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!Final Year > Acute Care and Trauma (2) > Flashcards

Acute Care and Trauma (2) Flashcards

1
Q

What is diabetic ketoacidosis (DKA)?

A

A serious complication or first presentation of type 1 diabetes mellitus (rarely type 2)

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2
Q

What is the pathophysiology of DKA?

A
  1. Uncontrolled lipolysis which results in the excess production of free fatty acids
  2. These are ultimately converted to ketone bodies
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3
Q

What is type 1 diabetes mellitus?

A
  1. Autoimmune disorder
  2. Insulin producing beta-cells in the in the Islet of Langerhans in the pancreas are destroyed
  3. Results in an absolute deficiency of insulin resulting in raised glucose levels
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4
Q

What are the presenting symptoms of type 1 DM?

A
  1. Weight loss
  2. Polydipsia
  3. Polyuria
    (2 and 3 are caused by the osmotic effects of excess blood glucose being excreted by the body, drawing water out)
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5
Q

What are the features of DKA?

A
  1. Abdominal pain
  2. Of type 1: polyuria, polydipsia, dehydration
  3. Kussmaul breathing: deep hyperventilation
  4. Acetone-smelling breathing
  5. Low GCS
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6
Q

What are the precipitating factors for DKA?

A
  1. Infection
  2. Missed insulin doses
  3. Myocardial infarction
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7
Q

What are the investigations for DKA?

A
  1. A to E approach
  2. Key investigations include VBG (pH, glucose) bloods for ketones, U&Es
  3. Urine dip
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8
Q

What is the diagnostic criteria for DKA?

A
  1. Glucose > 11 mmol/L or known DM
  2. pH < 7.3
  3. Bicarbonate < 15 mmol/L
  4. Presence of ketones:
    a. Ketones > 3mmol/L
    b. Urine ketones ++ on dipstick
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9
Q

What are the management principles of DKA?

A

MEDICAL EMERGENCY: A to E approach
1. Fluid resuscitation
2. Insulin
3. Correction of electrolyte disturbance
4. Long-term management e.g. insulin

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10
Q

What is the fluid replacement management in DKA?

A
  1. Most patients with DKA will be deplete of 5-8 L
  2. Isotonic saline is used initially (0.9% sodium chloride)
  3. Bolus of 500ml over 10-15 minutes
  4. Then replacement fluids: 100 ml/kg/day for the first 10kg, 50 ml/kg/day for the next 10kg, 20 ml/kg/day for weight over 20kg
  5. Plus maintenance fluids
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11
Q

What is the greatest risk in fluid resuscitation in children in the management of DKA?

A

Cerebral oedema:
1. Children and young adults are particularly vulnerable
2. Slower infusion rates may be indicated
3. Presents with headache, irritability, visual disturbance, focal neurology
4. If suspicion: CT head and senior review

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12
Q

What is the insulin management of DKA?

A
  1. Start an IV infusion at 0.1unit/kg/hour
  2. Once the blood glucose has been bought down to < 14mmol/L, continue the IV insulin and add 10% dextrose
  3. Infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
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13
Q

How are electrolyte disturbances corrected in the management of DKA?

A
  1. Serum potassium levels fall after the administration of insulin
  2. Therefore may need to add potassium to the fluids
  3. Of the rate of potassium infusion is > 20 mmol/hour then cardiac monitoring may be required
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14
Q

What is DKA resolution?

A
  1. pH > 7.3
  2. Blood ketones < 0.6 mmol/L
  3. Bicarbonate > 15 mmol/L
    If the patient is eating and drinking at this point = switch to S/C insulin
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15
Q

What must happen before a patient is discharged for an admission of DKA?

A

The patient must be reviewed by a diabetes specialist nurse

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16
Q

How quickly should ketonaemia and acidosis resolve in the management of DKA?

A
  1. Should resolve within 24 hours
  2. If not, requires senior review from endocrinologist
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17
Q

What are the complications of a DKA?

A

Can be from DKA or the management of it:
1. Gastric stasis
2. VTE
3. Arrhythmias secondary to hyperkalaemia
4. Incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
5. ARDS
6. AKI

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18
Q

What is the prognosis of DKA?

A

Although a serious condition, mortality has decreased significantly due to improved understanding of pathophysiology and close monitoring of electrolytes

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19
Q

What is Disseminated intravascular coagulation (DIC)?

A
  1. An acquired syndrome
  2. Characterised by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors
  3. Thrombi may lead to vascular obstruction/ischaemia and multi-organ failure
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20
Q

What are the common causes of DIC?

A
  1. Sepsis
  2. Trauma
  3. Obstetric complications e.g. amniotic fluid embolisation, elevated LFTs, HELLP syndrome
  4. Malignancy
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21
Q

What is the epidemiology of DIC?

A
  1. Many conditions can cause DIC, therefore, the overall incidence is difficult to determine
  2. Seen in any severely ill patient
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22
Q

What are the presenting symptoms of DIC?

A

Patient is severely unwell with symptoms of:
1. The underlying disease
2. Confusion
3. Dyspnoea
4. Evidence of bleeding

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23
Q

What are the signs of acute DIC?

A
  1. Signs of underlying cause e.g. sepsis, evidence of shock
  2. Petechiae
  3. Purpura
  4. Ecchymoses
  5. Epistaxis
  6. Mucosal bleeding
  7. Signs of end organ damage
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24
Q

What are the signs of chronic DIC?

A
  1. Signs of DVT or arterial thrombosis
  2. Superficial venous thrombosis
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25
Q

What is the difference between petechiae, purpura and ecchymosis?

A

Petechiae: bleeding into the skin from broken blood vessels, form tiny red dots
Purpura: blood can collect under the skin in larger flat reas
Ecchymosis: blood can collect under the skin and form a very large bruised area

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26
Q

What are the investigations for DIC?

A

FBC:
1. Decreased platelets (due to excessive consumption)
2. Decreased fibrinogen (excessive consumption)
3. Prolonged prothrombin time
4. Elevated D dimer
5. Raised fibrinogen degradation products
Peripheral blood film:
1. Red cell fragments: schistocytes
Causes for underlying cause e.g. blood cultures

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27
Q

How is DIC diagnosed?

A
  1. Low platelets
  2. Low fibrinogen
  3. Prolonged PT and APTT
  4. Raised fibrinogen degradation products
  5. Presence of schistocytes (red cell fragments) on blood film due to microangiopathic haemolytic anaemia
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28
Q

What is the management of DIC?

A
  1. Aggressive treatment of underlying disorder
  2. Restore normal coagulation: heparin
  3. Replacement of platelets and coagulation factors: Fresh frozen plasma, platelet concentrate, antithrombin III
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29
Q

What are the complications of DIC?

A
  1. Life threatening haemorrhage
  2. Acute renal failure
  3. Gangrene and loss of digits
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30
Q

What are the different causes of elbow pain?

A
  1. Lateral epicondylitis (tennis elbow)
  2. Medial epicondylitis (golfer’s elbow)
  3. Radial tunnel syndrome
  4. Cubital tunnel syndrome
  5. Olecranon bursitis
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31
Q

What is Lateral epicondylitis (tennis elbow)?

A
  1. Pain and tenderness to the lateral epicondyle
  2. Typically following unaccustomed activity e.g. house painting, play tennis
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32
Q

Who commonly is affected by Lateral epicondylitis (tennis elbow)?

A

Middle aged people: 45-55 years

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33
Q

Which are is typically affected in Lateral epicondylitis (tennis elbow)

A

The dominant arm

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34
Q

What are the features of Lateral epicondylitis (tennis elbow)?

A
  1. Pain and tenderness localised to the lateral epicondyle
  2. Pain worse on wrist extension against resistance when the elbow is extended
  3. Pain worse on supination of the forearm with the elbow extended
  4. Tends to be acutely painful for 6-12 weeks (can last up to 2 years as chronic pain)
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35
Q

What are the management options for Lateral epicondylitis (tennis elbow)?

A
  1. Avoid muscle overload
  2. Simple analgesia
  3. Steroid injections
  4. Physiotherapy
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36
Q

What is Medial epicondylitis (golfer’s elbow)?

A
  1. Pain and tenderness localised to the medial epicondyle
  2. Pain is aggravated by wrist flexion and pronation
  3. Symptoms may be accompanied by numbness / tingling in the 4th and 5th finger due to ulnar nerve involvement
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37
Q

What is radial tunnel syndrome?

A
  1. Symptoms are similar to lateral epicondylitis (so difficult to diagnose)
  2. Symptoms worsened by extending the elbow or pronating the forearm (opposite to lateral)
  3. Most commonly due to compression of the posterior interosseous branch of the radial nerve from overuse
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38
Q

What is Cubital tunnel syndrome?

A
  1. Tingling and numbness of the 4th and 5th finger
  2. Pain worse on leaning on the affected elbow
  3. Due to compression of the ulnar nerve as it passes through the cubital tunnel
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39
Q

What are the features of cubital tunnel syndrome?

A
  1. Tingling and numbness of the 4th and 5th finger which starts off intermittent and then becomes constant.
  2. Over time, may also develop weakness and muscle wasting
  3. Pain worse on leaning on the affected elbow
  4. Often a history of osteoarthritis or prior trauma to the area
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40
Q

What is the investigation for cubital tunnel syndrome?

A

Clinical diagnosis: however, in selected cases nerve conduction studies may be used

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41
Q

What is the management of cubital tunnel syndrome?

A
  1. Avoid aggravating activity
  2. Physiotherapy
  3. Steroid injections
  4. Surgery in resistant cases
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42
Q

What is olecranon bursitis?

A
  1. Swelling over the posterior aspect of the elbow
  2. May be associated warmth, pain and erythema
  3. Typically affects middle aged male patients
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43
Q

What is a radial head fracture?

