Acute and Emergency

Question 1

Metabolic acidosis is commonly classified according to what?

Answer 1

the anion gap

Question 2

Normal anion gap =

Answer 2

hyperchloraemic metabolic acidosis

Question 3

Metabolic acidosis= normal anion gap causes?

Answer 3

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula

renal tubular acidosis

drugs: e.g. acetazolamide

ammonium chloride injection

Addison’s disease

Question 4

Metabolic acidosis= raised anion gap causes?

Answer 4

lactate: shock, hypoxia

ketones: diabetic ketoacidosis, alcohol

urate: renal failure

acid poisoning: salicylates, methanol

Question 5

Metabolic alkalosis may be caused by what?

Answer 5

a loss of hydrogen ions or a gain of bicarbonate

Question 6

Metabolic alkalosis is mainly due to what?

Answer 6

problems of the kidney or GI tract

Question 7

Causes of metabolic alkalosis?

Answer 7

vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)

diuretics

liquorice, carbenoxolone

hypokalaemia

primary hyperaldosteronism

Cushing’s syndrome

Bartter’s syndrome

congenital adrenal hyperplasia

Question 8

Causes of respiratory acidosis?

Answer 8

COPD

decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema

sedative drugs: benzodiazepines, opiate overdose

Question 9

What drugs can cause resp acidosis?

Answer 9

sedative drugs: benzodiazepines, opiate overdose

Question 10

Common causes of respiratory alkalosis?

Answer 10

anxiety leading to hyperventilation

pulmonary embolism

salicylate poisoning

CNS disorders: stroke, subarachnoid haemorrhage, encephalitis

altitude

pregnancy

Question 11

How to calculate the anion gap?

Answer 11

(sodium + potassium) - (bicarbonate + chloride)

Question 12

Normal anion gap?

Answer 12

8-14 mmol/L

Question 13

Calculating the anion gap is useful to consider in who?

Answer 13

pts with metabolic acidosis

Question 14

Causes of a normal anion gap/hyperchloraemic metabolic acidosis?

Answer 14

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula

renal tubular acidosis

drugs: e.g. acetazolamide

ammonium chloride injection

Addison’s disease

Question 15

What drugs may cause a normal anion gap/hyperchloraemic metabolic acidosis?

Answer 15

acetazolamide

Question 16

Causes of a raised anion gap metabolic acidosis?

Answer 16

lactate: shock, hypoxia

ketones: diabetic ketoacidosis, alcohol

urate: renal failure

acid poisoning: salicylates, methanol

5-oxoproline: chronic paracetamol use

Question 17

What drugs may caused a raised anion gap metabolic acidosis?

Answer 17

5-oxoproline: chronic paracetamol use

Question 18

5 step approach to arterial blood gas interpretation?

Answer 18

1. How is the patient?
2. Is the patient hypoxaemic?
   the Pa02 on air should be >10 kPa
3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)
4. Respiratory component: What has happened to the PaCO2?
5. Metabolic component: What is the bicarbonate level/base excess?

Question 19

ABG interpretation= normal PaO2 on air?

Answer 19

> 10kPa

Question 20

ABG= acidaemic?

Answer 20

pH <7.35

Question 21

ABG= alkalaemic?

Answer 21

pH >7.45

Question 22

ABG= 4. Respiratory component: What has happened to the PaCO2?

Answer 22

PaCO2 > 6.0 kPa suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)

PaCO2 < 4.7 kPa suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)

Question 23

ABG= what suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)?

Answer 23

PaCO2 > 6.0 kPa

Question 24

ABG= what does PaCO2 > 6.0 kPa suggest?

Answer 24

a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)

Question 25

ABG= what suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)?

Answer 25

PaCO2 < 4.7 kPa

Question 26

ABG= what does PaCO2 < 4.7 kPa suggest?

Answer 26

respiratory alkalosis (or respiratory compensation for a metabolic acidosis)

Question 27

ABG= 5. Metabolic component: What is the bicarbonate level/base excess?

Answer 27

bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis) bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)

Question 28

ABG= what suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)?

Answer 28

bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l)

Question 29

ABG= what does bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggest?

Answer 29

metabolic acidosis (or renal compensation for a respiratory alkalosis)

Question 30

ABG= what suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)?

Answer 30

bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)

Question 31

ABG= what does bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggest?

Answer 31

a metabolic alkalosis (or renal compensation for a respiratory acidosis)

Question 32

Way to remember ABG interpretation?

Answer 32

ROME Respiratory = Opposite low pH + high PaCO2 i.e. acidosis, or high pH + low PaCO2 i.e. alkalosis Metabolic = Equal low pH + low bicarbonate i.e. acidosis, or high pH + high bicarbonate i.e. akalosis

Question 33

Metabolic acidosis= If a question supplies the chloride level then this is often a clue that...

Answer 33

the anion gap should be calculated.

Question 34

Anion gap normal range?

Answer 34

The normal range = 10-18 mmol/L

Question 35

Metabolic acidosis= Normal anion gap ( = hyperchloraemic metabolic acidosis) causes- gastrointestinal bicarbonate loss eg.

Answer 35

prolonged diarrhoea: may also result in hypokalaemia ureterosigmoidostomy fistula

Question 36

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:

Answer 36

lactic acidosis type A: sepsis, shock, hypoxia, burns lactic acidosis type B: metformin

Question 37

Metabolic acidosis secondary to high lactate levels= lactic acidosis type A?

Answer 37

sepsis, shock, hypoxia, burns

Question 38

Metabolic acidosis secondary to high lactate levels= lactic acidosis type B?

Answer 38

metformin

Question 39

Causes of metabolic alkalosis?

Answer 39

vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction) vomiting may also lead to hypokalaemia diuretics liquorice, carbenoxolone hypokalaemia primary hyperaldosteronism Cushing's syndrome Bartter's syndrome

Question 40

Mechanism of metabolic alkalosis?

Answer 40

activation of renin-angiotensin II-aldosterone (RAA) system is a key factor aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels in hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality

Question 41

Respiratory acidosis may be caused by a number of conditions: for example?

Answer 41

COPD decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema neuromuscular disease obesity hypoventilation syndrome sedative drugs: benzodiazepines, opiate overdose

Question 42

Common causes of resp alkalosis?

Answer 42

anxiety leading to hyperventilation pulmonary embolism salicylate poisoning (then met acidosis later) CNS disorders: stroke, subarachnoid haemorrhage, encephalitis altitude pregnancy

Question 43

Salicylate overdose leads to what metabolic disturbance?

