Acute Care & Trauma

Question 1

Define acute kidney injury (AKI).

Answer 1

An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.

Spectrum - mild to severe

Question 2

Explain the aetiology / risk factors of acute kidney injury (AKI).

Answer 2

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)

Question 3

Summarise the epidemiology of acute kidney injury (AKI).

Answer 3

10,400 per million
Seen in 10-20% of people admitted to hospital as emergencies
Inpatient mortality >20%
ICU incidence - 20-50%, mortality >50%

Question 4

Recognize the presenting symptoms of acute kidney injury (AKI).

Answer 4

• 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

Question 5

Recognise the signs of acute kidney injury (AKI) on physical examination.

Answer 5

• 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

Question 6

Identify appropriate investigations for acute kidney injury (AKI) and interpret the results.

Answer 6

• 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

Question 7

Generate a management plan for acute kidney injury (AKI).

Answer 7

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)

Question 8

Identify the possible complications of acute kidney injury (AKI) and its management.

Answer 8

• 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

Question 9

Summarise the prognosis for patients with acute kidney injury (AKI).

Answer 9

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

Question 10

What is Resuscitation, Replacement or Routine Maintenance, when you’re prescribing IV fluid therapy?

Answer 10

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.

Question 11

Define adrenal insufficiency.

Answer 11

Deficiency of adrenal cortical hormones - e.g. mineralcorticoids, glucocorticoids and androgens.

Question 12

Explain the aetiology / risk factors of adrenal insufficiency.

Answer 12

• 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

Question 13

Summarise the epidemiology of adrenal insufficiency.

Answer 13

Most common cause is iatrogenic - sudden cessation of long-term steroid therapy.
Primary cause is rare - 8 in 1 million

Question 14

Recognise the presenting symptoms of adrenal insufficiency.

Answer 14

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

Question 15

Recognise the signs of adrenal insufficiency on physical examination.

Answer 15

• 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

Question 16

Identify appropriate investigations for adrenal insufficiency and interpret the results.

Answer 16

1. Confirm Diagnosis
2. Identify level of defect ACTH.
3. Identify cause.
4. 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)

Question 17

Generate a management plan for adrenal insufficiency.

Answer 17

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

Question 18

Identify the possible complications of adrenal insufficiency and its management.

Answer 18

• Hyperkalaemia

- Death during Addisonian crisis

Question 19

Summarise the prognosis for patients with adrenal insufficiency.

Answer 19

• 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

Question 20

Define cardiac arrest.

Answer 20

Acute cessation of cardiac function.

Question 21

Explain the aetiology / risk factors of cardiac arrest.

Answer 21

4 H’s:

• Hypoxia
• Hypothermia
• Hypovolaemia
• Hypo or hyperkalaemia

4 T’s:

• Tamponade
• Tension pneumothorax
• Thromboembolism (TBE)
• Toxins (drugs, therapeutic agents, sepsis)

Question 22

Recognise the presenting symptoms of cardiac arrest.

Answer 22

Management precedes or is concurrent to history (e.g. from witnesses)

Question 23

Recognise the signs of cardiac arrest on physical examination.

Answer 23

• Unconscious
• Not breathing
• Absent carotid pulses

Question 24

Identify appropriate investigations for cardiac arrest and interpret the results.

Answer 24

1) Cardiac monitor - classifcation of rhythm directs management
2) Bloods - ABG, U&E, FBC, cross-match,clotting, toxicology screen, glucose

Question 25

Generate a management plan for cardiac arrest.

Answer 25

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

Question 26

Identify the possible complications of cardiac arrest and its management.

Answer 26

- Irreversible hypoxic brain damage | - Death

Question 27

Summarise the prognosis for patients with cardiac arrest.

Answer 27

- Less successful outside hospital | - Duration of inadequate effective cardiac output is associated with poor prognosis

Question 28

Define cardiac failure (acute and chronic).

Answer 28

Inability of the cardiac output to meet the body's demands despite normal venous pressures.

Question 29

Explain the aetiology / risk factors of cardiac failure (acute and chronic).

Answer 29

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

Question 30

Summarise the epidemiology of cardiac failure (acute and chronic).

Answer 30

10% of 65 year olds.

Question 31

Recognise the presenting symptoms of cardiac failure (acute and chronic).

Answer 31

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 1. No dyspnoea 2. Dyspnoea or ordinary activities 3. Dyspnoea on less than ordinary activities 4. Dyspnoea at rest

Question 32

Recognise the signs of cardiac failure (acute and chronic) on physical examination.

Answer 32

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

Question 33

Identify the appropriate investigations for cardiac failure (acute and chronic) and interpret the results.

Answer 33

1. Bloods 2. CXR 3. ECF 4. Echocardiogram 5. 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

Question 34

Generate a management plan for cardiac failure (acute and chronic).

Answer 34

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.

Question 35

Identify the possible complications of cardiac failure (acute and chronic) and its management.

Answer 35

- Respiratory failure - Cardiogenic shock - Death

Question 36

Summarise the prognosis for patients with cardiac failure (acute and chronic).

Answer 36

50% of patients with severe heart failure die within 2 years.

Question 37

Outline the mechanism of action of ACE-Inhibitors in heart failure patients.

Answer 37

- 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

Question 38

Outline the mechanism of action of Aldosterone Antagonists in heart failure patients.

Answer 38

- 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

Question 39

Outline the mechanism of action of Angiotensin Receptor Blockers in heart failure patients.

Answer 39

- May be added in pateints with persistent symptoms despite ACE inhibitors and B-blockers - Monitor K+ - may cause hyperkalaemia

Question 40

Outline the mechanism of action of Hydralazine and Nitrates in heart failure patients.

Answer 40

- May be added in patients (Afro-Carribeans) with persistent symptomsdespite therapy with ACE inhibitor and beta-blocker

Question 41

Outline the mechanism of action of Digoxin in heart failure patients.

Answer 41

- Positive ionotrope - Reduced hospitalisation - Does not improve survival

Question 42

Outline the mechanism of action of N-3 Polyunsaturated Fatty Acids in heart failure patients.

Answer 42

- Provide small beneficial advantage in terms of mortality

Question 43

Outline the mechanism of action of CRT in heart failure patients.

Answer 43

- 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

Question 44

Outline the mechanism of action of Beta-Blockers in heart failure patients.

Answer 44

- Block the effects of chronically activated sympathetic system - Slows progresion of heart failure and improves survival - Additive benefits of ACE inhibitors + Beta-blockers

Question 45

Define acute respiratory distress syndrome.

Answer 45

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)

Question 46

Explain the aetiology / risk factors for acute respiratory distress syndrome.

Answer 46

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

Question 47

Summarise the epidemiology of acute respiratory distress syndrome.

Answer 47

1 in 6000 per year in UK

Question 48

Recognise the presenting symptoms of acute respiratory distress syndrome.

Answer 48

- Rapid deterioration of respiratory function - Dyspnoea - Respiratory distress - Cough - Symptoms of aetiology

Question 49

Recognise the signs of acute respiratory distress syndrome on physical examination.

Answer 49

- Cyanosis - Tachypnoea - Tachycardia - Widespread inspiratory crepitations - Hypoxia refractory to oxygen treatment - Bilateral signs - May be asymptomatic in early stages

Question 50

Identify the appropriate investigations for acute respiratory distress syndrome and interpret the results.

Answer 50

1. CXR 2. Bloods 3. Echocardiography 4. Pulmonary artery catheterisation 5. 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

Question 51

Define arterial blood gas.

Answer 51

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.

Question 52

Summarise the indications for an arterial blood gas.

Answer 52

- 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.

Question 53

Identify the possible complications of an arterial blood gas.

Answer 53

- 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

Question 54

Define asthma.

Answer 54

Chronic inflammatory airway disease characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.

Question 55

Explain the aetiology / risk factors for asthma.

Answer 55

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

Question 56

Summarise the epidemiology of asthma.

