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Surgery > Peri-operative care > Flashcards

Peri-operative care Flashcards

1
Q

Definition of acute respiratory distress syndrome

A

Acute lung injury characterised by severe hypoxaemia in the absence of cardiogenic cause.
Criteria:
Acute onset within 7 days
PaO2:FiO2 ratio <300mmHg
Bilateral infiltrates on CXR
Alveolar oedema not explained by fluid overload or cardiogenic cause

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2
Q

Causes of acute respiratory distress syndrome

A

Direct causes: pneumonia, smoke, aspiration, fat embolus

Indirect causes: sepsis, acute pancreatitis, polytrauma

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3
Q

Pathophysiology of acute respiratory distress syndrome

A

Injury to the lung -> inflam -> breakdown of alveolar-capillary barrier -> fluid infiltration and pulm oedema -> impaired ventilation and gas exchange -> hypoxia.

Damage to type II alveolar cells -> reduced surfactant production -> reduced lung compliance which worsens ventilation

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4
Q

Clinical features of acute respiratory distress syndrome

A

Worsening dyspnoea, hypoxia, tachycardia, tachypnoea, inspiratory crackles on auscultation

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5
Q

Investigations for acute respiratory distress syndrome

A

Routine bloods (FBC, U+E, amylase, CRP)
Blood cultures
ABG
CXR (diffuse bilateral infiltrates similar to that of pulm oedema)

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6
Q

Management of acute respiratory distress syndrome

A

Supportive treatment with ventilation (most require ITU support, CPAP, etc)
Focused treatment of underlying cause
Circulatory support (inotropes, vasodilators)

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7
Q

What is post-op atelectasis ?

A

Partial collapse of the small airways. Typically occurs <24hrs post-op

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8
Q

Pathophysiology of atelectasis

A

Combination of airway compression, alveolar gas resorption intra-operatively and impairment of surfactant production
Atelectasis causes reduced airway expansion and subsequent accumulation of pulmonary secretions -> predisposes the patient to hypoxia, reduced lung compliance, pulm infection and acute respiratory failure

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9
Q

Risk factors for atelactisis

A

Age, smoking, general anaesthesia, duration of surgery, pre-existing lung/neuromuscular disease, porlonged bed rest, poor post-op pain control (= shallow breathing)

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10
Q

Clinical features of atelectasis

A

Varying degree of respiratory compromise
Tachypnoea
Reduced O2 sats

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11
Q

Investigations for atelectasis

A

Typically a clinical diagnosis (= new resp symptoms <24hrs post-op)
CXR may reveal small areas of airway collapse
CT may be done is CXR unhelpful (rare)

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12
Q

Management and prevention of atelectasis

A

Deep breathing exercises
Chest physiotherapy
Analgesia
Prevention = chest physiotherapy post-op

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13
Q

Post-op pneumonia (hospital acquired pnuemonia) aetiology

A

reduced mobility/bedridden -> inability to fully ventilate lungs -> accumulation of secretions -> infection
Hospital environment flora different to what patient is used to (E coli, S aureus, S pneumonia, Pseudomonas)
Surgical patients often have multiple comorbidities, compromising their immune system
Patients may require ITU intubation and ventilation which is a major risk factor

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14
Q

Risk factors for post-op pneumonia

A

Age, smoking, known respiratory disease or recent viral illness, poor mobility, mechanical ventilation, immunosuppression, underlying comorbidities

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15
Q

Differential diagnoses for pneumonia

A

Acute heart failure, acute coronary syndrome, PE, Asthma/COPD exacerbation, pleural effusion, empyema, anxiety

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16
Q

Investigations for pneumonia

A

Routine bloods (FBC, U+E, CRP), blood cultures, ABG (if sats are very low), sputum sample if cough is productive, CXR (consolidation with air bronchograms)

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17
Q

Management of post-op pneumonia

A

O2 (aim for 94%+, or 88-92% if CO2 retainers)
Manage any sepsis
Empirical antibiotics until sensitivities return (first-line co-amoxiclav or doxycycline, if severe/septic use tazocin, if MRSA use vancomycin)

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18
Q

Complications of pneumonia

A

Pleural effusion
Empyema
Respiratory failure
Sepsis

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19
Q

Risk factors for aspiration pneumonia in surgical patients

A

reduced GCS, iatrogenic interventions (eg. NG misplacement), prolonged vomiting without NG, underlying neuro condition, oesophageal stricture/fistula, post-abdo surgery

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20
Q

Virchow’s triad

A

Abnormality of blood flow (stasis) - immobility
Abnormality of blood components (hypercoagulability) - smoking, sepsis, malignancy, inherited disorder
Abnormality of vessel wall (endothelial damage) - atheroma, inflammation, direct trauma

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21
Q

Risk factors of VTE

A

Age, previous VTE, smoking, pregnancy, current active malignancy, COCP/HRT, immobility >3 days, recent surgery, inherited thrombophilia (factor V leiden, antiphospholipid syndrome), obesity

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22
Q

Management of VTE

A

DOAC first line - Factor Xa inhibitors (apixaban, rivaroxaban) or direct thrombin inhibitors (dabigatran). Dabigatran needs 5 days of LMWH before starting DOAC.
Some patients require warfarin instead of DOAC (needs LMWH until INR target is reached)
LMWH alone is recommended in cancer-associated VTE

Anticoagulation required for 3 months if provoked VTE. May require lifelong if proximal/persistent/high risk

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23
Q

Mechanical vs pharmacological thromboprophylaxis

A

Mechanical: Intermittent pneumatic compression (used in theatre), TED stockings (contraindicated in peripheral arterial disease, peripheral oedema, local skin conditions)

Pharmacological: LMWH (if eGFR<30 consider unfractionated heparin)

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24
Q

DVT clinical features

A

unilateral leg pain, swelling, erythema, warmth
Low grade pyrexia
Pitting oedema
Tenderness or prominent superficial veins
65% asymptomatic

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25
Q

Investigations for DVT

A

DVT Well’s score should be calculated
Score <= 1: DVT unlikely. Do D-Dimer to exclude.
Score >1: DVT likely. Do USS doppler to confirm.