Answer 43

leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

Question 44

Sensitivity to latex may cause a number of problems: (3)

Answer 44

type I hypersensitivity (anaphylaxis) type IV hypersensitivity (allergic contact dermatitis) irritant contact dermatitis

Question 45

Latex allergy is more common in who?

Answer 45

children with myelomeningocele spina bifida

Question 46

It is recognised that many people who are allergic to latex are also allergic to what?

Answer 46

fruits, particularly banana, pineapple, avocado, chestnut, kiwi fruit, mango, passion fruit and strawberry.

Question 47

Latex-fruit syndrome?

Answer 47

It is recognised that many people who are allergic to latex are also allergic to fruits, particularly banana, pineapple, avocado, chestnut, kiwi fruit, mango, passion fruit and strawberry.

Question 48

Allergy to penicillin based antibiotics is common although many patients who report an allergy may be describing what?

Answer 48

intolerance/side-effects (e.g. diarrhoea) or a coincidental rash (e.g. amoxicillin in patients with infectious mononucleosis).

Question 49

Around 0.5-6.5% of patients who are allergic to penicillin are also allergy to what?

Answer 49

cephalosporins

Question 50

The principal side-effect of the cephalosporins is

Answer 50

hypersensitivity and about 0.5-6.5% of penicillin-sensitive patients will also be allergic to the cephalosporins. Patients with a history of immediate hypersensitivity to penicillin should not receive a cephalosporin.

Question 51

Around 0.5-6.5% of patients who are allergic to penicillin are also allergy to cephalosporins. If a cephalosporin is essential in these patients because a suitable alternative antibacterial is not available, then what should be used?

Answer 51

cefixime, cefotaxime, ceftazidime, ceftriaxone, or cefuroxime can be used with caution; cefaclor, cefadroxil, cefalexin, cefradine, and ceftaroline fosamil should be avoided.

Question 52

It is important to be aware of other types of penicillin and their trade names to avoid accidental prescription. Types of penicillin?

Answer 52

phenoxymethylpenicillin benzylpenicillin flucloxacillin amoxicillin ampicillin co-amoxiclav (Augmentin) co-fluampicil (Magnapen) piperacillin with tazobactam (Tazocin) ticarcillin with clavulanic acid (Timentin)

Question 53

The symptoms of perforation secondary to peptic ulcer disease typically develop suddenly, what else?

Answer 53

epigastric pain, later becoming more generalised patients may describe syncope

Question 54

Ix for Peptic ulcer disease (perforation)?

Answer 54

Largely clinical. An upright ('erect') chest x-ray is usually required when a patient presents with acute upper abdominal pain This is a useful test, as approximately 75% of patients with a perforated peptic ulcer will have free air under the diaphragm.

Question 55

Idiopathic intracranial hypertension (also known as pseudotumour cerebri and formerly benign intracranial hypertension) is classically seen in who?

Answer 55

seen in young, overweight females

Question 56

Idiopathic intracranial hypertension RFs?

Answer 56

obesity female sex pregnancy drugs eg. combined oral contraceptive pill steroids tetracyclines retinoids (isotretinoin, tretinoin) / vitamin A lithium

Question 57

Idiopathic intracranial hypertension RFs- drugs?

Answer 57

combined oral contraceptive pill steroids tetracyclines retinoids (isotretinoin, tretinoin) / vitamin A lithium

Question 58

Idiopathic intracranial hypertension- features?

Answer 58

headache blurred vision papilloedema (usually present) enlarged blind spot sixth nerve palsy may be present

Question 59

Idiopathic intracranial hypertension- what nerve palsy may be present?

Answer 59

6th nerve palsy

Question 60

Idiopathic intracranial hypertension- Mx?

Answer 60

weight loss carbonic anhydrase inhibitors e.g. acetazolamide topiramate is also used, and has the added benefit of causing weight loss in most patients repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management surgery

Question 61

Idiopathic intracranial hypertension- Mx- weight loss?

Answer 61

whilst diet and exercise are important, medications such as semaglitide and topiramate may be considered by specialists. Topiramate is particularly beneficial as it also inhibits carbonic anhydrase

Question 62

Idiopathic intracranial hypertension- Mx- medication?

Answer 62

carbonic anhydrase inhibitors e.g. acetazolamide topiramate is also used, and has the added benefit of causing weight loss in most patients

Question 63

Idiopathic intracranial hypertension- Mx- surgery?

Answer 63

optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

Question 64

Papilloedema?

Answer 64

optic disc swelling that is caused by increased intracranial pressure. It is almost always bilateral.

Question 65

Fundoscopy in papilloedema?

Answer 65

venous engorgement: usually the first sign loss of venous pulsation: although many normal patients do not have normal pulsation blurring of the optic disc margin elevation of optic disc loss of the optic cup Paton's lines: concentric/radial retinal lines cascading from the optic disc

Question 66

Fundoscopy in papilloedema- 1st sign?

Answer 66

venous engorgement

Question 67

Fundoscopy in papilloedema- Paton's lines?

Answer 67

concentric/radial retinal lines cascading from the optic disc

Question 68

Causes of papilloedema?

Answer 68

space-occupying lesion: neoplastic, vascular malignant hypertension idiopathic intracranial hypertension hydrocephalus hypercapnia Rare causes include= hypoparathyroidism and hypocalcaemia; vitamin A toxicity

Question 69

How should I manage pain from raised intracranial pressure?

Answer 69

Consider whether a treatable underlying cause is present. Also consider a trial of dexamethasone at a dose of 8–16 mg daily (taken in the morning), titrated down to the lowest dose that controls symptoms.

Question 70

Respiratory failure?

Answer 70

inability of resp system to maintain adequate gas exchange

Question 71

2 types of resp failure?

Answer 71

type 1 and type 2

Question 72

Type 1 resp failure?

Answer 72

↓ pO2 with a normal or ↓ pCO2

Question 73

Type 2 resp failure?

Answer 73

↑ pCO2 with a normal or ↓ pO2 hypercapnia → ↓ pH → respiratory acidosis

Question 74

Result of hypercapnia in resp failure (type 2)?

Answer 74

hypercapnia → ↓ pH → respiratory acidosis

Question 75

Causes of type 1 resp failure?

Answer 75

pneumonia pulmonary embolism asthma pulmonary oedema acute respiratory distress syndrome

Question 76

Causes of type 2 resp failure?

Answer 76

chronic obstructive pulmonary disease decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema neuromuscular disease obesity hypoventilation syndrome sedative drugs: benzodiazepines, opiate overdose

Question 77

Non-invasive ventilation - key indications?