A
  1. Common in young adults
  2. It is usually caused by a fall on the outstretched hand
  3. O/E: there is marked local tenderness over the head of the radius, impaired movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination)
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44
Q

What is an epidural?

A
  1. An anaesthetic injected into the epidural space surrounding the fluid-filled sac (the dura) around the spinal cord
  2. It partially numbs the abdomen and legs and is most commonly used during childbirth
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45
Q

What are the indications for an epidural?

A
  1. Provide analgesia:
    a. intraoperative
    b. postoperative (v good for this)
    c. peripartum (labour analgesia, Caesarean section)
    d. end-of-life settings
  2. Can be used as the primary anaesthetic for surgeries from the mediastinum to the lower extremities
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46
Q

What are the possible complications of an epidural?

A
  1. Anaphylaxis due to anaesthetic
  2. Procedure related: back pain, pneumocephalus (presence of air in the cranial activity)
  3. Potentially life threatening:
    a. subdural injection
    b. Aseptic meningitis
    c. Cardiac arrest
    d. Spinal epidural abscess
    e. Epidural haematoma
    f. Permanent neurological injury
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47
Q

What is epilepsy?

A

A common neurological condition characterised by recurrent seizures

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48
Q

Are there any associated diseases with epilepsy?

A

Most commonly occurs in isolation
Can be associated with:
1. Cerebral palsy - 30% have epilepsy
2. Tuberous sclerosis
3. Mitochondrial diseases

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49
Q

How are seizures in epilepsy classified?

A

3 key features:
1. Where seizures begin in the brain
2. Level of awareness during a seizure
3. Any other features of seizures

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50
Q

What are the two main types of epilepsy?

A

Focal seizures
Generalised seizures

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51
Q

What are focal seizures?

A
  1. Start in a specific area on one side of the brain
  2. Level of awareness can vary
  3. Can be further classified into motor (e.g. Jacksonian march) or non-motor (e.g. deja vu) or other such as aura
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52
Q

What are generalised seizures?

A
  1. These engage or involve networks on both sides of the brain at onset
  2. Consciousness is lost immediately (no level of awareness)
  3. Can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)
  4. Specific types: tonic-clonic, tonic, clonic, typical absence and myoclonic (brief rapid muscle jerks)
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53
Q

What is a focal to bilateral seizure?

A

Where the seizure starts on one side of the brain in a specific area before spreading to both lobes

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54
Q

What are some of the signs and features of epilepsy?

A
  1. Seizure activity: level of awareness, motor vs non-motor
  2. Biting their tongue
  3. Incontinence of urine
  4. Post-ictal phase: drowsy and tired for around 15 minutes
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55
Q

What are the features of a seizure originating in the temporal lobe?

A
  1. May occur with or without impairment of consciousness
  2. An aura occurs in most patients (e.g. rising epigastric sensation, deja vu, less commonly hallucinations)
  3. Seizures typically last around 1 minute
  4. Automatisms are common (e.g. lip smacking, grabbing, plucking)
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56
Q

What are the features of a seizure originating in the frontal lobe?

A
  1. Head/leg movements
  2. Posturing
  3. Post-ictal weakness
  4. Jacksonian march
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57
Q

What are the features of a seizure originating in the parietal lobe?

A

Paraesthesia

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58
Q

What are the features of a seizure originating in the occipital lobe?

A

Floaters/ flashers

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59
Q

What are the investigations for epilepsy?

A

For any seizure: A to E approach, including blood glucose to exclude hypoglycaemia, think cardiac causes too
Following their first seizures, patients generally have both an EEG and imaging = MRI

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60
Q

What is the management of epilepsy?

A
  1. Most neurologists start anti-epileptics following a SECOND epileptic seizure
  2. Common medications include sodium valproate (not for females of reproductive age), Carbamazepine, Lamotrigine, Phenytoin
  3. Other considerations include:
    a. DVLA
    b. Other medications (enzyme inducers and inhibitors to need to check)
    c. women wishing to get pregnant or on contraceptives (talk to specialist neurologist)
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61
Q

What are the DVLA rules for patients who have epilepsy?

A

Patients cannot drive for 6 months following a seizure
Must be fit free for 12 months before being able to drive

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62
Q

What are the common anti-epileptic drugs?

A
  1. Sodium valproate: used for generalised seizures in men, P450 inhibitor
  2. Carbamazepine: used second line for focal seizures, P450 induced, side effects include leucopenia and agranulocytosis, dizziness
    *3. Lamotrigine: used for a variety of generalised and focal seizures with a limited side effect profile (other than Stevens-Johnson syndrome)
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63
Q

What is the acute management of seizures?

A
  1. Most seizures terminate spontaneously
  2. If they don’t after 5-10 minutes: appropriate to administer ‘rescue’ medication = benzodiazepines such as diazepam (intranasally or buccal midazolam)
  3. If a patient continues to fit despite such measures = status epilepticus = MEDICAL EMERGENCY
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64
Q

What is status epilepticus?

A

Either:
1. A single seizure lasting > 5 mins or
2. More than 2 seizures within a 5 minute period without the person turning normal between them
MEDICAL EMERGENCY

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65
Q

What is the priority in status epilepticus?

A

Termination of seizure activity, which if prolonged will lead to irreversible brain damage

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66
Q

What is the management of status epilepticus?

A
  1. ABC: airway adjunct, oxygen, check blood glucose
  2. First line medication = IV benzodiazepines e.g. diazepam or lorazepam - this can be repeated after 10-20 minutes
  3. If ongoing (or established) status, it is appropriate to start a second line agent e.g. phenytoin or phenobarbital infusion
  4. If no response (refractory status) within 45 minutes from onset = general anaesthesia (best way to achieve rapid control of seizure activity)
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67
Q

What are the complications of epilepsy?

A
  1. Fractures with tonic-clonic seizures
  2. Sudden death in epilepsy
  3. Side effects of AEDs e.g. neutropenia, osteoporosis with carbamazepine
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68
Q

What is an extradural haemorrhage?

A

A bleed between the dura mater and the inner surface of the skull

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69
Q

What is the difference between an extradural haemorrhage and a haematoma?

A

A haematoma is a collection of blood and a haemorrhage is an acute bleed (most commonly becomes a haematoma)

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70
Q

What is the aetiology of an extradural haematoma?

A
  1. Almost always caused by trauma and most typically ‘low impact trauma’
    E.g. a blow to the head or a fall
  2. The affected artery = middle meningeal artery: thin skill at the pterion overlies this and is vulnerable to injury
  3. Collection of blood is therefore in the temporal region
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71
Q

What are the features of an extradural haematoma?

A
  1. Patient initially loses, briefly regains and then loses consciousness again after a low-impact head injury
  2. As the haematoma expands: patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibres of the third CN
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72
Q

What is the brief regain in consciousness in an extradural haemorrhage known as?

A

The lucid interval
Consciousness is lost again due to the expanding haematoma and brain hernia
As the haematoma expands the uncut of the temporal love herniates = compression of parasympathetic fibres of CN3

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73
Q

What is the investigation of choice for an extradural haematoma?

A

Non-contrast CT:
1. Shows a biconvex (or lentiform), hyperdense collection around the surface of the brain
2. Looks like a lemon
3. Collection is limited by the suture lines of the skull

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74
Q

What is the management for an extradural haematoma?

A
  1. In patients with no neurological deficit: cautious clinical and radiological observation may be appropriate
  2. Definitive treatment: craniotomy and evacuation of the haematoma (if midline shift and brain stem herniate - needs early surgical intervention)
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75
Q

What is a head injury?

A
  1. Any sort of injury to your brain, skull, or scalp. 2. Can range from a mild bump or bruise to a traumatic brain injury. 3. Common head injuries include concussions, skull fractures, and scalp wounds
  2. Can be either closed or open (penetrating)- through the skull
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76
Q

What is the aetiology of head injuries?

A
  1. Accidents at home, work, outdoors, or while playing sports
  2. Falls (the most common cause of a skull fracture is a fall from a height)
  3. Physical assault
  4. Traffic accidents
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77
Q

What is the epidemiology of head injuries?

A

The most common causes in:
a. Infants are falls and abuse
b. Older children are falls and traffic accidents
c. Adults are falls, followed by traffic accidents, followed by assaults
1. Skull fractures occur in 2% to 20% of all head trauma
2. Occur most frequently between the ages of 20 and 50 years
3. Men are more commonly affected

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78
Q

How can head injury be divided?

A

Intracranial and extracranial

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79
Q

How can brain (intracranial) injury be classified?

A

Primary and secondary

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80
Q

What is a primary brain injury?

A
  1. Can be focal (contusion/haematoma) or diffuse
  2. Intracranial haematomas include extradural, subdural or intracerebral
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81
Q

What is a secondary brain injury?

A
  1. Occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury
  2. The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia
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82
Q

What is the Cushing’s reflex?

A
  1. Characterised by hypertension and bradycardia
  2. Often occurs late
  3. Usually a pre terminal event (occurring in the period before death)
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83
Q

What are they presenting symptoms of a head injury?

A
  1. Loss of consciousness (seconds to minutes)
  2. State of confusion or disorientated
  3. Headache
  4. Nausea and vomiting
  5. Fatigue/ drowsiness
  6. Problems with speech
  7. Sleeping problems (more or less than normal)
  8. Dizziness/ loss of balance
  9. Blurred vision
  10. Tinnitus
  11. Memory/ concentration problems
  12. Sensitivity to light or sound
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84
Q

What are some of the signs of a head injury on examination?

A
  1. GCS: altered mental state
  2. Evidence of trauma: bleeding, bruises
  3. Abnormal pupillary reflexes: suggests herniation/ brainstem injury
  4. Conductive hearing loss
  5. Open fracture
  6. Perioribital ecchymoses: (panda eyes), sign of basal skull fracture
  7. Battle’s sign: bruising over mastoid process
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85
Q

When does a patient with a head injury require a CT head within 1 hour?