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26
Q

Well’s Score

A 
Clinical signs
Heart rate >100
Recent surgery/immobilisation
Previous PE/DVT
Haemoptysis
Malignancy
Alternative diagnosis less likely than PE/DVT
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27
Q

PE clinical features

A 
Sudden onset dyspnoea
Pleuritic chest pain
Cough
Haemoptysis (rare)
Tachycardia
Tachypnoea
Pyrexia
Raised JVP (rare)
Pleural rub/ pleural effusion (rare)
Remember to examine for DVT
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28
Q

Investigations for PE

A

Calculate PE Well’s score
Score <=4: PE unlikely, D-dimer to exclude
Score >4: PE likely, CTPA to confirm (V/Q scan if poor renal function)

CXR to exclude other pathology
ECG to exclude MI

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29
Q

ECG changes for PE

A 
RBBB
RV strain (Inverted T waves V1-V4)
Rare S1Q3T3 (deep S wave lead 1, pathological Q wave lead 3, inverted T wave lead 3)
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30
Q

Surgical causes of hyperkalaemia

A

Post-op AKI
Repeated blood transfusions
Drugs (K+ sparing diuretics, ACE-I, ARB), excessive K+ treatment, dehydration, pre-existing conditions (addison’s)

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31
Q

Clinical features of hyperkalaemia

A

Asymptomatic, paraesthesia, muscle weakness, N+V, arrhythmias

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32
Q

Investigations of hyperkalaemia

A

Routine bloods (U+E, calcium and phosphate, magnesium), VBG (immediate K+ levels)< ECG, catheterisation (fluid balance), review obs/fluid status/medications

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33
Q

ECG changes with hyperkalaemia

A

Tall tented T waves, flattened P waves, QRS lengthening, heart block, BBB, axial deviation, sine wave, VF/asystole

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34
Q

Management of hyperkalaemia

A

Regular bloods and ECG monitoring
Alert senior +/- HDU support
Myocardium stabilisation (10ml 10% calcium gluconate) if ECG changes present or if mod/severe. Continuous cardiac monitoring required during calcium gluconate treatment.
Variable rate insulin with dextrose infusion (200ml 20% dectrose with insulin over 30 mins) to drive K+ intracellularly.
Salbutamol nebs to drive K+ intracellularly.
Oral calcium resonium to drive K+ into the bowel and out of the body.
Haemodialysis to drive K+ out of the body

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35
Q

Causes of hypokalaemia

A

Excess loss:
GI - vomiting, diarrhoea, distulae, laxative abuse
Urinary - diuretics, excess mineralocorticoid (Conn’s, cushing’s), hypomagnesaemia, polyuria, renal tubular acidosis
Skin - burns, excess sweating

Inadequate intake - malnutrition, inadequate IV K+

Intracellular shifts:
Alkalosis (H+ shifts out of cell to buffer pH and K+ shifts into cell to buffer electrical charge across membrane)
Excessive insulin (increased NaKATPase shifts K+ into cell)
Excessive beta agonists (salbutamol) increase NaKATPase

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36
Q

Clinical features of hypokalaemia

A

Asymptomatic
Muscle weakness, paraesthesia, ileus/pseudo-obstruction, hypotonia, hyporeflexia, hcramps, tetanus, resp failure, arrhythmia

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37
Q

ECG changes in hypokalaemia

A 
Cardiac hyperexcitability (re-entrant loops)
Elongated PR interval 
T wave flattening/inversion
Prominent U wave
ST depression
VT/VF
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38
Q

Investigations of hypokalaemia

A

ECG
Bloods (FBC, U+E, calcium and phosphate, magnesium)
VBG

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39
Q

Management of hypokalaemia

A

Treatment of underlying cause
If mild without ECG changes give oral Sando-K
If mod-severe with ongoing losses or unable to take oral give IV K+ replacement
IV K+ can normally be given at max 10mmol/hr, if aggressive replacement required consider central line
Regular bloods should occur during K+ replacement

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40
Q

Causes of hypernatraemia

A

Hypovolaemic - diuretics (loop), dehydration (diarrhoea, vomiting, burns, sweating), acute tubular necrosis, hyperosmolar hyperglycaemic state

Euvolaemic - diabetes insipidus

Hypervolaemic - excess hypertonic saline administration, steroid excess (conns, cushings)

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41
Q

Clinical features of hypernatraemia

A

Asymptomatic
Excessive thirst (due to thirst response, plus rise in Na+ drives fluid extracellularly)
Weakness
Lethargy
Confusion
If >180 –> ataxia, tremor, coma, seizure

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42
Q

Investigations for hypernatraemia

A

Bloods (glucose, U+Es)
ABG/VBG
Urine osmolality (hypertonic urine indicates vomiting/burns/diarrhoea, isotonic urine indicates diuretics, hypotonic urine indicates diabetes insipidus)
ADH levels and CT head may be needed to assess pituitary

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43
Q

Diabetes insipidus

-what is it, two different types, clinical features, investigations

A

Excessive excretion of dilute urine and increased thirst response
Cranial DI - impaired ADH secretion from posterior pituitary (post-pituitary surgery, or post-head injury)
Nephrogenic DI - impaired response to ADH
Clinical features - polyuria and compensatory polydipsia
Investigations - water deprivation test (pt deprived of fluids for 8 hours, urine osmolality checked, then desmopressin given, then urine osmolality checked again)

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44
Q

Management of hypernatraemia

A

Replace fluid deficit (enteral fluid replacement preferred, but if not possible 5% dextrose is preferred IV)
Correct serum sodium (dont correct too rapidly due to risk of cerebral oedema)
Manage underlying cause

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45
Q

Causes of hypo-osmotic hyponatraemia

A

Hypovolaemic - vomiting, diarrhoea, diuretic
Euvolaemic - acute fluid overload, SIADH
Hypervolaemic - CCF, liver failure, acute tubular necrosis

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46
Q

What are the complications post-op of hyponatraemia

A

hyponatraemia causes low plasma osmolality resulting in fluid shifting intracellulary -> cellular swelling/oedema
Tissue oedema impairs healing of wounds/anastamoses
Can also cause cerebral oedema and raised ICP

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47
Q

Why is hyponatraemia common post-op?