Answer 77

COPD with respiratory acidosis pH 7.25-7.35 - can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea cardiogenic pulmonary oedema unresponsive to CPAP weaning from tracheal intubation

Question 78

Non-invasive ventilation - indicated in COPD with resp...

Answer 78

respiratory acidosis pH 7.25-7.35 - can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used

Question 79

Recommended initial settings for bi-level pressure support in COPD?

Answer 79

Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O back up rate: 15 breaths/min back up inspiration:expiration ratio: 1:3

Question 80

The presentation of a ruptured abdominal aortic aneurysm (AAA) can be?

Answer 80

catastrophic (e.g. sudden collapse) or sub-acute (persistent severe central abdominal pain with developing shock).

Question 81

Mortality of ruptured AAA?

Answer 81

80%

Question 82

Features of ruptured AAA?

Answer 82

severe, central abdominal pain radiating to the back pulsatile, expansile mass in the abdomen patients may be shocked (hypotension, tachycardic) or may have collapsed

Question 83

Mx of ruptured AAA?

Answer 83

surgical emergency - patients with a suspected ruptured AAA require an immediate vascular review with a view to emergency surgical repair (endovascular repair)

Question 84

Ix of ruptured AAA?

Answer 84

unstable- clinical and straight to theatre stable= CT angiogram if diagnosis in doubt frail with multiple cormorbidities= may represent a terminal event and consideration should be given to a palliative approach.

Question 85

GCS how many points in Motor, verbal and eye opening?

Answer 85

E4 V5 M6

Question 86

GCS uses what 3 modalities?

Answer 86

Motor response Verbal response Eye opening

Question 87

GCS= motor response?

Answer 87

6. Obeys commands 5. Localises to pain 4. Withdraws from pain 3. Abnormal flexion to pain (decorticate posture) 2. Extending to pain 1. None

Question 88

GCS= verbal response?

Answer 88

5. Orientated 4. Confused 3. Words 2. Sounds 1. None

Question 89

GCS= eye opening?

Answer 89

4. Spontaneous 3. To speech 2. To pain 1. None

Question 90

What format is GCS normally expressed?

Answer 90

'GCS = 13, M5 V4 E4 at 21:30'.

Question 91

Normal GCS score?

Answer 91

15 lowest is 3

Question 92

GCS in children= motor?

Answer 92

6. Infant moves spontaneously or purposefully 5. Infant withdraws from touch 4. Infant withdraws from pain 3. Abnormal flexion to pain for an infant (decorticate response) 2. Extension to pain (decerebrate response) 1. No motor response

Question 93

GCS in children= verbal response?

Answer 93

5. Smiles, oriented to sounds, follows objects, interacts. 4. Cries but consolable, inappropriate interactions. 3. Inconsistently inconsolable, moaning. 2. Inconsolable, agitated. 1. No verbal response.

Question 94

GCS in children= eye opening?

Answer 94

4. Eyes opening spontaneously 3. Eye opening to speech 2. Eye opening to pain 1. No eye opening or response

Question 95

Recommended maintenance fluids?

Answer 95

25-30 ml/kg/day of water and approximately 1 mmol/kg/day of potassium, sodium and chloride and approximately 50-100 g/day of glucose to limit starvation ketosis

Question 96

Maintenance fluids for 80kg pt in 24hr period?

Answer 96

2 litres water 80mmol potassium & 80mmol sodium 50-100g glucose

Question 97

Fluids= Electrolyte concs (in millimoles/litre) in plasma?

Answer 97

Na+ = 135-145 Cl- = 98-105 K+ = 3.5-5 HCO3- = 22-28 Glucose= -

Question 98

Fluids= Electrolyte concs (in millimoles/litre) in 0.9% saline?

Answer 98

Na+ = 154 Cl- = 154 K+ = - HCO3- = - Glucose= -

Question 99

Fluids= Electrolyte concs (in millimoles/litre) in 5% glucose?

Answer 99

Na+ = - Cl- = - K+ = - HCO3- = - Glucose= 50g

Question 100

Fluids= Electrolyte concs (in millimoles/litre) in 0.18% saline with 4% glucose?

Answer 100

Na+ = 30 Cl- = 30 K+ = - HCO3- = - Glucose= 40g

Question 101

Fluids= Electrolyte concs (in millimoles/litre) in Hartmann's?

Answer 101

Na+ = 131 Cl- = 111 K+ = 5 HCO3- = 29 Glucose= -

Question 102

If large volumes of 0.9% saline are used then there is an increased risk of what?

Answer 102

hyperchloraemic metabolic acidosis

Question 103

Fluid types= NaCl 0.9% 1000ml?

Answer 103

150mmol Na

Question 104

Fluid types= KCl 0.3% 1000ml?

Answer 104

40mmol K

Question 105

Fluid types= KCl 0.15% 1000ml?

Answer 105

20mmol K

Question 106

Fluid types= glucose 5% 1000ml?

Answer 106

50g glucose

Question 107

Max rate of potassium can give?

Answer 107

10mmol/hr

Question 108

Maintenance fluids- aim for what volume and rate?

Answer 108

1000ml over 8-12hrs

Question 109

Maintenance and replacement fluids- aim for what volume and rate?

Answer 109

1000ml over 4-6hrs

Question 110

How to work out what maintenance fluids to give pt?

Answer 110

Work out what they need (daily requirements) Calculate what they have already been given Workout what they now need to be given to full-fill daily requirements Workout what fluid combo is best to give

Question 111

Fluids= how does K need to be given?

Answer 111

with Cl NOT on its own eg. KCl and alongside another fluid eg. saline or glucose

Question 112

Fluids for emergency resus?

Answer 112

sodium chloride 0.9% 500ml in less than 15m (10m)

Question 113

Fluids for emergency hypoglycaemia?

Answer 113

glucose 20% 100ml 15m

Question 114

Fluids for emergency hypokalaemia?

Answer 114

Sodium chloride 0.9% / Potassium chloride 0.3% 1000ml 4hr

Question 115

Fluids for emergency hypercalcaemia?

Answer 115

Sodium chloride 0.9% 1000ml 4hr

Question 116

Example fluids for maintenance without deficits or losses?

Answer 116

25-20ml/kg/24hr water 1mmol/kg/24hr Na & K 50-100g/24hr glucose aim 1000ml over 8-12hrs

Question 117

Example fluids for maintenance with deficits or losses eg. Na or K low, vomiting, diarrhoea?

Answer 117

min 30ml/kg/24hr water ensure electrolytes replaced aim 1000ml over 4-6hrs

Question 118

Fluids for emergency resus in children?