A
  1. GCS < 13 on initial assessment
  2. GCS < 15 at 2 hours
  3. Suspected open or depressed skull fracture
  4. Sign of basal skull fracture:
    haemotympanum (blood behind ear drum), ‘panda’ eyes, CSF leakage from the ear or nose, Battle’s sign
  5. Post-traumatic seizure
  6. Focal neurological deficit
  7. More than one episode of vomiting
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86
Q

When does a patient with a head injury require a CT head within 8 hours?

A

For adults who have experienced some loss of consciousness or amnesia since the injury with any of the following:
1. > 65 years
2. PMH of bleeding or clotting disorders incl anticoagulants
3. Dangerous mechanism of injury (RTCs)
4. More than 30 minutes retrograde amnesia of events before the head injury

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87
Q

What is the investigation of choice for a head injury?

A

CT Head: detects skull fractures and any associated intracranial pathology

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88
Q

What are the investigations for a head injury?

A
  1. A to E assessment
  2. GCS
  3. CT head > MRI (used secondary for increased detection of associated intracranial pathology such as diffuse axonal injury)
  4. MR angiography (vascular assessment)
  5. beta-2 transferrin assay: for any patient with head trauma and otorrhoea /rhinorrhoea to detect a CSF leak
  6. Audiogram: conductive or sensorineural hearing loss
  7. Skeletal scan for fractures
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89
Q

What is an important part of examining a patient with a head injury?

A

Pupillary findings

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90
Q

What are the causes of bilateral constriction of pupils on examination?

A

Main cause is opiates
Others: Pontine lesions, metabolic encephalopathy

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91
Q

What is the management of a head injury?

A
  1. Depends of type of injury e.g. extracranial vs intracranial, subdural vs extradural vs SAH
  2. Important to monitor ICP
  3. Where there is life threatening rising ICP (e.g. extradural haematoma), whilst theatre is prepared or transfer arranged, use of IV mannitol/ frusemide may be required
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92
Q

What are some of the specific surgical techniques used in the management of head injuries?

A
  1. Diffuse cerebral oedema may require decompressive craniotomy
  2. Depressed skull fractures that are open require formal surgical reduction and debridement
  3. Closed injuries may be managed nonoperatively if there is minimal displacement
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93
Q

What is the minimum cerebral perfusion pressure in adults and children?

A

Adults: 70mmHg
Children: 40-70mmHg

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94
Q

What is a hip fracture?

A

Fracture of the hip, which a common site especially in osteoporotic elderly females

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95
Q

What is the risk of neck of femur fractures?

A

Avascular necrosis: the blood supply to the femoral head runs up the neck of the femur
Risk is greater in displaced fractures

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96
Q

What are the features of hip fractures?

A
  1. Pain
  2. Shortened and externally rotated leg
  3. Patient with non-displaced or incomplete neck of femur fractures may be able to weight bear
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97
Q

How can hip fractures/ neck of femur fractures be classified?

A
  1. Location
  2. Garden system
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98
Q

What is the location classification for neck of femur fractures?

A
  1. Intracapsular: from the edge of the femoral head to the insertion of the capsule of the hip joint
    Lesser trochanter is the dividing line
  2. Extracapsular: these can either be trochanteric or subtrochanteric
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99
Q

What is the Garden system for hip fractures?

A

Type 1: Stable fracture with impaction in valgus
Type 2: Complete fracture but undisplaced
Type 3: Displaced fracture, usually rooted and angulated but still has boney contact
Type 4: Complete boney disruption

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100
Q

What Garden types most commonly have blood supply disruption and so greater risk of avascular necrosis?

A

Types 3 and 4

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101
Q

What is the management of an intracapsular hip fracture?

A

Depends if it is displaced or undisplaced:
1. Undisplaced = internal fixation or hermiarthroplasty if unfit
2. Displaced = replacement arthroplasty (either THR or hemirthroplasty), THR is favoured if:
a. Patients were able to walk independently with no more than the use of a stick
b. Not cognitively impaired
c. Medically fit for anaesthesia and procedure

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102
Q

What is the management for an extra capsular hip fracture?

A
  1. Stable intertrochanteric fracture = dynamic hip screw
  2. Reverse oblique, transverse or subtrochanteric features = intramedullary device
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103
Q

What advice should be given to patients who have had a hip replacement to minimise the risk of dislocation?

A
  1. Avoid flexing the hip > 90 degrees
  2. Avoid low chairs
  3. Do not cross your legs
  4. Sleep on their back for the first 6 weeks
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104
Q

What are the different surgical techniques in hip arthroplasty?

A
  1. Cemented hip replacement (most common): metal femoral component is cemented into the femoral shaft
  2. Uncemented hip: increasingly popular in younger and more active patients but more expensive
  3. Hip resurfacing: metal cap over the femoral head (advantage of preserving femoral neck in case conventional arthroplasty is needed later in life)
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105
Q

What sign is seen in pelvic fracture?

A

Positive Trendelenburg sign from superior gluteal nerve dysfunction

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106
Q

What is Ischaemic heart disease?

A
  1. Characterized by reduced blood supply (ischaemia) to the heart muscle resulting in chest pain known as angina pectoris
  2. Can present as:
    a. Stable angina
    b. Acute coronary syndrome (ACS)
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107
Q

What are the three types of acute coronary syndrome (ACS)?

A
  1. ST elevation myocardial infarction (STEMI)
  2. Non-ST elevation myocardial infarction (NSTEMI)
  3. Unstable angina
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108
Q

What is the difference between unstable angina and an NSTEMI?

A

Unstable angina:
1. Considered when there are symptoms of ischaemia but no elevation in troponins
2. Can be with or without ischaemic changes in ECG
3. Treated the same as an NSTEMI as troponins can take a while to increase

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109
Q

What is ischaemic heart disease also known as?

A

Coronary heart disease and coronary artery disease

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110
Q

What does ischaemic heart disease generally describe?

A

The gradual build up of fatty plaques within the walls of the coronary arteries

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111
Q

What are the two main consequences of ischaemic heart disease?

A
  1. Gradual narrowing of coronary arteries: stable angina (less oxygen reaches the myocardium at times of demand)
  2. Risk of sudden plaque rupture: ACS (rupture of fatty plaque leading to sudden occlusion of a coronary artery)
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112
Q

How are the risk factors for ischaemic heart disease divided?

A
  1. Unmodifiable:
    a. Increasing age
    b. Male gender
    c. FH
  2. Modifiable:
    a. Smoking
    b. DM
    c. Hypertension
    d. Hypercholesterolaemia
    e. Obesity
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113
Q

What is the most common cause of ischaemic heart disease?

A

Atherosclerosis

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114
Q

What is the pathophysiology of atherosclerosis?

A
  1. Endothelial injury (smoking, HTN, DM)
  2. Migration of monocytes into subendothelial space and differentiation into macrophages
  3. Macrophages accumulate LDL lipids in the subendothelium and become foam cells
  4. They release growth factors, which stimulate smooth muscle proliferation, production of collagen and proteoglycans = further propagate the inflammatory process
  5. This leads to the formation of an atheromatous plaque covered by a fibrous capsule
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115
Q

What is the epidemiology of ischaemic heart disease?

A

Common, prevalence > 2%
More common in males

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116
Q

What is stable angina?

A
  1. Occurs when myocardial oxygen demand exceeds oxygen supply
  2. The most common cause is atherosclerosis
  3. Other causes of coronary artery narrowing are: RARE
    a. Spasm (e.g. from cocaine)
    b. Arteritis
    c. Emboli
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117
Q

What are the features of stable angina/ chest pain?

A
  1. Constricting discomfort in the front of the best, shoulder, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in 5 minutes
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118
Q

How is stable angina classified?

A
  1. Typical angina: patients who have all three of the features of stable angina
  2. Atypical angina: patients with 2 features
  3. Non-anginal chest pain: patients with 1 or none of the features
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119
Q

What are the next steps in patients who present with typical/ atypical angina?

A
  1. CT coronary angiogram (first line)
  2. Non-invasive functional imaging (looking for reversible myocardial ischaemia) (second line)
  3. Invasive coronary angiography
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120
Q

What are some of the exmaples of non-invasive functional imaging in the investigation of anginal chest pain?

A
  1. Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT)
  2. Stress echocardiography
  3. First-pass contrast-enhanced magnetic resonance (MR) perfusion
  4. MR imaging for stress-induced wall motion abnormalities
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121
Q

What is the management of stable angina/ angina pectoris?

A
  1. Lifestyle measures
  2. Aspirin and statin
  3. Sublingual GTN
  4. Beta blocker or calcium channel blocker:
    a. If CCB as monotherapy, use a rate-limiting one verapamil or diltiazem
    b. If CCB plus B-blocker, use amlodipine
  5. Once patient is on both and doses have been increased: consider PCI and CABG, whilst waiting add a third drug e.g. a long-acting nitrate or ivabradine
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122
Q

What is nitrate tolerance in the management of stable angina?

A
  1. Many patients who take nitrates develop tolerance and experience reduced efficacy
  2. NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
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123
Q

What are the classic features of ACS?

A
  1. Centra/ left sided chest pain
  2. May radiate to the jaw or left arm
  3. ‘heavy’ or constricting sensation (like an elephant on their chest)
  4. Associations:
    a. Dyspnoea
    b. Sweating
    c. Nausea and vomiting
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124
Q

How can ACS present in older patients or those with diabetes?

A

Can be silent- experience no chest pain

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125
Q

What are the signs of ACS on examination?

A
  1. May have no signs
  2. May appear pale and clammy
  3. Mild changes to observations
  4. New arrhythmias/ murmurs
  5. Signs of complications e.g. acute HF, cardiogenic shock (hypotension, cold peripheries, oliguria)
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126
Q

When should a patient be referred with chest pain?