A

As part of the stress response, the hypothalamus and posterior pituitary produce cortisol and ADH –> increased free water resorption in excess of sodium –> hyponatraemia
Surgical patients also receive a lot of IV fluids, if the fluids are mostly dextrose there will be a dilutional effect on the sodium conc

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48
Q

Clinical features of hyponatraemia

A

Asymptomatic
Malaise, headache, confusion, LOC, seizures
Central pontine myelinolysis

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49
Q

Central pontine myelinolysis

A

In chronic hyponatraemic patients if there is a rapid sodium correction there will be a large change in extracellular osmolarity -> causes damage to myelin sheaths of the nerves to the brainstem -> confusion, balance problems, pseudobulbar palsy, quadriplegia
Diagnosed via MRI head. No cure.

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50
Q

Management of hyponatraemia

A 
Fluid balance (fluid monitoring +/- catheterisation)
IV fluids (0.9% saline) preferred over enteral replacement
Monitor renal function and electrolyte levels regularly
Urine osmolality and sodium conc may be required.

Dont increase sodium levels too rapidly due to risk of central pontine myelinolysis

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51
Q

Risk factors for hypoglycaemia

A

Overdose of insulin/hypoglycaemics
Diabetes mellitus
Post-gastrectomy/gastric bypass (lack of ghrelin which usually suppresses insulin)
Alcohol excess (reduced liver function -> reduced gluconeogenesis)
Renal dialysis (reduced clearance of insulin, reduced gluconeogensis, increased insulin sensitivity)
Beta blockers (inhibition of hepatic gluconeogenesis)
Decompensated liver disease (reduced gluconeogenesis)
Adrenal insufficiency/Addisons (low adrenaline/cortisol -> increased sensitivity to insulin)

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52
Q

Clinical features of hypoglycaemia

A

Sweating, tingling lips/extremeties, tremor, dizziness, slurred speech, confusion, tachycardia, tachypnoea, focal neurology/reduced conciousness

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53
Q

Management of hypoglycaemia

A

If conscious give 10g glucogel PO, then complex carbs and regular monitoring of BMs
If unconscious give IV glucose 100ml 20% over 5-15 mins. If unable to gain IV access give IM glucagon

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54
Q

Whats the pathophysiology of haemolytic disease of the newborn

A

RhD- female becomes exposed to RhD antigens (previous RhD+ pregnancy or previous blood transfusion) and creates anti-D antibodies. Female then becomes pregnant with RhD+ foetus. Mum’s anti-D antibodies cross the placenta and attack the foetus RBCs causing foetal anaemia

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55
Q

ABO blood grouping universal donor

A

O-

doesnt have any A/B/rhesus antigens on the RBC surface so nothing for the recipient to attack

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56
Q

ABO blood grouping universal recipient

A

AB+
Has all of the A, B and rhesus antigens in their circulation already so wont create any antibodies against the donor blood

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57
Q

Indications for CMV neg blood products

A

Pregnant women, intra-uterine transfusions, neonates (<28 days)
Because of risk of congenital cytomegalovirus

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58
Q

Indications for irradiated blood products

A

(treated with X-Rays to prevent remaining WBCs from dividing, reduces risk of GVHD).
Hodgkins lymphoma, intra-uterine transfusion, recent stem cell transplant, on chemo, if receiving blood from first/second degree fam members

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59
Q

Procedure for blood transfusion

A

3 points of identification
Gain consent
Label the bottles (handwrite) at bedside
Complete transfusion request form at bedside
Prescribe each unit individually
Specific observations before transfusion, at 15 mins, at 1 hours, at completion
Transfuse with green or grey cannula

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60
Q

Packed red cells

  • indications
  • duration of administration
  • how much it increases Hb by
A

Indications: acute blood loss, chronic anaemia (if symptomatic, if Hb<70 or <80 if cardiovascular disease)
Administered over 2-4 hours. Must be complete within 4 hours of coming out of store
1 unit increases Hb by 10

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61
Q

Platelets

  • Indications
  • Duration of administration
  • How much it increases platelets by
A

Indicated in haemorrhagic shock in a trauma patient, profound thrombocytopaenia (<10), bleeding with thrombocytopaenia (<30), or if pre-operative platelet level <50
Administered over 30 minutes
1 adult therapeutic dose should increase platelets by 20-40

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62
Q

Fresh frozen plasma

  • what does it contain
  • indications
  • duration of administration
A

consists mostly of clotting factors
indicated in DIC, and haemorrhage secondary to liver disease, all massive haemorrhage (usually after 2nd RBCs)
Administered over 30min

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63
Q

Cryoprecipitate

  • what does it contain
  • indications
  • duration of administration
A

Mostly contains fibrinogen, von willebrand factor, factor VIII and fibronectin
Indicated in DIC with low fibrinogen (<1g/L), vvWF disease, or massive haemorrhage
Administer stat

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64
Q

Fluid and electrolyte daily requirements for an adult

A

25ml/kg/day water
1mmol/kg/day sodium
1mmol/kg/day potassium
50g/day glucose

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65
Q

Hierarchy of feeding

A

insufficient calories -> oral nutritional supplements (ONS)
insufficient calories orally/dysfunctional swallow -> NG
Blocked/ dysfunctional oesophagus -> gastrostomy (PEG/RIG)
Stomach inaccessible/ outflow obstruction -> jejunostomy
Jejunum inaccessible/ intestinal failure -> parenteral nutrition

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66
Q

Peri-op nutrition advice

A

Reduce NBM time (6hrs for food and drink, 2 hours for clear fluid), pre-op loading, minimise drains and NG, rapid reintroduction of feeding post-op

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67
Q

Drugs to stop before surgery

A

(CHOW)
Clopidogrel 7 days before
Hypoglycaemics
Oral contraceptive pill/HRT 4 weeks before
Warfarin 5 days before and switch to LMWH

Ramipril stop 24 hours before (?)

