cardiac failure (acute and chronic).
10% of 65 year olds.
Recognise the presenting symptoms of cardiac failure (acute and chronic).
Left - caused by pulmonary congestion
- Dyspnoea
- Orthopnea
- Paroxysmal nocturnal dyspnoea
- Fatigue
Acute LVF
- Dyspnoea
- Wheeze
- Cough
- Pink frothy sputum
Right
- Swollen ankles
- Fatigue
- Increased weight - due to oedema
- Reduced exercise tolerace
- Anorexia
- Nausea
NB: New York Heart Association Classification
- No dyspnoea
- Dyspnoea or ordinary activities
- Dyspnoea on less than ordinary activities
- Dyspnoea at rest
Recognise the signs of cardiac failure (acute and chronic) on physical examination.
Left
- Tachycardia
- Tachypnoea
- Displaced apex beat
- Bilateral basal crackles
- 3rd heart sound - gallop rhythm, rapid ventricular filling
- Pansystolic murmuer - functional mitral regurgitation
Acute Left
- Tachyhypnoea
- Cyanosis
- Tachycardia
- Peripheral shutdown
- Pulsus alternans
- Gallop rhythm
- Wheeze cardiac asthma
- Fine crackles throughout the lung
Right
- High JVP
- Hepatomegaly
- Ascites
- Ankle/sacral pitting
- Oedema
- Signs of functional tricuspid regurgitation
Identify the appropriate investigations for cardiac failure (acute and chronic) and interpret the results.
- Bloods
- CXR
- ECF
- Echocardiogram
- Swan-Ganz Catheter
Bloods
- FBC
- U&E
- LFTs
- CRP
- Glucose
- Lipids
- TFTs
- Acute LVF - ABG, troponin, brain natriuretic peptide (BNP)
- High plasma BNP suggests cardiac failure
CXR (Acute LVF)
- Cardiomegaly - heart >50% of thoracic width
- Prominent upper lobe vessels
- Pleural effusion
- Intestitial oedema - Kerley B lines
- Perihilar shadowing - bat’s wings
- Fluid in fissures
ECG
- May be normal
- Ischaemic changes
- Arrhthmia
- Left ventricular hypertrophy
Echocardiogram
- LVEF <40% = systolic dysfunction
- Diastolic dysfunction - reduced compliance leading to a restrictive filling defect
Swan-Ganz Catheter
- Allows measurements of right atrial, right ventricular, pulonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Generate a management plan for cardiac failure (acute and chronic).
Acute LVF
- Cardiogenic shock - severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine), manage in ITU
- Pulmonary oedema - sit up patient, 60-10% oxygen, CPAP.
- Monitor BP, respiatory rate, sats, urine output, ECG
- Treat the cause - e.g. MI, arrythmia
Also consider: diamorphine (venodilator and axiolytic), GTN infusion (reduce preload) IV furosemide if fluid overloaded (venodilator and diuretic)
Chronic LVF
- Treat the cause - e.g. hypertension
- Treat exacerbating factors - e.g. anaemia
- ACE inhibitors - e.g. enalapril, perindopril, ramipril
- B-Blockers - e.g. bisprolol, carvidolol
- Loop diuretics - e.g. furosemide - and dietary salt restritcion to correct fluid overload
- Aldosterone Antagonists - e.g. spironolactone, eplerenone
- Angiotensin Receptor Blokcers - e.g. candesartan
- Hydralazine and Nitrate
- Digoxin
- N-3 Polyunsaturated Fatty Acids
- Cardiac Resynchroniszation Therapy (CRT)
- Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction - e.g. NSAIDs, non-dihydropyridine calcium channel blockers - e.g. diltiazem and verapamil.
Identify the possible complications of cardiac failure (acute and chronic) and its management.
- Respiratory failure
- Cardiogenic shock
- Death
Summarise the prognosis for patients with cardiac failure (acute and chronic).
50% of patients with severe heart failure die within 2 years.
Outline the mechanism of action of ACE-Inhibitors in heart failure patients.
- Inhibit intracardiac renin-angiotensin system that may contribute to myocardial hypertrophy and remodelling
- Slow progression of heart failure and improves survival
- Additive benefits of ACE inhibitors and beta-blockers
Outline the mechanism of action of Aldosterone Antagonists in heart failure patients.
- Improve survival in patients with NYHA class II/IV symptoms and on standard therapy
- Monitor K+ - may cause hyperkalaemia
- Used to assist with management of diuretic induced hypokalaemia
Outline the mechanism of action of Angiotensin Receptor Blockers in heart failure patients.
