Recall Flashcards

Question

Ways to reduce bleeding in hepatectomy?

Answer 1

Anaesthetic: Minimise CVP - decrease PEEP, insp pressure, keep patient dry, slight head up, GTN or epidural boluses Reduce coaguloapthy - warming, not acidotic, TEG guided transfusion, TXA Surgical: diathermy, ultrasonic scalpels, Pringle manoeuvre (clamping of hepato-duodenal ligament containing portal vein and hepatic artery)

Answer 2

Infection - 30% risk Liver failure (5 days onwards) Bile leaks (often early post op) Biliary fistula Haemorrhage Renal failure

Answer 3

BRAIN Bilirubin >300 Refractory ascites Albumin <28 INR >1.7 eNcephalopathy

Answer 4

Hepatopulmonary syndrome (worsened V/Q matching due to pulmonary vasodilation, orthodeoxia and +ve bubble study) Porto-pulmonary hypertension (increased CO and increased portal pressures --> pHTN) Mechanical (ascites, hepatosplenomegaly, hydrothorax) Infectious - increased risk of resp infections / ARDS

Answer 5

Ulcerative = gastric, oesophageal, infection (CMV, H pylori), drug induced (NSAIDs), Zollinger Ellison Portal hypertension = mallory-weiss tear, gastric / oesophageal varices, vascular malformations Tumours = benign, polyps, adeno, carcinoid, lymphoma

Answer 6

Restrictive (<80g/L) vs liberal (<100g/L) Hb transfusion in upper GI bleeding. No difference between groups (12% less blood transfused if 80g/L target but this wasnt statistically signfiicant)

Answer 7

For upper GI bleeding. Uses urea, Hb, systolic BP, HR, malena, syncope, hepatic disease and cardiac disease. 0 = manage as outpatient 5 = high risk, needs urgent intervention

Answer 8

Transjugular Intrahepatic Portosystemic Shunt. Shunt from portal vein to hepatic vein, accessed radiolgoically via jugular vein. allows blood to bypass gastric and oesophageal varices --> decreasing risk of recurrent bleeding. 90% success rates

Answer 9

DRinking, EAting, Mobilising and Sleeping

Answer 10

Cancer - anaemia, malnutrition, mets, mass effect, chemo, radiation, anxiety Other comorbidities - IHD, smoking common ERAS - Drinking, eating, mobilsing, sleeping. Reducing ileus. Analgesia + PONV. Lignocaine good evidence here Pneumoperitoneum Positioning (steep head down) Anastamosis - minimise fluids

Answer 11

Airway - history (stridor, voice changes, orthopnea, dyspnoea), exam (firm mass, tracheal deviation, retrosternal), investigations (CT, nasoendoscopy) Endocrine - history (palpitations, flushing, tremor, anxiety), exam (tremor, HTN, tachycardic, exopthalmos), investigations (TSH, T3/T4, ECG - AF, echo - CHF) Local structures - SVC, recurrent laryngeals Treatment - PTU, carbimazole, steroids, propanolol Aim euthyroid, no tremor, HR <80BPM for surgery

Answer 12

Propanolol 40mg Q6Hrly PTU 200mg Q6Hrly Hydrocortisone 100mg Q8hrly

Answer 13

Recurrent laryngeal palsy - if unilateral, hoarse voice. Bilateral needs urgent intubation Haematoma - oxygenate, evaluate, evacuate, intubate (from british association endocrine and thyroid surgeons) Hypocalcaemia - from parathyroid removal. Check serum Ca 24 hours post op then daily if low Tracheomalacia (if long standing large goitres) Pneumothorax (if large retrosternal goitres)

Answer 14

Aims to increase calcium. 1) Increases bone reabsorption 2) Increases Ca absorption at kidneys 3) Stimulates release of vitamin D (which also increases kidney Ca absorption, gut Ca absorption)

Answer 15

Primary - excess PTH from adenoma. Have high calcium. High vitamin D (due to PTH causing Vit D release). Low Phosphate Secondary - high PTH due to low calcium, most commonly from renal. Have high phosphate, low vitamin D Tertiary - high PTH but also high calcium, due to hypertrophy of parathyroid glands. End stage renal failure for a long time. High phosphate. Low vit D

Answer 16

Goals: Arterial pressure control (alpha blockade before beta), correct chronic intravascular depletion, heart rate and arrythmia control, assess and optimise cardiac function, correct electrolytes and BGLs Associated conditions: MEN2 (thryoid carcinoma, parathroid adenoma), neurofibromatosis 1 Diagnosis: urinary metanephrines / normetanephrines / homovanillic acid. CT or MRI or radionucleotide scan to find mass (+ mets) Investigations: bloods, ECG, echo. Electrolytes may be out of whack Treatment: phenoxybenazamine or doxazocin. PRESCRIPT trial found no difference mortality or issues post op. Phenoxybenzamine gave slightly better intraop control. High salt diet + rehydration Targets: Sys BP <140mmHg, Hr <100BPM, postural drop >20mmHg. No arrythmia on ECG (ST or T wave changes > 1 week)

Answer 17

High risk of mortality (17%). If found before 2nd trimester, should be resected early. Still alpha blockade first Highest risk is vaginal delivery - straining + possible catecholamine surge --> risk intracranial haemorrhage. If later in pregnancy and found, usually elective c section. Consider removal of phaeo in the same operation (under GA + epidural)

Answer 18

Neuroendocrine tumour embryonic origin. 70% in GI tract. Most common tumour of appendix. Can also form in lungs. Hormones release: 5HT, VIP, histamine, bradykinin, substance P, prostaglandins, dopamine Determine if mets: if mets, 5 year survival on 38% Symptoms: flushing, nausea, diarrhoea, postural hypotension, tachycardia, bronchospasm. right heart failure in late stage disease. May worsen with exercise, ingestion of alcohol or cheese (high tyramine foods). If GI, mass effect can cause obstruction. If lungs, can get haemoptysis, cough, recurrent pneumonia Two thirds will have right sided valvular disease - often TR and PS. Fixation of valves +/- right ventricular failure. Rarely may get valve procedure pre-op Diagnosis with 5-HIAA (metaboltie of 5HT) in urine Treatment: octreotide (50mcg/hour infusion) at least 12 hours preop. = somatostatin analogue

Answer 19

Monitoring: usual + arterial line. Consider PAC if right sided heart disease IV access: large bore + CVL Place: tertiary centre, familiar with surgery Octreotide infusion 50mcg/hr continued from preop + 50mcg IV boluses if bronchospasm or hypotension suspected from carcinoid Avoid histamine releasing drugs - morphine, atracurium If liver resection - usual liver things of low CVP Direct acting synthetic vasopressors (phenylephrine) ideal. Noradrenaline, ephedrine, adrenaline can cause synthesis of bradykinin --> paradoxical hypotension Monitor electrolytes, BGLs

Answer 20

Absolute: refusal, transmissible spongiform encephalopathies, diffusely spread metastatic malignancy Relative: lots

Answer 21

Three criteria are coma (GCS 3), apnoea and loss of brainstem reflexes (= zero chance of recovery) Preconditions: brain injury consistent with coma At least 4 hours with GCS 3, no cough and apnoea No sedation or paralysis No intoxication Normotensive, normothermic, normal electrolytes Not severely hypoxic (as can't test apnoea properly) Exam: Ideally by 2 clinicians TOF - rule out paralysis GCS exam - all 4 limbs and supraorbital Cranial nerve V (corneal reflex), IX and X (gag), CN II and III (pupils fixed and dilated) Apnoea test (preoygenate, then stop ventilation. If PaCO2 >60mmHg, then positive If can't be met. Then can use radiology: 4 vessel CT angio - no flow above carotids (anteriorly) or foreamen magnum (posteriorly) Radionucleiotide scintigraphy imaging

Answer 22

Main emphasis is on other organ perfusion, not brain. CVS - MAP 65-90mmHg (norad or vasopressin to treat hypotension, esmolol for hypertension). can have fluid but avoid excess as bad for lungs. DDVAP 4-8mcg IV if DI. Aim urine output 0.5-2ml/kg/hr. give 5% dextrose if sodium >150mmol/L. Amiodarone if tachyarrythmia. Hr 60-100BPM Resp - Lung protective ventilation (TV 6-8ml/kg, PEEP 5, plateau airway pressures <30cmH2O, SpO2 92-95%, normocarbia). Can still donate lungs if FiO2 100% Normothermia. 36-38c Haem. Hb >70g/L, Coag - Vit K if INR >1.5 Biochem: Sodium 135-150mmol, K 4-5, glucose 4-12. Insulin if BGLs high.

Answer 23

Organs are retrieved in order of cold ischaemia time (shortest first) Heart 4-6 hours Lungs 6-8 hours Liver, pancreas 12 hours Kidneys 24 hours

Answer 24

5 minutes of absence breath sounds, cardiac pulse and GCS 3. Abscence of pupil reflexes, corneal reflexes, supraorbital pressure response. In NZ, only lungs, kidneys and liver are major organs in DCD (in Aus, they do heart and pancreas too). Selection of patients important - DCD reliant on warm ischaemia times. Ideally want patient to die quickly after withdrawal of care (e.g. extubation, cessation of vasopressors). Warm ischaemia times start once systolic <50mmHg (but for heart it is once systolic <90mmHg, hence why not done in NZ) Warm ischaemia times acceptable: Heart 30mins Liver 30 mins Pancreas 30mins Kidney 60 mins Lungs 90 mins (LHP30 K60 L90)

Answer 25

Warm ischaemia times start once systolic <50mmHg (but for heart it is once systolic <90mmHg, hence why not done in NZ) Warm ischaemia times acceptable: Heart 30mins Liver 30 mins Pancreas 30mins Kidney 60 mins Lungs 90 mins (LHP30 K60 L90)

Answer 26

= removal of 2 or more out of 5 pelvic compartments. Total pelvic exenteration will include removal of all reproductive organs (penis / vulva, vagina, uterus), bladder, rectum, anus. Requires stoma and ileal conduit. Most commonly local spread malignancy. Rarely recurrent pelvic abscesses Psychological / PT / OT input preop. Pre op usual for major surgery Positoning - often need to be both supine and prone at various stages. Often abdominal phase in steep Trendelenburg + lithotomy Lines and monitoring - usual + art line, CVL. consider lumbar epi (load near end) Analgesia - everything + epidural Weirdly, may transport mid op to get intraop radiotherapy / brachytherapy Post op: ICU, pain team, PT / OT. Stoma input. Average length of stay 15 days postop

Answer 27

Xyelometazoline

Answer 28

Mid face: Le fort I = transverse maxillary fracture from rest of face, below nasal bone structures. Not mobile Le fort II = pyramidal, involving inferior orbit, nasal and maxilla bones. Reasonable mobile Le fort III = through nasal bridge, across orbits and through zygomatic arches. Entire midface dissociation base of skull. High risk of airway obstruction and lots of bleeding (patient better with face forward) TBI - 20-40% will have intracranial pathology C spine fracture Base of skull fracture Peribulbar haematoma Airway - more difficult if c spine, mandibular involvement (or zygomatic fracture causing decreased mandibular opening), bleeding in airway, retropharyngeal haematoma (suspect if stridor, dyspnoea, voice changes). Blood in stomach = not starved Haemodynamics (can bleed a lot, assess HR, BP)

Answer 29

= bilateral floor of mouth cellulitis, involving submandibular and sublingual spaces. Wood like rigid neck. Impending airway obstruction (asphixia most common cause of death). Usually from tracking dental infection Airway: Assess trismis, altered speech, stridor, rapidly worsening swelling Check for difficulty BMV, LMA, ETT, eFONA (eFONA can cause spread to mediastinum, high risk mortality) Get ENT nasoendoscopy Sepsis considerations - resuscitation and IV antibiotics. IV dexamethasone too

Answer 30

Headache, nausea, vomiting, blurred vision, papilloedema, seizures, ipslateral then bilateral fixed dilated pupils, hypertension, bradycardia, apnoea, coma Radiology: hydrocephalus, midline shift, cerebellar herniation

Answer 31

Brain tissue: Hyperosmolar saline / mannitol, dexamethasone Blood volume: hyperventilation, raise MAP, decrease CVP (head up, tape ETT), isoelectric EEG CSF volume: EVD Decompressive craniectomy

Answer 32

DECRA = NZ, Aus and Saudi Arabia. Decompressive crani reduced ICPs but less favourable neuro outcomes at 6 months RescueICP = 20 countries but 75% from UK. Surgery after failure tier 1 and 2 management. Improved survival (27 vs 49%) but survivors more likily in vegetative state (8 vs 2%)

Answer 33

Hypothermia after severe TBI (core temp 33c). Did not alter mortality or ICPs but increased risk pneumonia and bradycardia

Answer 34

Maintain CPP Avoid increases in ICP Good operating conditions, relaxed brain Facilitate rapid emergence for neurological assessment

Answer 35

90% are benign, 10% are malignant. Grade 1 = benign (fibrosis, angioblastic), grade 2 = atypical (clear cell, choroid), grade 3 = malignant (anaplastic, papillary). Can get mets, recurrence, may need radiation Associated syndromes: neurofibromatosis 2 (increased 8th cranial nerve schwannomas), li fraumeni syndrome (p53 tumour supressor mutation, increased risks most cancers), family history. Women 2x > men. Highly vascular, often nearby venous sinuses --> high propensity to bleed

Answer 36

Endocrine hypersecretion: GH (acromegaly), prolactin (prolactinoma), Cushings disease (ACTH), thyrotoxicosis (TSH) Endocrine hyposecretion: Adrenal insufficiency, hypothyroidism, diabetes insipidus (lack of ADH) Mass effects: visual changes, headaches, hydrocephalus

Answer 37

Usual neuro considerations with CPP, ICP, rapid emergence Prepare for massive bleeding as nearby carotid artery, venous sinuses Throat pack sometimes Topical nasal vasoconstrictor If supracellar extension of tumour, may get lumbar drain and anaesthetist pushes saline to advance tumour into operating field