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68
Q

Drugs to alter

A

Switch SC insulin to VRIII

Increase steroids and consider switching to IV

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69
Q

Drugs to start

A

LMWH
TED stockings
Antibiotic prophylaxis for orthopaedic, vascular and GI surgery

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70
Q

T1DM insulin management peri-op

and T2 insulin controlled

A

Put patient first on morning list
night before reduce SC basal insulin by 1/3
Omit morning insulin and commence VRIII
Whilst NBM give IV 5% dextrose and check BMs every 2hrs
Once eating and drinking, restart insulin with VRIII overlap. Give rapid acting insulin 20 mins before meal then stop VRIII 30-60 mins after meal

71
Q

T2DM management peri-op

if diet controlled and if on oral hypoglycaemics

A

diet controlled - no change
metformin - stop morning of
Other oral hypoglycaemics - stop 24hr before

72
Q

ASA grade

A

1 - normal healthy patient (0.1% mortality)
2 - mild systemic disease (0.2% mortality)
3 - severe systemic disease (1.8%)
4 - severe systemic disease constant threat to live (7.8%)
5 - moribund unexpected to survive without the op (9.4%)

73
Q

Pre-op investigations

A

Bloods - FBC, U+E, LFT, clotting screen, G+S, Xmatch
Imaging (if applicable) - ECG, echo, chest X-ray
Other tests - pregnancy test, sickle cell test (if applicable), MRSA swabs, urinalysis

74
Q

Clinical features of anaphylaxis

A

Hypotension unresponsive to IV fluid challenge, airway compromise (wheeze, stridor, desaturation), facial angioedema, urticarial rash, feeling of impending doom

75
Q

Pathophysiology of anaphylaxis

A

Allergen that has previously been encountered and sensitised to is re-introduced to the body -> binds to mast cells -> activates inflamm response -> releases histamine into tissues and blood -> systemic reaction.
Histamine is a vasodilator -> tissue oedema (-> airway obstruction) and hypotension (-> hypoperfusion of vital organs)

76
Q

Emergency drugs of anaphylaxis

A

IM adrenaline 1:1000 0.5mg
IV/IM chlorphenamine 10mg
IV hydrocortisone 200mg

77
Q

ABC for anaphylaxis

A

A - fast bleep on-call anaesthetist, ?nasopharyngeal airway or tracheal intubation depending on level of obstruction
B - 15L high flow O2 non-rebreathe, neb salbutamol and/or ipratropium
C - 2 large bore cannulae, routine bloods plus mast cell tryptase, fluid boluses, emergency drugs (adrenaline, chlorphenamine, hydrocortisone)

78
Q

Serum mast cell tryptase levels should be taken when?

A

As soon as possible after emergency treatment
then 1-2 hours after onset of symptoms
then >24 hours after event

79
Q

General complications specific to packed red cell transfusion

A

Clotting abnormalities due to dilutional effect as RBCs have no platelets or clotting factors. Reduce risk by giving FFP and platelets after 4 units of RBC.
Hypocalcaemia due to calcium binding agents in the preservative.
Hyperkalaemia due to partial haemolysis of RBCs releasing K+.
Hypothermia due to RBCs being stored in fridge and may not have time to warm up before administration.

80
Q

Acute haemolytic reaction

A

ABO incompatibility. Donor RBCs are destroyed by recipient antibodies causing haemolysis. –> urticaria, hypotension, fever, haemoglobinuria.
low Hb, low haptoglobin, high LDH, high bilirubin, positive direct antiglobulin test.
Urgently inform blood bank, stop transfusion, supportive measures, seek help.

81
Q

Transfusion associated circulatory overload

A

Due to fluid overload, esp in heart failure
Causes dyspnoea, peripheral/sacral/pulm oedema, etc.
Needs urgent CXR
Treat with high flow O2 and diuretics.
High risk patients may be given 20mg furosemide during transfusion prophylactically

82
Q

Transfusion related acute lung injury

A 
A form of ARDS
Causes dyspnoea and pulm oedema
High mortality
Urgent CXR needed
High flow oxygen, specialist advice and ITU input
83
Q

Acute complications of transfusions

A

Acute haemolytic reaction
TACO
TRALI
Mild allergic reaction (give chlorphenamine, continue transfusion once symptoms better)
Non-haemolytic febrile reaction (stop transfusion,give paracetamol and chlorphenamine)
Anaphylaxis - stop transfusion and treat
Infective/bacterial shock - stop transfusion, treat as sepsis

84
Q

Delayed transfusion complications

A

Infection (hep b, hep c, syphilis, HIV, malaria, vCJD)
Graft vs host disease
Iron overload

85
Q

Iron overload with blood transfusion

A

More common in repeated blood transfusions (thalassaemia)
Builds up in liver (cirrhosis), pancreas (bronze diabetes), heart (cardiomegaly, conduction disturbance), joints (arthralgia), skin (hyperpigmentation)

86
Q

Graft vs host disease

A

Due to HLA mismatch between donor and recipient. give irradiated blood to immunocomp patients.
symptoms range - fever, rash, toxic epidermal necrolysis, diarrhoea, vomiting