Answer 118

sodium chloride 0.9% 10ml/kg less than 15mins (10mins)

Question 119

Fluids for maintenance without deficits or losses in children?

Answer 119

100ml/kg/24hr= 0-10kg 50ml/kg/24hr= 11-20kg 20ml/kg/24hr= >20kg eg. weight 30kg so 1000ml for 1st 10kg 500ml for 2nd 10kg 200 for last 10kg so total 1700ml maintenance

Question 120

Hyperosmolar hyperglycaemic state (HHS)?

Answer 120

medical emergency that can be difficult to manage and has a significant associated mortality (up to 20%). Hyperglycaemia results in osmotic diuresis (more urine produced than normal), severe dehydration, and electrolyte deficiencies.

Question 121

Hyperosmolar hyperglycaemic state (HHS) typically presents in who?

Answer 121

the elderly with DMT2

Question 122

Pathophysiology of hyperosmolar hyperglycaemic state (HHS)?

Answer 122

hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion

Question 123

hyperosmolar hyperglycaemic state (HHS) precipitating factors?

Answer 123

intercurrent illness dementia sedative drugs

Question 124

DKA vs HHS in terms of features?

Answer 124

whilst DKA presents within hours of onset, HHS comes on over many days, and consequently, the dehydration and metabolic disturbances may be more extreme

Question 125

CP of HHS?

Answer 125

volume loss= dehydration, polyuria, polydipsia systemic= lethargy, N&V neuro= altered level on consciousness, focal neuro deficits haematological= hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)

Question 126

There is no precise diagnostic criteria for HHS but what is typically seen?

Answer 126

1) hypovolaemia 2) marked hyperglycaemia (>30 mmol/L) 3) significantly raised serum osmolarity (> 320 mosmol/kg)= can be calculated by: 2 * Na+ + glucose + urea 4) no significant hyperketonaemia (<3 mmol/L) 5) no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)

Question 127

DMT2 elderly pt with lethargy, N&V, dehyration, hyperglycaemia (>30mmol/L) but no raised ketones or acidosis?

Answer 127

HHS

Question 128

Mx of HHS?

Answer 128

1) Fluids= IV 0.9% saline, typically 0.5-1L/hr depending on assessment; monitor K levels and add to fluids if needed 2) Insulin should NOT be given unless blood glucose stops falling while giving IV fluids 3) VTE prophylaxis as at risk of thrombosis due to hyperviscosity

Question 129

Cx of HHS?

Answer 129

vascular complications may occur due to hyperviscosity: such as myocardial infarction and stroke

Question 130

Hyphema?

Answer 130

blood in the anterior chamber of the eye

Question 131

Hyphema (blood in the anterior chamber of the eye) - especially in the context of trauma needs what?

Answer 131

urgent referral to opthalmic specialist

Question 132

Risk of hyphema (blood in anterior chamber of eye)?

Answer 132

risk to sight due to raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes

Question 133

Hyphema (blood in the anterior chamber of the eye) - especially in the context of trauma Mx?

Answer 133

urgent referral to opthalmic specialist - strict bed rest so admit isolated hyphema (occurs without trauma) will require daily ophthalmic review and pressure checks initially as an outpatient.

Question 134

Hyphema/ocular trauma= An assessment should also be made for what?

Answer 134

orbital compartment syndrome, e.g. secondary to retrobulbar haemorrhage. This is true ophthalmic emergency

Question 135

Features of orbital compartment syndrome?

Answer 135

eye pain/swelling proptosis 'rock hard' eyelids relevant afferent pupillary defect

Question 136

eye pain/swelling proptosis 'rock hard' eyelids relevant afferent pupillary defect

Answer 136

orbital compartment syndrome eg. secondary to retrobulbar haemorrhage

Question 137

Mx of orbital compartment syndrome?

Answer 137

urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit

Question 138

Acute upper gastrointestinal (GI) bleeding most commonly due to what?

Answer 138

either oesophageal varices or peptic ulcer disease

Question 139

Clinical features of acute upper GI bleed?

Answer 139

- haematemesis (most common)= bright red or 'coffee ground' - melena= passage of blood per rectum, black and tarry - raised urea (due to 'protein meal' of blood) - Features associated with particular diagnosis eg. oesophageal varices: stigmata of chronic liver disease or peptic ulcer disease: abdominal pain

Question 140

What blood result may be seen in acute upper GI bleed?

Answer 140

a raised urea may be seen due to the 'protein meal' of the blood

Question 141

Oesophageal causes of acute upper GI bleed?

Answer 141

oesophageal varices oesophagitis ca mallory weiss tear

Question 142

Acute upper GI bleeding caused by oesophageal varices CP?

Answer 142

Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.

Question 143

Acute upper GI bleeding caused by oesophagitis CP?

Answer 143

Small volume of fresh blood, often streaking vomit. Melena rare. Often ceases spontaneously. Usually history of antecedent GORD-type symptoms.

Question 144

Acute upper GI bleeding caused by ca CP?

Answer 144

Usually small volume of blood, except as a preterminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until malignancy is managed.

Question 145

Acute upper GI bleeding caused by mallory weiss tear CP?

Answer 145

Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Melena is rare. Usually ceases spontaneously.

Question 146

Gastric causes of acute upper GI bleed?

Answer 146

Gastric ulcer Gastric ca Dieulafoy lesion Diffuse erosive gastritis

Question 147

Acute upper GI bleeding caused by gastric ulcer CP?

Answer 147

Small low low-volume bleeds are more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.

Question 148

Acute upper GI bleeding caused by gastric ca CP?

Answer 148

May be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia and may have constitutional symptoms. Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage.

Question 149

Acute upper GI bleeding caused by Dieulafoy lesion CP?

Answer 149

Often no prodromal features prior to haematemesis and melena, but this arteriovenous malformation may produce quite a considerable haemorrhage and may be difficult to detect endoscopically

Question 150

Acute upper GI bleeding caused by diffuse erosive gastritis CP?

Answer 150

Usually haematemesis and epigastric discomfort. Usually, there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise

Question 151

Duodenal causes of acute upper GI bleeding?

Answer 151

duodenal ulcer aorto-enteric fistual

Question 152

Acute upper GI bleeding caused by duodenal ulcer CP?

Answer 152

These are usually posteriorly sited and may erode the gastroduodenal artery. However, ulcers at any site in the duodenum may present with haematemesis, melena and epigastric discomfort. The pain of a duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours after eating. Periampullary tumours may bleed but these are rare.

Question 153

Duodenal ulcer may erode what artery and cause acute upper GI bleeding?

