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!Final Year > Acute Care and Trauma (1) > Flashcards

Acute Care and Trauma (1) Flashcards

1
Q

What is acute kidney injury (AKI)?

A

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

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2
Q

What is the aetiology of acute kidney injury (AKI)?

A

Pre-renal, renal and post renal
AKI may be due to various insults such as:
- impaired kidney perfusion
- exposure to nephrotoxins
- outflow obstruction
- intrinsic kidney disease

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3
Q

What are the risk factors of acute kidney injury (AKI)?

A

Advanced age
Underlying kidney disease
DM
Sepsis: may result in ATN, pre-kidney AKI from hypotension
Nephrotoxins e.g. aminoglycosides, NSAIDs, vancomycin

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4
Q

What are the pre-renal causes of an AKI?

A

Reduced renal perfusion:
1. Shock (hypovolaemic, septic, cardiogenic)
2. Hepatorenal syndrome (liver failure)

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5
Q

What are the renal causes of an AKI?

A
  1. Acute tubular necrosis: ischaemia, drugs and toxins
  2. Acute glomerulonephritis
  3. Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides
  4. Vessel obstruction:
    - Renal artery/vein thrombosis
    - Cholesterol emboli
    - Vasculitis
    Other causes: myeloma, haemolysis, nephropathy
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6
Q

What are the post renal causes of an AKI?

A

Stone
Tumour (pelvic, prostate, bladder)
Blood clots
Retroperitoneal fibrosis

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7
Q

What are the presenting symptoms of AKI?

A

Usually asymptomatic
Lower urinary tract symptoms:
- Urgency
- Frequency
- Hesitancy
Low urine output (oliguria)
Malaise
Anorexia
Nausea and vomiting
Pruritus (itching)
Drowsiness
Convulsions, coma (caused by uraemia)

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8
Q

What are the signs of acute kidney injury (AKI) on physical examination?

A
  1. Reduced urine output
  2. Pulmonary and peripheral oedema
  3. Arrhythmias (secondary to changes in potassium and acid-base balance)
  4. Features of uraemia (e.g. pericarditis or encephalopathy)
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9
Q

What are the appropriate investigations for AKI?

A
  1. U&Es: serum creatinine (rise of 26 micro mol/L in 48 hours or >50% in 7 days), potassium, sodium and urea
  2. Urinalysis: all suspected AKI patients, cellular casts (glomerulonephritis)
  3. Renal ultrasound: if no identifiable cause of deterioration or risk of obstruction
  4. ECG: changes associated with hyperkalaemia (tented T waves) and CXR
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10
Q

What is the management plan for AKI?

A

1.Assess hydration and fluid balance:
Pulse rate, lying and standing BP, JVP, skin turgor, chest auscultation, peripheral oedema, central venous pressure, fluid and weight charts. ECG monitoring (hyperkalaemia)

  1. If hypovolaemic (+ hyperkalaemia)
    - fluid resuscitation
    - review medications and stop nephrotoxins
    - identify and treat underlying cause
    others:
    - vasoactive drug
    - blood transfusion
  2. If hypervolaemic (+ pulmonary oedema and hyperkalaemia)
    - loop diuretic (under specialist supervision) and sodium restriction
    - identify and treat underlying cause
    consider: renal replacement therapy

Metabolic acidosis (if pH < 7.2): 50–100 mL of 8.4% bicarbonate via central line over 15–30 min

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11
Q

What medications can cause an AKI?

A

Acute tubular necrosis (ATN):
- Paracetamol
- Aminoglycosides
- Amphotericin B (anti-fungal)
- NSAIDs
- ACE-inhibtors
- Lithium
Acute interstitial nephritis:
- NSAIDs
- Penicillins
- Sulphonamides
Others: opioids, other antibiotics e.g. trimethoprim, vancomycin

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12
Q

What is the treatment for acute pulmonary oedema?

A

P- positioning (sit up)
O- oxygen
D- diuretic (furosemide) and fluid restriction
M- (dia)morphine
A- anti-emetics
N- nitrates (GTN infusion if SBP >110, or 2 puffs GTN spray if SBP >90)

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13
Q

What are the possible complications of acute kidney injury (AKI)?

A

Common and life-threatening:
- Hyperkalaemia
- Sepsis
- Metabolic acidosis
- Pulmonary oedema
- Hypertension
Less common:
Gastric ulceration, bleeding (platelet dysfunction), muscle wasting (hypercatabolic state), uraemic pericarditis, uraemic encephalopathy, acute cortical necrosis

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14
Q

What is acute respiratory distress syndrome?

A

A syndrome of acute and persistent lung inflammation with increased vascular permeability

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15
Q

What are the causes of acute respiratory distress syndrome?

A

(TOAST)
Transfusion
Overdose of drugs
Aspiration
Sepsis
Transplantation
(PIP)
Pneumonia
Injury/burns
Pancreatitis

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16
Q

What is ARDS characterised by?

A

A - Absence of raised capillary wedge pressure
R - Reduced blood oxygen (hypoxaemia)
D - Double-sided infiltrates (bilateral infiltrates)
S - sudden onset (acute- within 1 week)

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17
Q

What are the causes of ARDS?

A

Infection: sepsis, pneumonia
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
Covid-19
Cardio-pulmonary bypass

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18
Q

What is the aetiology of acute respiratory distress syndrome?

A

Severe insult to lungs
Inflammatory mediators released
Capillary permeability increases
Results in pulmonary oedema, reduced gas exchange and reduced lung compliance
(Injury, inflammation, increased permeability)

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19
Q

What are the pathological stages of ARDS?

A

Exudative
Proliferative
Fibrotic

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20
Q

What are the presenting symptoms of ARDS?

A

Rapid deterioration of respiratory function
Dyspnoea
Cough
Symptoms of cause

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21
Q

What are the signs of ARDS on physical examination?

A

Think SMURF: fast, blue, noisy:
Cyanosis
Tachypnoea
Tachycardia
Widespread crepitations
Hypoxia refractory to oxygen treatment
(Usually bilateral but may be asymmetrical in early stages)

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22
Q

What are the clinical features of ARDS?

A

Dyspnoea
Elevated respiratory rate
Bilateral lung crackles
Low oxygen saturations

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23
Q

What are the appropriate investigations for ARDS?

A

1st line:
CXR- bilateral infiltrates
ABG- low partial oxygen pressure
Sputum/ blood/ urine cultures- positive if underlying infection
Amylase- elevated in cases of acute pancreatitis
Others:
BNP- <100 nanograms/L make HF less likely, so ARDS more likely
Pulmonary artery catheterisation- Pulmonary artery occlusion pressure (PAOP) ≤18 mmHg suggests ARDS

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24
Q

What are the two key investigations for ARDS?

A

Chest x-ray and ABG

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25
Q

What is the criteria for ARDS (American-European Consensus Conference)?

A
  1. Acute onset (within 1 week of a known risk factor)
  2. Pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
  3. Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
  4. pO2/FiO2 < 40kPa (300 mmHg)
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26
Q

What is the management for ARDS?

A

Due to the severity of the condition patients are generally managed in ITU
Oxygenation/ventilation to treat the hypoxaemia
General organ support e.g. vasopressors as needed
Treatment of the underlying cause e.g. antibiotics for sepsis
Certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS

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27
Q

What is adrenal insufficiency?

A

Deficiency of adrenal cortical hormones (mineralocorticoids, glucocorticoids and androgens)

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28
Q

What is the aetiology of adrenal insufficiency?

A

Primary (Addison’s disease): Autoimmune (>70%)
Secondary: Pituitary or hypothalamic disease.

Surgical: After bilateral adrenalectomy.
Medical: (iatrogenic) sudden cessation of long-term steroid therapy

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29
Q

What are the risk factors for adrenal insufficiency?

A

4Is:
1. Infections: Tuberculosis, meningococcal septicaemia (Waterhouse–Friderichsen syndrome), Cytomegalovirus (HIV patients)
2. Infiltration: Metastasis (lung, breast, melanoma), lymphomas, amyloidosis
3. Infarction: Secondary to thrombophilia
4. Inherited: Adrenoleukodystrophy 1, ACTH receptor mutation

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30
Q

What is the most common cause of adrenal insufficiency?

A

Most common cause is iatrogenic- sudden cessation in long term steroid therapy
Primary causes are rare

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31
Q

What are the presenting symptoms of acute adrenal insufficiency?

A

(Addisonian crisis)
Acute adrenal insufficiency with major haemody-
namic collapse often precipitated by stress (e.g. infection or surgery)

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32
Q

What are the presenting symptoms of chronic adrenal insufficiency?

A

Non-specific vague symptoms such as dizziness, anorexia, weight loss, diarrhoea, vomiting, abdominal pain, lethargy, weakness, depression

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33
Q

What are the clinical features of adrenal insufficiency?

A

Postural hypotension
Increased pigmentation: more noticeable on buccal mucosa, scars, skin creases, nails, pressure points (resulting from melanocytes being stimulated by increased ACTH levels)
Loss of body hair in women (androgen deficiency)
Associated autoimmune conditions: e.g. vitiligo

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34
Q

What are the clinical features of an Addisonian crisis?

A

Hypotensive shock
Tachycardia
Pale
Cold and clammy
Oliguria

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35
Q

What are the appropriate investigations for adrenal insufficiency?

A

Definite investigation is ACTH stimulation (synACTHen) test
9am serum cortisol may also be helpful

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36
Q

What results would be seen in Addison’s disease on a synACTHen test/ 9am serum cortisol test?