87
Q

Three types of delirium

A

Hypoactive (most common) - lethargy and reduced motor activity
Hyperactive (most recognised) - agitation and increased motor activity
Mixed agitation - fluctuations throughout the day

88
Q

Risk factors for delirium

A

age>65, multiple comorbidities, underlying dementia, renal impairment, male, sensory impairment (hearing, visual)

89
Q

Causes fo delirium

A

hypoxia, infection, drugs (benzos, diuretics, steroids, opioids), drug withdrawal (alcohol, benzos), dehydration, pain, constipation, urinary retention, hyponatraemia, hypernatraemia, hypercalcaemia

90
Q

Investigations for delirium

A

Bloods (FBC, U+E, calcium, TFTs, glucose, B12, folate)
Blood cultures and/or wound cultures
Urinalysis and.or CXR
CT head (if relevent)

91
Q

Assessment of delirium

A

Collateral history
Abbreviated mental test, MMSE, confusional assessment method (CAM)
Review obs/drugs chart
Neuro exam to exclude pathology

92
Q

Management of delirium

A

Treat underlying cause
Quiet environment, regular routines, clocks in room
Encourage oral intake
Analgesia
Monitor bowels
Sedation not advised unless necessary (haloperidol PO first line)

93
Q

Classification of post-op haemorrhage

A

Primary bleed – occurs intra-op, should be resolved during the op
Reactive bleed – <24hrs post-op, usually from ligature that slips or a missed vessel (not noticed intra-op due to hypotension and vasoconstriction)
Secondary bleed – 7-10 days after, often due to vessel erosion from infection

94
Q

Management of post-op haemorrhage

A

A-E -> IV access (at least 18G cannula), rapid IV resus
Read operation notes
Direct pressure should be applied to the bleeding site
Urgent senior surgical review and appropriate imaging
Urgent blood transfusion in mod-severe post-op haemorrhage
If severe activate major haemorrhage protocol-> RBCs, plts, and FFP
May be appropriate to re-operative

95
Q

Post-op haemorrhage with neck surgery

A

Caution with thyroidectomy/ parathyroidectomy
Post-op haemorrhage causes airway obstruction because the pretracheal fascia can only distend a limited amount -> compression on venous return -> venous congestion -> laryngeal oedema -> asphyxiation
Any evidence of respiratory distress/ compromise requires emergency airway rescue – remove both skin clips and deep layer sutures, and suction the haematoma
Urgent senior surgical opinion and anaesthetist review

96
Q

Inferior epigastric artery injury

A

Arises from the external iliac artery, and runs vertically up the abdominal wall below the rectus muscle (approx. mid clavicular line)
Vulnerable to injury from laparoscopic surgery or pfannenstiel incision
May not be noticed during surgery due to gas insufflation

97
Q

Retroperitoneal bleeding post-angiography

A

Entry site for angiography is usually in groin (external iliac artery, above iliac ligament)
Any bleeding from this artery will go into the retroperitoneum
Unlikely be a large haematoma as it is hidden by the iliac ligament, and patients may bleed profusely because tamponading the injury is difficult
Apply pressure to the puncture side, resus the patient, ensure blood products are available immediately and call for senior support

98
Q

Risk factors for post-op N+V

A

Patient factors – female, age (incidence declines throughout adult life), previous PONV/motion sickness, use of opioids, non-smoker
Surgical factors – intra-abdominal laparoscopic surgery, intracranial or middle ear surgery, squint surgery, gynae surgery, prolonged op times, poor pain control
Anaesthetic factors – opiates, spinal anaesthesia, inhalational agents, prolonged anaesthetic time, intra-op dehydration or bleeding, over use of bag and mask ventilation (causes gastric dilatation)

99
Q

Pathophysiology of N+V

A

Vomiting centre in the medulla oblongata controls and coordinates the movements involved in vomiting
Chemoreceptor trigger zone in the postrema (inferoposterior aspect of the 4th ventricle), located outside the BBB and responds to stimuli in circulation
The vomiting centre receives input from the CTZ, GI tract, vestibular system and higher cortical structures (sight, smell, pain) -> acts on the diaphragm, stomach and abdo muscles -> initiates vomiting

100
Q

Neurotransmitters involved in N+V

A

Chemoreceptor trigger zone – dopamine and serotonin
Vestibular apparatus – acetylcholine and histamine
GI tract – dopamine
Vomiting centre – histamine and serotonin

101
Q

Alternative causes of N+V in post-op patients

A 
Infection
GI causes (post-op ileus, bowel obstruction)
Metabolic (hypercalcaemia, uraemia, DKA)
Medication (antibiotics, opioids)
CNS causes (↑ ICP)
Psychiatric causes (anxiety)
102
Q

Management of post-op N+V

A

Conservative management – Adequate fluid hydration, Adequate analgesia, Ensure no obstructive cause

Pharmaceutical management –
Impaired gastric emptying/stasis (NOT bowel obstruction) -> use a prokinetic agent like metoclopramide (D2 antagonist) or domperidone (D2 antagonist)
Bowel obstruction -> hyoscine (anti-muscarinic) can reduce secretions and subsequent N+V
Metabolic/biochemical imbalances (uraemia, electrolyte imbalance, cytotoxic agents, etc) -> metoclopramide
Opioid-induced N+V -> ondansetron (serotonin antagonist), cyclizine (antihistamine)

103
Q

Prophylaxis of post-op N+V

A

reduce opiates, reduce volatile gases, avoid spinal anaesthesia, prophylactic antiemetics, dexamethasone at induction of anaesthesia

104
Q

Side effects of NSAIDs

A

(I GRAB)
Interactions with other medications (warfarin, eg)
Gastric ulceration (consider PPIs when prescribing long-term NSAIDs)
Renal impairment (use NSAIDs sparingly in those with AKI/CKD)
Asthma sensitivity (occurs in 10% of asthmatics)
Bleeding risk (due to reduced platelet function)

