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MRCS A - Dr Bishoy > 17- Trouma & ER Explains 2 > Flashcards

17- Trouma & ER Explains 2 Flashcards

1
Q

What are the types of dislocations around the shoulder joint?

A

Glenohumeral dislocation, acromioclavicular joint disruption, and sternoclavicular dislocation (only glenohumeral dislocation will be covered here)

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2
Q

What is the initial management required for shoulder dislocation?

A

Emergent reduction to prevent lasting chondral damage

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3
Q

What imaging modalities are used to confirm the direction of dislocation in shoulder dislocation?

A

True anteroposterior (AP), axillary lateral, and/or scapula Y view

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3
Q

What should be assessed during the early assessment and management of shoulder dislocation?

A

Careful history, examination, and documentation of neurovascular status of the limb, particularly the axillary nerve; this should be reassessed post-manipulation

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3
Q

What is the recommended technique for emergent closed reduction of shoulder dislocation?

A

Gentle traction to adducted arm under entonox and analgesia, often requiring conscious sedation

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4
Q

What should be done after successful reduction of shoulder dislocation?

A

The arm should be immobilized in a polysling, and X-rays should be taken to confirm relocation

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5
Q

What are the features and causes of anterior shoulder dislocation?

A

Usually traumatic with an anterior force on the arm when the shoulder is abducted and externally rotated; loss of shoulder contour (sulcus sign), and the humeral head can be felt anteriorly

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6
Q

What are the features and causes of posterior shoulder dislocation?

A

50% missed in A&E; 50% traumatic, but classically associated with seizures or electrocution; the shoulder is locked in internal rotation, and X-rays may show a lightbulb appearance

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7
Q

What are the features and causes of inferior shoulder dislocation?

A

Rare; associated with pectoralis and rotator cuff tears, and glenoid fracture; similar to the management of the primary injury

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8
Q

What are the features and causes of superior shoulder dislocation?

A

Rare; associated with acromion/clavicle fracture; similar to the management of the primary injury

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9
Q

What is rotator cuff disease?

A

A spectrum of conditions ranging from subacromial impingement to rotator cuff tears and eventually to rotator cuff arthropathy (arthritis)

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10
Q

What are some associated injuries seen with shoulder dislocation?

A

Bankart lesion (avulsion of the anterior glenoid labrum), Hill Sachs defect (chondral impaction on posteriosuperior humeral head), rotator cuff tear, greater or lesser tuberosity fracture, and humeral neck fracture (should be discussed with orthopaedics prior to any attempted reduction)

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11
Q

What is the function of the rotator cuff muscles?

A

Important in shoulder movements and maintenance of glenohumeral stability

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12
Q

What are the four muscles of the rotator cuff?

A

Supraspinatus, Infraspinatus, Teres Minor, and Subscapularis

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13
Q

Which muscle is responsible for the external rotation of the humerus?

A

Infraspinatus and Teres Minor

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14
Q

Which muscle is involved in the internal rotation of the humerus?

A

Subscapularis

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15
Q

Which nerves innervate the rotator cuff muscles?

A

Suprascapular nerve (Supraspinatus and Infraspinatus), Axillary nerve (Teres Minor), Upper and Lower Subscapular nerves (Subscapularis)

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16
Q

What happens when there is an injury or tear in the inferior rotator cuff muscles?

A

Upward migration of the humeral head on the glenoid can be seen on an AP radiograph

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17
Q

How do the anterior muscles (subscapularis) and posterior muscles (infraspinatus, teres minor) of the rotator cuff balance each other?

A

The anterior muscles are balanced with the posterior muscles to maintain shoulder stability

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18
Q

What is subacromial impingement?

A

The most common cause of shoulder pain resulting from impingement of the superior cuff on the undersurface of the acromion, along with inflammatory bursitis

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19
Q

What is the presentation of subacromial impingement?

A

Insidious pain exacerbated by overhead activities

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20
Q

Which type of acromial morphology is associated with subacromial impingement?

A

Certain types of acromial morphology (Bigliani classification)

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21
Q

What is a rotator cuff tear?

A

Often presents as an acute event on the background of chronic subacromial impingement in older patients, and as an avulsion injury in younger patients

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22
Q

Which part of the rotator cuff is commonly affected by tears?

A

The majority of tears occur in the superior cuff (supraspinatus, infraspinatus, teres minor), although a tear to subscapularis is associated with subcoracoid impingement

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23
Q

What are the symptoms of a rotator cuff tear?