Answer 38

Commonly after pituitary surgery. Or brain death. Usually within 12-24 hours of surgery Symptoms: polyuria, polydipsia, thirst Rule out other causes of polyuria (diuretics, excess IV fluids, DKA) Diagnosis: urine output >3ml/kg/hour for at least 2 hours, sodium >145mmol/L, serum osmolarity >300mOsmol/L, urine osmolality <350mOsmol/kg (but often <200mOsmol/kg, dilute urine despite hyperosmolar serum). Urine specific gravity <1.005 Often triphasic post pituitary surgery (initial phase, then SIADH phase days 2-4, then permanent DI phase >1 week)

Answer 39

Monitoring inputs / outputs Awake, conscious patients: drink to thirst H2O IV fluids - match output with input. Usually plasmalyte is fine. May need 0.45% saline or 5% dextrose. Avoid dropping sodium more than 0.5mmol/L/hour NG H2O DDAVP - IV 0.25 - 4mcg IV, 10-20mcg IN. If urine output >1L over 4 hours or unable to tolerate oral H2O start DDAVP sodium checks Q4Hrly. Involve endocrine, especially if permanent DI

Answer 40

Posterior fossa = below tentorium cerebelli. contains cerebellum, pons, medulla and cerebral aquaduct. Risk of CSF obstruction and hydrocephalus. Also if raised ICP, risk of impaired brainstem function Resp: check for dysphagia, bulbar symptoms --> increased aspiration. May have impaired laryngeal reflexes. RSI and possible need for tracheostomy / ICU ventilation post op CVS: instability. Bradycardia, hyper / hypotension CNS: may present with low GCS. May get preop craniotomy EVD Increased risk of VAE - check for septal defect. Especially if plan for seated position (rare these days) High bleeding risk. Prepare accordingly

Answer 41

Same as craniotomy (CPP, ICP, good operating conditions and rapid emergence) AND: Positioning varied: supine, lateral (acoustic neuroma, lateral cerebellar tumours), prone, seated (rare, high risk VAE. Contraindicated if PFO, right to left shunting, ventriculoatrial shunt) High bleeding risk - sigmoid, transverse and occipital sinuses. High VAE risk. consider fenestrated CVL Surgical interference near brainstem may get hypotension, hypertension, bradycardia higher risk of PONV as near medulla and vomiting centre. 3x antiemetics probably Acoustic neuroma: facial nerve +/- 8th CN monitoring. single dose NDMR beginning of case

Answer 42

For having the aneurysm: HTN, smoking, family history, polycystic kidneys, connective tissue disorders (Ehlers-Danlos, Marfan) For dying from aneurysm rupture: increasing age, higher WFNS, rebleeding, vasospasm, hydrocephalus

Answer 43

World Federation of NeuroSurgeons. for SAH. Most important for morbidity and mortality scoring 1 = GCS 15, no motor deficit 2 = GCS 13-14. No motor deficit 3 = GCS 13 - 14 with motor deficit 4 = GCS 7-12 +/- motor 5 = GCS 3-6 +/- motor WFNS 1-3 should have definitive treatment within 48 hours presentation or diagnosis. Usually coiling

Answer 44

Neuro: Rebleeding (5-10% risk in first 72 hours, mostly in first 24 hours), delayed cerebral ischaemia (4-10 days post bleed, arterial vasospasm most common cause, hydrocephalus (blockage of CSF drainage. Put in EVD), seizures, cerebral oedema CVS: ECG changes (SVT, T wave inversion), heart failure (like Takotsubo, from massive SNS), APO Other: hyponatraemia (SIADH, cerebral salt wasting), hepatic / kidney dysfunction

Answer 45

Nimodipine 60mg Q4H for 21 days (CCB, crosses BBB) Hypertension and euvolaemia (AHA recommendation, not historical "hypertension, hypervolaemia, haemodilution). Aim systolic 160-180mmHg if secured aneurysm or 140mmHg if unsecured Endovascular verapamil or nimodipine Transluminbal balloon angioplasty

Answer 46

May be done electively or acutely. Less common these days as most done by coiling. Preop: Discuss with surgeon preop if wanting flow arrest - place on defib pads preemptively. Depends where surgery is - may be posterior or frontal craniotomy Intraop: usual craniotomy considerations (CPP, ICP, good operating conditions, rapid emergence) Optimal BP likely 110-160mmHg (too high = rupture risk, too low = poor CPP) Flow arrest with 24mg adenosine may be asked for. Push into big drip with large flush. Alternative is a temporary clip placed Have plan for intraop aneurysmal rupture (SNACC guidelines): may either abandon for endovascular approach (if before dura opened). If dura opened, usually have to continue in OT: Drop MAP to 50-60mmHg until secured, aim isoelectric EEG. Adenosine for flow arrest. Manage as per raised ICP (hyperventilate, give hypertonic saline

Answer 47

Remote location - emergency drugs, personnel, airway equipment, defib, help far away Access to patient = poor. Secure everything. Bed = not easy to manipulate Radiation exposure Can't use EEG as in way. Run some sevo Usual neuro considerations (ICP, CPP, rapid emergence, good conditions for proceduralist). don't need much analgesia (paracetamol + LA) Heparin use (ensure protamine available). May have DAPT if stent being placed Femoral vessel access - 4 hours flat post op. Avoid coughing on extubation. Risk of bleeding / AV fistula IV contrast use. Minimise nephrotoxics. Monitor urine output Plan for rupture (SNACC guidelines) - reduce MAP to pre-bleed levels with propofol / esmolol. Probably keep CPP >80mmHg - ICP management - hyperventilation, hypertonic saline, if EVD in then drain CSF. Increase fiO2 to avoid hypoxia, if able elevate head (unlikely - Minimise bleeding (reverse heparin with protamine, TEG and transfuse platelets if antiplatelet agents) - Most commonly just needs to be sorted in IR with coiling. Get neurosurgery to come place an EVD - Control seizures with midazolam and then levetiracetam - Once bleeding secure, raise BP to ensure CPP

Answer 48

Plan for rupture (SNACC guidelines) - reduce MAP to pre-bleed levels with propofol / esmolol. Probably keep CPP >60mmHg - ICP management - hyperventilation, hypertonic saline, if EVD in then drain CSF. Increase fiO2 to avoid hypoxia, if able elevate head (unlikely - Minimise bleeding (reverse heparin with protamine, TEG and transfuse platelets if antiplatelet agents) - Most commonly just needs to be sorted in IR with coiling. Get neurosurgery to come place an EVD - Control seizures with midazolam and then levetiracetam - Once bleeding secure, raise BP to ensure CPP

Answer 49

Hypernatraemia: - Diabetes insipidus (Lack of ADH. polydipsia, polyuria, thirst. Hyperosmolar serum, dilute urine. Especially if pitiutary surgery) - Iatrogenic (hypertonic fluids, excess osmotic diruetic (mannitol)) - Dehydration (excess fasting or reduced GCS and lack of intake) Hyponatraemia: - SIADH (excess ADH. Can be from any neuro pathology. Also surgical stress / other stress (sepsis). Drugs (morphine, SSRIs, antipsychotics, cyclosporin), paraneoplastic (small cell lung cancer). Euvolaemia. - Cerebral salt wasting (hypovolaemia, hyponatraemia with high urine sodium (>40mmol/L) - primary adrenal insufficnecy - Iatrogenic (fluid excess) - Cardiac failure (e.g. post SAH)

Answer 50

= excess ADH (stress (surgical / sepsis), drugs (morphine / SSRIs / antipsychotics), neuro pathology (tumours, ICH, SAH, raised ICP), paraneoplastic (small cell lung cancers). Hyponatraemia with urine sodium >20mmol/L (but not >40mmol/L which would be more indicative of CSW) Symptoms: fatigue, nausea, vomiting, headache, muscle weakness, seizure, coma --> death Fluid restrict 1-1.5L day (unless aneurysmal SAH and wanting euvolaemia) Hourly fluid input + output monitoring, IDC Withhold meds contributing to SIADH if appropriate Hypertonic saline (no more than 1-2mmol/L/hour correction or 10mmol/L/day). Aim sodium >130mmol/L and resolution of symptoms. Risk of central pontine demyelination (now called osmotic demyelinating syndrome) Vaptans (not used much due to risk of overshooting sodium correction) = V2 receptor antagonists

Answer 51

Hypovolaemia: - Cerebral salt wasting - Vomiting, diarrhoea - excess bleeding - Primary adrenal insufficiency - Excess diuretics Euvolaemia: - Hypothyroidism - SIADH - Secondary adrenal insufficiency Hypervolaemia: - Hepatic failure - Renal failure - Cardiac failure - Anaphylaxis - Excess hypotonic fluids - SAIDH again

Answer 52

Poorly understood, some think a continuum of SIADH Other theories: - increased ANP release centrally --> increased sodium and H2O loss at kidneys - Dysfunctional SNS --> decreased renin, excess ADH

Answer 53

Input and outputs fluids Increase sodium intake (salt tabs or hypertonic saline) Endocrine involvement, consideration of fludrocortisone (start 0.1mg PO, uptitrate to 0.4mg then cautiousless downtitrate).

Answer 54

Maternal request High likelihood of operational delivery (instrumental or C section) +/- risk factors for GA Maternal comorbidities: Cardiac (valvular lesions, heart failure, fontan, pulmonary HTN), resp (severe asthma, cystic fibrosis), obstetric (PET)

Answer 55

Absolute: 1) Maternal refusal 2) overlying infection 3) Uncorrected coagulopathy (SOAP, ASRA both suggest 70 platelet count for epi. Risk benefit between 50-70 for epi or spinal if high risk for GA. Ensure normal platelets). Based on LP data, 0.2% risk haematoma if plts 70-100. 3% risk if platelets 50-70. 4) Allergy / hypersensitivity to LA 5) Non-communicating obstructive raised ICP (fine if communicating idiopathic raised ICP) Relative: 1) stenotic valvular lesions 2) Hypovolaemia, massive haemorrhage. Uncorrected 3) Other cardiac lesions reliant on SVR (Fontan, HOCM) 4) Systemic sepsis 5) Spina bifidi, tethered cord 6) Previous spinal surgery (not really. One study of patients with previous scoliosis surgery still got 90% efficacy from an epidural)

Answer 56

Patient controlled epidural analgesia with programmed intermittent bolus. Prescrtiption: 0.0625% bupivacaine + 2mcg/ml fentanyl. 8ml PIB Q1Hrly. 5ml PCEA Q20mins Reduces overall LA used Improved maternal satisfaction Gives control to patient Reduced stage 2 labour Better spread of LA as bolus - better for breakthrough pain

Answer 57

Advantages: Rapid onset analgesia (10 mins faster than epi). Then similar advantage of epidural for prolonged analgesia with top ups Reduced pain scores, improved analgesia with less need for top ups. May be due to dural puncture and LA going intrathecally Can perform spinal component if patient unable to sit still for epidural - risk of dural puncture reduced Benefit of knowing you are in correct location due to LOR and confirmation with CSF Disadvantages: Longer proceedure, more technical Increased rates of maternal hypotension and pruritis May not be appropriate for high dose spinal in a labour room Test dosing for epi - still need to do. But need to wait 15 mins for spinal effects to become apparent.

Answer 58

Advantages: Rapid onset analgesia compared to epidural (not as fast as CSE but at least 5 mins faster). Also better quality of block with less patchy and unilateral analgesia Reduced hypotension compared to CSE. Similar to epidural Confirmation of correct epidural location with CSF present visually Disadvantages: More technically challenging than epidural or spinal Not as fast onset as CSE Higher rates of PDPH compared to epidural Need to use at least 25g spinal needle for benefit of analgesia. If 26g or smaller, then analgesia similar to epidural alone (hole too small). Meta analysis

Answer 59

Hypotension and associated nausea Pruritis (especially if intrathecal opioids) Motor block Indavertent dural puncture + PDPH Urinary retention Subdural block Total spinal LAST - if in epidural vein Temporary nerve injury - 1:3000 (neurapraxia - parasthesia, neuralgia, motor weakness) Permanent nerve injury - 1:80,000 - 1:200,000 Epidural abscess Epidural haematoma

Answer 60

History - Headache - worse standing, bilateral, frontal + posterior. From reduced CSF, stretch on meninges from brain being pulled downwards Associated symptoms - often visual accommodation changes. Rarely tinnitus and 6th nerve palsy Neuraxial insertion - difficult, multiple attempts, CSF noted, junior practitioner. Obese patient. Large gauge needle Previous headache risk factors - migraine. Idiopathic intracranaial hypertension Red flags - focal neurology. Seizure. PET with clonus. Fever. Backpain. Visual field deficit, sudden onset. Pain history - analgesia used, useful or not. Timing. Etc Exam - neuro basically + inspect insertion site Invest - MRI or CT head maybe

Answer 61

Prophylactic treatment not recommended - some women won't get PDPH even if 16g Tuohy needle (risk >50% though). risk of bacteraemia Conservative: Wait for dural puncture to heal + CSF volume to restore. Most PDPH will resolve without intervention (70% in first week, 85% within 6 weeks). Encourage oral fluids (increased CSF production) + simple analgesia (paracetamol, NSAIDs, tramadol). Bed rest if needed. Note this won't improve healing, just help symptoms. Will increase VTE risk (enoxaparin good idea if inpatient). Also limits ability to do daily activities, bond with neonate and breastfeed Caffiene: Controversial. Typically need 500-1000mg / day for benefit (from cerebral vasoconstriction). One cup coffee has 200mg. Not recommended to exceed 200mg in a day if breast feeding Sphenopalatine block: Temporising infilltration of LA. Through the nose. 1ml bilateral 0.5% ropivacaine. Minimal evidence this works. One RCT found no difference in pain scores between placebo and no reduction in epidural blood patches from placebo (but both placebo and LA group had reduction in EBP compared to control group by 50%?). Evidence is minimal. But safe, non invasive compared to EPB. High variability in terms of how block performed Epidural blood patch: Do not do in first 24-48 hours 30% of EPB get complete resolution of symptoms immediately. 50-80% get improvement of symptoms. Some need a second EBP. Contraindications: HIV, leukaemia, systemic and local infection, coagulopathy Risks: infection seeding, repeat dural puncture. Similar risks to usual epidural insertion Labour intensive, need 2x anaesthetists, aseptic field, theatre. Aim for 20ml blood or until back pain / fullness prevents further infiltration Bed resr 2 hours post EPB for clot formation + avoid heavy lifting for 2 days