A

> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed
ACTH stimulation test should show an increase in plasma cortisol levels 30 minutes after giving Synacthen 250ug IM

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37
Q

What are the appropriate investigations for an Addisonian crisis?

A

Bloods- Haematology (FBC for neutrophilic, CRP and ESR for infection)
Biochemistry (U&Es for hyperkalaemia, hyponatraemia, hypoglycaemia and metabolic acidosis)
Microbiology (blood cultures)
Urine- MCS

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38
Q

What are the causes of an Addisonian crisis?

A

Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
Steroid withdrawal

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39
Q

What is the management for Addisonian crisis?

A

Hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
Continue hydrocortisone 6 hourly until the patient is stable (no fludrocortisone is required because high cortisol exerts weak mineralocorticoid action)
Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
Treat the underlying cause e.g. Abx for sepsis

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40
Q

What is the management plan for adrenal insufficiency?

A

Replacement therapy of glucocorticoid and mineralocorticoid
Combination of: Hydrocortisone (usually given in 2 or 3 divided doses, 20-30 mg per day, with the majority given in the first half of the day) and fludrocortisone
Patient education: importance of not missing doses, MedicAlert bracelets, hydrocortisone injection for crisis
Management of intercurrent illness: glucocorticoid dose should be doubled with fludrocortisone staying the same

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41
Q

What precaution must be taken in a patient with adrenal insufficiency and hypothyroidism?

A

Give hydrocortisone before thyroxine to avoid precipitating an Addisonian crisis

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42
Q

What are the possible complications of adrenal insufficiency?

A

Hyperkalaemia
Death during an Addisonian crisis

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43
Q

What is the prognosis for patients with adrenal insufficiency?

A

Adrenal function rarely recovers, but normal life expectancy can be expected if treated

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44
Q

What is alcohol withdrawal?

A

A patient who is alcohol dependent and has stopped or reduced their alcohol intake within hours or days of presentation

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45
Q

What is the mechanism of alcohol withdrawal?

A
  1. Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
  2. Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
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46
Q

What is alcohol dependence?

A

Characterized by three or more of:
. Withdrawal on cessation of alcohol
. Tolerance
. Compulsion to drink, difficulty controlling termination or the levels of use
. Persistent desire to cut down or control use
. Time is spent obtaining, using, or recovering from alcohol
. Neglect of other interests (social, occupational, or recreational)
. Continued use despite physical and psychological problems

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47
Q

What are the features of alcohol withdrawal?

A

Symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety
Peak incidence of seizures at 36 hours
Peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

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48
Q

What are the presenting symptoms of alcohol withdrawal?

A

HAD A PINT
Headache
Anxiety/ agitation
Depression
Anorexia
Palpitations
Insomnia
Nausea
Tremor

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49
Q

What are the signs of chronic alcohol misuse?

A

Dupuytren’s contracture
Palmar erythema
Bruising
Spider naevi
Telangiectasia- widened venules cause threadlike red lines or patterns on the skin
Bilateral parotid enlargement
Gynaecomastia
Smell of alcohol

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50
Q

What are the appropriate investigations for alcohol withdrawal?

A

A to E approach
VBG: respiratory alkalosis with delirium tremens
Bloods: Increased MCV, thrombocytopenia, hypomagnesaemia, hypokalaemia, hypophosphataemia, elevated AST, ALT, and GGT
Coagulation studies: prolonged INR and prothrombin time
Drug screen: barbiturates, paracetamol

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51
Q

What is the management plan for a patient with alcohol withdrawal?

A

First-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam (lorazepam may be preferable in patients with hepatic failure) with a reducing dose protocol
B1 thiamine, pabrinex
Carbamazepine also effective in treatment of alcohol withdrawal
Patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised

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52
Q

What are the possible complications of alcohol withdrawal?

A

Seizures (generalised tonic-clonic) - cause of fatality
Delirium tremens

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53
Q

What are the complications of chronic alcohol use?

A

Cerebral atrophy and dementia
Cerebellar degeneration
Optic atrophy
Peripheral neuropathy
Myopathy

Indirect effects include hepatic encephalopathy, thiamine deficiency, causing Wernicke’s encephalopathy or Korsakoff’s psychosis

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54
Q

What is the prognosis for patients with alcohol withdrawal?

A

Depends on complications.
Alcoholic fatty liver is reversible on abstinence from alcohol
In general, 5-year survival rates in those with alcoholic cirrhosis who stop drinking are 60–75%, but < 40% in those who continue

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55
Q

What is anaphylaxis?

A

A severe, life-threatening, generalised or systemic hypersensitivity reaction

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56
Q

What cells are the drivers behind anaphylaxis?

A

There is sudden release of mast cell- and basophil-derived mediators into the circulation

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57
Q

What is anaphylaxis characterised by?

A

Rapidly developing life-threatening airway and/or breathing and/or circulation problems
Usually associated with skin and mucosal changes

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58
Q

What is the aetiology of anaphylaxis?

A

Immunologic: IgE-mediated or immune complex/complement-mediated
Non-immunologic: mast cell or basophil degranulation without the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)

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59
Q

What are the common identified causes of anaphylaxis?

A

Food (e.g. nuts) - the most common cause in children
Drugs
Venom (e.g. wasp sting)

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60
Q

What is the Resus Council UK’s definition of anaphylaxis?

A

The sudden onset and rapid progression of symptoms
Airway and/or Breathing and/or Circulation problems

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61
Q

What are the Airway and/or Breathing and/or Circulation problems seen in anaphylaxis?

A

Airway: swelling of the throat and tongue →hoarse voice and stridor
Breathing: respiratory wheeze and dyspnoea
Circulation: hypotension and tachycardia

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62
Q

What does it mean if a patient is not having an ABC symptoms in anaphylaxis?

A

That they are not in true anaphylaxis

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63
Q

What are the skin and mucosal changes seen in anaphylaxis?

A

Generalised pruritus
Widespread erythematous or urticarial rash

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64
Q

What are the appropriate investigations for anaphylaxis?

A

Clinical diagnosis
Later:
Serum mast cell tryptase (measured within 15 min–3 h after onset of symptoms)= elevated up to 12 hours post event
Histamine levels (measured preferably within 30 min after symptom onset) and urinary metabolites of histamine (which may remain elevated for several hours after symptom onset)
ABG: elevated lactate
ECG: Non-specific ST ECG changes are common post-adrenaline

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65
Q

What is the management plan for a patient with anaphylaxis?

A

Intramuscular adrenaline 500 micrograms (0.5ml 1 in 1,000)
Can be repeated every 5 minutes if necessary
Best site for IM injection is the anterolateral aspect of the middle third of the thigh
Other medications (not as important):
Oxygen
Chlorphenamine - only when patient is stabilised

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66
Q

What is refractory anaphylaxis?

A

Defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline
IV fluids should be given for shock
Expert help should be sought for consideration of an IV adrenaline infusion

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67
Q

What is the management plan for a patient with anaphylaxis following stabilisation?

A

Non-sedating oral antihistamines, in preference to chlorphenamine, may be given following initial stabilisation especially in patients with persisting skin symptoms (urticaria and/or angioedema)
Establish if it is true anaphylaxis: Serum tryptase levels
All patients with a new diagnosis of anaphylaxis should be referred to a specialist allergy clinic
An adrenaline injector should be givens an interim measure before the appointment

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68
Q

What should be given to patients with anaphylaxis post specialist allergy assessment?

A

Patients should be prescribed 2 adrenaline auto-injectors
Training should be provided on how to use it

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69
Q

How do you discharge patients following an anaphylactic reaction?

A

Risk-stratified approach to avoid biphasic reactions (can occur 1–72 h after the first reaction in up to 20% of patients)

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70
Q

What is the risk-stratified approach to discharge following anaphylaxis?

A
  1. Fast-track discharge (after 2 hours of symptom resolution):
    - good response to a single dose of adrenaline
    - complete resolution of symptoms
    - has been given an adrenaline auto-injector and trained how to use it
    - adequate supervision following discharge
  2. Minimum 6 hours after symptom resolution:
    - 2 doses of IM adrenaline needed, or previous biphasic reaction
  3. Minimum 12 hours after symptom resolution:
    - severe reaction requiring > 2 doses of IM adrenaline
    - patient has severe asthma
    - possibility of an ongoing reaction (e.g. slow-release medication)
    - patient presents late at night
    - patient in areas where access to emergency access care may be difficult
    - observation for at 12 hours following symptom resolution
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71
Q

What are the possible complications of anaphylaxis?

A

Respiratory failure
Shock
Death

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72
Q

What is the prognosis for patients with anaphylaxis?

A

Good if prompt treatment given

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73
Q

What is an arterial blood gas (ABG)?

A

A procedure to measure the acidity (pH) and the levels of oxygen and carbon dioxide in the blood from an artery

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74
Q

What are the indications for an arterial blood gas?

A

Respiratory failure - in acute and chronic states.
Any severe illness which may lead to a metabolic acidosis:
- Cardiac/ Liver/ Renal failure
- Hyperglycaemic states associated with diabetes mellitus
- Multiorgan failure
- Sepsis
- Burns
Poisons/toxins
Ventilated patients

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75
Q

What are the possible complications of an arterial blood gas?