Answer 56

``` 10% of children 5% of adults Increasing prevalence W > M 1000-2000 deaths from acute asthma per year ```

Question 57

Recognise the presenting symptoms of asthma.

Answer 57

- 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

Question 58

Recognise the signs of asthma on physical examination.

Answer 58

- 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

Question 59

Identify appropriate investigations for asthma and interpret the results.

Answer 59

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

Question 60

Generate a management plan for asthma.

Answer 60

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

Question 61

Identify the possible complications of asthma and its management.

Answer 61

- Growth retardation - Chest wall deformity - e.g. pigeon chest - Recurrent infections - Pneumothorax - Respiratory failure - Death

Question 62

Summarise the prognosis for patients with asthma.

Answer 62

Children usually improve when they grow older | Adult-onset asthma usually chronic

Question 63

Define COPD.

Answer 63

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.

Question 64

Explain the aetiology / risk factors of COPD.

Answer 64

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)

Question 65

Summarise the epidemiology of COPD.

Answer 65

Prevalence 8% Middle age or later Males Change due to increase in female smokers

Question 66

Recognise the presenting symptoms of COPD.

Answer 66

- Chronic cough - Sputum production - Breathlessness - Wheeze - Reduced exercise tolerance

Question 67

Recognise the signs of COPD on physical examination.

Answer 67

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)

Question 68

Identify appropriate investigations for COPD and interpret the results.

Answer 68

1. Spirometry and Pulmonary Function Tests 2. CXR 3. Bloods 4. ABG 5. ECG and Echocardiogram - for cor pulmonale 6. Sputum and Blood Cultures - acute exacerbations for treatment 7. 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

Question 69

Generate a management plan for COPD.

Answer 69

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

Question 70

Identify the possible complications of COPD and its management.

Answer 70

- Acute respiratory failure - Infections - e.g. Streptococcus pneumonia, Haemophilus influenzae - Pulmonary hypertension - Right heart failure - Pneumothorax - resulting from bullae rupture - Secondary polycythaemia

Question 71

Summarise the prognosis for patients with COPD.

Answer 71

- 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

Question 72

Define burns injury.

Answer 72

Predominantly to the skin and superficial tissues, caused by heat from hot liquids, flame, or contact with heated objects, electrical current or chemicals.

Question 73

Explain the aetiology / risk factors of burns injury.

Answer 73

Severity assess by burn size (% total body surface area) and depth (1st to 4th degree) Risk Factors: - Young children - Age > 60 years - Male sex

Question 74

Summarise the epidemiology of burns injury.

Answer 74

Very common injuries

Question 75

Recognise the presenting symptoms of burns injury.

Answer 75

- Dry and painful burns - Wet and painful burns - Dry and insensate burns

Question 76

Recognise the signs of burns injury on physical examination.

Answer 76

- Erythema - Clouded cornea - Cellulitis - Burns affecting subcutaneous tissue, tendon or bone

Question 77

Identify appropriate investigations for burns injury and interpret the results.

Answer 77

- 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

Question 78

Define alcohol withdrawal.

Answer 78

- 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

Question 79

Explain the aetiology / risk factors of alcohol withdrawal.

Answer 79

- 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

Question 80

Summarise the epidemiology of alcohol withdrawal.

Answer 80

2-9% of US (2004)

Question 81

Recognise the presenting symptoms of alcohol withdrawal.

Answer 81

CAGE - Cut-down? - Annoyed by criticism? - Guilt? - Eye-opener (wake up)? Withdrawal - Nausea - Sweating - Tremor - Restlessness - Agitation - Visual hallucination - Confusion - Seizures

Question 82

Recognise the signs of alcohol withdrawal.

Answer 82

- 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

Question 83

Identify appropriate investigations for alcohol withdrawal and interpret the results.

Answer 83

1. Bloods 2. 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

Question 84

Generate a management plan for alcohol withdrawal.

Answer 84

- I.V. Vitamin B complex (Pabrinex) - Reducing doses of chlordiazepoxide - Watch dehydration, electrolyte imbalances, infections - Nutritional support (malnourishment) - Lactulose & phosphate enemas - help encephalopathy

Question 85

Identify the possible complications of alcohol withdrawal and its management.

Answer 85

- Fits - Delirium tremors - coarse tremor, agitation, fever, tachycardia, confusion, delusions, hallucinations - Cerebral atrophy - Dementia - Cerebellar degeneration - Optic atrophy - Peripheral neuropathy - Myopathy - Hepatic encephalopathy - Thiamine deficiency - Wernicke's Encephalopathy - Korsakoff's Psychosis

Question 86

Summarise the prognosis for patients with alcohol withdrawal.

Answer 86

Depends on complications. Alcoholic fatty liver - reversible with abstinence. 5 year rate of alcoholic cirrhosis is 60-70% if stop drinking, <40% if continue.

Question 87

Define Wenicke's Encephalopathy.

Answer 87

- Nystagmus - Ophthalmoplegia - Ataxia - Apathy - Disorientation - Disturbed memory Treatment: Thiamine

Question 88

Define Korsakoff's Psychosis.

Answer 88

Profound impairment of retrograde and anterograde memory with confabulation, due to damage to mammillary bodies and hippocampus.

Question 89

Define epidural.

Answer 89

Opioids and anaesthetics are given into the epidural space by infusion or as boluses. Side effects are thought to be less, as the drug is more localized - watch for respiratory depression and local anaesthetic-induced autonomic blockade (drop in BP).

Question 90

Summarise the indications for an epidural.

Answer 90

- Blunt trauma - with or without rib fractures, thoracic, abdominal, orthopedic and vascular surgery - Non-surgical problems - intractable angina pectoris, acute pancreatitis. - Childbirth - Control pain after major surgery

Question 91

Identify the possible complications of an epidural.

Answer 91

- Patient refusal - Active maternal haemorrhage - Septicaemia - Infection at or near the site of needle insertion - Clinical signs of coagulopathy

Question 92

Define blood product transfusion (including red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate).

Answer 92

Whole Blood - Only option for first 250 years of transfusion history - Now rarely used Red Cell - Packed to make haematocrit approx 70% Platelet - says on the tin! FFP - Contains all coagulation factors except platelets - Fibrinogen, albumin, protein C, protein S, antithrombin, TFPI Cryoprecipitate - Source of fibrinogen Prothrombin Complex Concentrate (PCC) - Intermediate purity pooled plasma products containing a mixture of Vitamin K-dependent proteins

Question 93

Summarise the indications for a blood product transfusion (including red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate).

Answer 93

Red Cell - Use to correct anaemia or blood loss - 1 unit to increase Hb by 10-15g/L - Transfuse in anaemia until Hb >80g/L Platelet - Needed if bleeding or count is <20 x 10^9/L - 1 unit to increase platelet count by >20 x 10^9/L - Failure to increase platelet count = refractory cause - If surgery is planned, get advice if count is <100 x 10^9 / L FFP - Use to correct clotting defects - e.g. DIC, warfarin overdose where VitK is too slow, liver disease, thrombotic thrombocytopenic purpura - Expensive - Do not use as a simple volume expander Cryoprecipitate - Treatment of fibrinogen deficiency or dysfibrinogenaemia when there is clinical bleeding, an invasive proceedure, trauma or DIC Prothrombin Complex Concentrate (PCC) - Replacement therapy of congenital or acquired deficiency of Vitamin K-dependent clotting factors - Prophylaxis and treatment of bleeding (when specific coagulation factor products are not avaliable) - Urgent reversal of over-anticoagulation with warfarin

Question 94

Identify the possible complications of a blood product transfusion (including red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate).

Answer 94

EARLY (within 24h) - Acute haemolytic reactions - e.g. ABO or Rh incompatability - Anaphylaxis - Bacterial contamination - Febrile reactions - e.g. from HLA antibodies - Allergic reactions - e.g. itch, urticaria, mild fever - Fluid overload - Transfusion-related acute lung injury (TRALI, i.e. ARDS due to anti-leucocyte antibodies in donor plasma) DELAYED (after 24h) - Infections - e.g. viruses, heaptitis B or C, HIV, bacteria, protozoa, prions - Iron overload - GVHD - Post-transfusion purpura - potentially lethal fall in platelet count 5-7d post-transfusion requiring specialist treatment with IV immunoglobulin and platelet transfusions

Question 95

Define anaphylaxis.

Answer 95

Acute life-threatening multi-system syndrome caused by sudden release of mast cell- and basophil-derived mediators into the circulation.

Question 96

Explain the aetiology / risk factors of anaphylaxis.

Answer 96

Immunologic vs Non-immunologic. Immunologic: - IgE-mediated or immune complex /complement mediated Non-Immunologic: - Mast cell or basophil degranulation - No involvement of antibodies - e.g. reactions caused by vancomycin, codeine, ACE inhibitors Inflammatory Mediators: - Histamine - Tryptase - Chymase - Histamine-releasing factors - PAF - Prostaglandins - Leucotrienes --> result in bronchospasm, increased capillary permeability and reduced vascular tone --> tissue oedema Allergens: - Drugs - e.g. penicillins - Radiological contrast agents - Latex - Insect stings - Eggs - Peanuts - Shellfish - Fish - Following repeated administration of blood products in patients with selective IgA deficiency - as a result of formation of anti-IgA antibodies - Induced by exercise

Question 97

Summarise the epidemiology of anaphylaxis.

Answer 97

Relatively common. Approx 1 in 5000 exposures to parenteral penicillin or cephalosporins. 1-2% patients receiving IV radiocontrast experience a hypersensitivity reaction. 0.5-1% of children suffer from peanut allergy. 1 in 700 patients have selective IgA deficiency.

Question 98

Recognise the presenting symptoms of anaphylaxis.

Answer 98