A
  1. Emergency admission: current chest pain or chest pain in the last 12 hours with an abnormal ECG
  2. Refer to hospital for same day assessment: chest pain 12-72 hours ago
  3. Perform full assessment with ECG and troponin before referring: chest pain > 72 hours ago
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127
Q

What is the immediate management of suspected ACS in primary care?

A
  1. Glyceryl trinitrate (GTN)
  2. Aspirin 300 mg
  3. Do not routine give oxygen (only if sats < 94%)
  4. Perform an ECG ASAP but do not delay transfer to hospital
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128
Q

When would you offer a patient presenting with chest pain supplemental oxygen?

A
  1. If sats < 94% (those not at risk of hypercapnic respiratory failure)
  2. People with COPD to achieve their target of 88-92% until ABG available
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129
Q

What is the initial management of ACS in secondary care?

A
  1. Aspirin 300mg
  2. Oxygen if sats < 94%
  3. Morphine: only to patients in severe pain
  4. Nitrates: sublingually or IV, used in caution in patient hypotensive
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130
Q

What is the next step in the management of patients with ACS following initial treatment?

A

Determine what type of ACS they are having: ECG and biomarkers of myocardial damage

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131
Q

What is the criteria for a STEMI?

A
  1. Clinical symptoms consistent with ACS (generally > 20 mins duration)
  2. Persistent (>20 mins) ECG features in more than 2 contiguous leads
  3. ECG changes:
    a. 2.5 - 2.0mm ST elevation in V2-V3 (men, under 40, over 40 respectively)
    b. 1.5 mm ST elevation in V2-V3 in women
    c. 1mm ST elevation in other leads
    d. New LBBB
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132
Q

What is the management of a STEMI once it has been idnetified?

A
  1. Aspirin 300mg (if not previously given)
  2. Assess eligibility to coronary reperfusion therapy:
    a. PCI is first option if presenting within 12 hours and can be completed within 120 minutes
    b. Fibrinolysis: if primary PCI cannot be delivered within 120 minutes
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133
Q

What is PCI in the management of a STEMI?

A

Percutaenous coronary intervention:
1. Should be offered if the presentation is within 12 hours of onset and can be delivered within 120 mins
2. Radial access > femoral
3. Use drug-eluting stents
3. If presentation > 12 hours, but ongoing ischaemia PCI can be considered

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134
Q

What must be given to the patient before PCI for the management of a STEMI?

A
  1. Aspirin 300mg PLUS another antiplatelet e.g. clopidogrel or ticagrelor (known as dual antiplatelet therapy)
  2. Radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
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135
Q

What are the anticoagulants given to patients before PCI?

A

Aspirin 300mg plus:
1. Prasugrel/ ticagrelor (not high bleeding risk/ not on oral anticoagulants)
2. Clopidogrel (if high bleeding risk/ on oral anticoagulants)

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136
Q

What procedures can be offered during PCI?

A
  1. Main procedure is unblocking the affected coronary artery using a drug eluted stent
  2. Thrombus aspiration can be considered
  3. Complete revascularisation should be considered if with multivessel coronary artery disease without cardiogenic shock
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137
Q

What is fibrinolysis is the management of a STEMI?

A
  1. Less preferred to PCI, but used when it is the only form of reperfusion therapy available
  2. Patients should be given an antithrombin drugs
  3. Give ticagrelor following procedure
  4. ECG should be repeated after 60-90 minutes to see if ECG changes have been resolved
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138
Q

When should a PCI be considered after fibrinolysis in the management of a STEMI?

A

If patients have persistent myocardial ischaemia even after the treatment (on ECG)

139
Q

What is the management of a STEMI if reperfusion therapay cannot be offered (not eligible for it)?

A

Medical management:
1. Aspirin 300mg (if not previously given)
2. Another anticoagulant:
a. Ticagrelor (no high bleeding risk)
b. Clopidogrel (high bleeding risk)
3. Offer cardiology assessment and assessment of left ventricular assessment

140
Q

What is the management of an NSTEMI/ unstable angina?

A
  1. Initial antiplatelet therapy: aspirin 300mg
  2. Fondaparinux if no immediate PCI planned
  3. Estimate 6 month mortality (e.g. GRACE)
141
Q

What is the GRACE score used for in the management of NSTEMI/ unstable angina?

A

6 month mortality and risk of cardiovascular events: determine low risk (< 3%) or intermediate/ high risk (>3%)

142
Q

What is the management of an NSTEMI/ unstable angina with a low risk GRACE score?

A
  1. Conservative management (consider earl angiography is younger patient)
  2. Offer ticagrelor or clopidogrel (if high bleeding risk)
  3. Re-assess for ischamia and consider angiography if present
  4. Assess left ventricular function
143
Q

What is the management of an NSTEMI/ unstable angina with a intermediate/high risk GRACE score?

A
  1. PCI with dug eluting stents:
    a. Offer immediately if clinically unstable
    b. Offer within 72 hours if stable
  2. Given praugrel/ ticagrelor/ clopidogrel based of bleeding risk and oral anticoagulant use)
  3. Give UF heparin for radial access
144
Q

How is the GRACE score for NSTEMIs/ unstable angina calculated?

A

Online tools that take into account:
1. Age
2. Heart rate, BP
3. Cardiac and renal function (serum creatinine)
4. Cardiac arrest on presentation
5. ECG findings
6. Troponin levels

145
Q

What are the poor prognostic factors for ACS?

A
  1. Age
  2. Development or history of HF
  3. Peripheral vascular disease
  4. Reduced SBP
  5. Killip class: post MI
  6. Initial serum creatinine
  7. Elevated initial cardiac markers
146
Q

What is the Killip class of cardiac function post MI?

A

Used to stratify risk of 3- day mortality:
Class 1: No signs of HF = 6%
Class 2: Lung crackles, S3 = 17%
Class 3: Frank pulmonary oedema = 38%
Class 4: Cardiogenic shock = 81%

147
Q

What is primary vs secondary prevention in regards cardiovascular disease?

A

Primary prevention aims to prevent disease or injury before it has occured

148
Q

What are the drugs in primary prevention?

A
  1. Antihypertensive: Amlodipine 5mg (can be increased to 10mg)
  2. Statin: Atorvastatin 10mg
149
Q

What are the drugs in secondary prevention?

A
  1. Dual antiplatelet therapy: Aspirin 75mg plus second antiplatelet usually tacagrelor or prasugrel
  2. Statin: Atorvastatin 80mg
  3. ACE inhibitor
  4. Beta blocker
150
Q

What additional drug can be added for patients following an MI if they have developed signs of HF?

A

Aldosterone antagonists (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

151
Q

What lifestyle changes should be made in patients following an MI?

A
  1. Mediterranean lifestyle, switch butter and cheese for plant oil based products
  2. Exercise: 20-30 minutes daily
152
Q

What are the ECG changes associated with coronary arteries affected in ACS?

A

Anterior leads: V1-4: Left anterior descending
Inferior leads: II, III and aVF: Right coronary artery
Lateral leads: I, V5-6: Left circumflex artery

153
Q

What is the driving advice given to patients following an MI?

A

Not to drive one month post MI

154
Q

What are the complications of ischaemic heart disease?

A

Early complications (24-72hrs):
1. Death
2. Cardiogenic shock
3. HF
4. Ventricular arrhythmias
5. Heart block
6. Pericarditis
7. TE
Late complications (>72hrs):
1. Ventricular wall/septum rupture
2. Valvular regurgitation
3. Tamponade
4. Dresslers syndrome (pericarditis)
5. TE

155
Q

What are some of the simple positional manouvres which can open the airway?

A
  1. Head tilt/ chin lift
  2. Jaw thrust: preferred if there is concern about cervical spine injury
156
Q

What are the four types of airway adjuncts?

A
  1. Oropharyngeal airway
  2. Laryngeal mask
  3. Endotracheal tube
  4. Tracheostomy
157
Q

What is an oropharyngeal airway?

A
  1. Also known as a guedel
  2. Rigid plastic tube which sits at the top of the mouth and ends at the base of the tongue
  3. Easy to insert and use
  4. Ideal for short procedures
  5. No paralysis needed
  6. Most often used as a bridge for more definitive airway management
158
Q

What is a laryngeal mask?

A
  1. Commonly used as a supraglottic airway e.g. iGel
  2. Device sits in the pharynx and laigns to cover the airway
  3. Paralysis not usually needed
  4. Commonly used for wide range of anaesthetic uses, especially in day surgery
  5. Poor control against reflux of gastric contents
  6. Not suitable for high pressure ventilation
159
Q

What is a endotracheal tube?

A
  1. Provides optimal control of the airway once cuff is inflated
  2. Can be used for short and long term ventilation
  3. Paralysis often required
  4. Higher ventilation pressures can be used
  5. Errors in insertion can result in oesophageal intubation: must monitor end-tidal CO2 (capnography)
160
Q

What is a tracheostomy?

A
  1. Surgical opening into the trachea
  2. Reduces the work of breathing and dead space
  3. May be useful in slow weaning
  4. Percutaneous tracheostomy is widely used in ITU
  5. Dries secretions = humidified air is usually needed
161
Q

What is a nasopharyngeal airway?

A
  1. Come in a variety of sizes
  2. Inserted into the nostril to provide a patent airway in patients with low GCS
  3. Ideal for patients having seizures (unable to insert an oropharyngeal airway)
  4. Relatively contraindicated in base of skull fractures
162
Q

When are nasopharyngeal airways contraindicated?

A

In base of skull fractures- could cause further damage

163
Q

What is non-invasive ventilation?

A

Providing ventilatory support through a mask or similar device to the patient’s upper airway

164
Q

When is non-invasive ventilation indicated?