A

Pain and weakness when using the affected muscles

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24
Q

What is rotator cuff arthropathy?

A

Shoulder arthritis that occurs in the setting of rotator cuff dysfunction, resulting from superior migration due to the loss of rotator cuff function and integrity

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25
Q

What are the imaging modalities used for diagnosing rotator cuff pathology?

A

Plain radiographs (AP view and outlet view), ultrasound (USS), and MRI (combined with arthrogram for intra-articular pathology)

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26
Q

What are the treatment options for subacromial impingement?

A

Physiotherapy, oral anti-inflammatory medication, and subacromial steroid injection; arthroscopic subacromial decompression may be necessary

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27
Q

What are the management options for rotator cuff tears?

A

Conservative management for mild tears or tears in the elderly, arthroscopic repair for moderate tears, and open repair with tendon transfer for massive or retracted tears; subacromial decompression is often performed simultaneously

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27
Q

What factors should be considered when planning the surgical repair of a rotator cuff tear?

A

The age and activity of the patient, the nature, size, and retraction of the tear

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28
Q

What is calcific tendonitis?

A

It involves calcific deposits within tendons, most commonly in the rotator cuff (specifically the supraspinatus tendon)

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29
Q

Who is more commonly affected by calcific tendonitis?

A

Women aged 30-60 years

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29
Q

What are the associations of calcific tendonitis?

A

Diabetes and hypothyroidism

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30
Q

What are the three stages of calcification in calcific tendonitis?

A

Formative phase, resting phase, and resorptive phase

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31
Q

Which stage of calcific tendonitis is the most painful?

A

Resorptive phase

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32
Q

How does calcific tendonitis present?

A

Similar to subacromial impingement, with pain, especially with overhead activities, and it is atraumatic in nature

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33
Q

What does plain radiographs show in calcific tendonitis?

A

Calcification of the rotator cuff, usually within 1.5cm of its insertion on the humerus

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34
Q

What is the initial treatment for calcific tendonitis?

A

Non-operative management including NSAIDs, physiotherapy, and potentially steroid injections

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34
Q

How many cases of calcific tendonitis resolve with conservative management within 6 months?

A

Approximately 75%

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35
Q

What are the options for breaking down deposits and resolving symptoms in calcific tendonitis?

A

Ultrasound-guided or surgical needle barbotage, and occasionally surgical excision may be required

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36
Q

What is adhesive capsulitis (frozen shoulder)?

A

It is a condition characterized by pain and loss of movement in the shoulder joint, caused by fibroplastic proliferation of capsular tissue, leading to soft tissue scarring and contracture

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37
Q

What are the symptoms of adhesive capsulitis?

A

Patients present with a painful and decreased arc of motion in the shoulder

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38
Q

What are the factors associated with adhesive capsulitis?

A

Prolonged immobilization, previous surgery, thyroid disorders (AI), and diabetes

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39
Q

What are the three stages of adhesive capsulitis?

A

Stage one: the freezing and painful stage; Stage two: the frozen and stiff stage; Stage three: the thawing stage, where shoulder movement slowly improves

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40
Q

What imaging is used for adhesive capsulitis?

A

Plain radiographs to exclude other causes and MRI arthrogram to show capsular contracture and exclude cuff pathology, although it is often not performed as the diagnosis is mainly clinical

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41
Q

What are the treatment options for adhesive capsulitis?

A

Non-operative management including NSAIDs, steroid injections, and physiotherapy; operative options include manipulation under anesthesia (MUA) or arthroscopic adhesiolysis (release of adhesions) followed by intensive physiotherapy

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42
Q

What are the possible causes of glenohumeral arthritis?

A

It can be caused by osteoarthritis (primary or secondary to cuff tear or trauma), rheumatoid arthritis, or as part of a spondyloarthropathy

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43
Q

Who is more commonly affected by glenohumeral arthritis?

A

The elderly

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44
Q

How does glenohumeral arthritis present?

A

Similar to other types of arthritis, with pain at night and with movement

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45
Q

What imaging modalities are useful for diagnosing and classifying glenohumeral arthritis?

A

AP and axillary radiographs show features of arthritis, while CT/MRI can help classify the shape of the glenoid and assess extent of bone loss when considering arthroplasty; MRI is also essential to assess the integrity of the rotator cuff if shoulder replacement is being considered

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46
Q

What are the initial treatment options for glenohumeral arthritis?

A

Non-operative measures including NSAIDs, management of rheumatoid arthritis if present, physiotherapy, and steroid injection

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47
Q

What is the mechanism of injury for thoracic aorta rupture?