Answer 153

gastroduodenal artery (runs posteriorly)

Question 154

Acute upper GI bleeding caused by Aorto-enteric fistula CP?

Answer 154

In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of major haemorrhage associated with high mortality.

Question 155

Risk assessment for acute upper GI bleeding?

Answer 155

the Glasgow-Blatchford score at first assessment= helps clinicians decide whether patients can be managed as outpatients or not Rockall score is used after endoscopy= provides a percentage risk of rebleeding and mortality includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

Question 156

What risk assessment for upper GI bleed provides a percentage risk of rebleeding and mortality includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage?

Answer 156

Rockall score after endoscopy

Question 157

What risk assessment for upper GI bleed helps clinicians decide whether patients can be managed as outpatients or not?

Answer 157

the Glasgow-Blatchford score at first assessment

Question 158

Acute upper GI bleed= Glasgow-Blatchford score of what means pt may be considered for early discharge?

Answer 158

0

Question 159

Acute upper GI bleed= Glasgow-Blatchford score at first assessment?

Answer 159

Urea (mmol/L); - 6.6-8= score of 2 - 8-10= score 3 - 10-25= score 4 - >25= score 6 Hb (g/L): - men= 12-13 score 1; 10-12 score 3; <10 score 6 - women= 10-12 score 1; <10 score 6 Systolic BP (mmHg): - 100-109= score 1 - 90-99= score 2 - <90= score 3 Other markers: - Pulse >=100/min score 1 - Melaena score 1 - Syncope score 2 - Hepatic disease score 2 - Cardiac failure score 2 Patients with a Blatchford score of 0 may be considered for early discharge.

Question 160

Resuscitation in acute upper GI bleed?

Answer 160

ABC, wide-bore intravenous access * 2 platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal prothrombin complex concentrate to patients who are taking warfarin and actively bleeding

Question 161

Resuscitation in acute upper GI bleed= platelet transfusion when?

Answer 161

if actively bleeding platelet count of less than 50 x 10*9/litre

Question 162

Resuscitation in acute upper GI bleed= fresh frozen plasma when?

Answer 162

to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal

Question 163

Resuscitation in acute upper GI bleed= prothrombin complex concentrate to who?

Answer 163

patients who are taking warfarin and actively bleeding

Question 164

Acute upper GI bleed= what should be offered immediately after resus in all pts with a severe bleed?

Answer 164

endoscopy

Question 165

Acute upper GI bleed= all pts need what?

Answer 165

endoscopy within 24hrs

Question 166

Acute upper GI bleed= Mx of non-variceal bleeding?

Answer 166

- do NOT use PPI BEFORE ENDOSCOPY to pts with suspected variceal upper GI bleed - use PPI after - can be treated with clips, or thermal coagulation - if further bleeding then= repeat endoscopy, interventional radiology and/or surgery

Question 167

Acute upper GI bleed= Mx of variceal bleeding?

Answer 167

- terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy) - variceal band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices - transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

Question 168

Acute upper GI bleed= Mx of variceal bleeding- oesophageal varices?

Answer 168

band ligation

Question 169

Acute upper GI bleed= Mx of variceal bleeding- gastric varices?

Answer 169

injections of N-butyl-2-cyanoacrylate

Question 170

Acute upper GI bleed= Mx of variceal bleeding- what if bleeding still not controlled after Mx?

Answer 170

transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled

Question 171

Summarise how to manage acute upper GI bleed?

Answer 171

1) Risk assessment= Glasgow-Blatchford score at first assessment & Rockall score after endoscopy 2) ABATED mneumonic= A to E (resus); Bloods; Access (2x large bore cannula); Transfusions required; Endoscopy (within 24hrs); Drugs (stop anticoag and NSAIDs) 3) Endoscopy after resus (all pts should have within 24hrs) 4) Non-variceal bleeding= do not use PPI until after endoscopy; clips or thermal coagulation 5) Variceal bleeding= terlipressin and prophylactic antibiotics should be given to patients at presentation before endoscopy. - Oesophageal varices= variceal band ligation - Gastric varices= injections of N-butyl-2-cyanoacrylate - if fails= TIPS

Question 172

Upper GI bleeding involves bleeding from where?

Answer 172

oesophagus, stomach or duodenum

Question 173

Haematemesis (vomiting blood) Coffee ground vomit (caused by vomiting digested blood with the appearance of coffee grounds) Melaena (tar-like, black, greasy and offensive stools caused by digested blood)

Answer 173

Upper GI bleed

Question 174

Acute upper GI bleed causes= ..... associated with a history of epigastric pain and dyspepsia. They may be taking non-steroidal anti-inflammatory drugs (NSAIDs).

Answer 174

Peptic ulcers

Question 175

Acute upper GI bleed causes= .... tend to occur after heavy retching or vomiting, which may be caused by binge drinking, gastroenteritis or hyperemesis gravidarum (in early pregnancy).

Answer 175

Mallory-Weiss tear

Question 176

Acute upper GI bleed causes= ..... are associated with liver cirrhosis and portal hypertension. The patient will have signs of these conditions, such as ascites, jaundice and caput medusae.

Answer 176

Oesophageal varices

Question 177

Acute upper GI bleed causes= .... associated with a history of weight loss, epigastric pain, treatment-resistant dyspepsia, low haemoglobin (anaemia) and a raised platelet count.

Answer 177

Stomach ca

Question 178

Why do pts with upper GI bleed get high urea?

Answer 178

Acid and digestive enzymes break down blood in the upper GI tract. One of the breakdown products is urea, which is then absorbed in the intestines, causing a rise in blood urea. The association between upper GI bleeding and increased blood urea is a key fact worth remembering.

Question 179

Acute upper GI bleed= The Rockall score is used after endoscopy to estimate the risk of rebleeding and mortality. It takes into account what?

Answer 179

Age Features of shock (e.g., tachycardia or hypotension) Co-morbidities Cause of bleeding (e.g., Mallory-Weiss tear or malignancy) Endoscopic findings of recent bleeding (e.g., clots and visible bleeding vessels)

Question 180

Initial Mx of acute upper GI bleed?

Answer 180

ABATED mnemonic: A – ABCDE approach to immediate resuscitation B – Bloods A – Access (ideally 2 x large bore cannula) T – Transfusions are required E – Endoscopy (within 24 hours) D – Drugs (stop anticoagulants and NSAIDs)

Question 181

Acute upper GI bleed= send bloods for what during A to E resus?

Answer 181

Haemoglobin (FBC) Urea (U&Es) Coagulation (INR and FBC for platelets) Liver disease (LFTs) Crossmatch 2 units of blood

Question 182

Group and save vs crossmatch?