A
  1. COPD with acidosis
  2. Type 2 respiratory failure
  3. Cardiogenic pulmonary oedema unresponsive to CPAP
  4. Weaning from tracheal intubation
165
Q

How can knee problems be divided?

A

By age group:
1. Children and young adults
2. Older people

166
Q

What are the common knee problems in children and young adults?

A
  1. Chondromalacia patellae
  2. Osgood-Schlatter disease
  3. Osetochondritis dissecans
  4. Patella subluxation
  5. Patella tendonitis
167
Q

What is Chrondromalacia patellae?

A
  1. Softening of the cartilage of the patella
  2. Common in teenage girls
  3. Characteristically anterior knee pain on walking up and down stairs and rising from a seated position
  4. Usually responds to physiotherapy
168
Q

What is Osgood-Schlatter disease?

A
  1. Seen in sporty teenagers
  2. Pain, tenderness and swelling over the tibial tuberosity
  3. Management is supportive
169
Q

What is Oestochondritis dissecans?

A
  1. Pain after exercise
  2. Intermittent swelling and locking
  3. Feeling a painful ‘clunk’ when flexing or extending the knee (lateral femoral condyle)
170
Q

What are the signs for oestochondritis dissecans on examination?

A
  1. Joint effusion
  2. Tenderness on palpation of the articular cartilage of the medial femoral condyle when the knee if flexed
  3. Wilson’s sign
171
Q

What are the investigations for osteochondritis dissecans?

A
  1. X-ray (AP, lateral and tunnel views): may show subchondral crescent sign, loose bodies
  2. MRI: evaluate cartilage, visualise loose bodies, stage lesion
172
Q

What is the management of osteochondritis dissecans?

A
  1. Early diagnosis is important
  2. Clinical signs may be subtle in early stages- low threshold for imaging and/or orthopaedic opinion
173
Q

What happens if osteochondritis dissecans is left untreated?

A

Degenerative changes

174
Q

What is patella subluxation?

A
  1. Medial knee pain due to lateral subluxation of the patella
  2. Knee may give way
175
Q

What does subluxation mean?

A

Incomplete or partial dislocation of a joint or organ

176
Q

What is patella tendonitis?

A
  1. More common in athletic teenage boys
  2. Chronic anterior knee pain that worsens after running
  3. Tender below the patella on examination
177
Q

What is important to consider when a young adult presents with knee pain?

A

Referred pain may come from hip problems such as slipper upper femoral epiphysis

178
Q

What is the role of the patella?

A
  1. Sesamoid bone
  2. Protects the knee from physical trauma
  3. Plays an important role in the extensor mechanism of the knee
179
Q

How can patella injury be divided?

A

Direct or indirect injury

180
Q

What is a direct patella injury?

A
  1. Usually follows a direct blow or trauma to the front of the knee e.g. fall/ dashboard injury
  2. Usually an undisplaced crack with an intact extensor mechanism
181
Q

What is an indirect injury?

A
  1. When the quadriceps forcefully contracts against a block to knee extension e.g. catching their foot against a solid obstacle in order to stop themselves from falling
  2. Transverse patella fracture
  3. Possible disruption of the extensor mechanism
182
Q

What are the clinical features of a patella fracture?

A
  1. Considerable swelling and bruising
  2. Evidence of open wounds- open fractures require more urgent management
  3. Pain and tenderness around the knee, well localised to the patella and a palpable gap may be appreciable
  4. If the patient is able to straight leg raise = extensor mechanism is grossly intact (can lie sideways to ease pain)
183
Q

What are the investigations for a patella fracture?

A

Plain films are sufficient:
1. Minimum of two views: AP and lateral
2. If diagnosis is in doubt: skyviews can be taken but are uncomfortable and difficult to obtain

184
Q

What is the management of patella fractures?

A
  1. Undisplaced fractures (particualrly with intact extensor mechanism):
    a. non-operative management in a hinged knee brace for 6 weeks
    b. patients can fully weight bear
  2. Displaced fractures and loss of extensor mechanism:
    a. Considered for operative management with: tension band wire, inter-fragmentary screws or cerclage wires
    b. Then placed in a hinged knee brace for 4-6 weeks and allowed to fully weight bear
185
Q

What does the management of a patella fracture depend on?

A
  1. Displaced or undisplaced
  2. Intact or loss of extensor mechanism: tested through ability to straight leg raise
186
Q

What is a tibial plateau fracture?

A

Fracture at the proximal tibia

187
Q

What is the epidemiology of a tibial plateau fracture?

A

Occurs in the elderly

188
Q

What is the mechanism of injury in a tibial plateau fracture?

A

Knee forced into valgus or varus, but the knee fractures before the ligaments rupture

189
Q

Which movement is associated with which type of tibial plateau fracture?

A

Varus injury: medial plateau
Valgus injury: lateral plateau depressed fracture

190
Q

What is varus and valgus movement?

A

Varus: ‘run’ away, point outwards
Valgus: ‘together’, point inwards

191
Q

What is the classification system for tibial plateau fractures?

A

Schatzker Classification system, 6 types

192
Q

What are the signs of a tibial plateau fracture on examination?

A
  1. Joint deformity or shortening
  2. Swelling from effusion or haemarthrosis and/ or bruising
  3. Associated vascular or neurological signs of either affected
193
Q

What are the investigations and management for a tibial plateau fracture?

A

Plain x-rays:
1. AP and lateral x-rays
2. Oblique
Can also do CT scan
Management: open reduction internal fixation (ORIF)

194
Q

What is the anterior cruciate ligament?

A

Most commonly injured knee ligament

195
Q

What is the mechanism of injury in a ACL tear?

A

Any movement that involves a sudden twisting or awkward landing e.g. lateral blow to the knee, skiing (but non-contact injuries are most common overall)

196
Q

What are the symptoms of an ACL tear?

A
  1. Sudden ‘popping’ sound
  2. Knee swelling
  3. Instability: feeling that the knee will give way
197
Q

What are the two special tests performed for an ACL tear on knee examination?

A
  1. Anterior draw test:
    a. Patient lies supine with with knee at 90 degrees
    b. Examiners thumb on tibial tuberosity (other on thigh)
    c. Tibia is pulled forward to assess the amount of anterior motion of the tibia compared to femur
    d. Intact ACL = prevent forward translational movement
  2. Lachman’s test:
    a. Variant of anterior draw test
    b. Knee at 20-30 degrees
    c. Evaluate the anterior translation of the tibia in relation to the femur
    d. More reliable than anterior draw test
198
Q

What are the investigations for an ACL tear?

A
  1. Plain x-rays: AP, lateral ad skyline views
  2. MRI: to confirm clinical diagnosis
199
Q

What is the management of ACL tear?

A
  1. Non-operative options: physiotherapy focusing on range of motion and progressing to quad, hamstring, hip abductor and core strengthening
  2. Operative: ACL reconstruction
200
Q

What are the knee problems in older adults?

A
  1. Osteoarthritis: >50 years, overweight, intermittent swelling and crepitus
  2. Infrapatellar bursitis: associated with kneeling
  3. Prepatellar bursitis: associated with more upright kneeling
  4. ACL tear: twisting of knee, rapid onset of knee effusion, positive draw test
  5. PCL tear: caused by anterior force applied to the proximal tibia (knee hitting dashboard)
  6. Collateral ligament: tenderness over affected ligament, may have knee effusion
  7. Meniscal lesion: caused by twisting of the knee, locking and giving way, tender joint lines
201
Q

What are meniscal tears?

A

Typically result from twisting injuries

202
Q

What are the features of a meniscal knee tear?

A
  1. Pain worse on straightening the knee
  2. Knee may ‘give way’
  3. Displacement meniscal tears may cause knee locking
  4. Tenderness along the joint line
203
Q

What is the test for meniscal tears in the knee examination?

A

McMurray’s test:
1. Flex the knee and place a hand on medial side of knee, externally rotate the leg and bring the knee into extension
2. A palpable pop / click + pain is a positive test and can correlate with a medial meniscus tear

204
Q

What is the Thessaly test for meniscal knee tears?

A
  1. Standing at 20 degrees of knee flexion on the affected limb
  2. The patient twists with knee external and internal rotation with positive test being discomfort or clicking
205
Q

What is the most sensitive diagnostic test for meniscal tears?

A

MRI

206
Q

What are the management options for meniscal tears?

A
  1. Rest, NSAIDs and rehabilitation: first line for degenerative tears (older patients)
  2. Partial meniscectomy (if unable to be repaired)
  3. Meniscal repair
207
Q

What is Meningitis?

A

Inflammation of the meninges commonly caused by infection

208
Q

What are the common causative organisms for meningitis in 0-3 months old?

A
  1. Group B strep
  2. E.coli
  3. Listeria monocytogenes
209
Q

What are the common causative organisms for meningitis in 3 months -6 years old?

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
  3. Haemophilus influenzae
210
Q

What are the common causative organisms for meningitis in 6-60 years old?

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
211
Q

What are the common causative organisms for meningitis in the >60s?

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis
  3. Listeria monocytogenes
212
Q

What is the most common causative organism for meningitis in the immunosuppressed?

A

Listeria monocytogenes

213
Q

What are the symptoms of meningitis?

A
  1. Headache
  2. Fever
  3. Nausea/ vomiting
  4. Photophobia
  5. Drowsiness
  6. Seizures
214
Q

What are the signs of meningitis on physical examination?

A
  1. Neck stiffness
  2. Purpuric rash (particularly with invasive meningococcal disease)
215
Q

What are the investigations for meningitis?

A

All patients should be transferred to hospital for urgent treatment
1. ABC approach: including blood cultures
2. Senior review if there are any warning signs present
3. Lumbar puncture to confirm diagnosis (however should be delayed if there are certain circumstances e.g. signs of ICP)

216
Q

What are the warning signs in meningitis?