105
Q

Side effects of opiates

A

Most patients will experience constipation and nausea -> prescribe anti-emetics and laxatives concurrently
Other side effects may include sedation, confusion, resp depression, pruritis, tolerance and dependence

106
Q

Advantages of patient controlled analgesia

A

provides analgesia that is tailored to patient’s needs, risk of overdose is negligible, can accurately record how much opioid is being administered which can be converted to a regular dose

107
Q

Disadvantages of patient controlled analgesia

A

can be cumbersome and prevent patient mobilising, not appropriate for those with poor manual dexterity or learning difficulties

108
Q

Non-pharmacological and pharmacological management of neuropathic pain

A

Non-pharmacological treatment – cognitive behavioural therapy, transcutaneous electric nerve stimulation (TENS), or capsaicin cream (localised pain)
Pharmacological treatment – gabapentin, amitriptyline, pregabalin

109
Q

Causes of pyrexia in a post-op patient

A 
Infection
iatrogenic
VTE
Secondary to prosthetic implantation
Pyrexia of unknown origin
110
Q

Septic screen for post-op patients with pyrexia

A 
Bloods - FBC, U+E, CRP
Urine dipstick
Cultures - blood, urine, sputum, wound swab
Imaging - CXR
Consider CT or dopper US
111
Q

Management of pyrexia in the post-op patient

A

Empirical abx if there is infection (don’t start abx if no infection is identified)
Treat sepsis accordingly
Antipyrexials
Analgesia
Ensure patient remains hydrates (increase obs and start a fluid balance chart)

112
Q

Criteria for sepsis diagnosis

A

Presence of known or suspected infection

Clinical features of organ dysfunction (qSOFA score)

113
Q

qSOFA score

A

Any patient with a known or suspected infection and a qSOFA score of 2 or more should be investigated and managed for sepsis
qSOFA criteria – resp rate >= 22/min, altered mental state, systolic BP =< 100

114
Q

Sepsis six

A

Involve seniors early, and ask nurse for hourly obs

Oxygen – 15L non-rebreathe (94-98%, or 88-92% in chronic retainers)
Blood cultures – prior to abx
IV empirical abx – switch to targeted therapy when sensitivities are available
IV fluid resuscitation – 500ml fluid bolus and ongoing fluid status assessment
Lactate – ABG, plus routine bloods (FBC, U+E, LFT, clotting, CRP, glucose)
Urine output – aim for >0.5ml/kg/hr. Catheterise if necessary

115
Q

Escalation of sepsis management (criteria and treatment)

A

Involve ITU/clinical outreach team if - evidence of septic shock (hypotension despite fluid resus), lactate >4, failure to improve from initial Mx

ICU can then give vasopressors/inotrops to increase BP (eg. noradrenaline), renal replacement therapy, ventilator support

116
Q

Which surgeries require only a G+S (no cross match)?

A

Hysterectomy, appendicectomy, thyroidectomy, elective lower segment C section, lap chole

117
Q

Which operations have a likely chance of transfusion and require 2 units cross match?

A

salpingectomy for ruptured ectopic, total hip replacement

118
Q

Which ops have a definite chance of transfusion and require 6 units crossmatch?

A

total gastrectomy, oophorectomy, elective AAA repair, cystectomy, hepatectomy

119
Q

What is an anastomotic leak?

A

Leak of luminal content from a surgical join. Most important complication to exclude following GI surgery

120
Q

Risk factors for anastamotic leak

A

Patient - corticosteroids, imunosuppressants, smoking, alcohol, DM, obesity, malnutrition
Surgical - emergency surgery, longer intra-op time, peritoneal contamination with pus/faeces/gi content, oesophageal-gastric or rectal anastomoses

121
Q

Clinical features of anastomotic leak

A

Abdo pain and fever (usually 5-7 days post op)
Delirium, prolonged ileus
Examination - pyrexia, tachycardia, peritonism (tender, tense, distension, guarding, N+V), check for faeculent/purulent material or bile in any drains

122
Q

Investigations for anastomotic leak

A 
Urgent bloods (FBC, CRP, U+E, LFT, clotting, G+S)
VBG for lactate
Definitive investigation is CT abdo pelvis with contrast
123
Q

Management of anastomotic leak

A 
Urgent senior review
NBM
Broad spectrum abx
Iv fluids
Urinary catheter and fluid balance chart
Definitive management - 
minor leaks (<5cm) can be managed conservatively with IV abx, large leaks may need to be drained percutaneously
If septic/multiple collections, exploratory laparotomy required with washouts and drain insertion (and stoma if colo-rectal anastomosis)
124
Q

Incisional hernia pathophysiology

A

Weakness in the anterior abdominal wall muscles due to disruption by surgical incision. If intra-abdo pressure rises of risk factors are present, the abdo content can herniate through the weakness. May cause complications -> incarceration (irreducible), strangulation (compromised blood flow), or bowel obstruction

125
Q

Risk factors for incisional hernia

A 
Emergency surgery (doubles the risk)
Wound type
BMI >25
Midline incision
Wound infection
Pre-op chemo
Intra-op blood transfusion
Advancing age
Pregnancy
less common - chronic cough, DM, steroids, smoking, connective tissue disease
126
Q

Clinical features of incisional hernia

A

Non-pulsatile, reducible, soft and non-tender swelling at or near the site of a previous surgical wound
Incarcerated hernia is painful, tender and erythematous
Bowel obstruction causes abdo distension, vomiting and/or absolute constipation
Strangulation causes bowel iscahemia (rebound tenderness, involuntary guarding)

127
Q

Investigations for incisional hernia

A

Clinical diagnosis
US or CT if diagnosis unclear
Investigations may be required if complications are suspected