Answer 182

“Group and save” is where the lab checks the patient’s blood group and saves a blood sample to match blood if needed. “Crossmatch” is where the lab allocates units of blood, tests that it is compatible, and keeps it ready in the fridge.

Question 183

Acute upper GI bleed= transfusion needed is based on what?

Answer 183

individual presentation Blood, platelets and clotting factors (fresh frozen plasma) are given to patients with massive bleeding Transfusing more blood than necessary can be harmful Platelets are given in active bleeding plus thrombocytopenia (platelet count less than 50) Prothrombin complex concentrate can be given to patients taking warfarin that are actively bleeding

Question 184

Acute upper GI bleed= transfusion- what is given to pts with massive bleeding?

Answer 184

Blood, platelets and clotting factors (fresh frozen plasma)

Question 185

Fresh frozen plasma transfusion includes what?

Answer 185

blood, platelets and clotting factors

Question 186

Acute upper GI bleed= transfusion- when are platelets given?

Answer 186

in active bleeding plus thrombocytopenia (platelet count less than 50)

Question 187

Acute upper GI bleed= transfusion- what in active bleeding plus thrombocytopenia (platelet count less than 50)?

Answer 187

platelets

Question 188

Acute upper GI bleed= transfusion- what can be given to patients taking warfarin that are actively bleeding?

Answer 188

Prothrombin complex concentrate

Question 189

Acute upper GI bleed= transfusion- when can prothrombin complex concentrate be given?

Answer 189

to patients taking warfarin that are actively bleeding

Question 190

What is needed to diagnose and treat the source of bleeding in acute upper GI bleed?

Answer 190

Oesophago-gastro-duodenoscopy (OGD) (endoscopy)

Question 191

Acute upper GI bleed= Variceal Mx- what is given if there is uncontrolled haemorrhage? What if all measures fail?

Answer 191

Sengstaken-Blakemore tube Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail = connects the hepatic vein to the portal vein ; exacerbation of hepatic encephalopathy is a common complication

Question 192

Transjugular Intrahepatic Portosystemic Shunt (TIPSS) for acute upper GI variceal bleeding is all other Mx options fail?

Answer 192

connects the hepatic vein to the portal vein exacerbation of hepatic encephalopathy is a common complication

Question 193

Prophylaxis of variceal haemorrhage?

Answer 193

propanolol endoscopic variceal band ligation (EVL)= superior to endoscopic sclerotherapy; this is supported by NICE who recommends: 'Offer endoscopic variceal band ligation for the primary prevention of bleeding for people with cirrhosis who have medium to large oesophageal varices.'; it should be performed at two-weekly intervals until all varices have been eradicated; PPI cover is given to prevent EVL-induced ulceration TIPS if unsuccessful

Question 194

Carbon monoxide has a high affinity for...

Answer 194

haemoglobin and myoglobin resulting in a left-shift of the oxygen dissociation curve and tissue hypoxia

Question 195

There are approximately ..... per year deaths from accidental carbon monoxide poisoning in the UK.

Answer 195

50

Question 196

CO poisoning= questions may hint at what?

Answer 196

badly maintained housing eg. student houses

Question 197

Features of carbon monoxide toxicity?

Answer 197

headache: 90% of cases nausea and vomiting: 50% vertigo: 50% confusion: 30% subjective weakness: 20% severe toxicity: 'pink' skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death

Question 198

Signs of severe carbon monoxide posioning?

Answer 198

'pink' skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death

Question 199

Ix for carbon monoxide poisoning?

Answer 199

pulse oximetry may be falsely high due to similarities between oxyhaemoglobin and carboxyhaemoglobin therefore a venous or arterial blood gas should be taken for carboxyhaemoglobin an ECG is a useful supplementary investgation to look for cardiac ischaemia

Question 200

Carbon monoxide poisoning= typical carboxyhaemoglobin levels?

Answer 200

< 3% non-smokers < 10% smokers 10 - 30% symptomatic: headache, vomiting > 30% severe toxicity

Question 201

Mx of suspected carbon monoxide poisoning?

Answer 201

100% high-flow oxygen via a non-rebreather mask - should be administered as soon as possible, with treatment continuing for a minimum of six hours - target oxygen saturations are 100% - treatment is generally continued until all symptoms have resolved, rather than monitoring CO levels - Hyperbaric oxygen if indicated

Question 202

Mx of suspected carbon monoxide poisoning= when may hyperbaric oxygen be considered instead of standard 100% high flow oxygen?

Answer 202

discussion with a specialist should be considered for more severe cases (e.g. levels > 25%) in 2008, the Department of Health publication 'Recognising Carbon Monoxide Poisoning' also listed loss of consciousness at any point, neurological signs other than headache, myocardial ischaemia or arrhythmia and pregnancy as indications for hyperbaric oxygen

Question 203

Why is 100% high flow O2 given for the Mx of suspected CO poisoning?

Answer 203

from a physiological perspective, this decreases the half-life of carboxyhemoglobin (COHb)

Question 204

what should be considered in questions giving a combination of abdominal pain and neurological signs?

Answer 204

lead poisoning and acute intermittent porphyria

Question 205

Lead poisoning results in what?

Answer 205

defective ferrochelatase and ALA dehydratase function.

Question 206

Features of lead poisoning?

Answer 206

abdominal pain peripheral neuropathy (mainly motor) neuropsychiatric features fatigue constipation blue lines on gum margin (only 20% of adult patients, very rare in children)

Question 207

blue lines on gum margin?

Answer 207

may be lead poisoning

Question 208

Ix for lead poisoning?

Answer 208

the blood lead level is usually used for diagnosis. Levels greater than 10 mcg/dl are considered significant FBC: microcytic anaemia. Blood film shows red cell abnormalities including basophilic stippling and clover-leaf morphology raised serum and urine levels of delta aminolaevulinic acid may be seen making it sometimes difficult to differentiate from acute intermittent porphyria urinary coproporphyrin is also increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly increased) in children, lead can accumulate in the metaphysis of the bones although x-rays are not part of the standard work-up

Question 209

Mx of lead poisoning?

Answer 209

Various chelating agents are currently used: - dimercaptosuccinic acid (DMSA) - D-penicillamine - EDTA - dimercaprol

Question 210

One of the effects of organophosphate insecticide poisoning is?

Answer 210

inhibition of acetylcholinesterase leading to upregulation of nicotinic and muscarinic cholinergic neurotransmission. In warfare, sarin gas is a highly toxic synthetic organophosphorus compound that has similar effects.