A

Decelerating force, such as a road traffic accident or fall from a great height

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48
Q

What is the prognosis for most people with thoracic aorta rupture?

A

Most people die at the scene of the injury

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48
Q

What may survivors of thoracic aorta rupture have?

A

Survivors may have an incomplete laceration at the ligamentum arteriosum of the aorta

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49
Q

What are the clinical features of thoracic aorta rupture?

A

Persistent hypotension due to a contained hematoma; detected mainly by history and changes seen on chest X-ray

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50
Q

What changes can be seen on chest X-ray in thoracic aorta rupture?

A

Widened mediastinum, trachea/esophagus shifted to the right, depression of the left main stem bronchus, widened paratracheal stripe/paraspinal interfaces, obliteration of space between the aorta and pulmonary artery, and presence of rib fractures or left hemothorax

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50
Q

How is thoracic aorta rupture diagnosed?

A

Angiography, usually CT aortogram

51
Q

What is the treatment for thoracic aorta rupture?

A

Repair or replacement; ideally, patients should undergo endovascular repair

52
Q

How can the cause of hypocalcaemia be determined in most cases?

A

By combining the clinical history with parathyroid hormone levels

53
Q

What are some common causes of hypocalcaemia?

A

Vitamin D deficiency (osteomalacia), acute pancreatitis, chronic renal failure, hypoparathyroidism (e.g., post thyroid/parathyroid surgery), pseudohypoparathyroidism (target cells insensitive to PTH), rhabdomyolysis (initial stages), and magnesium deficiency (due to end organ PTH resistance)

54
Q

What is the preferred method for acute management of severe hypocalcaemia?

A

Intravenous replacement with calcium gluconate, given as 10 mL of a 10% solution over 10 minutes

55
Q

What is recommended during the acute management of severe hypocalcaemia?

A

ECG monitoring

56
Q

How should further management be approached for hypocalcaemia?

A

It depends on the underlying cause

57
Q

When do acute transfusion reactions typically present?

A

During or within 24 hours of a blood transfusion

57
Q

What should be avoided when administering calcium and bicarbonate for hypocalcaemia?

A

They should not be administered via the same route

58
Q

What are the most frequent reactions seen in acute transfusion reactions?

A

Fever, chills, pruritus, or urticaria, which usually resolve promptly without specific treatment or complications

59
Q

What signs may indicate a more severe potentially fatal transfusion reaction?

A

Severe dyspnea, pyrexia, or loss of consciousness occurring in temporal relationship with a blood transfusion

60
Q

What are the causes of adverse transfusion reactions?

A

They are multi-factorial, with immune-mediated reactions often resulting from component mismatch (commonly due to clerical error), and non-immune mediated complications potentially occurring due to bacterial or viral product contamination

61
Q

What are the proposed mechanisms underlying transfusion-related lung injury?

A

One involves the sequestration of primed neutrophils within the recipient pulmonary capillary bed, while the other suggests HLA mismatches between donor neutrophils and recipient lung tissue as the cause

62
Q

What are some examples of immune-mediated transfusion reactions?

A

Pyrexia, alloimmunization, thrombocytopenia, transfusion-associated lung injury, graft vs host disease, urticaria, acute or delayed hemolysis, ABO incompatibility, and Rhesus incompatibility

63
Q

What are some examples of non-immune mediated transfusion reactions?

A

Hypocalcemia, congestive heart failure (CCF), infections, and hyperkalemia

64
Q

What is the indication for fluid resuscitation in burns?

A

Burns involving >15% total body area in adults (>10% in children)

65
Q

What is the main aim of fluid resuscitation in burns?

A

To prevent the burn from deepening

66
Q

When is most fluid lost after a burn injury?

A

Within the first 24 hours

67
Q

What happens to fluid shifts in the first 8-12 hours after a burn injury?

A

Fluid shifts from intravascular to interstitial fluid compartments, potentially compromising circulatory volume

68
Q

Why is colloid fluid avoided in the first 8-24 hours of burn resuscitation?

A

Because it can cause more fluid to enter the interstitial compartment

69
Q

What is the current consensus guideline for fluid resuscitation in burns?

A

Fluid resuscitation should begin at 2 mL of lactated Ringers x patient’s body weight in kg x % TBSA for second- and third-degree burns

69
Q

What is a concern regarding the traditional Parkland formula for fluid resuscitation in burns?