128
Q

Management of incisional hernia

A

Majority are asymptomatic and can be managed conservatively
Surgery if hernia is painful and patient is clinically fit
Surgical repair - suture repair if small, laparoscopic mesh repair, or open mesh repair

129
Q

Prognosis of incisional hernia

A

Surgical repair often causes chronic pain (may also cause bowel injury, seroma)
Most hernias are asymptomatic life-long
about 10% incarcerate and 2% strangulate
They often come back after repair

130
Q

Causes of post-op constipation

A

Physiological - low fibre, poor fluid intake, low physical activity
Pathological - post-op ileus, obstruction, hypercalcaemia, hypothyroidism, neuromuscular
Iatrogenic - opioids, anticonvulsants, iron, antihistamines
functional - painful defaecation (eg. from anal fissures)

131
Q

Clinical features of post-op constipation

A

Lower abdo pain, abdo distension or tenderness, N+V, reduced appetite

DRE is essential to assess degree of faecal impaction

132
Q

Investigations for post-op constipation

A

Often a clinical diagnosis following DRE
Endoscopy if features of underlying sinister pathology
Routine bloods if no cause identified/resistant to treatment (inc TFT and calcium)
Imaging generally not needed

133
Q

Management of post-op constipation

A

Hydration, fibre, mobilisation, treat underlying cause
Laxatives -
If chronic with hard stool give an osmotic laxative (movicol) +/- glycerine suppository for the hard stool in the rectum
If soft stool (post-op ileus, opioid-induced) give stimulant (senna)

134
Q

Types of laxatives

A

Osmotics increase fluid in bowel which softens stool (lactulose, movicol, glycerin suppository)
Stimulants stimulate bowel contractions to expel stool (senna, sodium picosulfate, phosphate enema)
Bulk forming laxatives help stool to retain water, softening the stool (ispaghula husk)

135
Q

What is post-op ileus

A

Functional bowel obstruction due to deceleration/arrest in intestinal motility following surgery
(Delay in the return of normal bowel function)
Very common after abdo surgery or pelvic orthopaedic surgery

136
Q

Risk factors of post-op ileus

A

Patient - increased age, electrolyte abnormalities, neuro (dementia, parkinsons), anticholinergics
Surgery - opioids, pelvic surgery, extensive intra-op intestinal handling, peritoneal contamination (pus, faeces), intestinal resection

137
Q

Clinical features of post-op ileus

A 
Similar to mechanical obstruction
Failure to pass flatus or faeces
Sensation of bloating and distension
N+V/ high NG output
O/E - abdo distension, absent bowel sounds (mechanical obstruction causes tinkling bowel sounds)
138
Q

Investigations for post-op ileus

A

Rule out serious pathologies (eg. anastomotic leak)
Initial routine bloods (FBC, CRP, U+E inc calcium, phosphate, magnesium)
CT abdo pelvis with contrast (confirms diagnosis and rules out anastomotic leak)

139
Q

Management of post-op ileus

A

If serious pathology is excluded, manage conservatively
Daily bloods (correct abnormalities)
Encourage early mobilisation
Reduce opiates
Once ileus settles there will be diarrhoea for first 2-3 bowel movements (warn patient)
Some cases may need NG tube on free drainage, and catheter with fluid balance chart

140
Q

Pathophysiology of keloid scars

A

Prolonged inflammatory phase due to immune cell infiltration into the scar tissue, causing excess fibroblast activity and increased extracellular matrix deposition -> tissue projects beyond original wound margin

141
Q

Risk factors of keloid scars

A 
Black or asian
age 20-30
Cause of injury (burn most common)
Anatomical site (ear, shoulder, sternum)
Previous keloid formation
142
Q

Management of keloids

A

Intralesional steroids - anti–inflam. inhibits glucocorticoid receptors -> prevent fibroblast proliferation and collagen synth
Silicone gel may be used as an adjunct or on its own
Radiation therapy is helpful but carries risks

143
Q

Risk factors for surgical site infection

A

Patient - extremes of age, poor nutritional state, DM, renal failure, immunosuppression, smoker
Surgery - pre-op shaving, length of op, foreign material in wound, surgical drain, poor wound closure

144
Q

Clinical features of surgical site infection

A

typically 5-7 days post-op but may be up to 3 weeks.

Spreading erythema, localised pain, pus/discharge, wound dehiscence, persistent pyrexia

145
Q

Investigations for surgical site infection

A

Wound swabs for culture, FBC and CRP, blood cultures

146
Q

Management of surgical site infection

A

Remove sutures or clips to allow drainage of pus

Empirical abx

147
Q

Prevention

A

Pre-op: prophylactic abx, don’t shave hair, shower prior to surgery, encourage weight loss, optimise nutrition, good DM control, stop smoking
Intra-op: prepare skin immediately before incision, change PPE if contaminated, use appropriate interactive dressing
Post-op: monitor wound closely, consider using pads to separate wound from overlying skin and remove pressure on wound if wound is in difficult place, refer to tissue viability nurse, consider prophylactic topical abx

148
Q

What is wound dehiscence

A

A wound which fails to heal, and reopens a few days after surgery, usually after abdo surgery

149
Q

Classification of wound dehiscence

A

Superficial - only the skin wound fails. Often secondary to infection, poorly controlled DM, poor nutrition.
Full thickness - rectus sheath fails to heal and bursts with protrustion of small bowel and omentum. Secondary to raised IAP, poor surgical technique, critically ill patient

150
Q

Risk factors for wound dehiscence

A

Patient - age, male, comorbidities (DM), steroids, smoking, obese, malnutrition
Intra-op - emergency op, abdo surgery, length of op ?6hrs, wound infection, poor technique
Post-op - prolonged ventilation, post-op blood transfusion, poor tissue perfusion, excessive coughing, radiotherapy

151
Q

Clinical features of wound dehiscence

A

Visibly open wound, typically 5-7 days post-op
If full thickness, a new bulging of the wound and seepage of pink serous/blood-stained fluid.
A sudden increase in wound discharge should be deep dehiscence until proven otherwise

152
Q

Investigations for wound dehiscence

A

clinical diagnosis

wound swabs if ?infection

153
Q

Management of wound dehiscence

A

Superficial - wash out wound with saline, simple wound care, wound will heal by secondary intention (takes weeks)
Full thickness - analgesia, IV fluids, broad spec IV abx, cover wound in saline-soaked gause and arrange urgent return to theatre for wound closure.
Consider vacuum dressing.