Acute onset of symptoms: - Wheeze - Shortness of Breath - Sensation of choking - Swelling of lips and face - Pruritus - Rash The severity of previous reactions does not predict the severity of future reactions. Patients may have a history of other allergic hypersensitivity disorders - e.g. asthma, allergic rhinitis. Biphasic reactions occur 1-72h after 1st reaction in up to 20% of patients.

Question 99

Recognise the signs of anaphylaxis.

Answer 99

- Tachypnoea - Wheeze - Cyanotic - Swollen upper airways and eyes - Rhinitis - Conjunctival injection - Urticarial rash - erythematous wheals - Hypotension - Tachycardia

Question 100

Identify appropriate investigations for anaphylaxis and interpret the results.

Answer 100

Clinical diagnosis. - Serum tryptase - within 15 min-3h after onset of symptoms - Histamine levels - within 30 mins after symptom onset - Urinary metabolites of histamine - elevated for several hours after NB: Normal levels of these mediators do not exclude the possibility of anaphylaxis. After the Attack: - Allergen skin testing - identifies allergen, performed by allergy specialist due to risk and skill for interpretation - IgE immunoassays - e.g. radioallergosorbent tests (RASTs) to identify food-specific IgE in serum

Question 101

Generate a management plan for anaphylaxis.

Answer 101

Stop any suspected drugs. 1. Resuscitation - allow principles of ABCDE 2. Secure airway and give 100% O2 - intubation, transfer to ITU, inform anaesthetist early 3. Adrenaline IM (0.5mL of 1:1,000) - repeated every 10 mins according to pulse and BP 4. Antihistamine IV (10mg chlorpheniramine) 5. Steroids IV (100mg hydrocortisone) 6. IV Crystalloid or Colloid - maintain blood pressure, lie flat with head tilted down. 7. Treat bronchospasm with salbutamol and ipratropium inhaler (consider aminophylline IV infusion) Advice: - Educate on use of adrenaline pen for IM administration - Provide MedicAlert bracelet - Make note in drug charts and notes - Referral to an allergy specialist for identification of the culprit allergen and education in allergen avoidance

Question 102

Identify the possible complications of anaphylaxis and its management.

Answer 102

Respiratory failure, shock, death

Question 103

Summarise the prognosis for patients with anaphylaxis.

Answer 103

Good if prompt treatment given

Question 104

Define aspirin overdose.

Answer 104

Excessive ingestion of aspirin causing toxicity.

Question 105

Explain the aetiology / risk factors of aspirin overdose.

Answer 105

Causes: - Deliberate self-harm - Suicidal intent - Accident - e.g. children Ingestion of 10-20g can cause moderate-severe toxicity in adults. Aspirin (Acetylsalicylate): - Increases RR & depth - Stimulates CNS respiratory centre - Hyperventilation - Respiratory alkalosis in early phase - Compensation by increasing urinary bicarbonate and K+ excretion - Dehydration and hypokalaemia - Uncoupling of mitochondrial oxidative phosphorylation by salicyclic acid - Build up of lactic acid - Results in metabolic acidosis - CNS depression and respiratory failure

Question 106

Summarise the epidemiology of aspirin overdose.

Answer 106

One of most common drug overdoses.

Question 107

Recognise the presenting symptoms of aspirin overdose.

Answer 107

Key Facts: - How much aspirin? - When - Any other drugs? - Have you had any alcohol? May be asymptomatic. Early Symptoms: - Flushed appearance - Fever - Sweating - Hyperventilation - Dizziness - Tinnitus Late Symptoms: - Lethargy - Confusion - Convulsions - Drowsiness - Respiratory depression - Coma

Question 108

Recognise the signs of aspirin overdose on physical examination.

Answer 108

- Fever - Tachycardia - Hyperventilation - Epigastric tenderness

Question 109

Identify appropriate investigations for aspirin overdose and interpret the results.

Answer 109

Bloods - Salicylate levels - 500-750mg/L is moderate,>750mg/L is severe - FBC - U&E - low K+ if vomiting - LFT - high AST and ALT - Clotting screen - high PT - Glucose and other drug levels - e.g. paracetamol ABG - Mixed metabolic acidosis and respiratory alkalosis ECG - Hypokalaemia - small T-waves, U waves

Question 110

Define disseminated intravascular coagulation (DIC).

Answer 110

A disorder of the clotting cascade that can complicate a serious illness. 2 forms: 1) Acute overt form where there is bleeding and depletion of platelets and clotting factors 2) Chronic non-overt form where thromboembolism is accompanied by generalised activation of the coagulation system.

Question 111

Explain the aetiology / risk factors of disseminated intravascular coagulation (DIC).

Answer 111

ACUTE - Activation of coagulation due to endothelial damage and increased release of granulocyte / macrophage procoagulant substances - E.g. Tissue factor (secondary to endotoxin, membrane lipopolysaccharides, cytokines such as IL-6 and TNF-alpha) - Explosive thrombin generation - Depletion of clotting factors and platelets - Simultaneous activation of fibrinolytic system - Bleeding into the subcutaneous tissues, skin and mucous membranes - Occlusion of blood vessels by fibrin in microcirculation - Microangiopathic haemolytic anaemia and ischaemic organ damage as a result CHRONIC - Identical process, but slower rate - Time for compensatory responses - Diminishes likelihood of bleeding - Gives rise to hypercoaguable state and thrombosis can occur Causes: - Infection - gram-negative sepsis - Obstetric complications - missed miscarriage, severe pre-eclampsia, placental abruption, amniotic emboli - Malignancy - acute promyelocytic leukaemia (acute), lung, breast, GI malignancy (chronic) - Severe trauma or surgery - Haemolytic transfusion reaction - Burns - Liver disease - Aortic aneurysms - Haemangiomas

Question 112

Summarise the epidemiology of disseminated intravascular coagulation (DIC).

Answer 112

Seen in any severely ill patient

Question 113

Recognise the presenting symptoms of disseminated intravascular coagulation (DIC).

Answer 113

Severely unwell with symptoms of underlying disease, confusion, dyspnoea and evidence of bleeding

Question 114

Recognise the signs of disseminated intravascular coagulation (DIC) on physical examination.

Answer 114

Signs of underlying aetiology, fever, evidence of shock - hypotension and tachycardia. ACUTE - Petechiae - Purpura - Ecchymoses - Epistaxis - Mucosal bleeding - Overt haemorrhage - Signs of end-organ damage - e.g. local infarction or gangrene - Respiratory distress - Oliguria caused by renal failure CHRONIC - Signs of deep venous or arterial thrombosis or embolism - Superficial venous thrombosis, especially without varicose veins

Question 115

Identify appropriate investigations for disseminated intravascular coagulation (DIC) and interpret the results.

Answer 115

Bloods - FBC - low platelets, low Hb - Clotting - high APTT/ PT/TT, low fibrinogen, high fibrin degradation products and d-dimers Peripheral Blood Film - Red blood cell fragments - schistocytes

Question 116

Define encephalitis.

Answer 116

Inflammation of the brain parenchyma.

Question 117

Explain the aetiology /risk factors of encephalitis.

Answer 117

Causes: - VIRAL - e.g. HSV, herpes zoster, mumps, adenovirus, coxsackie, echovirus, enteroviruses, measles, EBV, HIV, rabies (Asia), Nipah (Malasia), arboviruses transmitted by mosquitos (Jap B encephalitis - Asia, St Louis and West Nile encephalitis - USA) - NON-VIRAL - e.g. syphillis, Staphylococcus aureus - IMMUNOCOMPROMISED - e.g. CMV, toxoplasmosis, Listeria - AUTOIMMUNE OR PARANEOPLASTIC - associated with antibodies - e.g. anti-NMDA or anti-VGKC

Question 118

Summarise the epidemiology of encephalitis.

Answer 118

7.4 in 100,000 in UK

Question 119

Recognise the presenting symptoms of encephalitis.

Answer 119

- Can be mild and self-limiting - Subacute onset (hours to days) - Headache - Fever - Vomiting - Neck stiffness - Photophobia - i.e. symptoms of meningism (meningoencephalitis) - Behavioural changes - Drowsiness - Confusion - History of seizures - Focal neurological symptoms - e.g. dysphagia, hemiplegia - DETAILED TRAVEL HISTORY

Question 120

Recognise the signs of encephalitis on physical examination.

Answer 120

- Reduced level of consciousness with deteriorating GCS - Seizures - Pyrexia - Neck stiffness - Photophobia - Kernig's test positive - Hypertension - Bradycardia - Papilloedema - Focal neurological signs - e.g. dysphagia, hemiplegia - Minimental examination may reveal cognitive or psychiatric disturbances NB: Raised intracranial signs and meningism signs.

Question 121

Identify appropriate investigations for encephalitis and interpret the results.

Answer 121

1. Bloods 2. MRI / CT 3. Lumbar Puncture 4. EEG 5. Brain Biopsy Bloods - FBC - high lymphocytes - U&E - SIADH may occur - Glucose - compare with CSF glucose - Viral serology - ABG MRI / CT - Excludes mass lesion - HSV produces characteristic oedema of the temporal lobe on MRI Lumbar Puncture - High lymphocytes - High monocytes - High protein - Glucose usually normal - CSF culture difficult - Viral PCR now first line EEG - Epileptiform activity - E.g. spiking activity in temporal lobes Brain Biopsy - Rarely performed

Question 122

Define extradural haemorrhage.

Answer 122

Aka epidural haematoma. Collection of blood that forms between the inner surface of the skull and outer layer of the dura, which is called the endosteal layer. Associated with a history of head trauma and associated skull fracture.

Question 123

Explain the aetiology / risk factors of extradural haemorrhage.

Answer 123

Causes: - Traumatic skull fracture - to a temple just lateral to the eye - temporal or parietal bone - Laceration of middle meningeal artery and vein - Tear in dural venous sinus Differentials - epilepsy, carotid dissection, carbon monoxide poisoning.

Question 124

Summarise the epidemiology of extradural haemorrhage.

Answer 124

2% of all head injuries | 15% of all fatal head traumas

Question 125

Recognise the presenting symptoms of extradural haemorrhage.

Answer 125

- Deteriorating consciousness after head injury - No initial loss of consciousness - Initial drowsiness post injury seems to have resolved - Lucid interval pattern - lasts a few hours to a few days before reducing GCS from raised ICP - Severe headache - Vomiting - Confusion - Seizures - Hemiparesis with brisk reflexes and upgoing plantar If bleeding continues: - Ipsilateral pupil dilation - Coma deepening - Bilateral limb weakness - Breathing becomes deep and irregular due to brainstem compression - Death following period of coma due to respiratory arrest - Bradycardia and high BP are late signs

Question 126

Recognise the signs of extradural haemorrhage on physical examination.