Answer 62

Drug - pKa (ion trapping if basic drugs e.g. opioids), molecular weight, lipid solubility. Most opioids have milk to maternal plasma concentration of 2:1 due to ion trapping Foetal - oral bioavailability (oral absorption + hepatic metabolism). Propofol BA <1%. Genetic polymorphisms (CYP2D6 and codeine) RID = relative infant dose. Percentage of drug in newborns serum compared to maternal. Most drugs have <2% RID. <10% acceptable

Answer 63

PG07 ANZCA document recommendation for breastfeeding to be encouraged. Pump and dump not needed. Benefits to for breast feeding include bonding, immunity, reduced dehydration and reduced mastitis Opioids - codeine and pethidine (SPANZA state tramadol is fine. Even though tramadol packet suggests not using). Most other opioids are fine, especially in hospital setting NSAIDs - only if duct depedent lesion Antibiotics - tetracyclines, cpirofloxacin, chloramphenicol Antipsychotics Anticonvulsants - avoid most of them. But carbemazipine is fine Cardiac - amiodarone (accumulates in breast milk), ACEis (except enalapril)

Answer 64

Increased rates of preterm delivery, VTE, maternal sepsis and c section CVS - Autonomic dysreflexia with labour + delivery. Labour with epidural and arterial line. C section with spinal or epi. If contraindicated for neuraxial, deep GA with remi. Poorly tolerate aortacaval compresion. Left tilt Caution that HTN could be from PET (get protein sample) Resp- May get worsening resp function with gravid uterus, reduced FRC. May need mechanical vent support Haem - anaemia chronic disease common MSK - challenging for positioning for spinal / neuraxial. May need multiple people to support Pharmacology - avoid sux

Answer 65

Prophylactic enoxaparin dose (as recommended by American college of Obs and Gynae) vs weight based intermediate dose (as recommended by Royal College of obs and gynae). No difference in VTE (did not include mechanical valves). But 40% of patients on higher dose were unable to have neuraxial compared to 20% with lower dose (need to wait 24 hours for treatment dose enoxaparin vs 12 hours for prophylactic dose)

Answer 66

(DOACs are avoid in pregnancy and breastfeeding. Unclear safety profile) Teratogenic, especially in weeks 6-12. Causes nasal hypoplasia and CNS abnormalities. Crosses placenta Much reduced risk in 2nd and 3rd trimesters It is SUPERIOR to LMWH for mechanical valves Reversal often preferred with prothrombinex or FFP as less thrombosis risk than vit K. Just prior to delivery. Alternative if planned IOL would be to stop 5 days prior and bridge with enoxaparin. Ensure INR <1.5 for neuraxial If mechanical valve, need to determine dose of warfarin they are on. If less than 5mg / day, low risk of teratogenicity. Continue warfarin throughout 1st, 2nd, 3rd trimester (as per AHA, ECS) If >5mg per day. Change to enoxaparin treatment dose between 6-12 weeks. Then warfarin again from there (level 1 recommendation AHA) Then from 36 weeks, change to 1mg/kg BD enoxaparin and stop warfarin. IOL at 38 weeks and cease LMWH 24 hours prior neuraxial. Cover with heparin infusion and cease this 4 hours before neuraxial if you want. Restart warfarin post delivery when reduced bleeding risk. Then enoxaparin cover until INR therapeutic

Answer 67

Baseline heart rate (110-160BPM) Variability (5-25). Too little may be foetal sleeping or compromise. High variabiltiy (sinusoidal) indicative of distress or foetal anaemia Accelerations (present = good. Not present = no worries) Decelerations (15BPM drop for >15 seconds). Early decels with contraction are fine (vagal response from head compression). Late decels and slow recovery = sign of hypoxia, cord compression, foetal distress. Decels >60s concerning. >3mins = bradycardia = very concerning. Variable decels can be concerning, more so if deep or >50% of contractions for 30 mins.

Answer 68

Foetal Doppler / US CTG Foetal scalp monitoring electrode Foetal scalp gases - pH and lactate

Answer 69

Empathy, compassionate, culturally safe / competant Determine cause for demise - sepsis, coagulopathy, PET all have implications for analgesia and delivery Timing of demise - high risk for sepsis, DIC if >2weeks. Check coags, HR, BP, temp Determine delviery mode preference - often vaginally with IOL. May need LSCS if breach + term Analgesia - non pharma - TENS, water labour, accupuncture. May be more acceptable if very premature Pharma - N2O, paracetamol, NSAIDs, PCA (can use fentanyl as no risk foetal resp depression), IV / IM opioids. Neuraxial - epidural

Answer 70

Miscarriage (highest in first trimester, risk of 10%. 1-3% risk 2nd trimester. 3-5% risk in third trimester). If surgery needs to happen during pregnancy, ideal in 2nd trimester. For acute surgery, there is often an increased risk of miscarriage if not operated (e.g. appendix). Discuss with mother, informed consent. Pre-term labour - increased risk for next 1 week post surgery. If contractions start, consider tocolysis. If high risk preterm labour, consider betamethasone IM steroids for foetal lung maturation. Volatile may be useful intraop as may cause uterine relaxation. Teratogenicity and drugs to avoid: NSAIDs (first trimester for renal, third due to PDA), N2O (methionine synthase theorectical risk), benzos and long term opioids. Improving foetal oxygenation / perfusion - ensure maternal Hb >70g/L - FiO2 controversial. Excess could cause retinopathy theoretically. Titrate to effect. Avoid hypoxia, SpO2 >94%. - Blood pressure. MAP >65mmHg or +/-20% of normal. Uterus perfusion dependent - Avoid acidaemia -Avoid hypothermia Foetal monitoring. - HR monitoring for any foetus before and after surgery (if heartbeat known to be present). At least from 10 weeks. (Royal College of obs and gynae) - contraction monitoring before and after surgery for any viable age (full CTG) - Intraoperative monitoring rarely done - need someone to interpret it. And needs to not interfere with surgery site. Then need decision for what to do with information if abnormalities detected

Answer 71

Airway - More difficult. Especially if PET - Increased aspiration risk, especially after 20 weeks or earlier if obese / GORD / multiple gestation - consider regional Breathing - Ventilation to PaCO2 of 32mmHg by term to avoid relative acidaemia (baseline maternal pH is alkalotic) - Reduced FRC, increased VO2. Increased risk of hypoxia with apnoea. Well preoxygenated. RSI. ETT. Consider HFNO - Use lowest possible pressures for pneumoperitoneum Circulation - aortocaval compression from 20weeks or earlier if obese, multiple gestation. Left lateral tilt always - Increase CO by term with increased HR, increased SV, decreased SVR and increased venous return. Poorly tolerated in heart failure, stenotic valve lesions, pulmonary hypertension - uteroplacental unit not able to autoregulate. Keep MAP >65mmHg CNS - Increased sensitivity to LA - reduced MAC requriements. But higher rates of awareness Haem - Anaemia common - dilutional - Increased thrombosis risk. Ensure prophylaxis Medications - Sugammadex controversial in pregnancy. Only use if needed. May bind progesterone (especially relevant in first trimester, avoid if possible (SOAP))

Answer 72

Orbit = 40-50mm deep, pyramidal shape. contains globe and retrobulbar space Retrobulbar space posterior to globe. Within extraoccular muscles (rectus muscles x 4 + superior / inferior oblique) Contents - connective tissue, fat. Optic nerve, CNIII, IV and VI, sensory neerves, ciliary ganglion, retinal artery and vein Sensory innervation of globe by V1 and V2 of trigeminal. Motor by III, IV, and VI. Visual by II. Pupil efferent by III Nearby retrobulbar space is peribulbar space. Target for peribulbar block. Lower risk compared to retrobulbar block

Answer 73

Retina --> choroid --> sclera --> tenons capsule (which contains subtenon space) --> conjunctiva

Answer 74

Aqueous / vitreous humour production / clearance - acetazolamide (reduces aqueous humour production) - mannitol (increases vitreous drainage) Intravascular volume - Head up - low normal PaCO2 Extra-occular eye muscle tone - Avoid coughing, straining, vomiting - avoid suxamethonium (increase IOP for up to 10 mins) Extra-occular compression - decompression haematoma - avoid excess LA volumes - avoid external pressure on eye

Answer 75

1) Avoid increases IOP - remi for intubation (avoiding coughing, straining, laryngosocpy response), maintenance and extubation - Paralysis with rocuronium not sux - Deep anaesthesia - Head up slightly if able 2) Good operating conditions - still patient - remifentanil +/- paralysis 3) PONV - high rates. Use TIVA, dex and ondans 4) Occulocardiac reflex - pretreatment with glyco before induction - atropine drawn up 5) Consider regional - cant do in ruptured globe. But otherwise, not many other contraindicated to subtenons block 6) Surgeon in vacinity to airway. ETT probably preferred. South RAE

Answer 76

Pre op - typically children 6 months to 6 years. But can be adults - Day case usually - Rarely may be part of syndrome (Down's, cerebral palsy, ring chromosome 14) Intraop - Usually 60 mins. GA - Don't use Sux. loose connection of squints with MH. And increases IOP - RAE or flexible LMA - PONV high rates. 2-3 antiemetics. Consider TIVA - surgical subtenons block performed so usually minimal analgesia requirements post op. Also reduces occulocardiac reflex - Atropine at the ready for occulocardiac reflex Post op - paracetamol + NSAID - Day stay considerations (Patient - ASA 1/2, eating + drinking, no PONV, oral tabs with no opioids Parental - sensible. Able to drive. Not too far from hospital. Cell phone. 2x adults while driving (one to drive, one to monitor child) Surgery - uncomplicated

Answer 77

Preop - Determine if sight saving or not. More urgent if chance to save eye. Otherwise often can wait til morning. Discuss with surgeon - Likely unfasted. Consider other trauma injuries (especially head trauma and c spine) - Anxiety around eye sight. Especially from children / parents. Children may be distressed or rub eye - If child, ametop on and aim for IV induction if able. - Pre-emptive antiemetic, want to reduce vomiting Intraop - Goals to avoid increases in IOP during induction, maintenance and emergence, still patient for surgeon - RSI if acute. Rocuronium rather than sux to reduce IOP. south RAE - Remifentanil / lignocaine are options to reduce larygnoscopy response + reduce coughing and straining - Pre-oxygenation and BMV may be challenging or impossible with injuries, especially with child - PONV high risk, give 3x antiemetics - Prepare for occulocardiac reflex. Pretreat with glyco. Have atropine drawn up - cant use blocks due to risk of increased IOP. Give opioids, NSAID, paracetamol Post op - extubate without coughing, on remi. Consider deep extubation if fasted child - Topical LA - Analgesia

Answer 78

Inputs are: age, Hb, comorbidities, mini cognitive test, malignancy presence and rest home status. Out of 10. Gives 30 day and 1 year mortality. Score 5 or more = high risk

Answer 79

Intracapsular: Sucapital and transcervical. Treatment with cannulated screws if non-displaced. Total hip replacement if displaced and not frail. Hemiarthroplasty if displaced and frail. Intracapsular have high rates of AVN due to blood supply interruption. Arterial supply from deep femoral artery --> branches to medial and alteral circumflex arteries. These send off retinacular arteries along neck of femur to head of femur (which can be disrupted by fracture) Extracapsular: intertrochanteric, subtrochanteric. simple intertrochanteric by dynamic hip screw. Complex intertrochanteric or subtrochanteric require IM nail. More likely to bleed pre-op (as capsule provides intracapsular fracture with localised tamponading)

Answer 80

1) Minimise delays to theatre. Aim to get mobilising as soon as possible - Surgery within 48 hours should be standard, some suggest within 36 hours (patients with pre-existing cognitive deficit, 2x increased risk of delirium if >24 hours wait) - Increased morbidity, mortality with delay (but most studies don't say why delay occurred. Some optimisation may be acceptable) - Reasons to delay: severe electrolyte abnormalities (K+ <2.7), decompensated heart failure, sepsis, coagulopathy, MI, complete heart block 2) Avoid hypotension - increases mortality, delirium 3) Utilise regional anaesthesia - reduces delirium, opioids 4) Minimise risk of delirium - Identify high risk patients. Reduce opioids. Reduce time to theatre. Avoid tramadol. Re-orientation. Use hearing / visual aids. Assessed by geriatrician. Defend MAP. Optimise electrolytes, Hb. Aggressively treat infection. Avoid urinary retention. Pre-op analgesia / regional. Post op screening for delirium (CAM tool)

Answer 81

If renal function >30ml/min, withhold riva. Give IV fluids. Proceed after 24 hours If eGFR <30ml/min, withhold riva. Check antiXa levels after 24 hours. If this is abnormal, at this point can either delay or give prothrombinex 25u/kg and proceed Can't spinal unless riva withheld for 3 days (normal renal function) or 5 days (eGFR <30ml/min) or normal anti-Xa levels. Check with haem If intraop bleeding, give prothrombinex 25-50IU/kg

Answer 82

Withhold dabi, check TCT on admission (ensure they have been taking dabi) Give IV fluids, wait 24 hours Recheck TCT 3 horus prior to surgery. If <40s can proceed with surgery. If >40, consider idarusuzimab 2.5-5mg IV and proceed Spinal only if TCT <20s