154
Q

Prevention of wound dehiscence

A

Optimisation of comorbidities
Treat surgical site infection
Avoid heavy lifting
Encourage adequate post-op nutrition

155
Q

Definition of AKI

A

Any of the following -
>= 50% rise in serum creatinine from baseline within last 7 days
Increase in serum creatinine by >= 26.5mmol/l within 48 hours
Urine output <0.5ml/kg/hr for more than 6 hrs

156
Q

Staging of AKI

A

Depends on creatinine level compared to baseline
Stage 1 – 1.5-2 times the baseline
Stage 2 – 2-3 times the baseline
Stage 3 - >3 times the baseline

157
Q

Pre-renal causes of AKI

A 
Sepsis
Dehydration (pre-op NBM, or bowel prep, etc)
Haemorrhage
Cardiac failure
Liver failure
Renal artery stenosis
Intra-op damage to renal arteries
158
Q

Intra-renal causes of AKI

A 
Nephrotoxins (NSAIDs, ACE-I, ARBs, chemo, abx/gentamicin)
Rhabdomyolysis
Multiple myeloma
Haemolytic uraemic syndrome
Other parenchymal diseases
159
Q

Post-renal causes of AKI

A

Ureters - retroperitoneal fibrosis, bilateral renal stones, tumours
Bladder - acute urinary retention, blocked catheter
Urethra – prostatic enlargement, renal stones

160
Q

Investigations for AKI

A

Assess fluid status
Bladder scan (?retention)
Review drug chart
Urine dip (urine specific gravity and osmolality will be higher in pre-renal causes, whilst Na excretion will be lower. Any glomerulonephritis will show blood and protein)
Initial bloods – U+E, FBC, CRP, LFT, calcium
ABG in severe cases due to acid-base disturbance secondary to AKI
Ultrasound kidneys, ureters and bladder

161
Q

Management of AKI

A

Resus pt and inform senior
Assess for dehydration (= more likely a pre-renal cause)
Give fluid bolus and reassess after 10-15 mins, monitoring UO after the bolus
Repeat boluses until patient is euvolaemic, then prescribe maintenance fluids

Ongoing monitoring –
Monitor UO (insert catheter and start fluid balance chart)
Regular bloods (U+Es to monitor creatinine)
In those who do not respond to fluid therapy, consider intrinsic/post-renal causes and manage accordingly
Daily weights if pt is fluid overloaded in AKI (eg. CCF)
Drug review

162
Q

Drug review in AKI (Which drugs to stop, which drugs to alter)

A

?Stop – ACE-I, ARBs, NSAIDs, aminoglycosides, K+ sparing diuretics
Alter/reduce – metformin (lactic acidosis), diuretics (intravasc fluid depletion), LMWH

163
Q

Clinical features of post-op acute urinary retention

A

Little/no urine passed in the post-op period
Sensation of needing to void but unable to do so (painless if chronic)
Suprapubic mass that is dull on percussion

164
Q

Common causes of post-op acute urinary retention

A

Uncontrolled pain
Constipation
Infection
Anaesthetic agents (eg. spinal or epidural)

165
Q

Risk factors for acute urinary retention

A 
Age >50 
Male
Previous retention
Type of surgery
Anaesthetic type (spinal/epidural)
Neurological or urological comorbidities
Medication (antimuscarinics, alpha agonists, opiates)
166
Q

Assessment of acute urinary retention

A

Clinical assessment/examination
US bladder scan (identify post-void residual urine vol)
Check for any underlying reversible causes
Ensure there is adequate pain control
Check renal function

167
Q

Management of acute urinary retention

A

Conservative in most patients as majority will resolve spontaneously given time and withdrawal of any causative agents
In those who do not results -> catheterisation (TWOC shortly after)
If TWOC fails and pt re-enters retention, a new catheter should be inserted and repeat TWOC 1-2 weeks later
Consider why TWOC may have failed

168
Q

Common causative organisms of UTI

A

E coli, Klebsiella sp, Enterobacteur, Proteus, Psuedomonas, Staphylococcus

169
Q

Risk factors for UTI

A 
Age >60
Female
Co-morbidities (CKD, DM, etc)
Catheter
Foreign body
Recent instrumentation
Pregnancy
Urinary retention or renal stones
170
Q

Clinical features of UTI

A

Frequency
Urgency
Dysuria
Suprapubic tenderness
Pyrexia
(+/- delirium, sepsis, urinary retention)
(pyelonephritis – loin pain, renal angle tenderness, pyrexia)

171
Q

Investigations for UTI

A

Urine dipstick (nitrites, leukocytes +/- blood)
Send urine off for MC+S (MSU)
Consider routine bloods – FBC, CRP, U+E
If systemically unwell -> blood cultures and VBG (lactate)
May need bladder scan if there is potential retention, if so -> catheterise
If ?pyelonephritis/recurrent UTIs -> renal US or further imaging

172
Q

Management of UTI

A

Hydration (PO or IV)
Maintain urine output >0.5ml/kg/hr
Empirical antibiotics (trimethoprim, nitrofurantoin, or co-amoxiclav)
Switch to correct abx when sensitivities are back

173
Q

Cannula sizes and colours

A

Orange (14g), grey (16g), green (18g), pink (20g), blue (22g)

Surgery (9 decks)

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