A

Local hematoma
Arterial vasospasm
Arterial occlusion
Air or thrombus embolism
LA anaphylactic reaction
Infection at the puncture site

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76
Q

What are the articulating surfaces of the ankle?

A

Tibia + fibula + talus

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77
Q

What are the two ligaments involved in the ankle joint?

A

Medial and lateral ligament (originating from the corresponding malleolus)

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78
Q

What are the muscle groups and movements of the ankle joint?

A

Plantarflexion: muscles in posterior compartment of leg (gastrocnemius, soleus, plantaris and posterior tibialis)
Dorsiflexion: muscles in anterior compartment of leg (tibialis anterior, extensor hallucis longus and extensor digitorum longus)

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79
Q

What is the neurovascular supply of the ankle?

A

Aterial supply = Malleolar branches of anterior tibial, posterior tibial and fibular arteries
Innervation is provided by tibial, superficial fibular and deep fibular nerves

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80
Q

What are the most common causes of posterior heel pain?

A

Achilles tendon disorders

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81
Q

What are the common achilles tendon disorders?

A

Tendinopathy (tendinitis)
Partial tear
Complete rupture of the Achilles tendon

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82
Q

What are some risk factors for Achilles tendon disorders?

A

Quinolone use (e.g. ciprofloxacin) is associated
Hypercholesterolaemia → predisposes to tendon xanthomata

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83
Q

What are the features of achilles tendinopathy (tendinitis)?

A
  1. Gradual onset of posterior heel pain that is worse following activity
  2. Morning pain and stiffness are common
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84
Q

What is the management of achilles tendinopathy (tendinitis)?

A

Typically supportive
1. Simple analgesia
2. Reduction in precipitating activities
3. Calf muscle eccentric exercises (self-directed or through physiotherapy)

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85
Q

What are the features of Achilles tendon rupture?

A

Suspected if the patient reports the following whilst playing a sport or running:
1. An audible ‘pop’ in the ankle
2. Sudden onset significant pain in the calf
2. Inability to walk or continue the sport

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86
Q

What is the examination for Achilles tendon rupture?

A

Simmond’s triad
1. Ask the patient to lie prone with their feet over the bed
2. Look for an abnormal angle of declination - there will be a greater dorsiflexion of the injured foot compared to the other
3. Feel for a gap in the tendon and gently squeeze the calf muscles: if there is a rupture the achilles tendon injured foot will stay in a neutral position

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87
Q

What is the imaging modality of choice for Achilles tendon rupture?

A

Ultrasound

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88
Q

What is the Thompson test?

A

Lack of plantar flexion when calf is squeezed

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89
Q

What is the management for Achilles tendon rupture?

A

Acute referral to orthopaedic specialist
1. Non-operative : functional bracing/ casting in resting equinus
2. Operative: open end-to-end achilles tendon repair (for acute ruptures < 6 weeks) or percutaneous repair

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90
Q

What are some complications of Achilles tendon rupture?

A

Re-rupture: higher with non-operative management
Wound healing complications
Sural nerve injury (percutaneous repair)

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91
Q

What are ankle fractures?

A

Very common injuries which generally occur due to a twisting mechanism

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92
Q

What are the locations of ankle fractures?

A

Breakdown by fracture type:
1. Isolated malleolus fracture = 70%
2. Bimalleolar = 20%
3. Trimalleolar = 7%

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93
Q

What are the risk factors for ankle fractures?

A

Male
Younger age (mainly 15-24 years)
Obesity
Smoking
Alcohol consumption

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94
Q

What is the main mechanism of injury for ankle fractures?

A

Twisting injuries

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95
Q

What are the three ligament complexes that stabilise the ankle?

A
  1. Deltoid
  2. Lateral ligament complex
  3. Syndesmosis
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96
Q

What are the two tendons which stabilise the ankle?

A
  1. Peroneal tendons: peroneus longus and brevis
  2. Posterior tibial tendon
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97
Q

What are the neurovascular structures surrounding the ankle?

A
  1. Anterior tibial artery and depot peroneal nerve
  2. Posterior tibial artery and tibial nerve
  3. Superficial peroneal nerve
  4. Sural nerve
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98
Q

What are the features of an ankle fracture?

A

Severe ankle pain
Difficulty or inability to walk

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99
Q

What are the findings of an ankle fracture of a physical exam?

A

Ecchymosis and swelling
Deformity
Limited ankle motion

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100
Q

What are the Ottawa ankle rules for an ankle fracture?

A

State that x-rays are only necessary if there is pain in the malleolar zone and:
1. Inability to weight bear for 4 steps
2. Tenderness over the distal tibia
3. Bone tenderness over the distal fibula

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101
Q

What is the Weber system in ankle fractures?

A

Describe ankle fractures related to the level of the fibular fracture:
Type A = below the syndesmosis
Type B = fractures start at the level of the tibial plafond and may extend proximally to the syndesmosis
Type C = above the syndesmosis which may itself be damaged

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102
Q

How is the Weber system for ankle fractures classified?

A

Type A: infrasyndesmotic
Type B: transsyndesmotic
Type C: Suprasyndesmotic

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103
Q

What are some differentials for an ankle fracture?

A

Ankle sprain
Syndesmotic injury
Achilles tendon rupture

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104
Q

What are some features of an ankle sprain?

A

May be able to weight bear
Positive anterior drawer or talar tilt test
Radiographs without fracture

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105
Q

What are the principles of management for ankle fractures?

A

Depends on the stability of the ankle joint and patient’s comorbidities
All fractures should be promptly reduced to remove pressure on the overlying skin and subsequent necrosis
Young patients = usually require surgical repair often using a compression plate
Elderly patients = usually fare better with conservative management as their thin bones do not hold metalwork well

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106
Q

What are some of the non-operative management options for ankle fractures?

A

Short-leg AO splint
Short-leg cast
CAM boot
(for stable ankle fractures and those unfit for surgery)

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107
Q

What are some of the operative management options for ankle fractures?

A

Open reduction internal fixation
External fixation

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108
Q

What are the Ottawa rules (ankle fractures)?

A

An x-ray is only required if there is any pain in the malleolar zone and one of the following:
1. Bony tenderness at the lateral malleolar zone
2. Bony tenderness at the medial malleolar zone
3. Inability to walk 4 weight bearing steps immediately after the injury

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109
Q

What is the management of ankle fractures according the Weber classification?

A

Type A: Usually stable → reduction and cast →ORIF occasionally needed
Type B: Stability variable → may require ORIF
Type C: Unstable fracture → ORIF

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110
Q

What is a lisfranc injury?

A

When bones in the midfoot are broken or ligaments that support the midfoot are torn

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111
Q

What is a metatarsal stress fracture?

A

Stress fracture = tiny cracks in the bone caused by repetitive force often from overuse
A hairline fracture in one of the long metatarsal bones in the foot from overly stressing the foot when using it in the same way repeatedly

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112
Q

What is aspirin (salicylate) overdose?

A

Excess ingestion of salicylates e.g. aspirin causing toxicity

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113
Q

What are the risk factors of aspirin overdose?

A

Deliberate self-harm
Suicidal intent
By accident e.g. in children

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114
Q

What are the features of aspirin overdose?

A

Hyperventilation (centrally stimulates respiration)
Tinnitus
Lethargy
Sweating, pyrexia
Nausea/vomiting
Hyperglycaemia and hypoglycaemia
Seizures
Coma

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115
Q

What is a key finding in aspirin overdose?

A

Mixed respiratory alkalosis and metabolic acidosis

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116
Q

How does aspirin overdose cause a mixed respiratory alkalosis and metabolic acidosis?

A
  1. Early stimulation of the respiratory centre leads to a respiratory alkalosis via hyperventilation
  2. Later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis
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117
Q

What is the aetiology of aspirin overdose?

A
  1. Aspirin increases respiratory rate and depth by stimulating the CNS respiratory centre
  2. This hyperventilation produces respiratory alkalosis in the early phase
  3. The body then compensates by increasing urinary bicarbonate and K+ excretion, causing dehydration and hypokalaemia
  4. Loss of bicarbonate together with the uncoupling of mitochondrial oxidative phosphorylation by salicylic acid and build up of lactic acid can lead to metabolic acidosis
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118
Q

What are the investigations for aspirin overdose?

A

ABC management
ABG: initially respiratory alkalosis; later concomitant metabolic acidosis
Salicylate levels - determines management
Bloods e.g. U&Es for hypokalaemia (and hypocalcaemia), FBC, LFTs
ECG: signs of hypokalaemia = flattening and inversion of T waves, visible U wave and some ST depression in severe

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119
Q

What are the salicylate levels in moderate and severe aspirin overdoses?

A

Moderate = 500- 750mg/L
Severe = >750mg/L
* >700mg/L is an indication for haemodialysis

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120
Q

What is the management of aspirin overdose?

A

ABC approach
Charcoal if early enough
Urinary alkalisation with IV sodium bicarbonate → enhances elimination of aspirin in the urine
Haemodialysis

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121
Q

What are the indications for haemodialysis in aspirin overdose?

A

Serum concentration > 700mg/L
Metabolic acidosis resistant to treatment
Acute renal failure
Pulmonary oedema
Seizures
Coma

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122
Q

What is asthma?

A

Chronic inflammatory airway disease characterised by:
1. Variable reversible airway obstruction
2. Airway hyper-responsiveness
3. Bronchial inflammation

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123
Q

What is the epidemiology of asthma?