- May be added in pateints with persistent symptoms despite ACE inhibitors and B-blockers
- Monitor K+ - may cause hyperkalaemia
Outline the mechanism of action of Hydralazine and Nitrates in heart failure patients.
- May be added in patients (Afro-Carribeans) with persistent symptomsdespite therapy with ACE inhibitor and beta-blocker
Outline the mechanism of action of Digoxin in heart failure patients.
- Positive ionotrope
- Reduced hospitalisation
- Does not improve survival
Outline the mechanism of action of N-3 Polyunsaturated Fatty Acids in heart failure patients.
- Provide small beneficial advantage in terms of mortality
Outline the mechanism of action of CRT in heart failure patients.
- Biventricular pacing
- Improves symptoms and survival in patients with LVEF<35%, cardiac dyssynchrony (QRS>120msec) and moderate to severe symptoms despite optimal medical therapy
- Most patients who meet these criteria are also candidates for implanatable cardiac defibrillator (ICD) and recieve combined device
Outline the mechanism of action of Beta-Blockers in heart failure patients.
- Block the effects of chronically activated sympathetic system
- Slows progresion of heart failure and improves survival
- Additive benefits of ACE inhibitors + Beta-blockers
Define acute respiratory distress syndrome.
Syndrome of acute and persistent lung inflammation with increased vascular permeability.
- Acute onset
- Bilateral infiltrates consistent with pulmonary oedema
- Hypoxaemia - PaO2 /FiO2 < 200mmHg regardless of the level of positive end-expiratory pressure (PEEP)
- No clinical evidence for increased left atrial pressure (pulmonary capillary wedge pressure PCWP <18mmHg)
- ARDS is the severe end of the spectrum of acute lung injury (ALI)
Explain the aetiology / risk factors for acute respiratory distress syndrome.
Severe insult to the lungs or other organs induces the release of inflammatory mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance.
Causes:
- Sepsis
- Aspiration
- Pneumonia
- Pancreatitis
- Trauma / Burns
- Transfusion - massive, transfusion-related lung injury
- Transplantation (bone marrow, lung)
- Drug overdose / reaction
- Alcohol misuse
- Smoke inhalation
- Drowning
- E-cigarette and vaping product use
Summarise the epidemiology of acute respiratory distress syndrome.
1 in 6000 per year in UK
Recognise the presenting symptoms of acute respiratory distress syndrome.
- Rapid deterioration of respiratory function
- Dyspnoea
- Respiratory distress
- Cough
- Symptoms of aetiology
Recognise the signs of acute respiratory distress syndrome on physical examination.
- Cyanosis
- Tachypnoea
- Tachycardia
- Widespread inspiratory crepitations
- Hypoxia refractory to oxygen treatment
- Bilateral signs
- May be asymptomatic in early stages
Identify the appropriate investigations for acute respiratory distress syndrome and interpret the results.
- CXR
- Bloods
- Echocardiography
- Pulmonary artery catheterisation
- Bronchoscopy
CXR
- Bilateral alveolar and interstitial shadowing
Bloods
- FBC
- U&E
- LFT
- ESR / CRP
- Amylase
- Clotting
- ABG
- Blood culture
- Sputum culture
- Plasma BNP < 100pg/mL may distinguish between ARDS and heart failure (cannot exclude if critically ill)
Echocardiography
- Severe aortic or mitral valve dysfunction or low left ventricular ejection fraction favours haemodynamic oedema over ARDS
Pulmonary Artery Catheterisation
- PCWP <18mmHg
- High PCWP does not exclude ARDS as patients may have concomitant left ventricular dysfunction
Bronchoscopy
- If cannot determine from history
- Exclude differentials - e.g. diffuse alveolar haemorrhage
- To lavage fluid for microbiology - mycobacteria, Legionella pneumophila
- For cytology - eosinophils, viral inclusion bodies, cancer cells
Diffuse Alveolar Haemorrhage
- Frothy blood in airways
- Haemosiderin-laden macrophage from lavage fluid
Define arterial blood gas.
A collective term applied to three separate measurements = pH, PCO2 and PO2.
They are generally made together to evaluate acid-base status, ventilation and arterial oxygenation.
Summarise the indications for an arterial blood gas.
- Respiratory failure - both acute and chronic states
- Any illness that may lead to a metabolic acidosis - e.g. cardiac failure, liver failure, renal failure, hyperglycaemic states (DM), multiorgan failure, sepsis, burns, poisons/ toxins
- Ventilated patients
- Sleep studies
- Severely unwell patients from any cause - affects prognosis.