Answer 83

Withhold warfarin Determine indication of warfarin ?AF ?mechanical valve (and type) ?antiphospholipid syndrome Check INR. Determine target INR If for AF and no stroke or VTE in last 3 months, give vit K 3-5mg IV (depending on INR). Recheck INR prior to surgery. If <1.5, can proceed and have spinal. If still raised, either delay or beriplex. But dont delay more than 48 hours, just give beriplex. BRIDGE trial demonstrates safety in withholding warfarin in AF patients without mechanical valves If mechanical valve (unless aortic St Judes = low risk), AF with recent stroke or VTE (within 3 months), likely better to have bridging. Give vitamin K 3-5mg IV. Then check INR Q6Hourly. Once INR

Answer 84

Cutaenous: Anterior thigh - femoral nerve (L2-4) Lateral thigh - lateral cutaenous nerve of thigh (L2-3) Superior-lateral - ilioinguinal and iliohypogastric (L1) Posterior - posterior cutaenous nerve of thigh Capsule: Anterior: femoral, obturator (L2-L4) and accessory obturator branches. Anterior most indicated for NOF fractures. Mainly blocked by PENG Medial: obturator articular branches. Blocked by PENG Posterior: nerve to quadratus femoris (L4-S1), contributions from sciatic and superior gluteal nerves. Variably blocked by PENG

Answer 85

11,000 hip fracture patients. Increased mortality based on single lowest recorded MAP during intraop. Aggresively defend MAP if spinal or GA. Prevent bleeding (TXA), tranfuse. Prepare for bone cementing with vasopressors and euvolaemia

Answer 86

No benefit for delirium between GA and spinal. n= 950

Answer 87

No benefit mortality or morbidity at 60 days for GA vs spinal in hip fractures. Also no difference delirium or post op ambulation at 60 days

Answer 88

Male CVS disease Diuretic use Increased age

Answer 89

Surgeon - inform anaesthetist before mixing (when femur being prepared) and when performing cementing, confirm they have heard - careful wash and prepare of femoral canal - lowest possible manual pressures Anaesthetist - Euvolaemia - Hb okay - Vasopressors - aim for MAP +/-10-20% pre induction values - Increase FiO2 - Invasive monitoring with arterial line if very high risk - Watch monitoring during cementing. Particularly etCO2, sats, HR and BP

Answer 90

Anterior-posterior compression (AP). Front on collision. Widening of pelvic ring. AP3 = complete SI joint disruption Lateral compression (LC). Impact from side. Cause internal rotation of pelvis. LC3 = open book = pubic rami, iliac crest and contralateral fracture / ligamentous disruption Vertical displacement. Usually fall from height. Displacement of fracture vertically (not well fixed by pelvic binder)

Answer 91

high mortality - 5-15%. Haemorrhage leading cause of death. then TBI (20%) - Bleeding can be entire blood volume before tamponading occurs in pelvis -Advanced trauma life support protocols. - 1G TXA then further 1G over 8 hours (CRASH 2) - Pelvic fractures rarely isolated. Use eFAST for PTX, tamponade, free fluid abdomen. CT trauma - Pelvic binders. OVer greater trochanters, approximates fractures to stop bleeding. Not good for vertical displacements. Will get in way of IR angiography but won't for laparotomy. Shouldnt be on longer than 24 hours - increases nerve injury, pressure sores - Log rolling contraindicated, may disrupt clots. Direct lifting prefered - Damage control surgery either pelvic packing with laparotomy or IR arterial embolisation - Usual damage control resus of avoiding coagulopathy, permissive hypotension and damage control surgery

Answer 92

Initial stabilisation - IR, ex fix or pelvic packing. May include bowel and ureter diversion if injury to reduce feculant material Definitive surgery. ORIF or percutaenous screws. May be anterior approach (pfennenstiel incision), lateral or prone - Posterior more likely if acetabular recon needed Post op, VTE prophylaxis. high rates of VTE 35-60%, 25-30% are proximal VTE. HDU post op at a minimum

Answer 93

systematic review and meta analysis. 94 studies, but not all included for each outcome. Mortality had n>200,000 Neuraxial has benefit over GA for: mortality, AKI, pulmonary complications, DVTs, strokes, blood transfusions, infections. Worse for urinary retention

Answer 94

108 RCTS, 21 meta analyses. GA or regional has minor impact on post op pain Grade A evidence for paracetamol, NSAIDs and 8-10mg IV dexamethasone Grade D for fascia iliaca and IT morphine

Answer 95

Absolute contraindications: moderate-severe HR, cirrhosis, ACEi + diuretics, entresto, eGFR <40ml/min Half dose: (=100mg celecoxib daily). single diuretic, age >85 and albumin <35, weight <50kg, eGFR 40-60 Fine to have if IHD, peptic ulcer or mild HF

Answer 96

Cochrane review 2024. 102 studies, N >8000. Reduce bleeding, transfusion requirments. Unclear on dose or method of delivery. Best seemed to be combination of oral and topical TXA

Answer 97

VTE risk is 0.6% of all patients. 0.3% will have a PE. 0.03% will die from VTE JAMA systematic review - aspirin vs traditional anticoagulants. No statistical significant difference (but note VTE is rare so hard to study) Benefits of aspirin - cheap, easy to administer, no monitoring needed, patients familiar with it some guidelines suggest aspirin or anticoagulant (ESA). some suggest anticoagulant for 10 days then 28 days of aspirin (NICE) CRISTAL trial (2022) in Australia. 31 hospitals elective hips and knees. symptomatic VTE 3.5% in aspirin group. 1.8% in enoxaparin. No mortality difference either way, early mobilisation is key. + TEDS, SCDs. Determine who is high risk or not

Answer 98

Grade A: paracetamol, NSAID, dexamethasone, adductor canal block Does not recommend gabapentinoids, ketamine, dexmed, fascia iliaca, femoral nerve blocks or epis

Answer 99

Decrease intraop bleeding, transfusion intraop and operation time. But didn't decrease overall bleeding. Increased risk of DVTs and slowed first time to mobilising Cochrane review - moderately associated with increased pain. Blood loss not particularly improved. Duration should be limited if used

Answer 100

Find apex of scoliosis. Then find most tilted vertebrae above and below the apex. Draw paralell lines across these vertebrae. Then from the two parallel lines, draw a perpendicular (90 degree) line off each so that these perpendicular lines intersect. Cobbs angle is the acute angle between these lines. Alternatively, the angle formed by drawing the two parallel lines until they intersect from the most tilted vertebrae will also be the Cobb's angle Usually Cobb's >40 degrees + skeletal immaturity + symptomatic (back pain, dyspnoea, CVS compromise) --> surgical correction. Cobb angle >65 degrees will cause reduced pulmonary function

Answer 101

Most common is adolescent idiopathic (80%) Secondary: - Muscular dystrophies - Cerebral palsy - Spina bifida - Friedreich's ataxia - Marfans

Answer 102

Indication: Usually Cobb's >40 degrees + skeletal immaturity + symptomatic (back pain, dyspnoea, CVS compromise) --> surgical correction. Cobb angle >65 degrees will cause reduced pulmonary function Complciations from scoliosis: - REsp - restrictive lung disease, pHTN, right heart failure. Impaired FRC, recurrent chest infections. - CVS - compression of great vessels - Neuro - chronic pain, spinal stenosis, nerve compression - MSK - arthritis - Psych - depression, anxiety - Determine surgery type - Magic or growing rods more common these days. Historically multi level fusion - Determine if idiopathic or associated conditions (cerebral palsy, muscular dystrophies, Friedreichs ataxia, spina bifida, Marfans) - Spirometry in most patients but especially if dyspnoea - If evidence right heart failure (SOBOE, raised JVP, peripheral oedema), get echo. Also get echo if congenital disease that may have cardiac implications - Usual paeds history - birth, congenital screening, developmental milestones - Airway assessment, may have difficult airway if c spine involvement - Informed consent with patient + parents. High risk bleeding, transfusion. Prolonged GA. Eyes

Answer 103

-Monitoring: usual + EEG + arterial line + CVL + nerve stimulator + temp +/- intraop neuro monitoring (SSEPs, MEPs) -TIVA if using neuro monitoring. Single dose NDMR beginning of case. Neurophysiologist present -Difficult airway possible - VL or asleep FOI. Reinforced ETT as prone. Reduced FRC possible, preoxygenate well. Rarely used but DLT if anterior approach to thoracic vertebrae -Positioning - superman if lumbar and lower thoracic, arms by sides if higher thoracic or c spine. Ensure arms well positioned to reduce nerve injury -Eyes are important -Bleeding risk high, average of 750ml. higher if congenital scioli. Ensure warming, 2x large bore IV, group + screen, TEG, monitor Hb, cell salvage. TXA (risk factors for bleeding are: female, smaller BMI, revision surgery, higher Cobbs angle, prolonged surgery) - Analgesia. Multimodal: paracetamol, NSAID, opioids, ketamine, dexamethasone. Consider surgical placed epi vs bilateral erector spinae. IV PCA Post op: - HDU - ERAS. Early mobilisation, PT / OT, anti emetics, early food and drinking, minimise drains and IDC out when mobilising. Nutritional support. Analgesia to support mobilising - Post op complications to watch for: 1) from prone (nerve injury, eye injury, airway swelling, venous air embolism, pressure wounds) 2) neurological (dural tears, epidural haematoma, spinal cord ischaemia) 3) Implant related (rod breakage, screw misplacement) 4) Other complications of prolonged surgery - PE, MI, pneumonia, AKI, DVT, coagulopathy, transfusion reactions

Answer 104

- If unstable, MILS. Consider options for difficult airway (awake bronchoscopic, VL, awake VL). No neck extension - Other injuries common with c spine trauma, especially TBI - consider risk of autonomic dysreflexia if trauma >3 weeks ago. Consider neurogenic shock if more recent injury. Avoid sux - Determine if anterior (Anterior cervical decompression and fusion = ACDF) or posterior approach (= prone) - Bleeding typically 500-1000ml. IV access, warming. Consider art line - Retraction of carotid sheath --> vagal, bradycardia - If prolonged C spine surgery or significant trauma, may need leak test before extubation due to supraglottic oedema or pharyngeal haematoma. 2% of c spine patients get re-intubated

Answer 105

Spinal surgery where increased chances of neurological injury e.g. deformity surgery, scoliosis. Needs a neurophysiologist to interpret. Tell this person the drugs you've given SSEPs = somatosensory evoked potentials. Small potentials evoked in somatosensory cortex when stimulation of peripheral nerve (e.g. posterior tibial nerve). NMBAs are actually useful here as small tremors can influence results (but not used). Decrease in latency by 10-15% or amplitude by 50% is signficant. Neurological deficit post surgery if SSEPs all normal = 0.063% MEPs = motor evoked potentials. Current with 300-700V applied to motor cortex, detect motor potentials (usually tib ant, abductor hallucus and vastus medialis). Influenced by NDMRs so don't use Both SSEPs and MEPs dose dependent reduction with volatile, N2O. MAC >0.5 incompatible with MEPs. Ketamine may enhance SSEPs. Opioids probably least likely to affect SSEPs and MEPs. Gold standard is "wake up test" but rarely used.

Answer 106

Sensory: - Axillary nerve (brachial plexus), posterior cord. Lateral cutaenous + inferior/anterior capsule - Suprascapular nerve (brachial plexus, superior trunk). Superior + posterior capsule - Subscapular (brachial plexus, posterior cord). Small contribution - Lateral pectoral (brachial plexus), minor contribution anterior + superior capsule - Supraclavicular (cervical plexus) - not the joint itself, but overlying cutaenous innervation for shoulder cape Motor: - Axillary. Deltoid + teres minor (abduction after 15 degrees, external rotation) - Lateral and medial pectoral. Pec major - Long thoracic nerve. Serratus anterior (protraction. Weakness causes medial winging) - Suprascapular - supraspinatus, infraspinatus (first 15 degrees of abduction. External rotation) - Subscapular - subscapularis, teres major (internal rotation) - Spinal accessory nerve (CN11). Trapezius, SCM. (Shrugging, weakness causes lateral winging) - Dorsal scapular nerve. Rhomboid major, minor. (retraction of scapula. Weakness causes lateral winging) Blood supply: From axillary artery. Anterior and posterior circumflex arteries. Subscapular artery From thyrocervical artery. Suprascapular artery

Answer 107

- Regional. Consider interscalene. Usually pretty sore so multimodal analgesia - Headup. Increased risk of VAE, stroke. Maintain BP. consider arterial line with transducer at head height. Will aid with ventilation - Surgeon near airway, use ETT - Bleeding risk -

Answer 108

Complex. Hard to block Mainly from supraclavicular nerve (cervical plexus, C3 + C4). Has medial, intermediate and lateral branches. Contributions by suprascapular, long thoracic and subclavian nerves (all from brachial plexus). Regional only technique would involve a cervical plexus block (e.g. superficial cervical plexus) and a brachial plexus block which covers the suprascapular nerve (interscalane)

Answer 109

Complex. Hard to block Intercostal nerves Superficial cervical plexus (supraclavicular nerve) Brachial plexus (suprascapular nerve + others probs)

Answer 110

Thoracic intercostal nerves. T2-T6. T4 for nipple. - lateral cutaenous branches of ventral rami for lateral breast. Anterior branches of ventral rami for medial breast Supraclavicular nerves (medial, intermediate, lateral). From cervical plexus -Superior portion of breast cutaenous innervation Intercostalbrachial nerve (T2) - Axilla, medial upper forearm Medial and lateral pectoral nerves (from brachial plexus). Between pec major and pec minor

Answer 111

Live autologous tissue taken from donor site and transfered / anastamosed into new location. Has both venous and arterial anastamoses

Answer 112

DIEPs and TRAMs both anastamosed to internal mammary artery - proximal to heart with good pressures -DIEP has no muscle - no abdominal muscle weakness, reduced hernia risk, less risk of ischaemia (as less tissue VO2 requirements) - Less pain Both DIEP and TRAM provide some level of cosmesis for abdomen (tummy tuck appearances)

Answer 113

Main goal is to provide improved O2 delivery to flap. O2 flux = blood flow x blood O2 content. Preop - smoking cessation (at least 4 weeks). Reduces CO, reduces vasoconstriction from SNS, less platelet activation - (sickle cell anaemia and polycythaemia are contraindications to free flap surgery) - Treat underlying anaemia Intraop - Avoid hypoxia, hypocapnia, acidaemia (hence also avoid hypercapnia) - ensure MAP acceptable. Likely +/-20% of normal - Avoid hypothermia, active warming + monitoring temp - Avoid excess CVP. Lower insp pressures, avoid excess PEEP - Euvolaemia. Excess fluid will cause oedema of free flap, venous congestion - Avoid anaemia. Hb >90g/L. Optimal HCt likely around 0.3-0.35 for optimal viscosity and O2 delivery - Some use of vasopressors are fine to maintain MAP (journal of microsurgery 2019 systematic review + meta analysis) - Regional to recipient site might be useful for vasodilation and improved perfusion. The blood vessels of the flap themselves don't respond to block as denervated but the supplying vessels do - Anaesthesia preconditioning with sevo might be a thing. Unclear Post op - avoid shivering (tramadol) - Keep warm - Regular checks, start at Q30 mins. HDU may be needed - Assess with doppler, CRT, colour of flap. Early return to theatre best if compromised flap

Answer 114

1L of 0.9% Nacl with 100ml 1% lignocaine (so 0.1% lignocaine) and 1mg adrenaline (so 1:1,000,000). Super wet technique = 1ml LA mix per 1ml fat sucked up. Peak LA absorption 12 hours Limit adrenaline to 6mg (peak effect is 4 hours post op). Monitor for cardiac ischaemia Max dose 35mg/kg lignocaine

Answer 115

1% blood loss per 1ml of LA used (so if 1L of LA used, then 100ml bleeding). Would be much higher (40%) if LA didn't have adrenaline in it.