A

Affects around 8% in the UK
More common in boys until teenage years
More common in women

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124
Q

What is the pathology of asthma?

A

Chronic airway inflammation (often eosinophilic inflammation)
Bronchial hyperreactivity to a variety of stimuli causing reversible airway obstruction

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125
Q

What are some of the stimuli in asthma?

A

Allergens e.g. pets, house dust mites
Emotion
Exercise
Change in air temperature
Pollution (indoors and outdoors)
Viruses
Occupational exposure e.g. flour dust, latex, chemicals (hairdresser)

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126
Q

What are some of the features in the history for asthma?

A

Wheeze
Chest tightness
Cough
Breathlessness
Symptoms can be diurnal e.g. nocturnal cough
Ask about triggers
Ask about smoking history which exacerbates asthma

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127
Q

What are the examination findings for asthma?

A

Mouth: oral candida (inhaled steroids without rinsing mouth out), nasal polyps
Hands: fine tremor (excess bronchodilator use)
HR: high (exacerbation or excess bronchodilator use)
Skin: eczema
Chest: audible expiratory wheeze, cough (poor control or acute exacerbation), high RR (acute), polyphonic expiratory wheeze (poor control or acute exacerbation)

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128
Q

What are the two types of wheeze heard in asthma patients?

A

Audible expiratory wheeze
Polyphonic expiratory wheeze = poor control or acute exacerbation

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129
Q

How is the diagnosis of asthma made in adults?

A
  1. Ask if their symptoms are better on days away from work/ during holidays - could be occupational asthma
  2. Spirometry with a bronchodilator reversibility (BDR) test
  3. All patients should have a FeNO test
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130
Q

What is a FeNO test for suspected asthma?

A

Fractional exhaled nitric oxide
Levels of NO correlate with levels of eosinophils inflammation which is found in asthma
Considered positive is equal to or above 40 parts per billion (35 ppb for children)

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131
Q

What are the spirometry findings for someone with asthma?

A

FEV1/FVC ratio less than 70% is considered obstructive

132
Q

What is a positive result in bronchodilator reversibility for patients with asthma?

A

Indicated by an improvement in FEV1 of 12% or more and increase in volume of 200ml or more

133
Q

What are the investigations for asthma?

A

No gold standard test
Evidence of airway obstruction:
1. Peak flow diary showing diurnal variation > 20%
2. Spirometry: FEV1/FVC < 0.7, after bronchodilation FEV1 improved by 12% and 200ml
3. FeNO > 40 ppb for eosinophil inflammation
Blood test: eosinophil count and IgE levels
Skin prick test (alternative to IgE blood tests)
Chest x-ray: should be normal, may show hyperinflation

134
Q

What are the two main differentials for a nocturnal cough?

A

Asthma
GORD

135
Q

What is the management of low probability asthma?

A

Investigate for other more likely diagnoses
Test for airway obstruction: spirometry and bronchodilator reversibility
If positive then follow intermediate possibility of asthma

136
Q

What is the management of intermediate probability of asthma?

A

Test for airway obstruction: spirometry and bronchodilator reversibility
Test for variability: reversibility, PEF charting, bronchial challenge
Test for eosinophilic inflammation or atopy: FeNO, IgE, eosinophil count
Then either watchful waiting if asthmatic or commence treatment

137
Q

What is the management for high probability of asthma?

A

Initiate treatment and assess response objectively e.g. lung function. validated system score
Adjust maintenance dose
Provide self-management advice
Arrange on-going review

138
Q

What are the principles of medical management of asthma?

A
  1. Short acting beta-2 agonist (SABA)
  2. SABA + low dose ICS
  3. SABA + low dose ICS + leukotriene receptor antagonist (LTRA)
  4. SABA + low dose ICS + Long acting beta-agonist (LABA) ± LTRA
  5. SABA ± LTRA + MART
  6. SABA ± LTRA + medium dose MART (or moderate dose ICS +LABA separately)
  7. SABA ± LTRA and either:
    a) high dose ICS
    b) trial of an additional drug e.g. LAMA
    c) Seeking advice from specialist
139
Q

What are examples of the medical management of asthma?

A

SABA = salbutamol
ICS = Flovent® (fluticasone) Pulmicort® (budesonide)
LTRA = montelukast
LABA = Serevent (salmeterol)

140
Q

What are some other considerations alongside medical management of asthma?

A

Regular asthma review - either GP or specialist
Trigger avoidance e.g. pets
Adherence
Inhaler technique
Asthma management (action) plan
Vaccinations = flu, covid
Smoking cessation
Cormorbid management e.g. obesity, allergic rhinitis

141
Q

What are some indications for severe asthma?

A

Frequent asthma exacerbations e.g 4 per year
Raised eosinophils/ FeNO/ IgE/ atopy

142
Q

What is MART in asthma management?

A

Maintenance and reliever therapy
Form of combined ICS and LABA treatment in which a single inhaler contained both
Used for both daily maintenance therapy and relief of symptoms as required

143
Q

What are the doses of inhaled corticosteroids in asthma management?

A

Low = < 400 mcg budesonide
Moderate = 400-800 mcg budesonide
High = > 800 mcg budesonide

144
Q

What are the principles of stepping down treatment in asthma?

A

Consider stepping down treatment every 3 months or so (taking into account duration of treatment, side effects and patient preference)
When reducing dose of ICS, do this by 25-50% at a time

145
Q

What are some differentials for asthma?

A

COPD (can have an overlap with asthma)
Allergic bronchopulmonary aspergillosis (ABPA)
Bronchiectasis
Bronchiolitis

146
Q

What are the typical features of asthma?

A

Wheeze
Cough (nocturnal)
Breathlessness
Chest tightness
History of triggers and diurnal variation

147
Q

What are the features of acute asthma?

A

History of asthma
Worsening dyspnoea, wheeze and cough that is NOT responding to salbutamol (SABA)
May be triggered by a respiratory tract infection

148
Q

How are patients with acute asthma stratified?

A

Moderate
Severe
Life-threatening

149
Q

What are the features of someone with moderate acute asthma?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25/ min
Pulse < 110 bpm

150
Q

What are the features of someone with severe acute asthma?

A

PEFR 33-50% at best
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

151
Q

What are the features of someone with life-threatening acute asthma?

A

PEFR < 33% at best
Oxygen saturations < 92%
PaO2 < 8kPa, “normal” PaCO2
Silent chest
Cyanosis
Poor respiratory effort
Bradycardia
Arrhythmia
Hypotension
Exhaustion
Altered conscious level (confusion or coma)

152
Q

What are the features of near-fatal asthma?

A

Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

153
Q

What is the management for severe or life-threatening asthma?

A

ABCDE assessment
Call for help: ITU/HDU
Oxygen: aim for sats 98%
Bronchodilators: nebuliser salbutamol ± ipratropium bromide, IV magnesium
Steroids: PO prednisolone, if not IV hydrocortisone
Re-assess
Later → ventilatory support

154
Q

What is the management for improved severe or life threatening asthma after initial management?

A

Continue bronchodilators and steroids (5-7 days)
Wean off oxygen
Serial PEF, discharge if PEF over 75%
TAME asthma:
1. Technique
2. Avoid triggers
3. Monitor PEF
4. Educate

155
Q

What are the doses of medical management for severe or life threatening acute asthma?

A

Oxygen (15L high flow or with nebulisers)
Nebulised beta agonists: 2.5 mg salbutamol every 15 minutes
Nebulised ipratropium: 0.5mg every max 4 hours
Steroids: Oral 40/50mg OD or 100mg IV hydrocortisone

156
Q

What is a blood product transfusion?

A

A lifesaving procedure to treat hemorrhages and to improve oxygen delivery to tissues

157
Q

What different blood products can be transfused?

A
  1. Packed red cells: for chronic anaemia
  2. Platelet rich plasma: for patients who are thrombocytopaenic and are bleeding or require surgery
  3. Platelet concentrate: for thrombocytopaenia
  4. Fresh frozen plasma: used in correcting clotting deficiencies in patients with hepatic synthetic failure who are due to undergo surgery
  5. Cryoprecipitate: Rich source of Factor VIII and fibrinogen
158
Q

Which blood products must be cross matched?

A
  1. Packed red cells
  2. Fresh frozen plasma
  3. Cryoprecipitate
  4. Whole blood
    (platelets can be ABO incompatible in adults)
159
Q

What blood products are used in warfarin reversal?

A
  1. Stop warfarin
  2. Vitamin K (reversal within 4-24 hours, IV is quicker than oral)
  3. Fresh frozen plasma
  4. Human prothrombin complex (now first line for warfarin reversal, reversal within 1 hour)
160
Q

What are the indications for red cell transfusions?

A
  1. Symptomatic anemia (causing shortness of breath, dizziness, congestive heart failure, and decreased exercise tolerance)
  2. Acute sickle cell crisis
  3. Acute blood loss of more than 30 percent of blood volume
161
Q

What is the Hb threshold to require a red blood cell transfusion?

A

Without ACS:
70 g/L (target for 70-90)
With ACS:
80 g/L (target for 80-100)

162
Q

What are the indications for fresh frozen plasma transfusion?

A

Can be used for reversal of anticoagulant effects e.g. warfarin (but less commonly used)

163
Q

What are the indications for platelet transfusion?

A

To prevent haemorrhage in patients with thrombocytopenia or platelet function defects

164
Q

What are the indications for cryoprecipitate transfusion?