Identify the possible complications of an arterial blood gas.
- Local haematoma
- Arterial vasospasm
- Arterial occlusion
- Air or thrombus embolism
- Local anaesthetic anaphylactic reaction
- Infection at the puncture site
- Needle-stick injury to healthcare personnel
- Vessel laceration
Define asthma.
Chronic inflammatory airway disease characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.
Explain the aetiology / risk factors for asthma.
Genetic Factors:
- Family history (twin studies)
- Atopy - tendency of TH2 cells to drive production of IgE on exposure to allergens
- Multiple chromosomal locations (genetic heterogeneity)
Environmental Factors:
- House dust mite
- Pollen
- Pets - e.g. urinary proteins, furs
- Cigarette smoke
- Viral respiratory tract infection
- Aspergillus fumigatus spores
- Occupation allergens (isocyanates, epoxy resins)
Early Phase (Up to 1h)
- Exposure to inhaled allergens in a pre-sensitized individual
- Cross-linking of IgE antibodies on mast-cell surface
- Release of histamine, PgD2, leukotrienes, TNF-alpha
- Smooth muscle contraction = bronchoconstriction
- Mucous hypersecretion
- Oedema
- Airway obstruction
Late Phase (After 6-12h)
- Recruitment of eosinophils, basophils, neutrophil and TH2 lymphocytes and products
- Perpetuation of inflammation and bronchial hyper-responsiveness
- Structural cells (e.g. bronchial epithelial cells, fibroblasts, smooth muscle, and vascular endothelial cells) release cytokines, profibrogenic and proliferative GFs
- Contribute to inflammation and altered function
- Contribute to the proliferation of smooth muscle cells and fibroblasts = airway remodelling
Summarise the epidemiology of asthma.
10% of children 5% of adults Increasing prevalence W > M 1000-2000 deaths from acute asthma per year
Recognise the presenting symptoms of asthma.
- Wheeze
- Breathlessness
- Cough
- Worse in the morning and at night
- Ask about interference with exercise, sleeping, days off school and work
- Acute attack - ask about whether admitted before or to ITU as a gauge of severity potential
Precipitating Factors:
- Cold
- Viral infection
- Drugs - e.g. B-blockers, NSAIDs
- Exercise
- Emotions
- History of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux, family history
Recognise the signs of asthma on physical examination.
- Tachypnoea
- Accessory muscle usage
- Prolonged expiratory phase
- Polyphonic wheeze
- Hyperinflated chest
Severe Attack:
- PEFR < 50% predicted
- Pulse >110/min
- RR >25/min
- Inability to complete sentences
Life-Threatening Attack:
- PEFR < 33%
- Chest silent
- Cyanosis
- Bradycardia
- Hypotension
- Confusion
- Coma
Identify appropriate investigations for asthma and interpret the results.
Acute
- Peak flow
- Pulse oximetry
- ABG
- CXR - to exclude pneumothorax, pneumonia etc
- FBC - high WCC if infective exacerbation
- CRP
- U&E
- Blood & sputum cultures
Chronic
- PEPR monitoring - diurnal variation (morning dip)
- Pulmonary function test - obstructive defect with improvement after trial of B2 agonist
- Blood - eosinophilia, IgE level, Aspergillus antibody titres
- Skin prick tests - identification of allergens
Generate a management plan for asthma.
SEE ALGORITHM.
Acute
- Resuscitate, monitor O2 sats, ABG, PEFR
- High-flow oxygen
- Nebulized B2-agonist bronchodilator salbutamol (5mg initially continuously, then 2-4 hourly), ipratropium (0.5mg QDS)
- Steroid therapy (100-200mg IV hydrocortisone followed by 40mg oral prednisolone for 5-7 days)
- If no improvement - IV magnesium sulphate
- Consider IV aminophylline infusion or IV salbutamol
- Summon anaesthetic if patient is getting exhausted - PCO2 increasing
- Treat any underlying cause (e.g. infection, pneumothorax)
- Give antibiotics if there is a chest infection - e.g. purulent sputum, abnormal CXR, high WCC fever
- Monitor electrolytes closely - as bronchodilators and aminophylline reduce K+
- May need ventilation in severe attacks
- If not improving or patient tiring then involve ITU early
Discharge
- PEF > 75% predicted or patient’s best diurnal variation <25%
- Inhaler technique checked
- Stable on discharge medication for 24h
- Own a PEF meter
- Steroid & bronchodilator therapy
- Arrange to follow up
Chronic Stepwise Therapy
- Review treatment every 3-6 months
STEP 1: Inhaled short-acting B2-agonist as needed, if used >1/day, move to STEP 2.