Answer 126

- Deteriorating consciousness after head injury - No initial loss of consciousness - Initial drowsiness post injury seems to have resolved - Lucid interval pattern - lasts a few hours to a few days before reducing GCS from raised ICP - Severe headache - Vomiting - Confusion - Seizures - Hemiparesis with brisk reflexes and upgoing plantar If bleeding continues: - Ipsilateral pupil dilation - Coma deepening - Bilateral limb weakness - Breathing becomes deep and irregular due to brainstem compression - Death following period of coma due to respiratory arrest - Bradycardia and high BP are late signs

Question 127

Identify appropriate investigations for extradural haemorrhage and interpret the results.

Answer 127

CT - Shows haematoma lens-shaped / biconvex - Rounded blood shape NB: Sickle-shaped subdural haematoma as touch dural attachments to skull keep it more localized Skull X-RAY - Normal - Fracture lines crossing course of middle meningeal vessels LUMBAR PUNCTURE IS CONTRAINDICATED.

Question 128

Define head injury.

Answer 128

A broad term that describes a vast array of injuries that occur to the scalp, skull, brain and underlying tissue and blood vessels in the head. TBI = traumatic brain injury

Question 129

Explain the aetiology / risk factors of head injury.

Answer 129

Causes: - Falls - Vehicle-related collisions - Violence - Sports injuries - Explosive blasts or other combat injuries Risk Factors: - Children - especially newborns to 4-year-olds - Young adults, especially 15-24 years - Adults >60 yrs - Males in any age group

Question 130

Summarise the epidemiology of head injury.

Answer 130

180-220 cases per 100,000 population.

Question 131

Recognise the presenting symptoms of head injury.

Answer 131

- Loss of consciousness for a few seconds to a few minutes to a few hours - No loss of consciousness, but a state of being dazed, confused or disorientated - Headache - Nausea - Vomiting - Fatigue - Drowsiness - Problems with speech - Difficulty sleeping - Sleeping more than usual - Dizziness or loss of balance - Sensory problems - e.g. blurred vision, ringing in heads, bad taste in mouth, changes in ability to smell - Sensitivity to light or sound - Memory or concentration problems - Mood changes or mood swings - Feeling depressed or anxious - Convulsions or seizures

Question 132

Recognise the signs of head injury on physical examination.

Answer 132

- Dilation of one or both pupils of the eyes - Clear fluids draining from the nose or ears - Weakness or numbness in fingers and toes - Loss of co-ordination - Profound confusion - Agitation, combativeness, unusual behaviour - Slurred speech - Coma

Question 133

Identify appropriate investigations for head injury and interpret the results.

Answer 133

CT Head <1h if: - GCS <13 on initial assessment or GCS <15 at 2h following injury - Focal neurological deficit - Suspected open or depressed skull fracture or signs of basal skull fracture - periorbital ecchymoses (panda eyes, racoon sign), postauricular ecchymosis (Battle's sign), CSF leak through nose / ears, haemotympanum - Post-traumatic seizure - Vomiting more than once Perform a CT Head <8h if: - Any loss of consciousness or amnesia - Any of : Age >65, coagulopathy, high-impact injury (e.g. struck by or ejected from motor vehicle, fall >1m or >5 stairs), retrograde amnesia of >30 mins CT Cervical Spine <1h if: - GCS <13 on initial assessment - Intubated patient - Definitive diagnosis needed urgently before surgery - Patient is having other body areas scanned - e.g. multi-region trauma - Clinical suspicion and any of: Age >65, high impact injury, focal neurological deficit, paraesthesia in upper or lower limbs NB: Alcohol unlikely caused of coma if plasma alcohol <44mmol/L.

Question 134

Define ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).

Answer 134

Reduced blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome. Acute coronary syndrome - divided into unstable angina (no cardiac injury), STEMI, NSTEMI. MI = cardiac muscle necrosis resulting from ischaemia. Atherosclerosis: - Endothelial injury - Migration of monocytes into sub-endothlial space - Differentiation into macrophages - Accumulation of LDL lipids insudated in subendothelium - Foam cells - Release of growth factors - Smooth muscle proliferation - Production of collagen and proteoglycans - Formation of atheromatous plaque

Question 135

Explain the aetiology / risk factors of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).

Answer 135

Angina pectoris = oxygen demand >> oxygen supply - Caused by atherosclerosis, spasm, arteritis, emboli MI - Caused by occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation Risk factors: - Male - DM - Family history - Hypertension - Hyperlipidaemia - Smoking - Previous history Atherosclerosis: - Endothelial injury - Migration of monocytes into sub-endothlial space - Differentiation into macrophages - Accumulation of LDL lipids insudated in subendothelium - Foam cells - Release of growth factors - Smooth muscle proliferation - Production of collagen and proteoglycans - Formation of atheromatous plaque

Question 136

Summarise the epidemiology of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).

Answer 136

2% Common More common in males MI 5 in 1000 incidence UK

Question 137

Recognise the presenting symptoms of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).

Answer 137

Acute Coronary Syndrome - Chest pain - Discomfort of acute onset - Central heavy tight gripping pain - Radiation to left arm, neck, jaw or epigastrum - Increase severity and frequency of previous stable angina - Breathlessness - Sweating - Nausea - Vomiting - Silent in elderly or patients with diabetes Stable Angina - Brought on by exertion - Relieved by rest

Question 138

Recognise the signs of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) on physical examination.

Answer 138

Acute Coronary Syndrome - No clinical signs - Pale - Sweating - Restless - Low-grade pyrexia - Check both radial pulses for aortic dissection - Arryhthmias - Disturbances of BP - New heart murmurs - e.g. pansystolic murmur of mitral regurgitation from papillary muscle rupture or ventricular septal defect - Signs of complications - e.g. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oligura) Stable Angina - Look for signs of risk factors

Question 139

Identfy appropriate investigations for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and interpret the results.

Answer 139

1. Bloods 2. ECG 3. CXR 4. Exercise ECG Testing 5. Radionuclide Myocardial Perfusion Imaging (rMPI) 6. Echocardiogram 7. Pharmacologic Stress Testing 8. Cardiac catheterization / angiography 9. Coronary Calcium Scoring Bloods - FBC - U&E - CRP - Glucose - Lipid profile - Cardiac enzymes - CK-MB and troponin -T or I1 (high after 12h) - Amylase - pancreatitis mimics MI - TFTs - AST & LDH - high after 24-48h ECG - Unstable Angina or NSTEMI - ST depression, T-wave inversion, Q waves (may indicate old MI) - STEMI - ST elevation (>1mm in limb leads, >2mm in chest leads), hyperacute T-waves, new-onset LBBB, hours later T-wave invesion, days later Q waves Location of infarct: - Inferior walls --> II, III, AVF - Anterior wall --> Septum (V1-2), Apex (V3-4), Anterolateral Wall (V5-6) - Lateral wall --> I, AVL - Posterior infarct --> Tall R wave, ST depression in V1-3 CXR - Look for signs of heart failure - Look for differentials - e.g. aortic dissection Exercise ECG - treadmill test - Indications - troponin-negative ACS, stable angina with intermediate or high pretest probability of CHD - Not on digoxin - false-positive result - Take into account chest pain, cardiac risk factors, age, gender - Positive Test = >1mm horizontal or downsloping ST-segment depression measured 80ms after end of QRS - Failed Test = failure to achieve at least 85% of the predicted maximal heart rate (220-age), negative otherwise - B-blockers reduce maximal heart rate Radionuclide Myocardial Perfusion Imaging (rMPI) - Tc-99m sestamibi or tetrofosmin - Under stress (exercise or pharmacological) or at rest - Show low uptake in ischaemic myocardium during stress - Rest testing - used in patient with ACS, no previous MI but non-diagnostic troponin and ECGs Echocardiogram - Measure LVEF - myocardial stunning misleading in early measurements - Exercise or dobutamine stress - detect inducible wall motion abnormalities Pharmacologic Stress Testing - Patients who cannot exercise or if exercise test is inconclusive - E.g. Dipyridamole, adenosine, dobutamine induces tachycardia - Detect ischaemic myocardium - e.g. rMPI, echocardiography - Contraindicated in AV block and reactive airway disease (dipyridamole, adenosine) Cardiac Catheterisation / Angiography - ACS with positive troponin or TIMI score 5-7 or if high risk on stress testing - Use Duke treadmill score based on exercise time, maximum ST-segment deviation and exercise angina Coronary Calcium Scoring - Using specialized CT - Role in outpatieints with atypical chest pain or in acute chest pain that is not clearly due to ischaemia - e.g. absence of CAC exclusdes obstructive coornary artery disease

Question 140

Generate a management plan for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).

Answer 140