A

It may result in the administration of excessive quantities of intravenous fluids

70
Q

How is the calculated fluid volume initiated in the first 24 hours of burn resuscitation?

A

One-half of the total fluid is provided in the first 8 hours, while the remaining one-half is administered during the subsequent 16 hours

71
Q

How is the efficacy of fluid replacement determined in burn resuscitation?

A

By monitoring urine output, with a target of around 0.5 mL/kg/hr for adults and 1 mL/kg/hr for children weighing less than 30 kg

72
Q

What is the recommended fluid rate for adults and children over 14 years with flames or scalding burns?

A

2 mL Hartmann’s solution x patient’s weight in kg x % TBSA

73
Q

What is the target urine output for adults and children over 14 years with flames or scalding burns?

A

0.3-0.5 mL/kg/hr or 30-50 mL per hour

74
Q

What is the recommended fluid rate for children less than 14 years with flames or scalding burns?

A

3 mL Hartmann’s solution x patient’s weight in kg x % TBSA

75
Q

What is the target urine output for children less than 14 years with flames or scalding burns?

A

1 mL/kg/hr

76
Q

What is the target urine output for children less than 30 kg and infants with flames or scalds burns?

A

1 mL/kg/hr

77
Q

What is the recommended fluid rate for children less than 30 kg and infants with flames or scalds burns?

A

3 mL Hartmann’s solution x patient’s weight in kg x % TBSA. Plus a sugar-containing solution at maintenance rate

78
Q

What is the recommended fluid rate for all ages with electrical injuries?

A

4 mL Hartmann’s solution x patient’s weight in kg x % TBSA until urine clears

79
Q

What is the target urine output for all ages with electrical injuries?

A

1-1.5 mL/kg/hr until urine clears

80
Q

What is the recommended fluid rate for maintenance crystalloid after 24 hours of burn injury?

A

1.5 mL x (burn area) x (body weight)

81
Q

What are some considerations for monitoring during fluid resuscitation?

A

Packed cell volume, plasma sodium, base excess, and lactate levels

82
Q

What can be used to minimize oxidant-mediated contributions to the inflammatory cascade in burns?

A

Antioxidants, such as vitamin C

83
Q

What are the possible causes of vascular injury?

A

Blunt, penetrating, or shearing injuries; fractures of bones close to vessels

84
Q

What signs should be checked to assess distal perfusion in vascular trauma?

A

Doppler signal distally (monophasic/biphasic/triphasic)

85
Q

What tests are considered the “gold standard” for assessing vascular trauma?

A

Duplex scanning and angiography

86
Q

How can simple lacerations of arteries be treated in vascular trauma?

A

Direct closure or application of a vein patch if there is a risk of subsequent stenosis

87
Q

What is the recommended management for vascular trauma?

A

Almost always operative; obtaining proximal and distal control of affected vessels is crucial

88
Q

How should transection of a vessel be treated in vascular trauma?

A

Either end-to-end anastomosis (if possible) or an interposition vein graft

89
Q

What should be avoided in traumatic open injuries to prevent infection?

A

Use of PTFE (polytetrafluoroethylene)

90
Q

What is torsades de pointes?

A

A rare arrhythmia associated with a long QT interval

90
Q

What can torsades de pointes deteriorate into?

A

Ventricular fibrillation

91
Q

What are some causes of a long QT interval?

A

Congenital conditions (Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome), certain medications (amiodarone, sotalol, class 1a antiarrhythmic drugs, tricyclic antidepressants, antipsychotics, chloroquine, terfenadine, erythromycin), electrolyte imbalances (hypocalcemia, hypokalemia, hypomagnesemia), myocarditis, hypothermia, subarachnoid hemorrhage

92
Q

What is the management for torsades de pointes?

A

IV magnesium sulfate

93
Q

What are the two main types of VT?

A

Monomorphic VT and polymorphic VT

93
Q

What is the most common cause of monomorphic VT?

A

Myocardial infarction

93
Q

What is the potential complication of VT?

A

Precipitation of ventricular fibrillation

94
Q

What is ventricular tachycardia (VT)?

A

Broad-complex tachycardia originating from a ventricular ectopic focus

95
Q

What are the causes of a long QT interval?

A

Congenital conditions, certain medications, electrolyte imbalances, myocarditis, hypothermia, subarachnoid hemorrhage

95
Q

What is the subtype of polymorphic VT that is precipitated by prolongation of the QT interval?

A

Torsades de pointes

96
Q

What is Jervell-Lange-Nielsen syndrome?