STEP 2: STEP 1 plus regular inhaled low-dose steroids (400mcg/day)
STEP 3: STEP 2 plus inhaled long-acting B2-agonist (LABA)
If inadequate control with LABA, then increase steroid dose to 800mcg/day. If no response to LABA then stop and increase steroid to 800mcg/day.
STEP 4: Increase inhaled steroid dose to 2000mcg/day, add 4th drugs (e.g. leukotriene receptor antagonist, SR theophylline or B2 agonist tablet)
STEP 5: Addition of regular oral steroids, maintain high-dose inhaled steroid, consider other treatments to minimize the use of oral steroids and refer for specialist care.
Advice
- Educate on proper inhaler technique
- Routine monitoring of peak flow
- Develop an individualized management plan with emphasis on avoidance of provoking factors
Identify the possible complications of asthma and its management.
- Growth retardation
- Chest wall deformity - e.g. pigeon chest
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death
Summarise the prognosis for patients with asthma.
Children usually improve when they grow older
Adult-onset asthma usually chronic
Define COPD.
Chronic, progressive lung disorder characterized by airflow obstruction, chronic bronchitis and emphysema.
Chronic Bronchitis - chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
Emphysema - pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles.
Explain the aetiology / risk factors of COPD.
Bronchial and alveolar damage as a result of environmental toxins - e.g. cigarette smoke.
Rare cause = alpha-1-antitrypsin deficiency (<1%)
- Young patients
- Non-smokers
- Co-presents with asthma
Chronic Bronchitis
- Narrowing of airways due to bronchiole inflammation = bronchiolitis
- Bronchi with mucosal oedema
- Mucous hypersecretion
- Squamous metaplasia
Emphysema
- Destruction and enlargement of alveoli
- Loss of elastic traction that keeps small airways open in expiration
- Larger spaces develop = bullae (>1cm)
Summarise the epidemiology of COPD.
Prevalence 8%
Middle age or later
Males
Change due to increase in female smokers
Recognise the presenting symptoms of COPD.
- Chronic cough
- Sputum production
- Breathlessness
- Wheeze
- Reduced exercise tolerance
Recognise the signs of COPD on physical examination.
Inspection
- Respiratory distress
- Use of accessory muscles
- Barrel-shaped overinflated chest
- Reduced cricosternal distance
- Cyanosis
Percussion
- Hyper-resonant chest
- Loss of liver and cardiac dullness
Auscultation
- Quiet breath sounds
- Prolonged expiration
- Wheeze
- Rhonchi and crepitations
Signs of CO2 Retention
- Bounding pulse
- Warm peripheries
- Flapping tremor of hands (asterixis)
- Late stages = signs of right heart failure (e.g. right ventricular heave, raised JVP, ankle oedema)
Identify appropriate investigations for COPD and interpret the results.
- Spirometry and Pulmonary Function Tests
- CXR
- Bloods
- ABG
- ECG and Echocardiogram - for cor pulmonale
- Sputum and Blood Cultures - acute exacerbations for treatment
- Consider alpha-1-antitrypsin Levels - in non-smokers, young patients
Spirometry & Pulmonary Function Tests
- Obstructive picture
- Reduced PEFR
- Reduced FEV1:FVC ratio - mild, 60-80%, moderate 40-60%, severe <40%)
- Increased lung volumes
- CO gas transfer coefficient reduced when significant alveolar destruction
CXR
- Normal
- Hyperinflation - >6 ribs visible anteriorly, flat hemi-diaphragms
- Reduced peripheral lung markings
- Elongated cardiac silhouette
Blood
- FBC - high Hb and PCV due to secondary polycythemia
ABG
- Hypoxia (reduced PaO2), normal or high PaCO2
Generate a management plan for COPD.