A
  1. Rapidly progressive rash
  2. Poor peripheral perfusion
  3. RR < 8 or > 30 / min or pulse rate < 40 or > 140 / min
  4. pH < 7.3 or WBC< 4 *109/L or lactate > 4 mmol/L
  5. GCS < 12 or a drop of 2 points
  6. Poor response to fluid resuscitation
217
Q

What are the circumstances in which you would delay a lumbar puncture in meningitis?

A
  1. Signs of severe sepsis or a rapidly evolving rash
  2. Severe respiratory/cardiac compromise
  3. Significant bleeding risk
  4. Signs of raised intracranial pressure:
    a. focal neurological signs
    b. papilloedema
    c. continuous or uncontrolled seizures
    d. GCS ≤ 12
218
Q

What are the CSF findings for bacterial meningitis?

A
  1. Cloudy appearance
  2. Low glucose (<1/2 plasma)
  3. High protein (>1g/L)
  4. 10-5,000 polymorph WCC
219
Q

What are the CSF findings for viral meningitis?

A
  1. Clear (maybe cloudy) appearance
  2. Normal glucose (60-80% of plasma glucose)
  3. Normal/ raised protein
  4. 15-1,000 lymphocytes
220
Q

What are the CSF findings for TB meningitis?

A
  1. Slightly cloudy appearance with a fibrin web
  2. Low glucose (< 1/2 plasma)
  3. High protein (>1g/L)
  4. 30-300 lymphocytes (not as raised as bacterial, which is also polymorphic)
221
Q

What are the CSF findings for fungal meningitis?

A
  1. Cloudy appearance
  2. Low glucose
  3. High protein
  4. 20-200 lymphocytes
222
Q

What additional test is used for suspected bacterial meningitis?

A

PCR, sensitivity of 75%
(Ziehl-Neelsen stain is only 20% sensitive)

223
Q

What is the management for meningitis (without indication for delayed LP)?

A
  1. IV access: take blood and cultures
  2. LP: if not within first hour, give IV antibiotics after blood cultures have been taken
  3. IV antibiotics
  4. IV dexamethasone as an adjunct (but avoid in septic shock, meningococcal septicaemia or if immunocompromised)
  5. CT scan is not normally indicated
224
Q

What are the IV antibiotic guidelines for bacterial meningitis?

A

3 months - 50 years: cefotaxime or cefrtriaxone
> 50 years: cefotaxime (or ceftriaxone) PLUS amoxicillin (or ampicillin) for adults (cover Listeria)

225
Q

What is the management of meningitis in patients with signs of raised ICP?

A
  1. Get critical care input
  2. Secure airway and give high flow oxygen
  3. IV access: take bloods and blood culture
  4. Give IV dexamethasone and IV antibiotics
  5. Arrange neuroimaging
226
Q

What is the management of meningitis in patients with signs of severe sepsis or a rapidly evolving rash?

A

Get critical care input
Sepsis 6 pathway:
1. Administer high flow oxygen
2. Take blood cultures
3. Give antibiotics: cefotaxime (or ceftriaxone) ± amoxicillin (depends on age)
4. Give IV fluid (bolus of 500ml crystalloid over less than 15 minutes)
5. Measure serum lactate
6. Measure hourly urine output

227
Q

What are the other additional investigations for meningitis?

A
  1. Bloods: FBC, renal function, glucose, lactate
  2. VBG/ ABG (depending on how ill the patient is)
  3. If LP has been performed: microscopy and culture, glucose and protein of CSF, PCR and HSV/ VZV
  4. Consider throat swab for meningococcal culture
228
Q

What is the management of contacts in meningococcal meningitis?

A

Prophylaxis needs to be offered to households and close contacts of patients affected with meningococcal meningitis if they were in close contact 7 days before onset
Oral ciprofloxacin or rifampicin may be used
Meningococcal vaccination should be offered

229
Q

What are the causes of viral meningitis?

A
  1. Non-polio enteroviruses e.g. coxsackie virus, echovirus
  2. Mumps
  3. Herpes simplex virus (HSV), cytomegalovirus (CMV), herpes zoster viruses
  4. HIV
  5. Measles
230
Q

What are the risk factors for viral meningitis?

A
  1. Patients at the extremes of age (< 5 years and the elderly)
  2. Immunocompromised, e.g. patients with renal failure, with DM
  3. Intravenous drug users
231
Q

What is the epidemiology of viral meningitis?

A

Much more common than bacterial meningitis and more benign
Patients do not often present to medical services

232
Q

What are the common features of viral meningitis?

A
  1. Headache
  2. Evidence of neck stiffness
  3. Photophobia (often milder than in in bacterial meningitis)
  4. Confusion
  5. Fevers
233
Q

What are the less common features of viral meningitis?

A
  1. Focal neurological deficits on examination
  2. Seizures: suggest meningoencephalitis
234
Q

What are the investigations for viral meningitis?

A
  1. LP: normal glucose, normal/ raised protein
  2. PCR for organism
235
Q

What is the management for viral meningitis?

A
  1. Supportive whilst awaiting results of LP
  2. If any suggestion of bacterial meningitis or encephalitis then treatment should be started (cefotaxime/ cefrtriaxone or aciclovir respectively)
  3. Aciclovir may be used if the patient has meningitis secondary to HSV
236
Q

What is the prognosis of viral meningitis?

A

Self-limiting
Symptoms should improve over the course of 7-14 days
Complications are rare in immunocompetent patients

237
Q

What is Multi-organ dysfunction syndrome?

A
  1. The presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention
  2. Defined as severe pain associated with failure of at least two of the following organs: liver, lung, and kidney
238
Q

What is the aetiology of Multi-organ dysfunction syndrome?

A

Widespread vaso-occlusion is thought to be responsible

239
Q

What is the epidemiology of Multi-organ dysfunction syndrome?

A
  1. Often associated with severe pain in patients with previously mild disease and a relatively high haemoglobin
  2. Death has been reported in up to 25% of patients
240
Q

What are the presenting symptoms and signs of Multi-organ dysfunction syndrome on physical examination?

A
  1. An atypically severe vaso-occlusion
  2. Fever
  3. Sudden deterioration including a drop in Hgb and platelets
  4. Diffuse encephalopathy
  5. Rhabdomyolysis
241
Q

What are the appropriate investigations for Multi-organ dysfunction syndrome?

A

The multiple organ dysfunction score:
Using physiological variables to determine the level of dysfunction
1. Resp: PO2/FiO2 ratio
2. Renal: serum creatinine
3. Hepatic: serum bilirubin
4. Cardiovascular: pulmonary artery to aorta ratio
5. Haematological: platelets
6. Neurological: GCS

242
Q

What are the clinical features of Multi-organ dysfunction syndrome?

A
  1. Lung: failure of normal gas exchange, reflected predominantly in arterial hypoxemia
  2. Kidney: reflected in impairment of normal selective excretory function, initially in oliguria despite adequate intravascular volume, but later in a rising creatinine level, and fluid and electrolyte derangements of sufficient magnitude that dialysis is required
  3. Liver: hyperbilirubinemia and cholestasis (reduction or stoppage of bile flow)
243
Q

What is the management of Multi-organ dysfunction syndrome?

A
  1. ICU admission and MDT approach
  2. Antibiotics for sepsis control
  3. Microcirculatory and respiratory support for reperfusion
  4. Organ-targeted drugs
  5. The correction of coagulation abnormalities and acid-base imbalance
244
Q

What is the prognosis of multi-organ dysfunction syndrome?

A

Mortality remains high, mainly from ARDS or sepsis

245
Q

What is neuroleptic malignant syndrome?

A

Rare but dangerous condition seen in patients taking anti-pyschotic medication

246
Q

What medications are involved in neuroleptic malignant syndrome?

A
  1. Anti-psychotics, can also occur in atypicals
  2. May also occur with dopaminergic drugs such as levodopa used in Parkinson’s disease- usually when the drug is suddenly stopped or the dose reduced
247
Q

What is the aetiology of neuroleptic malignant syndrome?

A
  1. Exact pathophysiology is unknown
  2. Theory that the dopamine blockade from the anti-psychotics triggers massive glutamate release
  3. There is subsequent neurotoxicity and muscle damage
248
Q

What are the features of neuroleptic malignant syndrome?

A

Occurs within hours to days of starting an anti-psychotic:
1. Pyrexia
2. Muscle rigidity
3. Autonomic lability: hypertension, tachycardia, tachypnoea
4. Agitated delirium with confusion

249
Q

What are the investigations for neuroleptic malignant syndrome?

A

Bloods:
1. Raised serum creatine kinase
2. AKI secondary to rhabdomyolysis (severe cases)
3. Leukocytosis may also be seen

250
Q

What is the management of neuroleptic malignant syndrome?

A
  1. Stop anti-psychotic
  2. Patients should be transferred to a medical ward (usually ITU)
  3. IV fluids to prevent renal failure
  4. Dantrolene may be useful in selected cases
  5. Bromocriptine (dopamine agonist) may also be used
251
Q

What are the main differences between serotonin syndrome and neuroleptic malignant syndrome?

A

SS:
1. Caused by SSRIs, MAOIs
2. Faster onset (hours)
3. Hyperreflexia, clonus, dilated pupils
4. Management: Cyproheptadine, chlorpromazine (plus IV fluids)
NMS:
1. Caused by anti-psychotics
2. Slower onset (hours-days)
3. Reduced reflexes, ‘lead pipe’ rigidity
4. Raised CK (risk of AKI)

252
Q

What are the similarities of serotonin syndrome and neuroleptic malignant syndrome?

A
  1. Drug reaction, often in young patients
  2. Tachycardia, hypertension
  3. Pyrexia, diaphoresis (excessive sweating)
  4. Rigidity
  5. Treat with IV fluids, maybe benzodiazepines
253
Q

What is opioid overdose?