Answer 116

FTSG contains epidermis + dermis in entirety. Must be excised by scalpel. Used in small areas where full thickness important for cosmesis or function (e.g. face, hands). Donor sites include posterior auricular skin, groin skin, antecubital skin. STSG has epidermis + variable amounts of dermis. Harvested by dermatome. Meshing done to expand graft. donor sites include thighs, abdomen. Can store skin for 2 weeks at 4c. Donor sites often sore.

Answer 117

Within 48 hours for debridement. But delayed by first 24 hours for resuscitation. Aim to debride burns to reduce sepsis risk and cover with silver coating dressings

Answer 118

3% of total blood volume per 1% TBSA debrided, more if infected or very deep burns (more than whole blood volume of over 30% TBSA burns)

Answer 119

4ml / kg / %TBSA = Iv fluids in 24 hours. First half of this total within 8 hours of the burn occuring (sometimes have to catch up if late presentation to hospital) Second half of this total over next 16 hours Doesn't include maintenance fluids. titrate to urine output between 0.5-1ml/kg/hour

Answer 120

-GA, ETT -Monitoring will need to be pragmatic - wherever you can get NIBP. May need arterial line and suture it in - Personnel- experienced tech, surgeon, anaesthetist - IV access similarly have to be pragmatic. May need central access - Avoid sux if >24 hours. Will "burn" through NDMRs due to extrajunctional receptors (up to 40% increased requirements if needing ongoing paralysis) - Lung protective ventilation, high RR. May have hypercapnia from high metabolic requirements - Avoid hypothermia. Active warming theatre and patient, HME filter, monitor temps. But can reduce temp if patient fine (surgeons will thank you) - analgesia with ketamine - Large volume bleeding can occur (3% total blood volume per 1% TBSA debrided). Ensure large bore access, group and screen. May need to stop surgery to go to ICU for resus - consider ICU if airway burns, burns >40% or haemodynamic issues

Answer 121

- ICU if haemodynamic issues, burns of airway or burns >40% - Sepsis. Loss of protective skin covering - 50% of mortality in burns due to infection. Most commonly staph aureus, streptococcus, enterococcus, klebsiella, pseudomonas. Antibiotics to cover these (often augmentin?) - Early nutrition. Often need 200% increase caloric requirements. Dietician. NG feeding (no more than 55% glucose or risk hyperglycaemia, no more than 30% fat or risk hepatic steatosis. Aim 1-2g/kg/day of protein). Often deplete of vitamines B, C, D and E and trace elements copper, zinc, selenium. Nutrition improves wound healing, reduces infection risk - Dressings silver impregnated. Dressings changes on ward with ketamine / midazolam PCA (10mg ket, 0.5mg midaz Q5mins) - PT / OT / hand therapy. analgesia to facilitate engagement with this

Answer 122

Thoracoscore. Based on demographics, type of surgery, comorbidities and functional status. Based on 15,000 French cases and validated in USA. c index of 0.85. Logistic regression

Answer 123

Predicted post op value. Usually for PFTs. Based on number of segments total (19) and number of segments to be removed (e.g. RUL would be 3 segments. RLL 5 segments) If PPO FEV1 <40% predicted, patient should get CPET testing for lobectomy Should also get CPET testing if DLCO <40% predicted

Answer 124

For lobectomy. VO2max <15ml/kg/min, then high risk surgery. Needs HDU bed. If VO2max <10ml/kg/min, alternative to surgery should be sought for pneumonectomy, VO2max should be >20ml/kg/min

Answer 125

(obviously non-pharma options in an SAQ) Systemic - Pdol - NSAIDs - Opioids +/- PCA - Ketamine - Lignocaine - Alpha 2 agonists Regional - Surgical placed intercostal chest wall catheters - ESP block - PVB - Serratus anterior plane block - thoracic epi Regional demonstrated to be useful for reducing post op chronic pain in thoracic surgery. In particular thoracic epis

Answer 126

RUL - 3 (hence the classic clover appearance). First to shoot off the right main bronchus. Occasionally from the trachea directly (1%) RML - 2 RLL - 5 Left lobes are annoying. Have between 4-5 segments each LUL - 4-5. Including 2x lingula segments LLL - also 4-5. Total usually somewhere between 18-20. With more variation on the left

Answer 127

Bottle 1 = fluid collection. Allows for blood / effusion / infected fluid removal from pleural space. Bottle 2 = underwater seal, basically a one way valve. Drain should always be 45cm below patient to prevent H2O and water entering patient. Tube into bottle 2 H2O usually 2cm submerged under water to provide seal. Air can escape but can't re-enter back to bottle 1 Bottle 3 = suction regulator bottle. Has a tubing that is open to air (vent tube). It is height of vent tube that determines the amount of suction transmitted to the pleura (so if 10cm submerged, then -10cmH2O maximal pressure no matter how much applied via wall suction) Usually 10-20cmH2O suction applied in lobectomy. Not pneumonectomy Bottle 4 = safety underwater seal. Relieves pressure in case of kinking or obstruction of tubing of main tubing

Answer 128

With insertion: - lung injury - cardiac perforation - liver perforation - Spleen - Kidney -Thoracic duct - Intercostal nerve / arterial / venous injury. Bleeding. Nerve pains Maintenance: - kinked, obstructed, disconnected chest drain - re-expansion pulmonary oedema - Infection, empyema With discontinuation - Plueral-cutaenous fistula - scarring - Chronic pain if nerve injury

Answer 129

<50ml output over 8 hours Pneumothorax <10% original size No ongoing bubbling, but still swinging (air leak stopped)

Answer 130

DLT (left and right) Bronchial blocker Univent tube (single lumen tube with a side arm for bronchus) EZ blocker tube Single lumen tube driven endobronchially

Answer 131

Surgical access (VATS lobectomy) Needing differential ventilation from each lung (e.g. one lung much higher compliance than other, risk of bullae rupture, severe air leak) Prevent contamination (abscess, pulmonary haemorrhage)

Answer 132

0.33 x Fr = external diameter. So 39Fr = 13mm external diameter DLT (but internal diameter in 6mm for each lumen)

Answer 133

Advantages: - easier to insert, more rapid to insert in emergence - Technically don't need bronchoscope. Can test clinically (bronchial blocker definitely needs bronchoscope) - Suctioning, toileting of each lung is possible - Easy to ventilate one lung then change and ventilate only the other lung (potentially useful if recruitment of each lung) - More secure once tied in than a BB, especially with change of position Disadvantages: - Risk of tracheal trauma, rupture - Increased sore throat, dental injury risk - More difficult to insert in difficult airway than SLT (which would be conduit for BB) - BB could block off a single lobe if poor lung function. so could ventilate the remaining 4 lobes - right sided tubes notoriously difficult to seat correctly

Answer 134

8 years old (as per SSH guidelines). Gets a 26Fr DLT. Otherwise needs a BB Use 5Fr BB in small children / infants. Use 2.2mm bronchoscope in paeds. Co-axial placement if >2 years (BB through endotracheal tube). Parallel placement if <2 years (outside the ETT) as ETT too small to ventilate through + have BB and bronchoscope through it

Answer 135

May be due to large (50%) shunt and subsequent V/Q mismatch. Need to optimise and rule out other potential contributions to hypoxaemia. Typically will get dip in SpO2 on one lung then return to normal due to HPV (occurs over 40 mins for first phase) If rapid decline, inform surgeons and call for help (anaesthesia assistant +/- senior anaesthetist with thoracic experience) Consider other causes hypoxaemia: PTX (especially if bullous emphysema in ventilated lung), PE, RV failure, anaphylaxis, bronchospasm ?what SpO2 is unacceptable for patient. E.g. 88-92% target for bleomycin exposed patient. - FiO2 100% - Machine to patient approach - Scan monitoring - EtCO2, Hr, BP, airway pressures. Check sats trace, rule out monitoring issue - Onto manual bag - check compliance, obvious secretions + eliminate ventilator - Ensure paralysis with NDMR (rest of the things will be easier if paralysed patient) - Back onto vent, may increase RR, TV or PEEP if able (lung protective ventilation ideal though) - Check DLT position, if shifted or twisted? - Suction down DLT for secretions - Bronchoscope - confirm position of DLT and remove secretions - Auscultate chest ?wheeze ?PTX. Treat bronchospasm with bronchodilators - Improve cardiac output if this is an issue (e.g. MAP +/- 20% of normal MAP) - Auxillary CPAP valve for lung on operative side (inform surgeons) - Intermittent two lung ventilation (inform surgeons) - consider TIVA (minimal evidence but sevo may impair HPV) - Rarely, clamping unilateral pulmonary artery to reduce shunting. May be for pneumonectomy

Answer 136

4Ts are teratoma, thyomoma, thyroid mass and terrible lymphoma In kids, may get neuroblastma and PNET (primitive neuroectodermal tumours Anterior medistinum bound by sternum anteriorly, pericarium posteriorly. Diaphragm inferrior. thoracic inlet superior

Answer 137

From tracheobronchial compression: dyspnoea (worse while flat), stridor, chronic cough, chest discomfort. Usually only symptoms if high degree of stenosis (>50%). children more often symptomatic as smaller airways From SVC obstruction: vein engorgment, pembertons +ve, headache, airway, facial and upper limb oedema, visual changes RA / RV compression: dyspnoea, peripheral oedema, raised JVP, ascites, hepatosplenomegaly (basically RHF) From the mass itself: Hyperthyroidism, myasthesnia gravis (thymoma), weightloss / night sweats (lymphoma), paraneoplastic

Answer 138

Best way to remember is that variable intrathoracic will look like asthma: the expiratory limb will be impaired. Extrathoracic will have the opposite (like stridor, impairs inspiration) Fixed obstruction will impair both inspiration and expiration Flow volume loops not really used any more as don't really change management / change anaesthetic technique

Answer 139

- Likely mass type - ?thyroid ?thyomoma ?lymphoma ?teratoma. And implications of these - Mass effects - airway obstruction (most concerning if >50% tracheal stenosis, especially if cant get passed with ETT. Or if symptomatic (stridor, dyspnoea, orthopnea). - SVC obstruction (airway swelling, face swelling, neck vein engorgement, upper limbs) - RA / RV obstruction (RV failure) - CT, echo, usual bloods. CT critical for knowing what is involved - know operative plan. ?biopsy ?resection ?approach (do they need OLV for resection?) - Depending on mass, could benefit from preop chemo, radiation or steroids - Risk stratification: - Low risk = asymptomatic, no compression of vessels and minimal airway stenosis. Usual GA fine - Mid risk = some symptoms or moderate compression of trachea (but <50%). Grey zone. Carefully titrated GA, consider spont breathing ETT placement. Arterial line - High risk = symptomatic + tracheal stenosis >50% or great vessel / cardiac compression. Preemptive ECMO for GA. Or LA only

Answer 140

- Always have backup plan B, C airway for if becomes hypoxic with plan A - Rigid bronch will need GA (flexible bronch could be done with light sedation). Aim spont ventilation TIVA (remi + propofol TCI) with open airway and HFNO initially. - Then plan for intermittent jet ventilation down rigid bronch - If needing apnoea, then apnoeic oxygenation with HFNO fine too (but usually only need paralysis for stent deployment) - LA to vocal cords to reduce response to rigid bronch - consider arterial line if needing to measure PaCO2 - Can get life threatening asphyxia from bleeding / clots Post op: -Often can be day stay. NSAID + Pdol - Jet ventilation issues - gas trapping, pneumothorax, pneumomediastinum - Shared airway issues - bleeding, dental injury, aspiration - Stent issues - migration, fracture, erosion of stent (can get fistula from trachea to oesophagus)

Answer 141

Endobronchial valves, placed via bronchoscopy. Basically one way valves that induce atelectasis in the diseased lung segments. Lung reduction surgery has high mortality (10%) with no obvious benefit. Sometimes interlobar collaterals (present in 2/3rds of COPD patients) limit endobronchial valve efficacy. But endobronchial coils may help in this case