1) Stop Smoking
2) Bronchodilators
3) Steroids
4) Pulmonary Rehabilitation
5) Oxygen Therapy
Bronchodilators
- Short-acting B2 agonists - e.g. salbutamol
- Anticholinergics - e.g. ipratropium
- Delivered by inhalers or nebulizers
- Long-acting B2 agonists if >2 exacerbations per year
Steroids
- Inhaled beclomethasone if FEV1 <50% predicted or those with >2 exacerbations per year
- Regular oral steroids avoided but may be necessary
Oxygen Therapy - only if stopped smoking = long-term home oxygen therapy has been shown to improve mortality
- More economical if used for >8h /day
Indications:
- PaO2 <7.3kPa on air during a period of clinical stability
- PaO2 7.3-8.0kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension
Treatment of Acute Infective Exacerbations:
- Provide 24% O2 via non-variable flow Venturi mask
- Increase slowly if no hypercapnia and still hypoxic (ABG)
- Corticosteroids (oral or inhaled)
- Start empirical antibiotic therapy if evidence of infection - follow trust policy
- Respiratory physiotherapy essential to clear sputum
- Consider non-invasive ventilation in severe cases
- Prevention = pneumococcal and influenza vaccination
Identify the possible complications of COPD and its management.
- Acute respiratory failure
- Infections - e.g. Streptococcus pneumonia, Haemophilus influenzae
- Pulmonary hypertension
- Right heart failure
- Pneumothorax - resulting from bullae rupture
- Secondary polycythaemia
Summarise the prognosis for patients with COPD.
- High level of morbidity
- 3 year survival rate of 90% if age < 60 years and FEV1 > 50% predicted, 75% if >60 years and FEV1 40-49% predicted
Define burns injury.
Predominantly to the skin and superficial tissues, caused by heat from hot liquids, flame, or contact with heated objects, electrical current or chemicals.
Explain the aetiology / risk factors of burns injury.
Severity assess by burn size (% total body surface area) and depth (1st to 4th degree)
Risk Factors:
- Young children
- Age > 60 years
- Male sex
Summarise the epidemiology of burns injury.
Very common injuries
Recognise the presenting symptoms of burns injury.
- Dry and painful burns
- Wet and painful burns
- Dry and insensate burns
Recognise the signs of burns injury on physical examination.
- Erythema
- Clouded cornea
- Cellulitis
- Burns affecting subcutaneous tissue, tendon or bone
Identify appropriate investigations for burns injury and interpret the results.
- FBC - low haematocrit, hypovolaemia, neutropenia, thrombocytopenia
- Metabolic panel - high urea, creatinine, glucose, hyponatraemia, hypokalaemia
- Carboxyhaemoglobin - high levels in inhalation injury
- Arterial blood gas - metabolic acidosis in inhalation injury
- Fluorescein staining - damaged corneal epithelial cells in corneal burns
- CT scan of head and spine - brain injury, fracture in head or spine trauma
- Wound biopsy culture - positive for the causative organism in wound infection sepsis
- Wound histology - show wound infection
Define alcohol withdrawal.
- Withdrawal on cessation of alcohol
- Tolerance
- Compulsion to drink, difficulty controlling termination or levels of use
- Persistent desire to cute down or control use
- Time spent obtaining, using or recovering from alcohol
- Neglect of other interests (social, occupational, recreational)
- Continued use despite physical and psychological problems
Explain the aetiology / risk factors of alcohol withdrawal.
- Genetic factors (twin & family history - 1 in 3 with parent)
- Cultural
- Parental
- Peer group influences
- Availability of alcohol
- Occupation - increased risk in publicans, doctors, lawyers
- Depression
- Anxiety
Summarise the epidemiology of alcohol withdrawal.
2-9% of US (2004)
Recognise the presenting symptoms of alcohol withdrawal.
CAGE
- Cut-down?
- Annoyed by criticism?
- Guilt?
- Eye-opener (wake up)?
Withdrawal
- Nausea
- Sweating
- Tremor
- Restlessness
- Agitation
- Visual hallucination
- Confusion
- Seizures
Recognise the signs of alcohol withdrawal.
- Dupuytren’s contracture
- Palmar erythema
- Bruising
- Spider naevi - spider veins with central red spot
- Telangiectasia - spider veins
- Facial mooning
- Bilateral parotid enlargement
- Gynaecomastia
- Smell of alcohol
Identify appropriate investigations for alcohol withdrawal and interpret the results.
- Bloods
- Acute Overdose
Blood
- Raised MCV
- Raised GGT
- Raised transaminases
- Raised uric acid, triglycerides, bilirubin, albumin, PT in liver
Acute Overdose
- Blood alcohol
- Glucose
- ABG - risk of ketoacidosis or lactic acidosis
- VBG
- U&E
- Toxic screen - e.g. barbiturates, paracetamol
Generate a management plan for alcohol withdrawal.
- I.V. Vitamin B complex (Pabrinex)
- Reducing doses of chlordiazepoxide
- Watch dehydration, electrolyte imbalances, infections
- Nutritional support (malnourishment)
- Lactulose & phosphate enemas - help encephalopathy