A

Used in cases of hypofibrinogenemia, which most often occurs in the setting of massive hemorrhage or consumptive coagulopathy

165
Q

How can the complications of blood product transfusions be classified?

A
  1. Immunological: acute haemolytic, non-haemolytic febrile, allergic/ anaphylaxis
  2. Infective
  3. Transfusion related acute lung injury (TRALI)
  4. Transfusion associated circulatory overload (TACO)
  5. Others: hyperkalaemia, iron overload, clotting
166
Q

What is non-haemolytic febrile reaction following a blood transfusion?

A

Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage
Features:
1. Fever
2. Chills
Management:
1. Stop or slow the transfusion
2. Paracetamol
3. Monitor

167
Q

What is a minor allergic reaction following a blood transfusion?

A

Thought to be caused by foreign plasma proteins
Features:
1. Pruritus
2. Utricaria
Management:
1. Temporarily stop the transfusion
2. Anti-histamine
3. Monitor

168
Q

What is an anaphylactic reaction following a blood transfusion?

A

Can be caused by patients with an IgA deficiency who have anti-IgA antibodies
Features:
1. Hypotension
2. Dyspnoea
3. Wheezing
4. Angioedema
Management:
1. Stop the transfusion
2. A to E approach (oxygen, fluids)
3. IM adrenaline

169
Q

What is an acute haemolytic reaction following a blood transfusion?

A

ABO incompatible blood e.g. secondary to human error
Features:
1. Fever
2. Abdominal pain
3. Hypotension
Management:
1. Stop the transfusion
2. Confirm diagnosis: check blood product against patient name, send blood for Coombs test
3. Supportive care: fluid resuscitation

170
Q

What is TACO following a blood transfusion?

A

Transfusion-associated circulatory overload from an excessive rate of transfusion/ pre-existing HF
Features:
1. Pulmonary oedema
2. Hypertension
Management:
1. Slow or stop transfusion
2. Consider IV loop diuretic e.g. furosemide and oxygen

171
Q

What is TRALI following a blood transfusion?

A

Transfusion related acute lung injury: non-cardiogenic pulmonary oedema from increased vascular permeability
Features:
1. Hypoxia
2. Pulmonary infiltrates on chest x-ray
3. Fever
4. Hypotension
Management:
1. Stop the transfusion
2. Supportive care and oxygen

172
Q

What transfusion reactions require stopping the transfusion ?

A
  1. Minor allergic reaction (only temporarily)
  2. Anaphylaxis
  3. Acute haemolytic reaction
  4. TRALI
173
Q

What is the key difference between TACO and TRALI following a blood transfusion?

A

TACO: hypertensive, TRALI: hypotensive
Both have pulmonary oedema but one is from circulatory overload (TACO) and one is non-cardiogenic (TRALI)

174
Q

What is a burns injury?

A

A very common injury predominantly to skin and superficial tissues caused by heat from hot liquids, flame or contact with hot objects

175
Q

How is the severity of burns injuries assessed?

A
  1. Burn size (% of total body surface area)
  2. Depth ( first to fourth degree)
176
Q

What symptoms and signs would be seen on physical examination for a burns injury?

A

Erythema
Dry/ wet and painful
Dry and lacking of physical sensation (insensate)
Cellulitis
If face affected- clouded cornea

177
Q

What are the risk factors for burn injuries?

A

Young children
Age > 60 years

178
Q

What are the investigations for burn injuries?

A
  1. A to E approach
  2. Assess carbon monoxide (ABG) and fluid loss (ABG, urinary catheter)
  3. Chest x-ray and ECG
  4. Bloods
  5. Wound biopsy and histology
179
Q

What is the management of burns injuries?

A
  1. Initial first aid as above
  2. Review referral criteria to ensure can be managed in primary care
  3. Superficial epidermal: symptomatic relief - analgesia, emollients etc
  4. Superficial dermal: cleanse wound, leave blister intact, non-adherent dressing, avoid topical creams, review in 24 hours
180
Q

What is the immediate first aid management in burns injuries?

A
  1. Airway, breathing, circulation
  2. Burns caused by heat:
    a. remove the person from the source
    b. within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes
    c. cover the burn using cling film, layered, rather than wrapped around a limb
  3. Electrical burns: switch off power supply and remove the person from the source
  4. Chemical burns:
    a. brush any powder off then irrigate with water
    b. attempts to neutralise the chemical are not recommended
181
Q

How do you assess the extent of a burn injury?

A
  1. Wallace’s Rule of Nines:
    head + neck = 9%
    each arm = 9%
    each anterior part of leg = 9%, each posterior part of leg = 9%
    anterior chest = 9%, posterior chest = 9%
    anterior abdomen = 9%, posterior abdomen = 9%
  2. Lund and Browder chart: the most accurate method
    the palmar surface is roughly equivalent to 1% of total body surface area (TBSA). Not accurate for burns > 15% TBSA
182
Q

How do you assess the depth of a burns injury?

A
  1. Superficial epidermal (first degree) = Red and painful, dry, no blisters
  2. Partial thickness (superficial dermal) (second degree) = Pale pink, painful, blistered. Slow capillary refill
  3. Partial thickness (deep dermal) (second degree) = Typically white but may have patches of non-blanching erythema. Reduced sensation, painful to deep pressure
  4. Full thickness (third degree) = White (‘waxy’)/brown (‘leathery’)/black in colour, no blisters, no pain
183
Q

What is the criteria for referral to secondary care for a burns injury?

A
  1. All deep dermal and full-thickness burns
  2. Superficial dermal burns of more than 3% TBSA in adults, or more than 2% TBSA in children
  3. Superficial dermal burns involving the face, hands, feet, perineum, genitalia, or any flexure, or circumferential burns of the limbs, torso, or neck
  4. Any inhalation injury
  5. Any electrical or chemical burn injury
  6. Suspicion of non-accidental injury
184
Q

What is the pathophysiology of severe burns injuries?

A
  1. Local response with progressive tissue loss and release of inflammatory cytokines
  2. Systemically, there are cardiovascular effects resulting from fluid loss and sequestration of fluid into the third space
  3. There is a marked catabolic response
  4. Immunosupression is common with large burns and bacterial translocation from the gut lumen is a recognised event → Sepsis is a common cause of death following major burns.
185
Q

What is the management of severe burn injuries?

A

The initial aim = stop the burning process and resuscitate the patient

  1. Airway:
    Smoke inhalation can result in airway oedema
    Early intubation should be considered e.g. if deep burns to the face or neck, blisters or oedema of the oropharynx, stridor etc
  2. IV fluids will be required for adults with burns greater than 15% (10% for children) of TBSA = Parkland formula, half of the fluid is administered in the first 8 hours
  3. Urinary catheter should be inserted and analgesia should be given
  4. Complex burns, burns involving the hand, perineum and face and burns >10% in adults and >5% in children should be transferred to a burns unit, circumferential burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the burnt tissue (improve ventilation)
186
Q

What is the prognosis of a burns injury?

A

Conservative management is appropriate for superficial burns and mixed superficial burns that will heal in 2 weeks
More complex burns may require excision and skin grafting

187
Q

What is the fluid resuscitation formula used for burns injuries?

A

Parkland formula:
1. (Crystalloid only e.g. Hartman’s solution/Ringers’ lactate)
2. Total fluid requirement in 24 hours =
4 ml x (total burn surface area (%)) x (body weight (kg))
3. 50% given in first 8 hours, then 50% given in next 16 hours
4. Resuscitation endpoint:Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this)
Points to note: Starting point of resuscitation is time of injury, deduct fluids already given

188
Q

What is the indication for fluid replacement in burns injuries?

A
  1. Indication = >15% total body area burns in adults (>10% children)
  2. The main aim of resuscitation is to prevent the burn deepening
  3. Most fluid is lost 24h after injury
  4. First 8-12h fluid shifts from intravascular to interstitial fluid compartments
    a. Therefore circulatory volume can be compromised
    b. However fluid resuscitation causes more fluid into the interstitial compartment especially colloid (therefore avoided in first 8-24h)
189
Q

What is cardiac arrest?

A

Acute cessation of cardiac function

190
Q

What are the reversible causes for a cardiac arrest?

A

4 Hs and 4Ts:
Hs:
1. Hypo/ hyperkalaemia
2. Hypothermia
3. Hypovolaemia
4. Hypoxia
Ts:
1. Tamponade
2. Tension pneumothorax
3. Thromboembolism
4. Toxins

191
Q

What signs would be seen on physical examination for a patient in cardiac arrest?

A

Unconscious
Patient is not breathing
Absent carotid pulses

192
Q

What are the ‘shockable’ rhythms in cardiac arrest?

A

Ventricular fibrillation (VF)
(Pulseless) Ventricular tachycardia (VT)

193
Q

What are the ‘non-shockable’ rhythms in cardiac arrest?

A

Asystole
Pulseless-electrical activity (PEA)

194
Q

What is the management for a cardiac arrest?

A

Crash call 2222
MEDICAL EMERGENCY
Adult advanced life support:
1. Determine rhythm via cardiac monitor
2. Begin chest compressions to ventilation at a ratio of 30:2
3. Defibrillate if shockable rhythms
4. Adrenaline 1mg
Management depends on cardiac rhythm

195
Q

What is the management of a shockable rhythm in cardiac arrest?

A

A to E assessment/ 2222/ medical emergency
1. Deliver shock
2. Resume chest compressions 30:2
3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus (anti-arrhythmic)

196
Q

What is the management for a non-shockable rhythm in a cardiac arrest?