Stable Angina - Mimize cardiac risk factors - e.g. BP, hyperlipidaemia, diabetes, advice on smoking, exercise, weight loss, low-fat diet --> ASPIRIN 75mg/day - Immediate symptoms relief --> GTN as a spray or sublingually - Long-term --> B-BLOCKERS (e.g. atenolol), CALCIUM CHANNEL BLOCKERS ( e.g. verapamil, diltiazem), NITRATES (e.g. isosorbide dinrate) - Percutaneous Coronary Intervenion (PCI) - for localised areas of stenosis, in patients with angina not controlled by therapy, restenosis rate 25% at 6 months, drug-eluting coronary stents reduce rates (release sirolimus or paclitaxel) - Coronary Artery Bypass Graft (CABG) - for 3-vessel disease, rate of MI and survival similar betwen PCI and CABG NB: Contraindications of B-blockers - e.g. acute heart failure, cardiogenic shock, bradycardia, heart block, asthma, Unstable Angina / NSTEMI - Admit to CCU - Oxygen - IV access - Monitor vitals - Serial ECG - Analgesia - e.g. GTN, morphine sulphate / diamorphine, antiemetic (metoclopramide) - Aspirin - 300mg chewed, 75mg maintenance indefinite - Clopidogrel - 300mg, 75mg maintenance for 1 year if troponin positive or high risk - Low molecular weight heparin - e.g. enoxaparin, dalteparin - B-blocker - e.g. metoprolol - Glucose-insulin infusion if blood glucose >11 mmol/L - Glycoprotein IIb/IIIa inhibitors - e.g. tirofiban (initiated on presentation, continued for 48-72h or until PCI) --> for patients undergoing PCI, high risk for further cardiac events - Urgent angiography & revascularisation if no improvement High Risk for further cardiac events: - Troponin positive - TIMI risk score >4 - Continuing ischaemia STEMI - Admit to CCU - Oxygen - IV access - Monitor vitals - Serial ECG - Analgesia - GTN, morphine sulphate / diamorphine, antiemetic (metoclopramide) - Aspirin - 300mg chewed, 75mg maintenance indefinite - Clopidogrel - 600mg if patient going to primary PCI, 300mg if thrombolysis, <75yrs, 75mg if thrombolysis, >75yrs, 75mg maintenance for 1 year - B-Blocker - e.g. metoprolol - Primary PCI route - needs IV heparin + GP IIb/IIIa inhibitor OR bivalirudin (antithrombin) - Thrombolysis route with recobinant tissue plasminogen activator (rtPA) - IV heparin - Glucose-insulin infusion if blood glucose>11mmol/L NB: Primary PCI with goal <90 mins Thrombolysis with goal of 30 mins Rescue PCI if continued pain or elevation after thrombolysis of initial ST-segment elevation on follow up ECG 60-90min after fibrinolytic reaction Thrombolysis - Fibrinolytics - e.g. streptokinase, rtPA (alteplase, reteplase, tenecteplase) if within 12h of chest pain with ECG changes Secondary Prevention: - Antiplatelet agents - e.g. aspirin, clopidogrel - ACE inhibitors - B-Blockers - Statins - Control risk factors - e.g. smoking, diabetes, hypertension Advice - Do not drive for a month following MI - Education by cardiac rehabilitation team - Lifestyle changes - e.g. exercise, stop smoking, changing diet CABG - For patients with left main stem or three-vessel disease

Question 141

Identify the possible complications of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and its management.

Answer 141

At risk of MI and other vasuclar diseases - e.g. stroke, peripheral vascular disease Cardiac injury can lead secondarily to heart failure and arrhythmias Early Complications (24-72h) - Death - Cardiogenic shock - Heart failure - Ventricular arrythmias - Heart block - Pericarditis - Myocardial rupture - Thromboembolism Late Complications - Ventricular wall or septum rupture - Valvular regurgitation - Ventricula aneurysms - Tamponade - Dressler's syndrome (pericarditis) - Thromboembolism

Question 142

Summarise the prognosis for patients with ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction).

Answer 142

Acute Coronary Sydnrome: - TIMI score used for risk stratification (0-7) - High score = high risk of cardiac events within 30 days 1) >65 yrs 2) Known CAD 3) Aspirin in last 7 days 4) Severe angina (>2 episodes in 24h) 5) ST deviation >1mm 6) Elevated troponin levels 7) >3 coronary artery disease risk factors - e.g. hypertension, hyperlipidaemia, family history, diabetes, smoking Killip Classification of Acute MI: - Class I - no evidence of acute heart failure - Class II - mild to moderate heart failure (S3, crepitations

Question 143

Define meningitis.

Answer 143

Inflammation of the leptomeningeal (pia mater and arachnoid) coverings of the brain, most commonly caused by infection. Aseptic meningitis - characterised by clinical and laboratory evidence for meningeal inflammation and negative routine bacterial culture Mollaret's meningitis - recurrent benign lymphocytic meningitis

Question 144

Explain the aetiology / risk factors of meningitis.

Answer 144

Bacterial - Neonates - Group B streptococci, Escherichia coli, Listeria monocytogenes - Children - Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae - Adults - Neisseria meningitidis (meningococcus), Streptococcus pneumonia, tuberculosis - Elderly - Streptococcus pneumoniae, Listeria monocytogenes Viral - Enteroviruses - Mumps - HSV - VZV - HIV Fungal - Cryptococcus - associated with HIV infection Aseptic Meningitis - Enterovirus, mycobacteria, fungi, spirochetes - Autoimmune - e.g. Sarcoidosis, Behcet's disease, Systemic lupus erythematosus - Malignancy - lymphoma, leukaemia, metastatic carcinomas - Medication - NSAIDs, trimethoprim, azathioprine Mollaret's Meningitis - 50% exhibit transient neurological manifestations - HSV-2 - Large granular plasma cells on Papnicolaou's stain, PCR for HSV DNA - Treat with acyclovir Risk Factors: - Close communities - e.g. dormitories - Basal skull fractures - Mastoiditis - Sinusitis - Inner ear infections - Alcoholism - Immunodeficiency - Splenectomy - Sickle cell anaemia - CSF shunts - Intracranial surgery

Question 145

Summarise the epidemiology of meningitis.

Answer 145

Variation according to geography, age, social conditions. UK Public Health Laboratory Service receives approx 2500 notifications / year. Recent visitors to Haj (meningococcal serogroup W135). Epidemics occur in the meningitis belt of Africa (meningococcal serogroup A).

Question 146

Recognise the presenting symptoms of meningitis.

Answer 146

- Severe headache - Photophobia - Neck or backache - Irritability - Drowsiness - Vomiting - High-pitched crying or fits (common in children) - Clouding of consciousness - Fever Check travel and exposure history: - Rodents - lymphocytic choriomeningitis virus - Ticks - Lyme borrelia, Rocky Mountain spotted fever - Mosquitoes - West Nile virus, St. Louis encephalitis virus - Sexual activity - HSV-2, HIV, syphilis - Travel - C.immitis, A.cantonensis - Contact with other individuals with vrial exanthems - enteroviruses

Question 147

Recognise the signs of meningitis on physical examination.

Answer 147

Signs of Meningism: - Photophobia - Neck stiffness - Kernig's sign - with hips flexed, pain / resistance on passive knee extension - Brudzinski's sign - flexion of hips on neck flexion Signs of Infection - Fever - Tachycardia - Hypotension - Skin rash - petechiae with meningococcal septicaemia - Altered mental state

Question 148

Identify appropriate investigations for meningitis and interpret the results.

Answer 148

1. Bloods 2. Imaging 3. Lumbar Punctre 4. viral 5. TB Bloods - 2 sets of blood cultures - do not delay antibiotics Imaging - CT scan to exclude a mass lesion or raised intracranial pressure before LP - LP may lead to cerebral herniation due to subsequent CSF removal - CT head before LP in patents with immunodeficiency, history of CNS disease, reduced consciousness, fit, focal nerologic deficit, papilloedema LP - Note opening CSF pressure - Send for microscopy with culture, sensitivity, Gram staining, biochemistry, cytology - Streptococcus pneumoniae - Gram-positive diplococcic - Neisseria Meningitidis - gram-negative diplococcic Bacterial - Cloudy CSF - Increased neutrophils - Increased protein - Reduced glucose - CSF serum glucose ratio of <0.5 Virus - Increased lymphocytes - Increased protein - Normal glucose TB - Fibrinous CSF - Increased lymphocytes - Increased protein - Reduced glucose Staining of petechiae scrapings may detect meningococcus in 70%. Additional studies - e.g. viral PCR, staining / culture for mycobacteria and fungi, HIV test depending on the clinical presentation / CSF findings.

Question 149

Generate a management plan for meningitis.

Answer 149

1. IMMEDIATE ANTIBIOTICS IV or IM - If meningitis suspected before lumbar puncture or CT - 3rd generation cephalosporin - cefotaxime 2g QDS or ceftriaxone 2g BD - Benzylpenicillin - initial blind therapy, sensitive meningococci and pneumococci - Listeria = amoxicillin + gentamicin - Penicillin & Cephalosporin resistant pneumococci = + vancomycin + rifampicin - History of anaphylaxis to penicillin or cephalosporins = chloramphenicol - Patients treated with benzylpenicillin or chloramphenicol = 2 days rifampicin (eliminate nasopharyngeal carriage) 2. DEXAMETHASONE IV - 10mg QDS for 4 days - Given shortly before or with first dose of antibiotics - Continue in pneumococcal or H. influenzae meningitis - reduce complications of death (pneumococcal) and hearing loss (H.influenzae) - Avoid dexamethasone if HIV suspected 3. RESUSCITATION - ITU 4. PREVENTION - Notify public health services - Consult a consultant in communicable disease control for advice regarding chemoprophylaxis - e.g. rifampicin for 2 days - Vaccination for close contacts - Vaccination against meningococcal serogroups A and C (none for B)

Question 150

Identify the possible complications of meningitis and its management.

Answer 150

- Septicaemia - Shock - DIC - Renal failure - Fits - Peripheral gangrene - Cerebral oedema - Cranial nerve lesions - Cerebral venous thrombosis - Hydrocephalus - Water house - Friderichsen Syndrome - bilateral adrenal haemorrhage

Question 151

Summarise the prognosis for patients with meningitis.

Answer 151

Bacterial meningitis mortality at 10-40% with meningococcal sepsis. In developing countries - higher mortality rate Viral meningitis - self-limiting

Question 152

Define multi-organ dysfunction syndrome.

Answer 152

Evidence of two or more organs failing in addition to systemic inflammatory response syndrome (SIRS) - e.g. confusion due to cerebral hypo-perfusion, renal failure, respiratory failure, liver failure.

Question 153

Explain the aetiology / risk factors of multi-organ dysfunction syndrome.

Answer 153

Causes: - Sepsis - Major trauma - Major surgery - Burns - Pancreatitis - Shock - Aspiration syndromes - Blood transfusions - Autoimmune disease - Acute heart failure - Poisons / toxins Risk Factor: - Reduced renal blood flow due to systemic hypotension - Altered regional renal perfusion - Increased intra-abdominal pressure - Nephrotoxic drugs - Advancing age - Prior chronic conditions - Malnutrition - Injury severity score (ISS) - Coma on admission - Use of H2-Receptor Antagonists - Use of antacids - Number of blood transfusions - Intra-abdominal infection

Question 154

Recognise the signs of multi-organ dysfunction syndrome on physical examination.

Answer 154

- Acute kidney injury (AKI) - Uraemic acidosis - Acute respiratory distress syndrome (ARDS) - Cardiomyopathy - Encephalopathy - Gastrointestinal dysfunction - Hepatic dysfunction - Coagulopathy - Bone marrow suppression - Acute neurological dysfunction

Question 155

Identify appropriate investigations for multi-organ dysfunction syndrome and interpret the results.

Answer 155

- Urinalysis | - Bloods - raised urea, creatinine, reduced eGFR

Question 156

Identify appropriate investigations for multi-organ dysfunction syndrome and interpret the results.

Answer 156

- CXR - pneumonia - Supine and upright or lateral decubitus abdominal film - US - if biliary tract infection source - CT - intra-abdominal, retroperitoneal source - CT head - if raised intracranial pressure (papilloedema), focal mess lesion, meningitis - LP - meningitis - Bloods - FBC (low Hb?), Clotting (DIC), WCC (>15,000 - bacterial infection), Neutrophils (>1500 - bacterial infection) - Metabolic assessment - Mg, Ca, PO4, glucose - Urinalysis - raised urea, creatinine - LFTs - bilirubin (high), ALP (high), ALT (high), albumin (low) - depends on cause - ABG - lactate (high in hypoperfusion)