Question 211

Features of organophosphate insecticide poisoning can be predicted by?

Answer 211

the accumulation of acetylcholine as one of the effects of organophosphate poisoning is inhibition of acetylcholinesterase leading to upregulation of nicotinic and muscarinic cholinergic neurotransmission.

Question 212

Features of organophosphate insecticide poisoning?

Answer 212

Features can be predicted by the accumulation of acetylcholine (mnemonic = SLUD) Salivation Lacrimation Urination Defecation/diarrhoea cardiovascular: hypotension, bradycardia also: small pupils, muscle fasciculation

Question 213

Mx of organophosphate insecticide poisoning?

Answer 213

atropine the role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear benefit

Question 214

Thoracic trauma= tension pneumothorax?

Answer 214

Often laceration to lung parenchyma with flap Pressure develops in thorax Most common cause is mechanical ventilation in patient with pleural injury Symptoms overlap with cardiac tamponade, hyper-resonant percussion note is more likely in tension pnemothorax

Question 215

Thoracic trauma= Flail chest?

Answer 215

Chest wall disconnects from thoracic cage Multiple rib fractures (at least two fractures per rib in at least two ribs) Associated with pulmonary contusion Abnormal chest motion Avoid over hydration and fluid overload

Question 216

Pulmonary contusion?

Answer 216

bruise to the lung that can occur after chest trauma

Question 217

Thoracic trauma= pneumothorax?

Answer 217

Most common cause is lung laceration with air leakage Most traumatic pneumothoraces should have a chest drain Patients with traumatic pneumothorax should never be mechanically ventilated until a chest drain is inserted

Question 218

Thoracic trauma= Haemothorax?

Answer 218

Most commonly due to laceration of lung, intercostal vessel or internal mammary artery Haemothoraces large enough to appear on CXR are treated with large bore chest drain Surgical exploration is warranted if >1500ml blood drained immediately

Question 219

Thoracic trauma= pts with traumatic pneumothorax should never be what?

Answer 219

mechanically ventilated until a chest drain is inserted

Question 220

Thoracic trauma= haemothorax- Surgical exploration is warranted if...

Answer 220

>1500ml blood drained immediately

Question 221

Beck's triad?

Answer 221

elevated venous pressure, reduced arterial pressure, reduced heart sounds. In cardiac tamponade

Question 222

Cushing's triad?

Answer 222

bradycardia, irregular respirations, and widened pulse pressures in response to raised ICP

Question 223

Thoracic trauma= pulmonary contusion?

Answer 223

Most common potentially lethal chest injury Arterial blood gases and pulse oximetry important Early intubation within an hour if significant hypoxia

Question 224

Thoracic trauma= pulmonary contusion- what if signif hypoxia?

Answer 224

early intubation within an hr

Question 225

Thoracic trauma= blunt cardiac injury?

Answer 225

Usually occurs secondary to chest wall injury ECG may show features of myocardial infarction Sequelae: hypotension, arrhythmias, cardiac wall motion abnormalities

Question 226

Thoracic trauma= aortic disruption?

Answer 226

Deceleration injuries (injury to the body that occurs when a moving object suddenly stops or slows down) Contained haematoma Widened mediastinum

Question 227

Thoracic trauma= Diaphragm disruption?

Answer 227

Most due to motor vehicle accidents and blunt trauma causing large radial tears (laceration injuries result in small tears) More common on left side Insert gastric tube, which will pass into the thoracic cavity

Question 228

Thoracic trauma= Mediastinal traversing wounds?

Answer 228

Entrance wound in one hemithorax and exit wound/foreign body in opposite hemithorax Mediastinal haematoma or pleural cap suggests great vessel injury Mortality is 20%

Question 229

Following trauma there is a trimodal death distribution?

Answer 229

Immediately following injury. Typically as result of brain or high spinal injuries, cardiac or great vessel damage. Salvage rate is low. In early hours following injury. In this group deaths are due to phenomena such as splenic rupture, sub dural haematomas and haemopneumothoraces In the days following injury. Usually due to sepsis or multi organ failure.

Question 230

Aspects of trauma management?

Answer 230

ABCDE approach. Tension pneumothoraces will deteriorate with vigorous ventilation attempts. External haemorrhage is managed as part of the primary survey. As a rule tourniquets should not be used. Blind application of clamps will tend to damage surrounding structures and packing is the preferred method of haemorrhage control. Urinary catheters and naso gastric tubes may need inserting. Be wary of basal skull fractures and urethral injuries. Patients with head and neck trauma should be assumed to have a cervical spine injury until proven otherwise.

Question 231

Patients with head and neck trauma should be assumed to have what until proven otherwise?

Answer 231

C-spine injury GOLD is to neck CT

Question 232

Trauma= what will deteriorate with vigorous ventilation attempts?

Answer 232

tension pneumothorax

Question 233

Trauma Mx= types of Thoracic injuries?

Answer 233

Simple pneumothorax Mediastinal traversing wounds Tracheobronchial tree injury Haemothorax Blunt cardiac injury Diaphragmatic injury Aortic disruption Pulmonary contusion

Question 234

Mx of thoracic trauma= simple pneumothorax?

Answer 234

insert chest drain. Aspiration is risky in trauma as pneumothorax may be from lung laceration and convert to tension pneumothorax.

Question 235

Mx of thoracic trauma= Mediastinal traversing wounds?

Answer 235

These result from situations like stabbings. Exit and entry wounds in separate hemithoraces. The presence of a mediastinal haematoma indicates the likelihood of a great vessel injury. All patients should undergo CT angiogram and oesophageal contrast swallow. Indications for thoracotomy are largely related to blood loss.

Question 236

thoracotomy?

Answer 236

surgical procedure that involves making an incision in the chest wall to access the lungs or other organs. It's a major operation that's usually only performed in serious cases

Question 237

Mx of thoracic trauma= Tracheobronchial tree injury?

Answer 237

Unusual injuries. In blunt trauma most injuries occur within 4cm of the carina. Features suggesting this injury include haemoptysis and surgical emphysema. These injuries have a very large air leak and may have tension pneumothorax.

Question 238

Mx of thoracic trauma= haemothorax?

Answer 238

Usually caused by laceration of lung vessel or internal mammary artery by rib fracture. Patients should all have a wide bore 36F chest drain. Indications for thoracotomy include loss of more than 1.5L blood initially or ongoing losses of >200ml per hour for >2 hours.

Question 239

Mx of thoracic trauma= Cardiac contusions?

Answer 239

Usually cardiac arrhythmias, often overlying sternal fracture. Perform echocardiography to exclude pericardial effusions and tamponade. Risk of arrhythmias falls after 24 hours.