A
  1. An opioid is any synthetic or natural agent that stimulates opioid receptors and produces opium-like effects - naturally derived from the opium poppy, Papaver somniferum, and include morphine and codeine
  2. An overdose occurs when larger quantities than physically tolerated are taken
254
Q

What can an opioid overdose result in?

A
  1. CNS and respiratory depression
  2. Miosis (bilateral pupil constriction)
  3. Apnoea
    These can be fatal if not treated rapidly
255
Q

What is the aetiology of opioid overdose?

A
  1. Substance abuse in regular users/abusers of illicit or prescription opioids
  2. Unintentional overdose in patients prescribed opioids for pain by taking larger amounts than tolerated
  3. Intentional overdose and intent of self-harm (suicidality)
  4. Therapeutic drug error
256
Q

What is the epidemiology of opioid overdose?

A
  1. Opioid abuse and overdose is a growing problem worldwide
  2. Common cause of death in prisoners one released due to loss of tolerance
257
Q

What are the presenting symptoms of opioid overdose?

A
  1. Miosis
  2. Altered mental state
  3. Fresh needle marks
  4. Old tracks on arms and legs
258
Q

What are the signs of opioid overdose on physical examination?

A
  1. Miosis (constricted pupils)
  2. Bradypnoea: RR of <12 breaths/minute
  3. Altered mental state
  4. Fresh needle marks
  5. Old tracks on arms and legs
259
Q

What are the appropriate investigations for opioid overdose?

A
  1. Dramatic response to naloxone: diagnostic of opioid overdose
  2. ABG: respiratory acidosis
  3. Urine drug screen
  4. ECG: In patients with significant respiratory compromise, look for abnormal ECG (e.g. signs of myocardial ischaemia)
  5. CXR: Look for ARDS features e.g. non-cardiogenic pulmonary oedema, perihilar, basilar, or diffuse alveolar infiltrates
260
Q

What is the management of opioid overdose?

A

Naloxone

261
Q

What is cocaine toxicity?

A

Recreational stimulant that has lead to adverse effects e.g. coronary artery spasm

262
Q

What is the mechanism of action of cocaine?

A

Cocaine blocks the uptake of dopamine, serotonin and noradrenaline

263
Q

What are the cardiovascular adverse effects of cocaine toxicity?

A
  1. Coronary artery spasm: lead to MI
  2. Tachycardia and bradycardia
  3. Hypertension
  4. Widening of QRS
  5. Aortic dissection
264
Q

What are the neurological adverse effects of cocaine toxicity?

A
  1. Seizures
  2. Mydriasis
  3. Hypertonia
  4. Hyperreflexia
265
Q

What are the psychiatric adverse effects of cocaine toxicity?

A
  1. Agitation
  2. Psychosis/ hallucinations
266
Q

What are the investigations for cocaine toxicity?

A
  1. Urine drug screen
  2. ABG
  3. ECG
267
Q

What is the management of cocaine toxicity?

A

1.Benzodiazepines are usually first line
2. Chest pain: benzodiazepines and glyceryl trinitrate (GTN), management of ACS
3. Hypertension: benzodiazepines + sodium nitroprusside

268
Q

What is paracetamol overdose?

A

Excessive ingestion of paracetamol causing toxicity

269
Q

What is the aetiology of paracetamol overdose?

A
  1. Maximum recommended dose: 2x 500 mg tablets 4 times in 24 h
  2. Intake of > 12 g or > 150 mg/kg can cause hepatic necrosis
270
Q

What is the epidemiology of paracetamol overdose?

A
  1. Most common intentional drug overdose in the UK, 70,000/year
  2. Women more than men
  3. Deaths reduced by legislation in 1998 restricting pack sizes
271
Q

What are the associations/risk factors for paracetamol overdose?

A
  1. Commonly associated with ingestion of other substances, e.g. alcohol
  2. Patients on enzyme-inducing drugs (which increase cytochrome P450 activity, e.g. anticonvulsants or anti-TB drugs)
  3. Malnourished
  4. Anorexia nervosa
  5. HIV
    These patients are more susceptible to toxic effects of paracetamol
272
Q

Why type of alcohol excess is associated with an increased risk of developing hepatotoxicity?

A

Chronic alcohol excess (acute alcohol excess may be protective)

273
Q

What are the presenting symptoms of paracetamol overdose?

A

Very important to ascertain timing and quantity of overdose, and presence of risk factors
0–24 h: Asymptomatic or mild nausea, vomiting, lethargy, malaise
24–72 h: RUQ abdominal pain, vomiting
> 72 h: Increasing confusion (encephalopathy), jaundice

274
Q

What are the signs of paracetamol overdose on physical examination?

A

0–24 h: No signs are evident
24–72 h: Liver enlargement and tenderness
> 72 h: Jaundice, coagulopathy, hypoglycaemia and renal angle pain

275
Q

What are the appropriate investigations for paracetamol overdose?

A
  1. A to E assessment
  2. ABG and lactate: degree of acidosis, monitor severity of hepatic failure
  3. Serum paracetamol levels at 4 h post ingestion (absorbed rapidly, hence peak plasma levels are usually within 4h)
  4. Bloods:
    a. LFTS, serum AST and ALT: elevated
    b. U&Es: may show renal impairment
    c. Serum prothrombin time and INR: PT may be prolonged and INR may be increased
276
Q

What is the management for paracetamol overdose?

A
  1. If present within 1 hour: may benefit from activated charcoal to reduce absorption of the drug
  2. N- Acetylcysteine:
    a. Plasma paracetamol concentration > 100 mg/L at 4 hours and 15 mg/L at 15 hours
    b. Patient presents 8-14 hours after ingestion of > 150mg/kg
    c. Patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
277
Q

How is N-Acetylcysteine given to patients int he management of paracetamol overdose?

A
  1. Infused over 1 hour (rather than the previous 15 mins)
  2. This is to reduce the number of adverse effects e.g. anaphylactoid reactions
  3. These reactions are generally treated by stopping the infusion and restarting at a slower rate
278
Q

What is the criteria for liver transplantation in paracetamol overdose?

A
  1. Arterial pH < 7.3, 24 hours after ingestion
  2. Or all of the following:
    a. Prothrombin time > 100 seconds
    b. Creatinine > 300 µmol/l
    c. Grade 3 or 4 encephalopathy
279
Q

What are benzodiazepines?

A

Medications used for sedation, muscle relaxant, hypnotic and anxiolytic effects

280
Q

How long should benzodiazepines be used for and why?

A

Used for 2-4 weeks
Short term risks:
1. Drowsiness
2. Reduced concentration
Long term risks:
1. Cognitive impairment
2. Anxiety and dpression
3. Dependence

281
Q

What are the signs and symptoms of benzodiazepine overdose?

A

Signs of respiratory depression:
1. Low GCS
2. Hypotensive
3. Mydriasis
4. Hyporeflexia

282
Q

What is the management of benzodiazepine overdose?

A

IV flumazenil

283
Q

What is the greatest risk of tricyclic antidepressants?

A

Can be fatal in overdose, therefore not to be given in patients with a risk of suicide

284
Q

What is Lithium used for and what are the side effects of it?

A

Used as a mood stabiliser e.g. BPAD
Side effects:
1. Mild tremor
2. Nausea and vomiting
3. Arrhythmias
4. Hypothyroidism
5. Weight gain
6. Eyebrow hair loss

285
Q

What happens in Lithium overdose?

A

> 1.2 mmol/L
1. Coarse tremor
2. Hyperreflexia
3. Nystagmus
4. CNS signs: seizures, ataxia
5. GI: nausea and vomiting

286
Q

What can lead to Lithium overdose?

A
  1. Dehydration
  2. Other drugs: NSAIDs, ACE inhibitors, diuretics (interrupts normal renal excretion)
  3. Deliberate overdose
287
Q

What can methanol poisoning lead to?

A

Metabolic acidosis

288
Q

What are the signs and symptoms of digoxin toxicity?

A
  1. Anorexia
  2. Nausea and vomiting
  3. Neurological symptoms
  4. Can trigger fatal arrhythmias
289
Q

What is the most common cause of digoxin toxicity?

A

Hypokalaemia

290
Q

What is sepsis?

A

Defined as life threatening organ dysfunction caused by a dysregulated host response to an infection

291
Q

How can sepsis be classified?

A

Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection
Septic shock: more severe form sepsis in which circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone

292
Q

How are patients with suspected sepsis stratified?

A

Red and amber flag criteria

293
Q

What is the amber flag criteria for suspected sepsis?

A
  1. Relatives concerned about mental status
  2. Acute deterioration in functional ability
  3. Immunosuppressed
  4. Trauma/ surgery/ procedure in last 6 weeks
  5. RR 21-24
  6. SBP 91-100mmHg
  7. HR 91-130 or a new dysrhythmia
  8. Not passed urine in last 12-18 hours
  9. Temperature < 36ºC
  10. Clinical signs of wound, device or skin infection
294
Q

What is the red flag criteria for suspected sepsis?

A
  1. Responds only to voice or pain/ unresponsive
  2. Acute confusional state
  3. SBP < 90mmHg (or drop >40mmHg)
  4. HR > 130
  5. RR >25
  6. Needs O2 to keep sats > 92%
  7. Non-blanching rash, mottled/ ashen/ cyanotic
  8. Not passed urine in last 18h/ UO < 0.5ml/kg/hr
  9. Lactate > 2 mmol/L
  10. Recent chemotherapy
295
Q

What should be initiated if any of the red flags are present in suspected sepsis?

A

‘Sepsis six’:
1. Administer oxygen (aim >94%)
2. Take blood cultures
3. Give broad spectrum antibiotics
4. Give IV fluids (500ml crystalloid over 10-15 mins)
5. Measure serum lactate
6. Measure accurate hourly urine output (catheter)

296
Q

What is the SOFA score?