A

Medical emergency/ 2222
1. CPR for 2 min at 30:2, and then return to assessing rhythm
2. Administer adrenaline (1 mg IV) every 3–5 min

197
Q

What is the management of return of spontaneous circulation (ROSC) in a cardiac arrest?

A

A to E approach
Aim for SpO2 sats of 94-98%
2 IV wide bore cannulas
ABG
12 lead ECG
Treat precipitating cause
Targeted temperature management

198
Q

What is the management for shockable cardiac rhythms?

A
  1. Defibrillate once
  2. Resume CPR immediately for 2 min, and then defibrillate
  3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
  4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus (anti-arrhythmic)
199
Q

What is the management for non- shockable cardiac rhythms?

A
  1. CPR for 2 min, and then return to assessing rhythm
  2. Administer adrenaline (1 mg IV) every 3–5 min
    No longer give atropine!
200
Q

What is the treatment for the 4 H reversible causes of cardiac arrest?

A
  1. Hypothermia: Warm slowly
  2. Hypo- or hyperkalaemia: Correction of electrolytes
  3. Hypovolaemia: IV colloids, crystalloids or blood products
  4. Hypoxia: oxygen
201
Q

What is the treatment for the 4 T reversible causes of cardiac arrest?

A
  1. Tamponade: Pericardiocentesis under xiphisternum up and leftwards
  2. Tension pneumothorax: Aspirate: needle into second intercostal space, mid-clavicular line
  3. Thromboembolism: management for PE, MI
  4. Toxins: antidotes
202
Q

What are the complications of a cardiac arrest?

A

Irreversible hypoxic brain damage → death

203
Q

What is the prognosis for patients with a cardiac arrest?

A
  1. Resuscitation is less successful in the arrests that occur outside hospital
  2. Duration of inadequate effective cardiac output is associated with poor prognosis
204
Q

What is cardiac failure?

A

Defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body

205
Q

How can heart failure be classified?

A
  1. By ejection fraction
  2. Acute or chronic
  3. Left or right
  4. High-output
206
Q

What is high-output HF?

A

Refers to a ‘normal’ heart is unable to pump enough blood to meet the metabolic demands of the body

207
Q

What are the causes of a high-output HF?

A
  1. Anaemia
  2. Arteriovenous malformation
  3. Paget’s disease
  4. Pregnancy
  5. Thyrotoxicosis
  6. Thiamine deficiency (Beri-Beri)
208
Q

What are the common causes of left sided HF?

A
  1. Increased left ventricular afterload e.g. arterial hypertension, aortic stenosis
  2. Increased left ventricular preload e.g. aortic regurgitation
209
Q

What is a common feature of left sided HF?

A

Pulmonary oedema:
1. Dyspnoea
2. Orthopnoea
3. Paroxysmal nocturnal dyspnoea
4. Bibasal fine crackles

210
Q

What are the causes of right sided HF?

A
  1. Increased right ventricular afterload e.g. pulmonary hypertension
  2. Increased right ventricular preload e.g. tricuspid regurgitation
211
Q

What are the common features of right sided HF?

A
  1. Peripheral oedema e.g. pedal/sacral oedema
  2. Raised jugular venous pressure
  3. Hepatomegaly
  4. Weight gain due to fluid retention
  5. Anorexia ‘cardiac cachexia’
212
Q

How is ejection fraction in HF measured?

A

By echocardiography

213
Q

What is the terminology for ejection fraction in HF?

A
  1. Reduced ejection fraction (HF-rEF) = < 35-40%
  2. Preserved ejection fraction (HF-pEF)
214
Q

What are the general causes of reduced and preserved ejection fraction HF?

A

Reduced EF:
1. Ischaemic heart disease
2. Dilated cardiomyopathy
3. Myocarditis
4. Arrhythmias
Preserved EF:
1. Hypertrophic obstructive cardiomyopathy
2. Restrictive cardiomyopathy
3. Cardiac tamponade
4. Constrictive pericarditis

215
Q

What is the epidemiology of HF?

A

10% of those over 65 years, usually presents at this age

216
Q

What is acute HF?

A
  1. A life threatening emergency
  2. Used to describe the sudden onset or worsening of symptoms of HF
  3. Usually has a background of pre-existing HF: decompensated
  4. If there is no history of HF: de-novo AHF
217
Q

What are the causes of decompensated HF (background of pre-existing HF)?

A
  1. Acute coronary syndrome
  2. Hypertensive crisis
  3. Acute arrhythmia
  4. Valvular disease e.g. AS
218
Q

What are the causes of de novo acute HF?

A
  1. Usually ischaemia
  2. Other causes e.g. viral myopathy, toxins, valve dysfunction
219
Q

How can patients with acute HF be broadly categorised?

A
  1. With or without hypoperfusion
  2. With or without fluid congestion
220
Q

What are the general symptoms of acute HF?

A
  1. Breathlessness
  2. Reduced exercise tolerance
  3. Oedema
  4. Fatigue
221
Q

What are the general signs of acute HF?

A
  1. Cyanosis
  2. Tachycardia
  3. Elevated jugular venous pressure
  4. Displaced apex beat
  5. Chest signs: bibasal crackles (pulmonary oedema), may have wheeze
  6. S3 heart sound
    *Over 90% of patients with have a normal or increased BP
222
Q

What are the investigations for acute HF?

A

Medical emergency- A to E approach
1. Bloods: look for underlying abnormality e.g. anaemia, infection
2. Chest x-ray: cardiomegaly, pulmonary oedema: venous congestion, interstitial oedema, Kerley B lines
3. Echocardiogram: ejection fraction, pericardial effusion, cardiac tamponade
4. BNP (B-type natriuretic peptide): > 100mg/L is supportive of dx

223
Q

What is the recommended management for all patients with acute HF?

A

IV loop diuretics e.g. furosemide

224
Q

What are some of the other management options for acute HF?

A

(Sit patient up)
1. Oxygen: aim for saturations 94-98%
2. Vasodilators e.g. nitrates (not to all patients)
3. Opiates (again not to all patients)
4. Continue any regular medication for HF e.g. ACE inhibitors

225
Q

When are nitrates used in the management of HF?

A

If patients have concomitant myocardial ischaemia, severe hypertensionor regurgitant aortic or mitral valve disease

226
Q

What is the major side effect/ contraindication to the use of nitrates in the management of acute HF?

A

Hypotension (cardiogenic shock)

227
Q

What is the management of cardiogenic shock (hypotension) in acute HF?

A
  1. < 10% of patients- seek senior support
  2. IV loop diuretics and nitrates may worsen hypotension
  3. Consider inotropic agents e.g. dobutamine
  4. Vasopressors e.g. norepinephrine
  5. Mechanical circulatory assistance e.g. intra-aortic balloon
228
Q

What routine mediations for HF should be continued or stopped in the management of acute HF?

A
  1. Continue ACE inhibitors
  2. Continue B blockers (but if HR is < 50 bpm, second or third degree heart block or shock then stop)
229
Q

What are the features of chronic HF?

A
  1. Dyspnoea
  2. Cough: worse at night, associated with pink/ frothy sputum
  3. Orthopnoea
  4. Paroxysmal nocturnal dyspnoea
  5. ‘Cardiac’ wheeze
  6. Weight loss: ‘cardiac cachexia’/ weight gain secondary to oedema
  7. Bibasal crackles on examination
  8. Signs of right sided HF: raised JVP, ankle oedema, hepatomegaly
230
Q

What is the New York Heart Association (NYHA) for chronic HF?

A

Used to classify the severity of HF:
Class 1: No symptoms/ no limitation
Class 2: Mild symptoms, some limitation of physical activity
Class 3: Moderate symptoms, marked limitation of physical activity (less than normal activity results in symptoms)
Class 4: Severe symptoms, unable to carry out any physical activity without discomfort (symptoms present even at rest)

231
Q

What is the first-line blood test for chronic HF diagnosis?

A

N-terminal pro-B-type natriuretic peptide (NT‑proBNP)

232
Q

How are the N-terminal pro-BNP tests interpreted in chronic HF diagnosis?

A
  1. If ‘high’: arrange specialist assessment (incl echo) within 2 weeks
  2. If ‘raised’: arrange specialist assessment (incl echo) within 6 weeks
233
Q

What is B-type natriuretic peptide (BNP)?

A
  1. Hormone produced mainly by the left ventricular myocardium in response to strain
  2. Very high levels are associated with a poor prognosis:
    a. High = > 400pg/ml
    b. Raised = 100-400ph/ml
    c. Normal = < 100pg/ml
234
Q

What can increase BNP levels?

A
  1. Left ventricular hypertrophy
  2. Ischaemia
  3. Tachycardia
  4. Hypoxaemia (including PE)
  5. GFR < 60ml/min
  6. Sepsis
  7. COPD
  8. DM
  9. Aged > 70 years
  10. Liver cirrhosis
235
Q

What can decrease BNP levels?

A
  1. Obesity
  2. Diuretics
  3. ACE inhibitors
  4. B blockers
  5. ARBs
  6. Aldosterone antagonists e.g. spironolactone
236
Q

What is the first line management for chronic HF?

A

(manage lifestyle and optimise comorbidities)
1. ACE inhibitors (ARB if intolerant)
2. Beta Blockers
(start one at a time)

237
Q

What is the second line management for chronic HF?