Question 240

Contusion?

Answer 240

bruise

Question 241

Mx of thoracic trauma= Diaphragmatic injury?

Answer 241

Usually left sided. Direct surgical repair is performed.

Question 242

Mx of thoracic trauma= Traumatic aortic disruption?

Answer 242

Commonest cause of death after RTA or falls. Usually incomplete laceration near ligamentum arteriosum. All survivors will have contained haematoma. Only 1-2% of patients with this injury will have a normal chest x-ray.

Question 243

ligamentum arteriosum?

Answer 243

a fibrous band that connects the aorta to the pulmonary artery. It's a remnant of a blood vessel that shunts blood from the lungs to the body before birth.

Question 244

Mx of thoracic trauma= Pulmonary contusion?

Answer 244

Common and lethal. Insidious onset. Early intubation and ventilation.

Question 245

Causes of abdominal trauma?

Answer 245

Deceleration injuries are common. In blunt trauma requiring laparotomy the spleen is most commonly injured (40%) Stab wounds traverse structures most commonly liver (40%) Gunshot wounds have variable effects depending upon bullet type. Small bowel is most commonly injured (50%) Patients with stab wounds and no peritoneal signs- up to 25% will not enter the peritoneal cavity Blood at urethral meatus suggests a urethral tear High riding prostate on PR = urethral disruption Mechanical testing for pelvic stability should only be performed once

Question 246

High riding prostate on PR =

Answer 246

urethral disruption

Question 247

Blood at urethral meatus suggests...

Answer 247

a urethral tear

Question 248

In blunt trauma requiring laparotomy the ... is most commonly injured (40%)

Answer 248

spleen

Question 249

Stab wounds transverse structures, most commonly...

Answer 249

liver (40%)

Question 250

What injuries are common in abdo trauma?

Answer 250

deceleration injuries

Question 251

Ix in abdo trauma= diagnostic peritoneal lavage?

Answer 251

Indication= Document bleeding if hypotensive Early diagnosis and sensitive; 98% accurate Invasive and may miss retroperitoneal and diaphragmatic injury

Question 252

Ix in abdo trauma= Abdominal CT scan?

Answer 252

Indication= Document organ injury if normotensive Most specific for localising injury; 92 to 98% accurate Location of scanner away from facilities, time taken for reporting, need for contrast

Question 253

Ix in abdo traum= USS?

Answer 253

Indication= Document fluid if hypotensive Early diagnosis, non invasive and repeatable; 86 to 95% accurate Operator dependent and may miss retroperitoneal injury

Question 254

What may be normal following pancreatic trauma?

Answer 254

amylase

Question 255

Ix in abdo trauma= what if suspected urethral injury?

Answer 255

urethrography

Question 256

Ix in abdo trauma= name 4?

Answer 256

Diagnostic Peritoneal Lavage = Document bleeding if hypotensive Abdominal CT scan= Document organ injury if normotensive USS= Document fluid if hypotensive Urethrography= suspected urethral injury

Question 257

There are various complications associated with admission and treatment on ICU. These include:

Answer 257

Ventilator-associated lung injury Ventilator-associated pneumonia Catheter-related bloodstream infections (e.g., from central venous catheters) Catheter-associated urinary tract infections Stress-related mucosal disease (erosion of the upper gastrointestinal tract) Delirium Venous thromboembolism Critical illness myopathy Critical illness neuropathy

Question 258

Multiple organ dysfunction syndrome (MODS)?

Answer 258

progressive organ dysfunction whereby homeostasis cannot be maintained without intervention. also known as multi-organ failure (MOF), is a severe clinical syndrome that is seen in critically ill patients.

Question 259

Multiple organ dysfunction syndrome (MODS) is common in what setting?

Answer 259

intensive treatment unit (ITU) setting and usually present at the time of ITU admission and/or at the time of death

Question 260

Multiple organ dysfunction syndrome (MODS) types?

Answer 260

primary and secondary

Question 261

Primary Multiple organ dysfunction syndrome (MODS)?

Answer 261

direct, identifiable injury (e.g. liver failure due to a hepatotoxic agent)

Question 262

Secondary Multiple organ dysfunction syndrome (MODS)?

Answer 262

no direct attributable cause. Due to host response to an injury (e.g. severe bacterial sepsis)

Question 263

Multi-organ dysfunction syndrome is commonly the result of what?

Answer 263

sepsis

Question 264

Multi-organ dysfunction syndrome represents what?

Answer 264

the end stage of a severe illness, which may be infectious or non-infectious: Infectious (e.g. bacterial sepsis, severe COVID-19) Non-infectious (e.g. necrotising pancreatitis, thyroid storm)

Question 265

Multi-organ dysfunction syndrome pathophysiology?

Answer 265

complex process and the exact underlying mechanisms remain unknown. However, it is suggested that MODS is the result of a proinflammatory response with the release of many immunological mediators (e.g. tumor necrosis factor-α and interleukin (IL)-1β) that promote inflammation and leads to organ dysfunction. This overwhelming immune response causes free radicals to be generated that can damage tissue, as well as promoting hypoperfusion and hypoxia that further cause cellular damage.

Question 266

Multi-organ dysfunction syndrome diagnosis?

Answer 266

Scoring systems are used to help define organ dysfunction in the setting of MODS.

Question 267

There is no universal definition for individual organ dysfunction in MODS, which is broadly defined as?

Answer 267

dysfunction of ≥2 organs that occurs simultaneously. Consequently, scoring systems have been derived in an attempt to categorise and diagnose the organ dysfunction in MODS.

Question 268

Scoring system to help define organ dysfunction in multi-organ dysfunction syndrome?

Answer 268

Sequential Organ Failure Assessment (SOFA) score.

Question 269

Sequential Organ Failure Assessment (SOFA) score to help define organ dysfunction in multi-organ dysfunction syndrome looks at what parameters to determine the presence and severity?

Answer 269

Respiratory dysfunction: Pa02, Fi02, need for ventilation Cardiovascular dysfunction: Blood pressure, need for inotropes Renal dysfunction: Acute kidney injury Haematological dysfunction: Platelet count, coagulation Liver dysfunction: Bilirubin Neurological dysfunction: Glasgow coma score

Question 270

Tx for multi-organ dysfunction syndrome?

Answer 270

No specific Tx. Management of MODS largely comprises organ support in an ITU setting with the treatment of the underlying disease process and any secondary complications (e.g. secondary infection). Scoring systems used to help define organ dysfunction may also be used to help predict mortality and can be sequentially monitored to provide prognostic information.