Question 157

Define opiate overdose.

Answer 157

Opioid - any synthetic or natural agent that stimulates opioid receptors and produces opium-like effects. Papver somniferum - e.g. morphine, codeine. Overdose - when larger quantities than physically tolerated are taken, resulting in CNS and respiratory depression, miosis, apnoea.

Question 158

Explain the aetiology / risk factors of opiate overdose.

Answer 158

Risk Factors: - Opioid abuse and dependence - Recent abstinence in chronic users - Chronic pain

Question 159

Summarise the epidemiology of opiate overdose.

Answer 159

Leading cause of accidental death in the US. x4 increase in prescriptions for opioid containing medications in early 10s, x4 increase in overdose deaths due to opioids. Majority due to heroin and other synthetic opiates other than methadone.

Question 160

Recognise the signs of opiate overdose on physical examination.

Answer 160

- CNS depression - altered mental status - Respiratory depression - bradypnoea - Miosis - Apnoea - Dramatic response to naloxone - Fresh needle marks, old track marks on arms and legs - Drug paraphernalia nearby - Decreased gastrointestinal motility - Pulmonary rales - Frothy pink sputum - Seizures - Dysrhythmias

Question 161

Identify appropriate investigations for opiate overdose and interpret the results.

Answer 161

- Therapeutic trail of naloxone - results in reversal of overdose signs - ECG - QRS prolongation, signs of myocardial ischaemia - CXR - ARDS, perihilar, basilar or diffuse alveolar infiltrates - AXR - drug-filled packets - CT Abdomen - drug-filled packets - Opioid urine screen - positive for opioids (morphine) - Gas chromatography / mass spectrometry - positive for specific opioid (but long turn-around time)

Question 162

Define paracetamol overdose.

Answer 162

Excessive ingestion of paracetamol causing toxicity.

Question 163

Explain the aetiology / risk factors of paracetamol overdose.

Answer 163

Maximum recommended dose - 500mg x2 tablets QDS. Intake of >12g or >150mg/kg can cause hepatic necrosis. Risk Factors: - Chronic alcohol abusers - Enzyme-inducing drugs that increase cytochrome P450 activity - e.g. anti-convulsants, anti-TB drugs - Malnourished - Anorexia nervosa - HIV - more susceptible to toxic effects of paracetamol Pathogenesis - Metabolised in conjugation with glucuronate or sulphate - Excreted in kidneys - <7% metabolised by Cytochrome P450 mixed function oxidases - Highly toxic reactive intermediate N-acetyl-p-benzoquinoneimine (NAPQI) - Toxic intermediate inactivated by conjugation with glutathione - Cogulation pathway and glutathione stores are overwhelmed - NAPQI-induced oxidative damage - Acute liver necrosis

Question 164

Summarise the epidemiology of paracetamol overdose.

Answer 164

Most common intentional drug overdose in the UK. 70,000 / year F>M 100 deaths a year Reduced by legislation in 1998 restricting pack sizes.

Question 165

Recognise the presenting symptoms of paracetamol overdose.

Answer 165

Very important to ascertain timing and quantity of overdose, and presence of risk factors. 0-24h - asymptomatic, mild nausea, vomiting, lethargy, malaise 24-72h - RUQ abdominal pain, vomiting >72h - increasing confusion (encephalopathy), jaundice

Question 166

Recognise the signs of paracetamol overdose on physical examination.

Answer 166

0-24h - no signs evident 24-72 - liver enlargement and tenderness >72h - jaundice, coagulopathy, hypoglycaemia, renal angle pain

Question 167

Identify appropriate investigations for paracetamol overdose and interpret the results.

Answer 167

- Paracetamol levels - 4h post ingestion - absorbed rapidly, peak levels within 4h - Assess need to treat based on normogram - see UK National Poisons Information Service guidelines - FBC - U&E - Glucose - LFTs - Clotting screen - Lactate - ABG - for degree of acidosis

Question 168

Define subarachnoid haemorrhage.

Answer 168

Arterial haemorrhage into the subarachnoid space.

Question 169

Explain the aetiology / risk factors for subarachnoid haemorrhage.

Answer 169

- Rupture of a saccular aneurysms at the base of the brain - usually at Circle of Willis (85%). - Permesencephalic haemorrhage - e.g. parenchymal haemorrhages tracking onto surface of brain (10%) - Arteriovenous malformations - Bleeding diatheses - Vertebral or carotid artery dissection with intracranial extension - Mycotic aneurysms - Drug abuse - e.g. cocaine, amphetamines Associated with: - Hypertension - Smoking - Excess alcohol intake - Polycystic kidney disease - Marfan's Syndrome - Peseudoxanthoma elasticum - Ehlers-Danlos Syndrome

Question 170

Summarise the epidemiology of subarachnoid haemorrhage.

Answer 170

Incidence 10 in 100,000 | Peak incidence = 50-60 years

Question 171

Recognise the presenting symptoms of subarachnoid haemorrhage.

Answer 171

- Sudden onset severe headache - hit at the back of the head - Nausea - Vomiting - Neck stiffness - Photophobia - Reduced level of consciousness

Question 172

Recognise the signs of subarachnoid haemorrhage on physical examination.

Answer 172

Meningism - Neck stiffness - Kernig's sign - resistence or pain on knee extension when hip is flexes - Irritation of meninges by blood - Pyrexia GCS - Assess and regularly monitor for deterioration Increased intracranial pressure - Papilloedema - IV or III cranial nerve palsy - Hypertension - Bradycardia Fundoscopy - Subhyaloid haemorrhage - between retina and vitreous membrane Focal Neurological Signs - 2nd day - Ischaemia from vasospasm and reduced brain perfusion - Aneurysms - pressure on cranial nerves causing opthalmoplegia (III or VI nerve palsy)

Question 173

Identify appropriate investigations for subarachnoid haemorrhage and interpret the results.

Answer 173

- Bloods - FBC, U&E, ESR, CRP, Clotting (?bleeding diathesis) - CT - Angiography (CT or intra-arterial) - LP CT - Hyperdense area in basal regions of the skull - due to blood in subarachnoid space - Identifies any intraparenchymal or intraventricular haemorrhages Angiography - To detect the source of bleeding if the patient is a candidate for surgery or endovascular treatment LP - Increased opening pressure - Increased red cells - Few white cells - Xanthochromia - straw-coloured CSF due to Hb breakdown - Confirmed by spectrophotometry of CSF supernatant after centrifugation

Question 174

Define subdural haemorrhage.

Answer 174

A collection of blood that develops between the surface of the brain and the dura mater. Acute - within 72h Subacute - 3-20 days Chronic - 3 weeks

Question 175

Explain the aetiology / risk factors of subdural haemorrhage.

Answer 175

Trauma causing rapid acceleration and deceleration of the brain results in shearing forces which tear veins (bridging veins) that travel from the dura to the cortex. Bleeding occurs between the dura and arachnoid membranes. In children, non-accidental injury should always be considered.

Question 176

Summarise the epidemiology of subdural haemorrhage.

Answer 176

Acute - Younger patients - Associated with major trauma (5-25% of cases in severe head injury) More common than extradural haemorrhage. Chronic - Elderly - 1-5 per 100,000

Question 177

Recognise the presenting symptoms of subdural haemorrhage.

Answer 177

Acute - History of trauma with head injury - Patient has reduced conscious level Subacute - Worsening headaches 7-14 days after injury - Altered mental status Chronic - Headache - Confusion - Cognitive impairment - Psychiatric symptoms - Gait deterioration - Focal weakness - Seizures May not be a history of fall or trauma, hence low index of suspicion especially in elderly and alcoholics.

Question 178

Recognise the signs of subdural haemorrhage on physical examination.

Answer 178

Acute - Low GCS - Midline shift haematoma - ipsilateral fixed dilated pupil (compression of ipsilateral third nerve parasympathetic fibres) - Pressure on brainstem results in reduced consciousness and bradycardia Chronic - Neurological examination may be normal - Focal neurological signs - III or VI nerve dysfunction, papilloedema, hemiparesis, reflex asymmetry

Question 179

Identify appropriate investigations for subdural haemorrhage and interpret the results.

Answer 179

CT Head - Crescent or sickle-shaped mass - Concave over brain surface - extradural is lentiform in shape - CT appearance changes with time - Acute - hyperdense, become isodense over 1-3 weeks (presence may be inferred from effacement of sulci, midline shift, ventricular compression, obliteration of basal cisterns) - Chronic - hypodense - approach that of CSF MRI Brain - Higher sensitivity for isodense or small SDH

Question 180

Generate a management plan for subdural haemorrhage.

Answer 180

Acute - ALS protocol with priorities of cervical spine control and ABC - GCS, pupillary reactivity - If signs of raised ICP, head elevation and consider osmotic diuresis with mannitol or hyperventilation - Stabilise - then CT head Conservative - Especially if small and minimal midline shift - SDH <10 mm thickness - Midline shift <5mm Surgical Chronic - If symptomatic or mass effect on imaging - surgical treatment with Burr hole, craniotomy, drainage (24-72h) - If asymptomatic or no significant mass effect - conservative management, serial imaging to monitor for spontaneous resorption - May require craniotomy with membranectomy if haematoma does not fully liquify Children - Percutaneous aspiration via open fontanelle - Placement of subdural to peritoneal shunt

Question 181

Identify the possible complications of subdural haemorrhage and its management.

Answer 181

- Raised ICP - Cerebral oedema - Secondary ischaemic brain damage - Mass effect - transtentorial or uncal herniation Post-Op - Seizures - Recurrence (33% for SDH) - Intracranial haemorrhage - Subdural empyema - Brain abscess - Meningitis - Tension pneumocephalus

Question 182

Summarise the prognosis for patients with subdural haemorrrhage.

Answer 182

Acute - Underlying brain injury most important factor on outcome Chronic - Generally better outcome than acute - Lower incidence of underlying brain injury - Good outcomes in 3/4 of those treated by surgery

Question 183

Define urinary catheterisation.

Answer 183

A flexible tube used to empty the bladder and collect urine in a drainage bag. Urethral or suprapubic (small opening in tummy).

Question 184

Summarise the indications for urinary catheterisation.