A
  1. ACE inhibitors + beta blockers
  2. Add an aldosterone antagonist e.g. spironolactone
238
Q

What should be monitored alongside the management of chronic HF?

A

Potassium levels: both ACE inhibitors and aldosterone antagonists cause hyperkalaemia

239
Q

What other drugs can be given as second line management in chronic HF?

A

SGLT-2 inhibitors:
1. For patients with a reduced EF
2. Reduce glucose reabsorption and increase urinary glucose excretion
3. E.g. dapagliflozin

240
Q

What is the third line management for chronic HF?

A
  1. Only initiated by a specialist
  2. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
241
Q

When is digoxin indicated in the management of chronic HF?

A

If there is coexistent atrial fibrillation

242
Q

When is cardiac resynchronisation therapy indicated in the management of chronic HF?

A

Widened QRS (e.g. left bundle branch block) complex on ECG

243
Q

What are add on treatments for patients with chronic HF?

A
  1. Annual influenza vaccination
  2. One-off pneumococcal vaccine (if the patient has asplenia, splenic dysfunction or chronic kidney disease they need a booster every 5 years)
244
Q

When should ivabradine be added in the management of chronic HF?

A
  1. Third line specialist treatment
  2. If sinus rhythm > 75/min and a left ventricular EF < 35%
245
Q

When should sacubitril-valsartan be added in the management of chronic HF?

A
  1. Third line specialist treatment
  2. When left ventricular EF < 35% and still symptomatic on ACE inhibitors and ARBs
  3. Should be initiated following ACEi/ ARB wash-out period
246
Q

How do beta blockers work in the management of chronic HF?

A
  1. Block the effects of chronically activated sympathetic system, slow progression of the heart failure and improve survival
  2. The benefits of ACE inhibitors and b-blockers are additive*
247
Q

How to ACE inhibitors work in the management of chronic HF?

A

e.g. enalapril, perindopril, ramipril)
1. Inhibit intracardiac renin-angiotensin system which may contribute to myocardial hypertrophy and remodelling
2. ACE inhibitors slow progression of the heart failure and improve survival

248
Q

When should Hydralazine and a nitrate be added in the management of chronic HF?

A

May be added in patients (particularly in Afro-Caribbeans) with persistent symptoms despite therapy with an ACE inhibitor and b-blocker

249
Q

Which drugs should be avoided in chronic HF?

A

Drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil)

250
Q

What are the complications of HF?

A
  1. Respiratory failure
  2. Cardiogenic shock
  3. Death
251
Q

What is the prognosis of heart failure?

A

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

252
Q

What is carbon monoxide poisoning?

A
  1. Type of poisoning
  2. Carbon monoxide has a high affinity for haemoglobin and myoglobin leading to tissue hypoxia
253
Q

What is the epidemiology of carbon monoxide poisoning?

A

Around 50 deaths per year in the UK from accidental carbon monoxide poisoning

254
Q

What is the pathophysiology of carbon monoxide poisoning?

A
  1. Carbon monoxide has a high affinity for haemoglobin and myoglobin
  2. This leads to a decrease in the oxygen saturation of haemoglobin leading to an early plateau in the oxygen dissociation curve
  3. Resulting in tissue hypoxia
255
Q

What may be a key feature in the history of carbon monoxide poisoning?

A

Badly maintained housing e.g student housing

256
Q

What are the features of carbon monoxide poisoning?

A
  1. Headache (90%)
  2. Nausea and vomiting (50%)
  3. Vertigo (50%)
  4. Confusion (30%)
  5. Subjective weakness (20%)
257
Q

What are the signs of severe toxicity in carbon monoxide poisoning?

A
  1. ‘Pink’ skin and mucosae
  2. Hyperpyrexia
  3. Arrhythmias
  4. Extrapyramidal features
  5. Coma
  6. Death
258
Q

What is the best investigation for carbon monoxide poisoning?

A

ABG/ VBG
Pulse oximetry may be falsely high because of similarities between oxyhaemoglobin and carboxyhaemoglobin

259
Q

What are the carboxyhaemoglobin levels in normal patients and in severe toxicity of carbon monoxide poisoning?

A
  1. Non-smokers = < 3%
  2. Smokers = <10%
  3. Symptomatic poisoning (headache, vomiting) = 10-30%
  4. Severe toxicity = >30%
260
Q

What are the investigations for carbon monoxide poisoning?

A

A and E management:
1. ABG/VBG for carboxyhaemoglobin levels
2. ECG: look for cardiac ischaemia

261
Q

What is the management for carbon monoxide poisoning?

A
  1. Managed in A&E
  2. 100% high flow oxygen via a non-rebreather mask (generally given until all symptoms have resolved)
262
Q

What is the reasoning for giving high flow oxygen in the management of carbon monoxide poisoning?

A
  1. Decreases the half-life of carboxyhemoglobin (COHb)
  2. Should be administered as soon as possible, with treatment continuing for a minimum of six hours
  3. Target oxygen saturations are 100%
  4. Given until symptoms resolve
263
Q

What can also be given under specialist input for carbon monoxide poisoning management?

A
  1. Hyperbaric oxygen
  2. For more severe cases: if carboxyhaemoglobin levels are > 25%
  3. Indications also include:
    a. Loss of consciousness at any point
    b. Neurological signs other than headache
    c. Myocardial ischaemia or arrhythmia
    d. Pregnancy
264
Q

What are central venous cannulas?

A
  1. Thin flexible tubes which are used to draw blood and give treatments
  2. Inserted into usually the superior vena cava
  3. Can stay in place for weeks or months
265
Q

Which central venous cannula is preferred and why?

A

Internal jugular route is preferred over femoral lines:
Femoral lines are easier to insert and iatrogenic injuries easier to manage in this site however they are prone to high infection rates

266
Q

How should central venous cannulas be inserted?

A

Ultrasound guided

267
Q

What can be given via central venous cannulas?

A

IV fluids, drugs, blood products (lumens are relatively narrow so do not allow particularly rapid rates of infusion)

268
Q

When are central venous lines preferred over peripheral cannulas?

A

Peripheral cannulas are unsuitable for the administration of vasoactive drugs, such as inotropes and irritant drugs such as TPN

269
Q

What are some of the complications of central venous cannulas?

A
  1. Failure to place catheter
  2. Arterial puncture/ iatrogenic arterial injury
  3. Catheter malposition
  4. Pneumothorax
  5. Subcutaneous haematoma
  6. Haemothorax
  7. Cardiac arrest (<1%)
270
Q

What is a PICC line?

A

Peripherally inserted central cannula: popular methods for establishing central venous access whilst minimising major complications relating to device insertion than conventional central lines

271
Q

What is a chest drain?

A

A tube inserted into the pleural cavity which creates a one way valve: allows the movement of air or liquid out of the cavity

272
Q

What are the indications for a chest drain?

A
  1. Pleural effusion
  2. Pneumothorax not suitable for aspiration or conservative management
  3. Empyema
  4. Haemothorax/ haemopneunomothorax
  5. Some cases of penetrating chest wall injuries in ventilated patients
273
Q

What are the relative contraindications for a chest drain?

A
  1. INR > 1.3
  2. Platelet count < 75
  3. Pulmonary bullae
  4. Pleural adhesions
274
Q

How is a chest drain inserted?

A
  1. Patient positioned in a supine position or at 45 degrees
  2. Identify the 5th intercostal space in the mid-axillary line
    (can be ultrasound guided especially if fluid in the pleura)
  3. LA (lidocaine max 3mg/kg)
  4. Drainage tube inserted using a Seldinger technique
  5. Drain tubing should then be secured using either a straight stitch or an adhesive dressing
275
Q

What is a Seldinger technique?

A
  1. The desired vessel is punctured with a sharp hollow needle
  2. The syringe is detached and a guide wire is advanced through the lumen of the needle
  3. The needle is then withdrawn
276
Q

How can the position of a chest drain be confirmed?

A
  1. Aspiration of fluid from the drainage tube
    ‘2. Swinging’ of the fluid within the drain tubing when the patient inspires
  2. On chest x-ray
277
Q

What are the complications of a chest drain?

A
  1. Failure of insertion (may go into the wrong place- should be removed and re-sited)
  2. Bleeding: around the site of the drain or into the pleural space
  3. Infection
  4. Penetration of the lung
  5. Re-expansion pulmonary oedema
278
Q

What is re-expansion pulmonary oedema?

A
  1. Uncommon complication following drainage of a pneumothorax or pleural effusion
  2. Features: Cough and/or shortness of breath
279
Q

How can re-expansion pulmonary oedema be prevented and managed?

A

Prevention: the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours)
Management: the chest drain should be clamped and an urgent chest x-ray should be obtained

280
Q

When should a chest drain be removed?

A

Dependent on the indication for insertion:
1. If for fluid drainage = the drain should be removed when there has been no output for > 24 hours and imaging shows resolution of the fluid collection
2. For pneumothorax = the drain should be removed when it is no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution of the pneumothorax

281
Q

What is COPD?

A

An umbrella term encompassing chronic bronchitis and emphysema

282
Q

What is the most common cause of COPD?

A

Smoking

283
Q

What is COPD characterised by?

A
  1. Airflow limitation that is not fully reversible
  2. Chronic bronchitis + emphysema
284
Q

What is the aetiology of COPD?

A
  1. Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke)
  2. Overlaps and may co-exist with asthma
285
Q

What is the second common cause of COPD?