A

Sequential (Sepsis-related) Organ Failure Assessment Score: helps to identify and categorise patients by organ system and accounts for clinical interventions

297
Q

What is the prognosis of sepsis?

A
  1. An increasingly important cause of mortality in the UK
  2. Even patients with modest dysfunction can deteriorate further: need or prompt and appropriate intervention
298
Q

What is the prognosis of septic shock?

A

Patients with severe sepsis have a mortality rate in excess of 40%, with organ failure in 6-65% of those admitted to ICU

299
Q

What type of surgical patients are are greater risk of septic shock?

A

Those with anastomotic leaks, abscesses and extensive superficial infections such as necrotising fasciitis (these patients do not fare well with prolonged surgery)

300
Q

What is shock?

A

When there is insufficient tissue perfusion

301
Q

What are the different types of shock?

A
  1. Septic
  2. Haemorrhagic
  3. Neurogenic (spinal cord transection)
  4. Cardiogenic (ischaemic heart disease)
  5. Anaphylactic
302
Q

Where is the best site for IM adrenaline in the management of anaphylactic shock?

A

500mcg IM in the anterolateral aspect of the middle third of the thigh

303
Q

What are the two common shoulder problems?

A
  1. Adhesive capsulitis (frozen shoulder)
  2. Supraspinatus tendonitis (subacromial impingement, painful arc)
304
Q

What is adhesive capsulitis?

A
  1. Also known as frozen shoulder
  2. Common cause of shoulder pain
  3. Inflammatory process, most commonly idiopathic
305
Q

What is the epidemiology of adhesive capsulitis?

A

Common in middle-aged females and in diabetics

306
Q

What is associated with adhesive capsulitis?

A

Diabetes mellitus: up to 20% of diabetics may have an episode of frozen shoulder

307
Q

What are the features of adhesive capsulitis?

A

Typically develop over days:
1. External rotation is affected more than internal rotation or abduction
2. Patients have a painful freezing phase, an adhesive phase and a recovery phase
3. Bilateral in up to 20% of patients

308
Q

What are the signs of adhesive capsulitis on examination?

A
  1. External rotation is more affected than internal rotation and abduction
  2. Both active and passive movement is affected
  3. Bilateral in up to 20% of patients
309
Q

How long can an episode of adhesive capsulitis last?

A

6 months to 2 years

310
Q

How is adhesive capsulitis diagnosed?

A
  1. Usually clinically
  2. Imaging may be required for atypical and persistent symptoms
311
Q

What is the management of adhesive capsulitis?

A

Conservative-medical-surgical
1. Prolonged course of physical therapy
2. Medical management of underlying disease if present (e.g. DM, thyroid disease)
3. NSAIDs, oral corticosteroids and intra-articular corticosteroids may be beneficial
4. Manipulation under anesthesia or arthroscopic capsular release is indicated in patients with progressive loss of motion having failed a prolonged course of physical therapy

312
Q

What are the different types of rotator cuff injuries?

A
  1. Subacromial impingement (also known as impingement syndrome, painful arc syndrome)
  2. Calcific tendonitis
  3. Rotator cuff tears
  4. Rotator cuff arthropathy
313
Q

What is the main symptom of a rotator cuff injury?

A

Shoulder pain worse on abduction

314
Q

What are the signs of a rotator cuff injury on examination?

A
  1. Painful arc of abduction
  2. Tenderness over the anterior acromion
315
Q

What is the painful arc of abduction in subacromial impingement?

A

Between 60 and 120 degrees

316
Q

What is the painful arc of abduction in rotator cuff tears?

A

May be in first 60 degrees

317
Q

What is subacromial impingement?

A
  1. Most common cause of shoulder pain
  2. Occurs as a result of compression of the rotator cuff muscles by superior structures leading to inflammation and development of bursitis
318
Q

What are the features of subacromial impingement?

A
  1. Shoulder pain
  2. Exacerbated by overhead activities and lifting objects away from the body (abduction)
319
Q

What are the special tests to investigated subacromial impingement on shoulder examination?

A
  1. Painful arc test
  2. Neer test
  3. Hawkins test
320
Q

How is subacromial impingement diagnosed?

A

Diagnosis can be made on physical examination with a positive Neer and Hawkins tests, and can be supplemented with MRI studies

321
Q

What is the management of subacromial impingement?

A
  1. Trial of nonoperative measures including NSAIDs, physical therapy and corticosteroid injections
  2. Arthroscopic subacromial decompression with possible acromioplasty is indicated in patients who fail conservative measures
322
Q

What are rotator cuff tears?

A
  1. A very common source of shoulder pain and decreased motion
  2. Can occur due to both:
    a. traumatic injuries in young patients
    b. degenerative disease in the elderly patient
323
Q

How are rotator cuff tears diagnosed?

A

Diagnosis can be suspected clinically with provocative tests of the supraspinatous, infraspinatous, teres minor and subscapularis, but confirmation requires an MRI of the shoulder

324
Q

What is the management of rotator cuff tears?

A

Can be nonoperative or operative depending on the chronicity of symptoms, severity of the tear, degree of muscle fatty atrophy, patient age and patient activity demands

325
Q

What is a biceps rupture?

A
  1. When one of the biceps tendons separates from its attachment site or is torn across it’s full width
  2. This most frequently occurs at the long tendon (90%), but rarely can occur in the distal tendon (10%)
326
Q

What are the attachment sites for the the long and short biceps tendons?

A
  1. The long tendon attaches to the glenoid 2. 2. The short tendon attaches to the coracoid process
  2. The biceps inserts distally via another tendon onto the radial tuberosity
327
Q

What is the epidemiology of biceps rupture?

A
  1. Men more than women (3:1)
  2. Proximal biceps tendon ruptures generally occur in older patients, over the age of 60 and account for 90% of biceps tendon ruptures
328
Q

What are the risk factors for biceps rupture?

A
  1. Heavy overhead activities
  2. Shoulder overuse or underlying shoulder injuries which may stress the biceps tendon
  3. Smoking
  4. Corticosteroids; these weaken tendons
329
Q

What is the mechanism of injury in biceps rupture?

A
  1. Proximal biceps long tendon ruptures: typically occurs when the biceps are lengthened and contracted and a load is applied. e.g. the descent phase of a pull-up.
  2. Distal biceps tendon ruptures: Usually when a flexed elbow is suddenly and forcefully extended whilst the biceps muscle is already contracted
330
Q

What is the main feature of a biceps rupture?

A

A sudden ‘pop’ or tear either at the shoulder (long tendon), or at the antecubital fossa (distal tendon) which is followed by pain, bruising and swelling

331
Q

What biceps tendon is ruptured when a ‘popeye’ deformity can be seen on examination?

A
  1. Rupture of the proximal tendon
  2. The muscle bulk results in a bulge in the middle of the upper arm
332
Q

What are the special tests for biceps rupture on shoulder examination?

A
  1. Start with a basic examination:
    a. palpate the long head and distal biceps tendon
    b. assess neurovascular function of the upper extremities
  2. The biceps squeeze test: If it is intact then a squeeze will cause forearm supination
333
Q

What should be the first investigation for a suspected biceps tendon rupture?

A

Musculoskeletal ultrasound by a skilled clinician

334
Q

What is the management for a suspected long head biceps tendon rupture?

A
  1. Little role for further imaging (MRI can be considered if there is a limited examination or other pathology)
  2. Conservative management: physiotherapy, analgesia
335
Q

What is the management for a suspected distal biceps tendon rupture?

A
  1. An urgent MRI should be performed as a diagnosis on clinical signs alone is challenging
  2. Usually requires surgical intervention
336
Q

What is biceps tendonitis?

A
  1. Well recognised source of anterior shoulder pain
  2. May be associated with subscapularis tears and subacromial impingement
  3. Diagnosis can be suspected clinically with anterior shoulder pain made worse with provocative tests and confirmed with MRI studies to evaluate for concurrent pathology
  4. Management: an initial trial of NSAIDs, activity modification and physical therapy
  5. If recurrent symptoms: Arthorscopic versus open biceps tenodesis/tenotomy is indicated
337
Q

What is shoulder dislocation?

A

Occur when the humeral head dislodges from the glenoid cavity of the scapula

338
Q

What is the epidemiology of shoulder dislocation?

A

The shoulder is the most common joint in the body to dislocate, accounting for approximately 50% of all major joint dislocations

339
Q

What is the most common type of shoulder dislocation?

A

Anterior shoulder dislocation: accounts for > 95% of cases

340
Q

What is the mechanism of injury in shoulder dislocation?

A

An anterior force to the shoulder while its abducted and externally rotated and may lead to recurrent anterior shoulder instability

341
Q

How is shoulder dislocation diagnosed?

A
  1. Made clinically with the presence of positive anterior instability provocative tests
  2. Confirmed with MRI studies that may reveal labral and/or bony injuries of the glenoid and proximal humerus (Hill-Sachs lesion)
342
Q

What is the management of shoulder dislocation?

A
  1. Large number of different techniques for reducing shoulders
  2. If the dislocation is recent then reduction may be attempted without any analgesia/sedation
  3. However, other patients may require analgesia +/- sedation to ensure the rotator cuff muscles are relaxed
343
Q

What is acromioclavicular joint injury?

A

Injury to the AC joint is relatively common and typically occurs during collision sports such as rugby following a fall on to the shoulder or a FOOSH (falls on outstretched hand)

344
Q

How are acromioclavicular joint injuries graded?

A
  1. AC joint injuries are graded I to VI depending on the degree of separation
  2. Grade I and II injuries are very common and are typically managed conservatively including resting the joint using a sling
  3. Grade IV, V and VI are rare and require surgical intervention
  4. The management of grade III injuries is a matter of debate and often depends on individual circumstances

!Final Year (26 decks)

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