Answer 142

Pre op - Need to be very fit. PPO (predicted post op) values will effectively be half (worse if right lung being removed) pre op values. Need FEV1 >80% for PPO to be >40%. CPET VO2max >20ml/kg/min - Always need bloods, ECG, PFTs, echo, CPET - mortality 5-10%, need to inform patient high risk and get informed consent - Usual cancer considerations - mass effect, chemo, radiation, paraneoplastic, anaemia, nutrition, cachexia, mets Intraop - Montoring - standard + art line + EEG + CVP - Lines - CVL, 2x large bore. Ensure CVL on same side as pneumonectomy (as won't tolerate PTX on opposite side) - Airway. DLT. Can use a left DLT even for left pneumonectomy. but prefer to place correct sided DLT. Bronchoscope available - Breathing. Lung protective vent of one lung. Need to avoid excess fluids, airway pressures (high risk for oedema post op) - Circulation. Avoid excess fluids. CVP low (<5cmH2O). Most common cause death post op = APO. Maintain BP with vasopressors. Goal directed fluid challenges. Prepare for PVR doubling with PA clamping. Have normal PaCO2, avoiding hypxoa, avoiding acidosis, normothermia - Disability - GA with TIVA or volatile fine - analgesia - Multimodal. Regional with PVB - Positioning = lateral decubitus. Long op. Pad well Postop - ICU or HDU - Watch for complications: APO, infection, atelectasis, PE, bronchopleural fistula, bleeding, cardiac herniation - Acute lung injury occurs in 4% of pneumonectomies, has 30-50% mortality. Risk factors are alcohol abuse, >4L Iv fluids, high insp pressures

Answer 143

High risk if right sided pneumonectomy. Present with obstructive shock (compression of great vessels) Flip patient so operative side facing upwards. Consider injecting 1L air into operative site Return to theatre

Answer 144

Empyema = infected fluid (pus) in pleural space. Causes: pneumonia, chest wall trauma (especially penetrating), bronchial tumours. Decortication = pealing off thickened, disease, pleural membrane High risk for bleeding (>1-2L), pain. Often 2-3 hour surgery. Can develop bronchopleural fistulae too. Need DLT if air leak and PPV only once isolated Check for sepsis if pneumonia Cant do PVB if pleura being removed (can do epi, erector spinae or SA plane blocks)

Answer 145

Preop - Causes: Recent surgery - pneumonectomy, lobectomy. Most common cause (5-20% risk post pneumonectomy, typically 1-2 weeks post op) Infection - pneumonia, empyema, pulmonary abscess, TB Chest drain insertion Malignancy - primary or metastatic lung Ca Trauma - penetrating chest wall injury Radiation to chest wall - Risk factors - right sided pneumonectomy, malnutrition, diabetes, persistent empyema, residual lung tumour - Symptoms: Fevers, dyspnoea, haemoptysis, subcut emphysema, persistent air leak, falling fluid level on CXR post pneumonectomy - CT chest to assess size, location, lung remaining and any mediastinal shift - Assess for sepsis, respiratory compromise. Some patients on death's door. Ropey anaesthetic to follow - Active resuscitation and chest drain prior to induction of anaesthesia Intraop - Most experienced thoracic practitioner available + senior surgeon + anaesthesia assistant - Goal is to get DLT in and isolate so no contamination of good lung from bad lung. confirm isolation before PPV. If PPV before isolation, could worsen air leak and cause tension pneumothorax too - Depends on size of fistula and how unwell. If small (<5mm), IV induction with gentle PPV via bag mask and DLT with quick-ish isolation acceptable - If very unwell, large air leak or fistula >8mm, described technique is 3 anaesthetists. One for laryngoscopy + place DLT, one with a bronchoscope and one to watch anaesthetic - Could also consider AFOI with spont ventilation and SLT endobronchially. Would be challenging to do spont ventilation with DLT - As well preoxygenated as possible + RSI with high dose rocuronium Postop - Extubate as soon as possible - HDU -

Answer 146

Previous PTX Connective tissue disease (e.g. Marfans) Severe asthma Positive pressure ventilation, high airway pressures (e.g. obesity) Smoking COPD. Especially bullous emphysema Males, especially younger <30 years old. Tall, thin stature Lung malignancy Air travel or scuba diving after previous PTX

Answer 147

Concerns regarding inhibition of inflammatory changes from chemical (talc) or mechanical pleurodesis --> may reduce efficacy. One study from 2024 suggested use of NSAIDs >48 hours increased risk of recurrent pneumothorax Pleurodesis is usually very sore post op. Cant use PVB as pleura not intact. Alternatives are epidural or ESP block or intercostal catheter by surgeons

Answer 148

STUMBL score - based on age, comorbidities, number of ribs broken Lower risk if <15, give oral opioids or PCA If 15-30, consider regional anaesthesia 30 or more, regional unless reason not to. HDU admission

Answer 149

Always mention non-pharma options - incentive PT - Functional assessment pain - rib fixation (especially flail segments) - Pain team review Pharma - PDol - NSAIDs - Opioids + PCA + tramadol - Regional: ESP block, SA block, PVB, thoracic epi

Answer 150

Very commonly fatal prehospital -Signs / symptoms. neck SC emphysema, pneumothorax not responding to chest drain / ongoing air leak, respiratory distress - Goal is to intubate beyond injury. If tracheal injury, aim distal. If bronchial, aim for OLV - Options to intubate include: VL - VAFI - AFOI - If ventilation fine, may do a flexible bronch to assess injury prior to GA - If carinal disruption, high risk of dying. May need ECMO preemptive (CPB might be tricky as need heparin which could cause massive haemorrhage) - If intrathoracic injury, surgery is thoractomy

Answer 151

Suspect if sternal fracture, rapid deceleration - 12 lead ECG (may have St changes, arrythmia, heart blocks or SVT - Spectrum from minor myocardial contusion through to wall / valve rupture - If ECG changes or trop rise, admit for 48 hours. Get inpatient echo - Admit HDU - Sometimes need inotropy

Answer 152

1-2% risk if 5-5.9cm. Becomes 15% risk if >6cm

Answer 153

No difference mortality, MI, Trop T levels between TIVA and sevo (but pretty underpowered for mortality)

Answer 154

1) Bleeding - get surgeons to sort it out 2) Drop in systemic vascular resistance from clamp 3) Response to metabolic byproducts - K+, H+, lactate. CO2 increases from Haldane effect (increase H+). Negative inotropy from H+ too

Answer 155

Prepare for 3 causes of hypotension: 1) Bleeding 2) Metabolic byproducts (H+, K+, lactate and subsequent vasodilation, negative inotropy) 3) reduced SVR Ensure electrolytes normal. Correct K+ so <5.0. Ca2+ Correct acidaemia, ensure normal bicarb. Hyperventilate slightly as PaCO2 will increase with H+ load Increase FiO2. Will get drop in sats from Bohr effect Hb >90g/L Euvolaemia Normoglycaemia Normothermia Turn off vasodilators (e.g. GTN infusion) Turn on vasopressors (e.g. noradrenaline or metaraminol) Communicate with surgeons. May be best for partial release from single iliac vessel. Especially if high clamp or long duration

Answer 156

Improved 30d mortality for EVAR compared to open (4% vs 2%). But similar 2 year mortality. DREAM and EVAR-1 for elective IMPROVE was for ruptured AAA, showed similar mortality at 30d for open and EVAR. But women did better with EVAR. Also reduced hospital costs, reduced LOS with EVAR. Also more likely to go home (rather than rest home) IMPROVE also showed LA alone for ruptured AAA improved mortality (13%) vs GA (34%).

Answer 157

AKI - pre-renal mainly from hypotension, hypovolaemia and aortic ballooning. Also nephrotoxicity from contrast Lower limb ischaemia - from atherosclerotic lesions + prolonged aortic ballooning Ischaemic colitis (less common than open AAA, 6% vs 20%). Mortality 25-50% Vascular access issues - pseudoaneurysm, haematoma, retroperitoneal bleeding Spinal cord ischaemia Stent migration. Endoleak MI, stroke, PE

Answer 158

Female, rapidly expanding AAA, connective tissue disease, smoking, hypertension, large AAA

Answer 159

Aneurysm = enlargement of all 3 layers of blood vessel (intima, media and adventitia) Dissection = disruption of intima, bleeding into wall of vessel Pseudoaneurysm = rupture through layers of vessels but held together by other external structures

Answer 160

Risk is 4-10% of cases for spinal ischaemia, most commonly due to cross clamping above artery of Adamkiewica (largest segmental medullary artery, typically from T8-L1 in 80% of people). Risks for SCI: long operation, long cross clamp times, extent of aneurysm, hypotension, diabetes, advanced age, smoking, anaemia Spinal cord ischaemia due to lack of O2 to spinal cord. O2 flux = arterial O2 content x spinal blood flow O2 content - SpO2, Hb concentration Blood flow - Perfusion pressure / vascular resistance MAP - +/- 20% of normal, aim spinal cord perfusion pressure >70mmHg Avoid excess CVP, PEEP Lumbar spinal drains (Khan 2016 metaanalysis, 50% reduction in SCI in open repair). aim CSF pressure <10mmHg. Drain off 20-30mlhr. Then post op keep for 2 days (aim 5-12mmHg). AHA states level 1A evidence. SSEPs, MEPs monitoring

Answer 161

Stanford type B = descending aorta only. Most commonly medical management Aggressive BP management. ICU admission. Decrease wall stress by decreasing afterload and HR. Arterial line + ECG 1) esmolol. 50mcg/kg/min +/- bolus IV loading. Or labetalol. Usually BB first so dont get the reflex tachy from vasodilators 2) GTN 3) SNP 4) Nicardipine Targets are Systolic BP 100-120mmHg, HR 60-80BPM. MAP >65mmHg. Surgical management often for failed medical management, expansion of dissection or complex dissection. TEVAR most commonly.

Answer 162

Stroke (especially if near arch) MI AKI Spinal cord ischaemia Lower limb ischaemia Vascular access issues - haematoma, bleeding, pseudoaneurysm Aortic rupture Stent - migration, endoleak, infection

Answer 163

TIA or stroke within 2 weeks for evidence of improvement. Internal carotid with >70% stenosis, likely contributary to the neurological insult.

Answer 164

Stroke, TIA 1-5% risk MI (due to risk factors) Haematoma - airway, recurrent laryngeal, carotid sinus compression (bradycardia, hypertension) Hyperaemia (aim BP 100-160mmHg), risk of haemorrhagic stroke or transformation of existing ischaemic stroke Regional complications - recurrent laryngeal block, phrenic nerve block, brachial plexus block Delirium

Answer 165

Inform surgeons Augment BP, increase MAP >10% of baseline (fluids, pressors) Increase FiO2 Ensure normal Hb Ensure not hyperventilation, normal PaCO2 Isoelectric EEG, increase anaesthesia (but don't drop MAP) Surgical placement of shunt. May need to convert to Ga if not protecting airway

Answer 166

From axilliary artery tunneled extraperitoneal trouser graft to both femoral arteries. Often last ditch surgery before palliation, patients may have infected graft or aorta occlusion

Answer 167

Risk factors: bilateral amputations, recurrent limb surgeries, high dose opioids / pain levels prior, increasing age (not sex or mental health issues, unlike other chronic pain issues. But if someone with mental health issues gets phantom limb pain, more likely to report as severe) Pathophysiology - unclear exactly. But includes peripheral nerve sensitisation, neuroma formation, central sensitisation / wind up Treatment: No evidence for opioids, gabapentinoids, TCAs, clondine Ketamine does not reduce risk of phantom limb pain. But does reduce severity Salmon calcitonin. Give 100-200U subcut daily for 5-7 days. Unclear mechanism. Neuropeptide, inhibits prostaglandins / cytokines, enhances beta endorphin production. ?Regional?? not shown to reduce risk of chronic pain or chronic phantom limb pains. But epidural likely to reduce risk of severe post amputation pain. One study had perineural catheter for 80 days, very low rates of phantom limb pains

Answer 168

Preop - surgery is for hyperhydrosis, sweaty palms and axillae. Or for Raynauds (prevent excess vasoconstriction) cut thoracic sympathetic trunk at T2-3 - Usually young, well (I guess may not be if systemic sclerosis = CREST = Calcinosis, Raynauds, Esophageal dysfunction, Sclerodactyly and Telangectasia) Intraop - Traditionally done with DLT and OLV. Patient reverse trendelenburg (head up). If doing this and doing bilateral surgery, can be challenging as alternating OLV - Modern way is with spont ventilation on LMA, surgeron pushes lung out way by insuflating with CO2. Aim for no PPV until end of case. Post op complications: - Atelectasis - Haemothorax - Pneumothorax - Compensatory sweating other locations - Horners syndrome

Answer 169

Pre op - thoracic outlet syndrome. Due to compression of brachial plexus = neurogenic (95%), venous compression (5%) or arterial (1%). Msot commonly from compression of 1st rib and clavicle. May be from excess muscle (body building) or from extra cervical rib - Symptoms: Neurogenic: parasthesia, weakness, numbness of upper limb / hand. Atrophy of muscles Venous: oedema of hand / arm, blue discolouration, DVT Arterial: pale, pulseless. Surgery urgent Intraop - Consider superficial cervical plexus block - ETT, IPPV, SLT - Surgeons may want to test brachial plexus - short acting NDMR or no NDMR - Check for lung air leak Psot op - CXR

Answer 170

Fistula have better long term patency, less thrombosis (6x less risk) and less infection (10x less risk). Less morbidity and mortality

Answer 171

-Monitoring: usual stuff, no arterial line ideally - IV access - aim for hand on other limb. Avoid ACF or forearm which are likely future AV fistula targets - Regional. Systematic review of 4 RCTs in 2017 showed AV fistula under regional had OR of 0.28 for failure compared to LA alone (likely from sympatholysis and reduced vasospasm). Reduce LA max dose by 25% due to renal stuff (less protein to bind) - all patients have ESRF - considerations in theater will include whether to intubate (gastroparaesis). And pharmacokinetics - Give minimal fluids. No K+ - Day stay possible. Fistula can be used for 4-6 weeks