Answer 184

- Acute urinary retention - e.g. BPH, blood clots - Chronic obstruction that causes hydronephrosis - Initiation of continuous bladder irrigation - Intermittent decompression for neurogenic bladder - Hygienic care of bedridden patients

Question 185

Identify the possible complications of urinary catheterisation.

Answer 185

- Allergy or sensitivity to latex - Bladder stones - Blood infections (septicaemia) - Blood in urine (haematuria) - Kidney damage (long-term) - Urethral injury - Urinary tract or kidney infections

Question 186

Define epilepsy.

Answer 186

>2 seizures. Seizure = paroxysmal synchronised cortical electrical discharges. Focal Seizures - Localised to specific cortical regions - Temporal lobe, frontal lobe, occipital, complex partial - Simple partial - does not affect consciousness - Simple complex - does affect consciousness Generalised Seizures - Affect consciousness - Tonic clonic, absence attacks, myoclonic, atonic (drop attacks), tonic seizures

Question 187

Explain the aetiology / risk factors of epilepsy.

Answer 187

Result from an imbalansce in the inhibitory and excitatory currents (Na+ or K+) or neurotransmittors (glutamate or GABA) in the brain. Can be precipitated or are cryptogenic. Precipitants: - Flashing lights - Drugs - Sleep deprivation - Metabolic Idiopathic. Primary Syndromes - Idiopathic generalized epilepsy - Temporal lobe epilepsy - Juvenile myoclonic epilepsy Secondary Seizures (Symptomatic) - Tumour - Infection - meningitis, encephalitis, abscess - Inflammation - vasculitis, multiple sclerosis - Toxic / metabolic - sodium imbalance, hyperglycaemia, hypoglycaemia, hypocalcaemia, hypoxia, porphyria, liver failure - Drugs - alcohol withdrawal, benzodiazepine withdrawal - Vascular - haemorrhage, infarction - Congenital anomalies - cortical dysplasia - Neurodegenerative disease - Alzheimer's disease - Malignant hypertension or eclampsia - Trauma Common Seizure Mimics - Syncope - Migrane - Non-epileptiform seizure disorder (e.g. dissociative disorder)

Question 188

Summarise the epidemiology of epilepsy.

Answer 188

Common. 1% of general population. Peak age of onset is in early childhood or in elderly.

Question 189

Recognise the presenting symptoms of epilepsy.

Answer 189

Obtain history from a witness as well as a patient. Key features from history to determine seizure semiology: - Rapidity of onset? - Duration of episode? - Any alteration of consciousness? - Any tongue-biting or incontinence? - Any rhythmic synchronous limb jerking? - Any post-ictal period? - Drug history - alcohol, recreational drugs FOCAL SEIZURES - Frontal lobe focal motor seizures - motor convulsions, Jacksonian march (spasm spreads from mouth or digit), post-ictal flaccid weakness (Todd's paralysis) - Temporal lobe seizures - aura (visceral and psychic symptoms, fear or deja-vu sensation), hallucinations (olfactory, gustatory) - Frontal lobe complex partial seizures - loss of consciousness, automatisms, rapid recovery GENERALISED SEIZURES - Tonic-clonic (grand mal) - vague symptoms before attack (irritability), tonic phase (generalised muscle spasm), clonic phase (repetitive synchronous jerks), faecal or urinary incontinence, tongue biting, impaired consciousness, lethargy, confusion, headache, back pain, stiffness afterwards - Non-convulsive status epilepticus - acute confusional state, fluctuating, difficult to distinguish from dementia

Question 190

Recognise the signs of epilepsy on physical examination.

Answer 190

Depends on aetiology, usually normal between seizures. Look for focal abnormalities indicative of brain lesions.

Question 191

Identify appropriate investigations for epilepsy and interpret the results.

Answer 191

Bloods - FBC, U&E, LFTs - Glucose, Ca2+, Mg2+ - ABG, toxicology screen - Prolactin - transient increase shortly after a true seizure EEG - Helps confirm or refute the diagnosis - Assists in clarifying the epileptic syndrome - Usually performed inter-ictally and often normal and does not rule out epilepsy - Ictal EEGs combined with video telemetry are more useful but requires adequate facilities CT / MRI - For structural, space-occupying and vascular lesions Others - Particularly for secondary seizures according to suspected aetiology - E.g. lumbar puncture, HIV serology

Question 192

Generate a management plan for epilepsy.

Answer 192

STATUS EPILEPTICUS: seizure lasting longer than 30 minutes, failure to regain consciousness - Early treatment has higher success - give at 5-10 minutes - Resuscitate and protect airway, breathing and circulation - Check glucose and give if hypoglycaemic - Consider thiamine - IV lorazepam or IV/PR diazepam - repeat once after 15 minutes if needed - Reoccur or fail to respond- give IV phenytoin (15mg/kg) under ECG monitoring - Alternative IV agents - phenobarbitone, levetiracetam, sodium valproate - If these measures fail, consider general anaesthesia - requires intubation and mechanical ventilation - Treat cause - e.g. correct hypoglycaemia or hyponatraemia - Check plasma levels of all anticonvulsants PHARMACOLOGICAL TREATMENT - Only start anti-convulsant therapy after >2 unprovoked seizures - Lamotrigine or carbamazepine - 1st line focal seizures - Sodium valproate - 1st line generalised seizures - Others - phenytoin, levetiracetam, clobazam, topiramate, gabapentin, vigabatrin, ethosuximide (absence) - Start treatment with single anti-epileptic drug (AED) PATIENT EDUCATION - Patient education - Avoid triggers - e.g. alcohol - Encourage seizure diaries - Recommend supervision for swimming or climbing - Driving only permitted if seizure free for 6 months - Women of childbearing age should be counselled regarding possible teratogenic effects of AEDs and should consider taking supplemental folate to limit the risk - Drug interactions can limit the effectiveness of oral contraception SURGERY - For refractory epilepsy - Removal of definable epileptogenic focus - determined from detailed EEG, intra-cortical recordings, ictal SPECT, neuropsychometry - Vagus nerve stimulator

Question 193

Identify the possible complications of epilepsy (including status epilepticus) and its management.

Answer 193

- Fractures with tonic-clonic seizures - Behavioural problems - Sudden death in epilepsy (SUDEP) - Complications of AEDs SE of phenytoin = gingivial hypertrophy SE of carbamazepine = neutropenia, osteoporosis SE of lamotrigine = Stevens-Johnson syndrome

Question 194

Summarise the prognosis for patients with epilepsy.

Answer 194

50% remission at 1 year Mortality 2 in 100,000 per year Directly related to seizure or secondary to injury

Question 195

Define diabetic ketoacidosis.

Answer 195

An acute metabolic complications of diabetes that is potentially fatal and requires prompt medical attention for successful treatment. Characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complications of T1DM.

Question 196

Explain the aetiology/risk factors of diabetic ketoacidosis.

Answer 196

Triad - hyperglycaemia, ketonaemia and metabolic acidosis. Risk factors: - Inadequate or inappropriate insulin therapy - Infection - Myocardial infarction - Pancreatitis - Stroke - Acromegaly - Hyperthyroidism - Drugs - e.g. corticosteroids, thiazides, pentamidide, sympathomimetics, second-generation antipsychotics, cocaine, immune checkpoint inhibitors, SGLT2 inhibitors - Cushing's syndrome - Hispanic or black ancestry - Bariatric surgery

Question 197

Summarise the epidemiology of diabetic ketoacidosis.

Answer 197

While the exact incidence is not known, it is estimated to be 1 out of 2000. DKA occurs primarily in patients with type 1 diabetes. The incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with DKA.

Question 198

Recognize the presenting symptoms of diabetic ketoacidosis.

Answer 198

- Thirst - Polyuria - Weight loss - Excessive tiredness - Nausea and vomiting - Dehydration - Abdominal pain - Hyperventilation - Reduced consciousness

Question 199

Recognise the signs of diabetic ketoacidosis on physical examination.

Answer 199

- Acetone smell on breath | - Hypothermia

Question 200

Identify appropriate investigations for diabetic ketoacidosis and interpret the results.

Answer 200

- VBG - pH>7 mild, pH <7 severe, hyperkalaemia, plasma osmolality = metabolic acidosis with raised anion gap (>16) - Serum ketones - >3.0 mmol/L ketonaemia - Blood glucose - hyperglycaemia >11.1 mmol/L - U&E - hyponatraemia, hyperkalaemia (hypokalaemia = severe), hypermagnesaemia, hypophosphataemia - FBC - leukocytosis To consider: - Urinalysis - ketonuria, glycosuria, leukocytes & nitrites in presence of infection, myoglobinuria or haemoglobinuria in rhabdomyolysis - ECG - abnormal T or Q waves or ST segment changes in MI, hypokalaemia (U waves), hyperkalaemia (peaked tall T waves) - Pregnancy - Amylase & lipase - Cardiac enzymes - Creatinine kinase - high with rhabdomyolysis - Chest X Ray - signs of pulmonry oedema, consolidation in pneumonia - Liver function tests - Blood, urine, sputum cultures

Question 201

Generate a management plan for diabetic ketoacidosis.

Answer 201