A

Alpha -1 antitrypsin deficiency (not as common as smoking)

286
Q

Aside from smoking and alpha-1 antitrypsin deficiency, what are the other causes of COPD?

A

Not as common
1. Cadmium (used in smelting)
2. Coal
3. Cotton
4. Cement
5. Grain

287
Q

What are the features of COPD?

A
  1. Cough, often productive
  2. Dyspnoea
  3. Wheeze
  4. In severe cases = right-sided HF may develop leading to peripheral oedema
288
Q

What are the investigations for suspected COPD?

A
  1. Spirometry with bronchodilator: demonstrate airflow obstruction, FEV1/FVC < 70%
  2. Chest x-ray
  3. Bloods: FBC to exclude secondary polycythaemia
  4. BMI index
289
Q

What are the signs of COPD on a chest x-ray?

A
  1. Hyperinflation
  2. Bullae: if large can mimic a pneumothorax
  3. Flat hemidiaphragm
  4. Exclude lung cancer
290
Q

Why is peak expiratory flow (PEF) of limited value in COPD?

A

May underestimate the degree of airflow obstruction

291
Q

What is the severity of COPD categorised by?

A

FEV1: forced expiratory volume in 1 second

292
Q

When should COPD diagnosis be considered in patients?

A

If over 35 years who are smokers or non-smokers and have symptoms such as:
1. Exertional breathlessness
2. Chronic cough
3. Regular sputum production

293
Q

What value of post-bronchodilator spirometry FEV1/FVC is needed to make a diagnosis of COPD?

A

< 0.7 (< 70%)

294
Q

What are the stages of severity of COPD based on the FEV1?

A

Stage 1 (>80%): Mild, symptoms should be present to diagnose COPD in these patients
Stage 2 (50-79%): Moderate
Stage 3 (30-49%): Severe
Stage 4 (<30%): Very severe

295
Q

What stage of COPD does a patient have if their post-bronchodilator FEV1/FVC is < 0.7 but their FEV1 is greater than 80%?

A

Stage 1, mild COPD (even though their FEV1 is over 80% it is still COPD, but must have symptoms for diagnosis)

296
Q

What is the general management of COPD?

A
  1. Smoking cessation advice (includes offering nicotine replacement therapy)
  2. Annual influenza vaccination, one-off pneumococcal vaccination
  3. Pulmonary rehabilitation
  4. Bronchodilator therapy, first-line SABA or SAMA
297
Q

What is the medical management of COPD?

A
  1. SABA or SAMA
  2. Determine whether they have asthmatic/ steroid responsive features
    a. If yes: SABA or SAMA as required, LABA + ICS (often one inhaler)
    b. If no: SABA as required, LABA + LAMA regularly
  3. If patient remains breathlessness or have exacerbations:
    SABA as required, triple therapy regularly = LABA + LAMA + ICS
298
Q

What are the NICE criteria to determine whether a COPD patient has asthmatic/ steroid responsive features?

A
  1. Any previous secure diagnosis of asthma/ atopy
  2. Higher blood eosinophil count (as part of the recommended FBC)
  3. Substantial variation in FEV1 over time ( at least 400ml)
  4. Substantial diurnal variation in PEF (at least 20%)
299
Q

When would oral theophylline be recommended in COPD management?

A
  1. Only after trials of short and long-acting bronchodilators or to people who cannot use inhaled therapy
  2. The dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
300
Q

When are oral prophylactic antibiotic therapy recommended in the management of COPD?

A
  1. Azithromycin in select patients
  2. Patients should not smoke, have optimised standard treatments and continue to have exacerbations
  3. Need to have a CT thorax to exclude bronchiectasis
  4. Need to have a sputum culture to exclude atypical infections and TB
  5. ECG prior to starting to exclude QT prolongation (as azithromycin can cause this) and LFTs
301
Q

When would mucolytic be considered in COPD management?

A

Should be considered in patients with a chronic productive cough and continued if symptoms improve

302
Q

What are the features of cor pulmonale in the context of COPD?

A
  1. Peripheral oedema (due to right-sided heart failure)
  2. Raised jugular venous pressure
  3. Systolic parasternal heave
  4. Loud P2
303
Q

What is the management of cor pulmonale in COPD patients?

A
  1. Use a loop diuretic for the oedema
  2. Consider long-term oxygen therapy
    (NOT ACEi, CCB or alpha blockers)
304
Q

What are the factors which may improve survival in patients with stable COPD?

A
  1. Smoking cessation
  2. Long-term oxygen therapy in patients who fit the criteria
  3. Lung volume reduction surgery in selected patients
305
Q

What is the single most important intervention in COPD patients who are still smoking?

A

Smoking cessation

306
Q

What is chronic bronchitis?

A

Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years

307
Q

What is emphysema?

A

Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles

308
Q

What is the aetiology of chronic bronchitis?

A

Narrowing of the airways resulting from:
1. Bronchiole inflammation (bronchiolitis) and
2. Bronchi with mucosal oedema
3. Mucous hypersecretion

309
Q

What is the aetiology of ephysema?

A
  1. Destruction and enlargement of the alveoli
  2. Results in loss of the elastic traction that keeps small airways open in expiration
  3. Progressively larger spaces develop, termed bullae (diameter is >1 cm)
310
Q

Which COPD patients should be assessed for long-term oxygen therapy?

A
  1. Very severe outflow obstruction, FEV1 <30% (considered if FEV1 is 30-49%)
  2. Cyanosis
  3. Polycythaemia
  4. Peripheral oedema
  5. Raised jugular venous pressure
  6. Oxygen saturations < 92% on room air
311
Q

What is the assessment for long-term oxygen therapy in COPD patients?

A

Measure ABG on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management

312
Q

When should COPD patients be offered long-term oxygen therapy?

A
  1. ABG: pO2 of <7.3 kPa
  2. ABG pO2 of 7.3-8 kPa and one of the following:
    a. Secondary polycythaemia
    b. Peripheral oedema
    c. Pulmonary hypertension
313
Q

What is the advice on long-term oxygen therapy and smoking?

A

Do not offer long-term oxygen therapy to people who continue to smoke despite being offered smoking cessation advice and treatment and referral to specialist

314
Q

What is important in regards to the risk assessment for long-term oxygen therapy?

A
  1. Risk of falls from tripping over the equipment
  2. Risk of burns and fires (increased risk for people who live in homes where someone smokes)
315
Q

What is an acute exacerbation of COPD?

A

Where patients with COPD experience more severe symptoms, often due to an infective cause

316
Q

What are the most common bacterial causes of acute exacerbation of COPD?

A
  1. Haemophilus influenzae (most common)
  2. Streptococcus pneumoniae
  3. Moraxella catarrhalis
317
Q

What is the most common bacterial causative organism for an acute exacerbation of COPD?

A

Haemophilus influenzae

318
Q

What are the viral causes of an acute exacerbation of COPD?

A
  1. Respiratory viruses, account for 30% of exacerbations
  2. Human rhinovirus is most important
319
Q

What are the features of an acute exacerbation of COPD?

A
  1. Increase in dyspnoea, cough and wheeze
  2. May be increase in sputum (suggestive of infective cause)
  3. Patients may be hypoxic and in some cases have acute confusion
320
Q

What is the criteria for admission of an acute exacerbation of COPD?

A
  1. Severe breathlessness
  2. Acute confusion or impaired consciousness
  3. Cyanosis
  4. O2 sats < 90% on pulse oximetry
  5. Social reasons e.g. inability to cope at home/ living alone
  6. Significant comorbidity e.g. cardiac disease, insulin dependent DM
321
Q

What is the management of non-severe acute exacerbation of COPD?

A
  1. Increase the frequency of bronchodilator use (and consider giving via a nebuliser)
  2. Give prednisolone 30mg daily for 5 days
  3. Antibiotics if sputum is purulent or clinical signs of pneumonia: oral amoxicillin, clarithromycin or doxycycline
322
Q

What is the management of severe acute exacerbation of COPD (requiring secondary care admission)?

A
  1. Oxygen therapy
  2. Nebulised bronchodilator
  3. Steroid therapy: prednisolone 30mg daily for 5 days or IV hydrocortisone
  4. Consider IV theophylline
  5. Non-invasive ventilation if T2RF development
323
Q

What is the oxygen therapy in the management of severe exacerbation of COPD?

A
  1. Risk of hypercapnia therefore aim for oxygen target of 88-92%
  2. Initially use 28% Venturi mask at 4L/min, aim for 88-92% whilst waiting for ABG results
  3. Adjust target range to 94-98% if the pCO2 is normal
324
Q

What nebulised bronchodilators are used in the management of severe exacerbation of COPD?

A
  1. Beta adrenergic agonist: salbutamol
  2. Muscarinic antagonist: ipratropium bromide
325
Q

When is IV theophylline therapy considered in severe exacerbations of COPD?

A

For patients not responding to nebulised bronchodilators

326
Q

When is non-invasive ventilation used in the management of severe exacerbations of COPD?

A
  1. If the patient develops type 2 respiratory failure: low O2 and high CO2
  2. Typically used for COPD with respiratory acidosis: pH 7.25-7.35 (can be for <7.25 but require more monitoring and has a lower threshold of intubation and ventilation)
327
Q

What type of non-invasive ventilation is used in severe exacerbations of COPD?

A

Bi-level positive airway pressure (BiPAP), initial settings:
1. Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
2. Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O

!Final Year (26 decks)

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