A

A congenital condition characterized by a long QT interval and deafness due to an abnormal potassium channel

97
Q

What is Romano-Ward syndrome?

A

A congenital condition characterized by a long QT interval without deafness

98
Q

Which drugs can cause a long QT interval?

A

Amiodarone, sotalol, class 1a antiarrhythmic drugs, tricyclic antidepressants, fluoxetine, chloroquine, terfenadine, erythromycin

99
Q

What are the features of an oculogyric crisis?

A

Restlessness, agitation, involuntary upward deviation of the eyes

100
Q

What are some other causes of a long QT interval?

A

Electrolyte imbalances (hypocalcemia, hypokalemia, hypomagnesemia), acute myocardial infarction, myocarditis, hypothermia, subarachnoid hemorrhage

100
Q

What is an oculogyric crisis?

A

A dystonic reaction to certain drugs or medical conditions

101
Q

Which drugs can cause an oculogyric crisis?

A

Phenothiazines, haloperidol, metoclopramide

101
Q

Which medical condition can cause an oculogyric crisis?

A

Postencephalitic Parkinson’s disease

102
Q

What is the management for an oculogyric crisis?

A

Procyclidine

102
Q

Which side of the diaphragm is more prone to rupture?

A

Left side (due to the presence of the liver on the right, which shields the diaphragm)

103
Q

How are penetrating injuries to the diaphragm typically discovered?

A

During surgery performed for another more significant injury

104
Q

What can happen if diaphragmatic injuries are missed during initial assessment?

A

They can present later with symptoms of herniation

105
Q

What are the characteristics of diaphragmatic injuries caused by blunt trauma?

A

They tend to be larger and result in more obvious herniation

106
Q

What is the recommended management for diaphragmatic rupture?

A

Surgical repair

106
Q

What should be considered when deciding whether to use mesh during surgical repair?

A

Intra-peritoneal contamination and the potential risks associated with mesh placement

107
Q

What is compartment syndrome?

A

A complication that can occur following fractures or ischemia re-perfusion injury, characterized by raised pressure within a closed anatomical space

107
Q

Which fractures are commonly associated with compartment syndrome?

A

Supracondylar fractures and tibial shaft injuries

108
Q

How is compartment syndrome diagnosed?

A

By measuring intracompartmental pressure, with pressures exceeding 20mmHg considered abnormal and >40mmHg being diagnostic

108
Q

What are the symptoms and signs of compartment syndrome?

A

Pain (especially on movement), paresthesiae, pallor, arterial pulsation may still be felt, paralysis of the muscle group

109
Q

What is the treatment for compartment syndrome?

A

Prompt and extensive fasciotomies

110
Q

What should be considered during fasciotomies in the lower limb?

A

Ensuring adequate decompression of the deep muscles by experienced operators

111
Q

What complications can occur following fasciotomy?

A

Myoglobinuria, which can result in renal failure, requiring aggressive IV fluids

112
Q

How soon can muscle groups die in compartment syndrome?

A

Within 4-6 hours

112
Q

What should be done if muscle groups are necrotic at fasciotomy?

A

They should be debrided, and amputation may be necessary

113
Q

What can cause an Addisonian crisis?

A

Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism), adrenal hemorrhage (e.g., Waterhouse-Friderichsen syndrome), steroid withdrawal

114
Q

What is the recommended management for an Addisonian crisis?

A

Hydrocortisone 100 mg IM or IV, 1 liter of normal saline infused over 30-60 minutes (or with dextrose if hypoglycemic), continue hydrocortisone 6 hourly until the patient is stable

114
Q

Is fludrocortisone required for an Addisonian crisis?

A

No, because high cortisol exerts weak mineralocorticoid action

114
Q

When can oral replacement therapy be initiated for an Addisonian crisis?

A

After 24 hours, and then gradually reduced to maintenance over 3-4 days

115
Q

What percentage of trauma-related deaths are due to uncontrolled hemorrhage?

A

Up to 39%

116
Q

What is considered massive transfusion?

A

Replacement of a patient’s total blood volume in less than 24 hours or acute administration of more than half the patient’s estimated blood volume per hour

117
Q

What is the recommended initial administration for hemorrhaging patients following trauma?

A

Tranexamic acid

118
Q

What is the principle of hemostatic resuscitation?

A

Transfusing blood components in fixed ratios, such as packed red cells, FFP, and platelets in a ratio of 1:1:1

MRCS A - Dr Bishoy (58 decks)

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