SBP <90 mmHg 1) Serum K+ <3.5mmol/L - IV fluids - 500ml bolus 0.9% saline over 10-15mins (repeat if needed), 1L 0.9% saline over 1 hour once SBP >90mmHg - K+ replacement - add to 2nd litre of IV fluids, give 10% glucose if level <14.0mmol/L - Supportive care and referral to critical care - Insulin - dose per kg per hour, start at fixed-rate IV insulin infusion 0.1 units / kg /hour - Identify and treat any precipitating acute illness - e.g. MI, sepsis, pancreatitis - Monitor biochemical markers - ketones, glucose, bicarbonate, K+, pH - Monitor and treat complications - Sodium bicarbonate - if pH <6.9 - Thromboprophylaxis - LMWH 2) Serum K+ 3.5-5.5mmol/L - IV fluids - 500ml bolus 0.9% saline over 10-15mins (repeat if needed), 1L 0.9% saline over 1 hour once SBP >90mmHg - K+ replacement - add to 2nd litre of IV fluids, give 10% glucose if level <14.0mmol/L - Supportive care and referral to critical care - Insulin - dose per kg per hour, start at fixed-rate IV insulin infusion 0.1 units / kg /hour - Identify and treat any precipitating acute illness - e.g. MI, sepsis, pancreatitis - Monitor biochemical markers - ketones, glucose, bicarbonate, K+, pH - Monitor and treat complications - Sodium bicarbonate - if pH <6.9 - Thromboprophylaxis - LMWH 3) Serum K+ >5.5 mmol/L - IV fluids - 500ml bolus 0.9% saline over 10-15mins (repeat if needed), 1L 0.9% saline over 1 hour once SBP >90mmHg - Supportive care and referral to critical care - Insulin - dose per kg per hour, start at fixed-rate IV insulin infusion 0.1 units / kg /hour - Identify and treat any precipitating acute illness - e.g. MI, sepsis, pancreatitis - Monitor biochemical markers - ketones, glucose, bicarbonate, K+, pH - Monitor and treat complications - Potassium replacement (once <5.5 mmol/L) - Sodium bicarbonate - if pH <6.9 - Thromboprophylaxis - LMWH SBP >90mmHg 1) Serum K+ <3.5mmol/L - IV fluids - 1L 0.9% saline over 1 hour - K+ replacement - add to 2nd litre of IV fluids, give 10% glucose if level <14.0mmol/L - Supportive care and referral to critical care - Insulin - dose per kg per hour, start at fixed-rate IV insulin infusion 0.1 units / kg /hour - Identify and treat any precipitating acute illness - e.g. MI, sepsis, pancreatitis - Monitor biochemical markers - ketones, glucose, bicarbonate, K+, pH - Monitor and treat complications - Sodium bicarbonate - if pH <6.9 - Thromboprophylaxis - LMWH 2) Serum K+ 3.5-5.5mmol/L - IV fluids - 1L 0.9% saline over 1 hour - K+ replacement - add to 2nd litre of IV fluids, give 10% glucose if level <14.0mmol/L - Supportive care and referral to critical care - Insulin - dose per kg per hour, start at fixed-rate IV insulin infusion 0.1 units / kg /hour - Identify and treat any precipitating acute illness - e.g. MI, sepsis, pancreatitis - Monitor biochemical markers - ketones, glucose, bicarbonate, K+, pH - Monitor and treat complications - Sodium bicarbonate - if pH <6.9 - Thromboprophylaxis - LMWH 3) Serum K+ >5.5 mmol/L - IV fluids - 1L 0.9% saline over 1 hour - Supportive care and referral to critical care - Insulin - dose per kg per hour, start at fixed-rate IV insulin infusion 0.1 units / kg /hour - Identify and treat any precipitating acute illness - e.g. MI, sepsis, pancreatitis - Monitor biochemical markers - ketones, glucose, bicarbonate, K+, pH - Monitor and treat complications - Potassium replacement (once <5.5 mmol/L) - Sodium bicarbonate - if pH <6.9 - Thromboprophylaxis - LMWH Resolution of DKA defined as: - pH >7.3 - blood ketone level <0.6 mmol/L - bicarbonate >15mmol/L

Question 202

Identify the possible complications of diabetic ketoacidosis and its management.

Answer 202

- Hypokalaemia - Cerebral oedema - Pulmonary oedema - AKI - Hypoglycaemia - ARDS (acute respiratory distress syndrome)

Question 203

Summarise the prognosis for patients with diabetic ketoacidosis.

Answer 203

2-10% mortality rate.

Question 204

Define stroke (ischaemic and hemorrhagic).

Answer 204

Rapid permanent neurological deficit from cerebrovascular insult. Focal or global impairment of CNS function developing rapidly and lasting >24h.

Question 205

Explain the aetiology / risk factors of stroke (ischaemic and hemorrhagic).

Answer 205

INFARCTION (80%) - Thrombosis - lacunar and large vessel atherosclerosis, prothrombotic states - Emboli - intimal flap of carotid dissection, atherosclerosis in carotids, heart pathology (AFib, right-left heart defect) - Hypotension - If below the autoregulatory range maintaining cerebral blood flow, infarction results in watershed zones between different cerebral artery territories - Vasculitis - Cocaine ``` HAEMORRHAGE (10%) - Hypertension - Charcot-Bouchard microaneurysm rupture - Amyloid angiopathy - AV malformation Trauma - Tumours - Vasculitis ``` Ischaemic brain becomes soft due to vasogenic oedema from breakdown of BBB and prone to haemorrhagic transformation - secondary damage to CNS.

Question 206

Summarise the epidemiology of stroke (ischaemic and hemorrhagic).

Answer 206

2/1000. Common. 3rd most common cause of death in industrialized countries. 70yrs + most patients. Young stroke (<50) merit extensive investigations.

Question 207

Recognise the presenting symptoms of stroke (ischaemic and hemorrhagic).

Answer 207

Sudden onset - deterioration within seconds. - Weakness, sensory, visual or cognitive impairment - Impaired coordination - Impaired conscioussness - Head and neck pain in carotid or vertebral artery dissection - Enquire time of onset as critical for management (if <4.5h) - Enquire if history of atrial fibrillation, MI, valvular heart disease, carotid artery stenosis, recent neck trauma or pain

Question 208

Recognise the signs of stroke (ischaemic and hemorrhagic) on physical examination.

Answer 208

Examine for underlying cause -e.g. AFib, heart murmurs, carotid bruit, fundoscopy. ANTERIOR CIRCULATION - Anterior cerebral = lower limb weakness (motor cortex), confusion (frontal lobe) - Middle cerebral = facial weakness, hemiparesis (motor cortex), hemisensory loss (somatosensory cortex), apraxia, hemineglect (parietal lobe), receptive or expressive dysphasia (language centres), quadrantanopia (superior or inferior optic radiations) SMALL VESSELS (LACUNAR) - Internal capsule or pons = pure sensory or motor deficit, or combination of both - Thalamus = LOC, hemisensory deficit - Basal ganglia = hemichorea, hemiballismus, parkinsonism POSTERIOR CIRCULATION - Posterior cerebral = hemianopia - Anterior inferior cerebellar artery = vertigo, ipsilateral ataxia, ipsilateral deafness (or tinnitus), ipsilateral facial weakness - Posterior inferior cerebellar artery (lateral medullary syndrome of Wallenberg) = vertigo, ipsilateral ataxia, ipsilateral Horner's syndrome, ipsilateral hemifacial sensory loss, dysarthria and contralateral spinothalamic sensory loss - Basilar artery - combination of cranial nerve pathology, impaired consciousness (emergency) MULTIPLE LACUNAR INFARCTS - Vascular dementia - Urinary incontinence - Gait apraxia - marche a petits pas - Shuffling small-stepped gait - Upright posture - Normal or excessive arm-swing HAEMORRHAGE - Intracerebral = headache, meningism, focal neurological signs, N&V, signs of raised ICP, seizures - Subarachnoid

Question 209

Identify appropriate investigations for stroke (ischaemic and hemorrhagic) and interpret the results.

Answer 209

1. Bloods 2. ECG - identify arrhythmias 3. Echo - identify source of embolism (bubble contrast for right-to-left shunt) 4. Carotid Doppler - exclude carotid artery disease 5. CT Head - see haemorrhages, normal in lacunar infarct or <6h into stroke 6. MRI brain - higher sensitivity, diffusion-weighted imaging to determine whether recent or old 7. CT-Cerebral Angiogram - detect dissections or intracranial stenosis (MRA with T1-fat-saturation useful alternatively) Bloods - FBC - U&E - Glucose - Clotting profile - Lipids - Thrombophilia screen ISCHAEMIC STROKE 1st line: - Non-contrast CT head - if indications for thormbolysis or thrombectomy, on anti-coag / bleeding tendency, GCS <13, raised ICP, severe headache Result: Hypoattenuation (dark in brain parenchyma), loss of grey matter-white matter differentiation, sulcal effacement, hyperattenuation (brightness) in artery (clot) - Glucose - normal, hypoglycaemia (stroke mimic), hyperglycaemia (bleeding, worse outcomes) - Electrolytes - normal - Urea & Creatinine - normal, renal failure - Cardiac enzymes - normal, cardiac ischaemia - FBC - normal, anaemia, thrombocytopenia - ECG - may show arrhythmia or signs of ischaemia - PT/PTT with INR - normal, coagulopathy HAEMORRHAGIC STROKE - Non-contrast CT head - if indications for thormbolysis or thrombectomy, on anti-coag / bleeding tendency, GCS <13, raised ICP, severe headache Result: Hyperattenuation, suggesting acute blood surrounding hypoattenuation due to oedema. - Glucose - normal, hypoglycaemia (stroke mimic), hyperglycaemia (intracerebral bleeding risk) - Electrolytes - normal - Urea and Creatinine - normal, renal failure - LFTs - normal, liver dysfunction (bleeding risk) - FBC - normal, anaemia, thrombocytopenia - Clotting screen - normal or high INR / FXa levels - ECG - normal, arrhythmia or signs of ischaemia

Question 210

Generate a management plan for stroke (ischaemic and hemorrhagic).

Answer 210

SUSPECTED ISCHAEMIC STROKE - A to E approach - ET intubation GCS <8, Oxygen if Sats <93% - Admit to hyperacute stroke unit within 4 hours of presentation - swallow assessment, nutrition support CONFIRMED ISCHAEMIC STROKE Within 4.5 hours + Thrombolysis IS NOT contraindicated (Must exclude intracerebral haemorrhage by imaging first) - Supportive care + monitoring - GCS, blood glucose 4-11mmol/L, BP <185/110mmHg, O2 if Sats <93%, hydration, temperature, ECG monitoring, ICP (low LOC, headache, N&V, high BP), seizures - Alteplase IV - Consider mechanical thrombectomy (endovascular intervention) - Antiplatelet agent - 24h after alteplase, give aspirin or clopidogrel daily for 2 weeks - VTE prophylaxis - intermittent pneumatic compression, NOT LMWH or Teds - Early mobilization - High-intensity statin - atorvastatin given after 48h Outside 4.5 hours OR Thrombolysis IS contraindicated - Supportive care + monitoring - Mechanical thrombectomy (endovascular intervention) - Anti-platelet agent - give aspirin or clopidogrel daily for 2 weeks - VTE prophylaxis - intermittent pneumatic compression, NOT LMWH or Teds - Early mobilization - High-intensity statin - atorvastatin given after 48h SUSPECTED HAEMORRHAGE - A to E approach - ET intubation GCS <8, Oxygen if Sats <93% - Admit to hyperacute stroke unit within 4 hours of presentation - swallow assessment, nutrition support CONFIRMED HAEMORRHAGE - Supportive care plus monitoring - GCS, glucose 4-11 mmol/L, BP, O2, hydration, temperature, cardiac monitoring, ICP (haematoma mass effect, transtentorial herniation, intraventricular haemorrhage, hydrocephalus), seizures - Immediate referral for neurosurgery assessment - medical management for small deep haemorrhages, lobar haemorrhages without hydrocephalus or neurological deterioration, large haemorrhage and comorbidities, posterior fossa haemorrhage, GCS <8 unless hydrocephalus - Rapid blood pressure control - aim for 130-140 SBP mmHg for 7 days within 1h of starting treatment - Urgent reversal of anticoagulation Warfarn/Vit K antagonist = PCC AND Phytomenadione Dabigatran = Idarucizumab Factor Xa Inhibitor = PCC - VTE prophylaxis - intermittent pneumatic compression, NOT LMWH or Teds - Early mobilisation SECONDARY PREVENTION - Aspirin - Dipyridamole - Warfarin (if AFib) - Stop smoking - Control hypertension and hyperlipidaemia - Treatment of carotid artery disease

Question 211

Identify the possible complications of stroke (ischaemic and hemorrhagic).

Answer 211

- Cerebral oedema - raised ICP and local compression - Immobility - Infections - e.g. pneumonia, UTI, pressure sores - DVT - Cardiovascular events - e.g. arrhythmias, MI, cardiac failure - Death

Question 212

Summarise the prognosis for patients with stroke (ischaemic and hemorrhagic).

Answer 212

10% mortality in first months. Up to 50% of those who survive remain dependent. 10% recurrence in 1 year. Poorer for haemorrhages than infarction.