Answer 172

Preop - 20% will have congenital heart disease - 30% mortality risk from lung hypoplasia, pHTN - Usually already intubated. May be on high frequency oscillatory ventilation - Needs NG prior to surgery - Often diagnosed antenatally on US Intraop - Surgery will be either suturing a small defect. Or using synthetic graft - 2xIV access. Arterial line (right radial) - Avoid N2O (will worsen pHTN and expand gas filled spaces) - Avoid high airway pressures. Risk of PTX due to lung hypoplasia - High dose fentanyl (15-25mcg/kg) then back to NICU. Fenties avoid sympathetic stimulation Psot op - At risk for pHTN crisis. May need sildanfil, NO

Answer 173

Gastroschisis = defect of anterior abdominal wall. More commonly right of the umbilicus. Herniation of bowel contents without sac covering. More common in prem babies. Bowel wall may be thickened due to exposure to amniotic fluid Exompthalos = Persistent herniation of bowel through umbilical cord. Bowel covered by amniotic sac. High rates cardiac disease associated

Answer 174

1:3500 births. 85% have oesophageal atresia with a distal fistula to the trachea (so oesophagus is blind ending proximal. and then distal to this blind ending is the fistula and remaining is attached to the stomach) Preop - Most diagnosed in utero. If polyhydramnios present, needs to be excluded (as child not drinking the amniotic fluid due to TOF). If diagnosis in uterus, have birth at hospital with NICU and surgery within 24 hours - Increased risk if prem. 25% of TOF kids have congenital heart disease. More common in trisomy 18 and 21 - VACTERL association = Vertebrae, Anorectal, Cardiac, Trachea / Esophagus, Renal, Limbs - PResent with choking, inability to feed, cyanosis with feeding. Unable to pass NG - Needs echo before surgery. - Spitz classification 1 = if >1.5kg and normal heart, >98% chance of living 2 = <1.5kg or abnormal heart, 82% chance living 3 = <1.5kg and abnormal heart, 50% chance of living Intraop - Either done with thoracoscope or thoracotomy. thoracoscope uses CO2 into chest, like pneumoperitoneum here. - Can be done SV or with IPPV. - IPPV risks - need ETT distal to fistula before PPV to prevent aspiration. If unable to ventilate, likely due to ventilating fistula. In urgent setting, may need surgeon to do gastrotomy and block fistula. Bronchoscope may be needed to drive ETT - SV risks - dont do this if pHTN or cardiac disease. Risk of vicious cycle deterioration - high dose fentanyl GA. 15mcg/kg - May need to hand ventilate at times to assess compliance of lungs Post op - back to NICU intubated - sedation with 0.01mg/kg/hr morphine or 0.1mg/kg/hr midaz

Answer 175

Pyloric stenosis from hypertrophy of smooth muscle of pyrlorus. 1:300-1000 births. 80% males. 10% are in prems not a surgical emergency. Medical emergency only Present with dehydration, hypokalaemia, hyponatraemia, hypochloraemia metabolic alkalosis Resuscitation bolus 10-20ml/kg 0.9% NaCl IV (most wont need boluses) Maintenance fluids = 0.9% NaCl + 5% glucose (10% glucose if <4 weeks) +/- 20mmol/L Kcl (add potassium once UO greater than 1ml/kg/hour) Starship guidelines suggest maintenance fluids at 6ml/kg/hour (more than 4:2:1 rule), decreases risk of overload compared to giving boluses Replace NG losses ml:ml with NaCl 0.9% Targets: pH < 7.45, chloride >100mmol/L, K+ >4, HCO3 <26mmol/L. Main risks are apnoea post op if persistent alkalosis. And arrythmia

Answer 176

Only minimal K+ in gastric fluids (10mmol/L) so minimal losses there. Alkalosis will increase Na+/K+ ATPase, drive K+ intracellularly dehydration will cause increase in aldosterone. Will cause further loss of K+ in kidneys to preverse Na+ and H2O. Will also get paradoxical acidification of urine (loss of protons), despite alkalosis, due to preserving Na+ and H2O at expense of pumping H+ out

Answer 177

Trisomy 21, Treacher collins, diGeorge, Pierre robin Sequence, Goldenhar

Answer 178

Cleft lip: 6 weeks to 6 months Cleft palate: 6 months to 12 months

Answer 179

Blood Access (hard to get to face cause a surgeon is there) Dislodgement (of ETT or monitoring) Debris (teeth going down the airway. May get throat pack)

Answer 180

If in upper airway, then high risk if giving PPV. Especially if ball-valve mechanism --> complete airway obstruction. 5mcg/kg glyco to dry out secretions Ideally SV GA. Can be either with TIVA or gas induction Optimal would probably be with a TIVA, as then shared airway and hard to deliver volatile. Can technically attach circuit to rigid bronch and deliver ventilation + volatile here but unreliable due to open nature of bronch IV dexamethasone 0.4mg/kg airway dose

Answer 181

Mild = 1-5, moderate 6-10 and severe >10. Any AHI is abnormal due to higher pharnygeal tone expected in paeds.

Answer 182

Hot = diathermy. More pain. Less intraop bleeding. More post op bleeding (2-3x risk) cold = scalpel. More intraop bleeding. Less post op

Answer 183

Intracapsular = less sore. More likely for OSA, especially in kids. Less nausea if less bleeding swallowed. Higher rates of recurrence Extracapsular. Bascially for recurrent tonsilitis. More sore, therefore more opioids. more bleeding. Less recurrence. More risk post tonsil bleed.

Answer 184

Pre op - Either primary haemorrhage (within 24 hours of surgery) or secondary (5-10 days post op, from loss of fibrin clot) - 1-2% risk - Assess from haemodynamic point of view. Resus with blood if needed - And airway - Paeds considerations - cooperation, anxiety, parental presence, viral illness, - TXA Intraop - RSI. ENT in room. Consider 2nd anaesthetist + most experienced paeds anaesthetist. Ideally in OT - ETT. Suctions x2. Plan B, C, D. - Induction if stable 2mcg/kg fentanyl, 2-3mg/kg propofol, 1.2mg/kg rocuronium Induction if unstable 1mcg/kg fentanyl, 1mg/kg ketamine, 1.2mg/kg rocuronium - Decompress stomach with NG - Usual bleeding considerations Post op - Extubate awake. Admit - Hb >70g/L

Answer 185

Preop - Typical presentation 3 years old. Most common childhood abdo malignancy. Most are unilateral - Can be massive - may invade IVC and up to RA and therefore needs bypass. May cause resp impairment, impaired ventilation. Get echo - 10% are associated with syndromes e.g. trisomy 18. Difficult airways, congenital heart disease - Some tumours may get chemo beforehand if unresectable (check cardiac, renal impairment from this) - Massive bleeding possible if IVC invaded - Often hypertensive due to impaired renin and renal artery compression. Often on ACEi - Can get paraneoplastic aldosteronism, acquired VWD Intraop - Open surgery due to risk of tumour lysis and spreading with laparoscopy - Arterial line. Consider CVL - RSI, ETT. May be difficult airway if syndromic - 2x large bore iv. If IVC invasion, make sure these are in upper limbs Post op - epidural - HDU - extubate awake

Answer 186

ICP - normal in neonate is 2-6mmHg (in all children, should be less than 15mmHg) Can subjectively assess ICP with fontanelles. Fontanelles also provide expansion ability until fusion (around 12-18 months for anterior one) Assessment obviously different with GCS and paeds. -CMRO2 double adults (6mlo2/100g/min). Also higher cerebral blood flow in children than adults. Neonates = 40ml/100g/min, infants 90ml/100g/min, children 3-12 = 100ml/100g/min, adults 50ml/100g/min Autoregulation of CBF impaired in neonates, matures around 33 weeks (hence increased risk intraventricular haemorrhage) Check for congenital heart disease - ASD, VSD at risk of paradoxical air embolism

Answer 187

Congenital: - Chiari malformation - Aquaductal stenosis - Miningomyelocele Acquired: - Infection (meningitis) - Intraventricular, subarachoid haemorrhage - tumours (especially posterior fossa and CSF secreting)

Answer 188

Refractory seizures on medical managment, medically optimised Usual seizure things: AEDs, adverse effects of meds, seizure type / response to treatment, timing of last AED, ensure AED continued. Avoid pro epileptic agents (tramadol) Options include vagal nerve stimulators, resection of epileptiform foci, hemispherotomy. Functional hemisepherotomy + temporal lobe resection can resolve 60-90% of epilepsy. May need cortical mapping

Answer 189

Meningiocoele = herniation of dural sac which has CSF but no neural tissue. Spinal cord may be tethered but neurology usually normal Meningiomyelocoele = sac with spinal cord, nerves, meninges and CSF. Associated with chiari malformations and at risk of hydrocephelus needing VP shuntings Encephalocele = defect of cranium with brain tissue present. Usually these need closure within 24 hours as high risk infection if no skin overlying CNS. Latex free ideally

Answer 190

Most pathological murmurs will be picked up perinatally. If murmur in <1 year old, refer. Need to do history, exam of child to determine if murmur significant. 50% of children will have murmur at some point. Concerning history = failure to thrive, weight loss, cyanosis, dyspnoea on exertion (not able to keep up with peers), orthopnoea, syncope, syndromic child (CHARGE, DiGeorge, Trisomy 21), sudden deaths in family Concerning exam = low SPO2, peripheral oedema, 7 S's of innocent (flow) murmur = flow murmur. From high CO and thin walled ventricles: Soft (grade 1 or 2) Sweet (not harsh, no associated heave or thrill) Systolic (diastolic = bad) Short (not pan systolic) Single (no additional sounds) Sensitive (to position changes)

Answer 191

Primum = lower down septum, more associated with valve issues, AVSDs, and syndromes. Often need surgical repair which can cause complete heart block Secondum = septal defect from foramen ovale. 80% of ASDs. Often asymptomatic. Surgical or transcatheter repair. Both can cause left to right shunting (causing RV overload). If PVR goes up, could cause right to left shunting and hypoxaemia (/eisenmengers syndrome). Bubble precautions with both

Answer 192

Minor = cardiac condition with or without medications (e.g. ASD, small VSD) or repaired congenital heart disease with normal CVS function post op. Moderate = Repaired congenital heart disease with residual haemodynamic abnormalities (e.g. TOF with some degree of pulmonary regurg) Severe. Uncorrected cyanotic heart disease. pHTN. list for heart transplant. Ventricular dysfunction One study with NSQIP showed normal children had 7% risk of any complication. If mino cardiac then 20% if severe then 35%. Combine with Faraoni score for deciding location and anaesthetist for surgery. Faraoni score gives 30d mortality for congenital heart disease (includes emergency surgery, kidney disease, single ventricle...) If moderate-high risk then should be done in paeds cardiac centre with paeds cardiac anaesthetist + PICU available

Answer 193

Right to left shunting from raised PVR, causing hypoxaemia, acidosis. Hypoxaemia / acidosis causes worsening of PVR --> further worsening of right to left shunting. Hypoxaemia also worsens ventricular function. Vicious cycle with eventual collapse. High mortality

Answer 194

1) RVOTO. Such as pulmonary valve stenosis. Can be fixed but are often dynamic (e.g. infundibular muscles) 2) VSD. Often get right to left shunting 3) RV hypertrophy 4) Overriding aorta (aorta has input from both left and right ventricles)

Answer 195

Distress / increased sympthatetic outflow --> spasm of infundibular muscle sub-pulmonary valve --> worsening of RVOTO --> increased right to left shunting --> hypoxaemia / cyanosis (can then go into Eisenmengers like vicious cycle with hypoxaemia and worsening right to left shunting)

Answer 196

At delivery, likely to need alprostadil (PGE1 analogue prostaglandin) to maintain PDA for pulmonary perfusion Management of Tet Spells: Aim to reduce PVR, increase SVR and reduce right to left shunting. Most are self limiting over 15 mins. But can lead to cerebral ischaemia - Avoid triggers(distress, pain, exercise, Valsalva) - Squat position (older kids only). Knee to chest to increase SVR, reduce right to left shunting - High flow O2 - Fluid boluses (improves venous return) - Alpha 1 agonists. Increase SVR - Intubation, ventilation. Drop PaCO2 - Urgent surgery if above fails Surgery - Usually only get a single repair. Without repair life expectancy around 20-30 years old. With repair, longer - May get a Blalock-Taussig shunt (PA to subclavian) which acts as a PDA, if DA is not Patent - Usually surgeyr within 6 months of age. On bypass. Closure of VSD. Separation of aorta to only be conenct to LV. Reduction of RVOT muscle bundles. Often leads to ongoing pulmonary regurg

Answer 197

Decide if surgery urgent or can do transfer. With availability of paeds cardiac anaesthesia and PICU. Discuss with them If not: - Reduce PVR (usual things for this - avoid hypoxia, hypercapnia, insp pressures, acidosis, hypothermia, SNS) - Maintain SVR (alpha agonists. well filled) Aim to reduce right to left shunting which could lead to Eisenmengers syndrome and death

Answer 198

Hypoplastic left heart, tricuspid atresia, pulmonary atresia. Nowadays Fontans have 93% survival to 20 years old. 1st stage = Norwood procedure or a Blalock-Taussig shunt. Norwood procedure combines aorta to PA to allow for shunting. Blalock-Taussig shunt = goretex conduit between PA and subclavian artery Both allow for right ventricle to pump blood to systemic circulation 2nd stage = Hemifontan or bidirectional Glenn procedure. SVC connected to PA. Done in stages to prepare PA for blood flow. Increases survival doing stages 3rd = Fontan. Where IVC and SVC connected to PA. Nowadays most commonly have IVC and SVC directly (total cavo-pulmonary connection = TCPC) into PA which improves mortality. Previously uses the RV as an intermediary pump but found this dilated out and became arrythmogenic and developed thromboses.

Answer 199

-Cardiac output depedent on gradient from systemic arterial --> venous --> pulmonary circulation --> single atrium. With pulmonary vasculature most rate limiting step. 30% of blood flow from changes in thoracic pressure from respiration. - Loss of pulsatility thought to contribute to increased PVR from reduced NO - Single ventricle - less able to regulate cardiac output than normal heart. Cardiac output determined by venous return. Increasing inotropy won't increase CO - High arrythmia risk - Heart failure common - SpO2 usually in low 90s. Less than 90 is abnormal - High VTE mortality risk (8%) due to low flow, arrythmia - Liver disease common due to raised CVP

Answer 200

Cavo-atrial extension of tumour for renal cellular carcinoma Level 1= thrombus into ICD but <2cm above renal vein Level 4 = thrombus involving RA If level 4, often needs CPB, cardiac surgeon involvement. May need vascular surgeon to remove from thoracic IVC and hepatobilliary surgeon to remove from hepatic veins

Answer 201

Rationale for robot - improved post op pain, less bleeding, reduced LOS compared to open prostatectomy Positioning - 2-3 hours with steep trendelenburg. Can get nerve injury (brachial plexus, common peroneal). Airway swelling. Facial swelling. Increased ICP and IOP (caution in glaucoma). At risk for gastric fluids leaking. Lots of tapes for eyes Access - poor. Ensure multiple IVs plus extensions. team need to be able to rapidly remove robot Movement- dangerous with robot in place. Ensure high dose remi or paralysis communication alterations with surgeon. Sometimes using audio tech Patients often aggitated post op from mild cerebral oedema. Ensure leak test prior to extubation

Answer 202

Pathophys: Hypotonic (220mmol/L), high volume fluid (typically glycine historically to allow for monopolar diathermy as non-conducting), absorption by prostatic vessels. Can cause fluid overload and hyponatraemia Symptoms: Aggitation, nausea, headache, increased RR, confusion, seizures, resp distress, hypxia, coma, death (hard to detect a lot of these under GA hence spinal preference) Management: - Inform surgeon. Aim to minimise fluids and wrap up surgery - Airway - consider intubation, ventilation. Or CPAP to help with APO - Breathing: fiO2 100%. Consider 40mg IV frusemide if APO (especially if not hypontraemic) - Circulation. Stop Iv fluids. Place art line for serial Na monitoring. Send of ABG - Disability - give midaz if seizring. - Electrolytes. If Na <120mmol/L, give 1-2ml/kg of 3% NaCl until Na >125mmol/L and free of symptoms. aim for correction 1-2mmol/L/hour. No more than 12 mmol/L in a day (risk of central pontine myeolysis - HDU

Answer 203

Percutaneous nephrolithotomy. Perc option for removing stones - especially large ones (>1.5cm) and staghorn ones Starts off lithotomy, ureteric stents placed. Then nephrostomy placed in prone position in outstretched position. Needs reinfored ETT as going prone (not really amenable to spinal). Positioning outstrethed = risk for nerve injury Sometimes surgeon will ask for lungs off when nephrostomy placed under x ray guidence under 12th rib. could get pneumothorax if accidental puncture of lungs (or hydrothorax if irrigating fluid into pleural space)

Answer 204

- CKD considerations. Dialysis (frequency, last timing, volume removed, haemo?, site used, ports?), medications, anaemia, calcium, K+. Cause for CKD (?HTN ?diabetes ?IgA). ?last seen by renal physician - May be from live donor or from deceased. Timing can be elective or semi-acute. May not get dialysis day before surgery due to this. May be fluid overloaded, K+ high and acidotic - Usually get full work up - beforehand with FBC, U+E, coags, ECG, CXR. Consider echo

Answer 205

Monitoring - Usual + arterial line. Can get big swings in BP (may have autonomic neuropathy fromm DM, HTN, hypovolaemia if dialysis, bleeding etc) Lines - ideally avoid A-V fistula sites (if transplant fails). consider CVL (CVP monitoring useful too). Vascath if surgeon thinks likely delayed graft function GA + ETT. Consider RSI if delayed gastric emptying Bleeding - usually no more than 500ml. Hb target 70g/L. dont over transfuse. Use CMV negative blood Pharmacology - propofol, remi, sevo all fine. No sux. roc is aiight. Atracurium is good. No NSAIDs or morphine. Fentanyl is good. Regional with TAP block Haemodynamics - aim for MAP 90mmHg. Normotension at time of graft arterial clamp removal with CVP 12-14cmH2O for graft perfusion. Some centres use 0.5g/kg Iv mannitol for graft to promote function (no evidence this works). Same for dopamine. Immunosuppresion often given intraop. Methylpred +/- biological agent (commonly basiliximab = IL2 antagonist (risk of opportunistic infection and anaphylaxis, arrythmia, SJS) Post op: Fentanyl PCA + paracetamol Mild hypervolaemia to promote diuresis. follow guidelines Immunosupression commenced Monitor for bleeding, urine output. If drop in UO, may be sign of graft failure and require return to theatre

Answer 206

CVS - initially vagal causing decreased HR for 15 seconds or so, may get asystole briefly. then sympathetic with increase HR, BP. risk of tachyarrythmia, May strain IHD patients. Also increased VO2 from seizures, increased demand so increased ischaemia risk Resp - increase VO2, increased risk of desaturation. Ensure preoxygenation CNS - increased ICP Eyes - increased IOP GI - increased tone, risk of aspiration MSK - movement, may harm self or staff. Ensure paralysis Other - hypersalivation

Answer 207

-Seizure causes increased neurotransmitters - 5HT, NA - Neurogenesis. may promote synaptogenesis via growth factors, particularly in mood centres and hippocampus - Unclear if electricity or the seizure that is the treatment. But works with Lancet meta analysis showing improvment

Answer 208

MI in last 3 months, phaeo, raised ICP, unstable angina, aortic aneurysm, incracranial masses, intracranial aneurysms, recent stroke

Answer 209

- Ionising radiation. To staff and patient (protect both as able). Audit radiation - Access to patient = limited, ensure lines and ETT secure - Bed is narrow. Risk of falls. Hard to manipulate bed - Remote location - access to emergency equipment, drugs, other staff in emergency, unfamiliarity of staff there. - Often paeds or have reason they need a GA - Contrast media. Risk of renal stuff

Answer 210

Magnet risks (staff and patient) - projectiles - macro and micro - implanted devices - malfunction, move position - Inductance heating - loud noises Remote location considerations - access to drugs, equipment, defib, other staff Monitoring / equipment - MRI compatible. Pumps. Anaesthesia machine Emergency situations - quench (risk hypoxia). No one into room Often paeds. Or medically unwell / undifferentiated Gadolinium IV contrast. Risk of nephrogenic sclerosing fibrosis (NSF) if group 1 gadollinium agents Access to patient. Secure Iv, tubes. Long etCO2 so delayed response

Answer 211

Vascular access - haematoma, pseudoaneurysm, AV fistula formation, retroperitoneal bleed. 1:100 Cardiac tamponade. 1:100-200 Pericardial effusion 1:100-200 Stroke: 1:250 Atrial oesophageal fistula Oesophageal perforation

Answer 212

PARTNER was for patients that weren't candidates for SAVR. Randomised to TAVI or medical management. TAVI did better PARTNER 3, SAVR vs TAVI RCT n=1000. TAVI mortality 1.5% less than AVR at 1 year but no difference at 5 years. TAVIs have high rates of re-interventions. Higher paravalvular leaks. High rates of needing PPM. But faster recovery. Faster discharge. Lower mean gradients for TAVIs.

Answer 213

-Monitoring - Usual + arterial line (severe AS) -IV access. Usually a 20g is fine. Then can have large bore extension on venous sheath - know where access is going to be done by. If femoral vessels no good, rarely could be trans-apical, transcarotid, from IVC into aorta etc - could be done with ETT or LMA. But probs ETT - Volatile or TIVA fine. Minimal stimulating so need vasopressors (metaraminol good for AS) - IV heparin. ACT >250s - Rapid atrial pacing (200BPM) to facilitate TAVI placement. Have adrenaline 10mcg ready for potential myocardial stunning - Post deployment may get massive increase BP due to improved CO and ongoing high SVR. Have GTN and MgSO4 ready. Or phentolamine. - TTE or TOE may be used to check placement and check for paravalvular leak, may need 2nd prosthesis placement if unsatisfactory - Usual remote location, radiation exposure, cathlab things

Answer 214

-Access site issues - haematoma, retroperitoneal bleeding, AV fistula, pseudoaneurysm - Valve malposition, rotation, paravalvular leak - Stroke (2% risk, was previously 8%) - Tamponade - Complete heart block. Arrythmia. May need PPM - Coronary artery occlusion (<1% risk but high mortality). commonly from native valve covering coronary ostia, needs stenting - Rupture of aortic annulus (<1% but mortality very high. May need SAVR or palliation)

Answer 215

Major adverse cardiac event = MACe = largest cause of peroop deaths (30%) High risk: MI <2 months of surgery Unstable angina Ischaemia ongoing after MI LVEF <40% Significant arrythmia (uncontrolled SVT, complete heart block) Severe valve disease PCI (BMS <1 month, DES < 1 year, angioplasty < 2 weeks) Intermediate: History of ischaemia Well heart failure Diabetes CKD Minor: Smoking obesity advanced age Poor functional capacity

Answer 216

SIC SIC = Surgery (high risk are intraperitoneal, thoracic, suprainguinal vascular) Ischaemia history Congestive heart failure Stroke / TIA Insulin depedent diabetes Creatinine (>177umol/L) Each gets a point. All comers have 4% risk. 1 has 6%. 2 has 10%. 3 or more then 15% No age in RCRI. Also was developed for major elective surgery not minor stuff

Answer 217

High sensitivity troponin change with at least 1 >99th centile + (any of the following) ECG changes suggestive of ischaemia (ST, arrythmia, T wave) TTE / TOE (RWMAs) Clinical (CP, SOBOE, APO, cardiogenic shock / hypotension) Thrombosis seen

Answer 218

Myocardial injury after non-cardiac surgery Any trop change after non cardiac surgery, not due non-ischaemic pathology (rapid AF, anaemia, sepsis). Within 30 days of surgery. Includes MI but commonly asymptomatic (only 20% of MINS are MI). 20% of patients get MINS If high risk for MINS (based on high risk for ischaemia + intermediate to high risk surgery), should get preop trop + daily trops for 3 days (european cardiac society). Could start aspirin, statin, BB, refer to cardio

Answer 219

1 = Chamber paced (A, V or D) 2 = Chamber sensed (A, V or D) 3 = response to sensing (O, I, T or D). I = inhibit. T = triggered 4 = Rate modulation, programmability (O, P, R or M). P = programmable, R = rate modulation, M = multi-programmable 5 = antitachycardia functions (O, S, P or D). S = shock. P = programmable. D = dual

Answer 220

LVEF <35%, on maximal medical therapy. Usually with QRS >120ms and LBBB. CRT aims to improve coordination of contraction for both LV and RV (which will obviously be out of whack with a LBBB or prolonged QRS)

Answer 221

- Device type (PPM, CRT, ICD, loop recorder) - Reason for device - ?primary prevention ?event ?ischaemic heart disease vs arrythmia vs family history - Device function, generic pacemaker code (e.g. VVI, DDD) - Last check, when next due for check. Usually 12 months for PPM, 6 months for ICD (but more frequent if nearing end of battery life) - Battery life - Lead impedence - underlying rythym (?pace dependent) - Response to magent - Inappropriate pacing, sensing, shocks - CP, SOB, syncope, heart failure - Anti arrythmic medications, anticoagulation

Answer 222

New York Heart Association 1= cardiac disease but no effect on function 2 = mild functional limitation to activity 3 = comfortable at rest, limited activity due to symptoms 4 = symptoms at rest

Answer 223

1) ACEi / ARB / neprolysin inhibitors 2) BB 3) Spironolactone 4) SGLT2i all improve symptoms and mortality Other meds: loop diuretics, digoxin. Anticoagulation if AF Non pharma - low salt diet, fluid restriction, cardiac rehab, regular follow up cardiologist, CRT No treatment has been demonstrated to improve mortality for HFpEF. spironolactone reduces hospital admissions. Others treat symptoms only

Answer 224

Pulmonary HTN - 1) Pulmonary arterial hypertension 2) Left sided heart disease 3) Lung disease 4) PE / chronic VTE / tumours 5) misc Ventricular / valvular disease - ischaemia of RV, myocarditis, pulmonary valve stenosis, tricuspid regurg, cardiomyopathy Pericardial disease - effusions, pericarditis

Answer 225

Peripheral oedema Elevated JVP Ascites Hepatosplenomegaly Low CO - hypotension, tachycardia, cyanosis

Answer 226

Tricuspid annular plane systolic excursion = displacement of lateral tricuspid annulus during systole towards apex. If <16mm, then RV systolci dysfunction

Answer 227

Hypertension = systolic >140mmHg or diastolic > 90mmHg. Increases risks of IHD, stroke, heart failure, renal failure. But HTN alone does not increase mortality perioperatively Secondary = 5%, HTN from another aetiology. Endocrine - Conns (=hyperaldosteronism), Cushings (excess ACTH --> excess cortisol), thyrotoxicosis, phaeochromocytoma Renal - HTN, diabetes, IgA nephropathy, pre renal (renal artery stenosis), post renal Medication - serotonin syndrome, neuroleptic malignant syndrome, methamphetamine Neurogenic - raised ICP Obstetric - preeclampsia, gestational hypertension

Answer 228

If aortic valve, 1.5-2 (as long as on aspirin too) If mitral, still 2.5 - 3.5

Answer 229

Increasing in calcification / narrowing of AV --> increased afterload --> increased LV pressures, increased end diastolic volume --> concentric LV hypertrophy, reduced diastolic ventricular compliance More reliant on atrial kick for LV filling Worsened supply to LV due to increased LV pressures required for afterload, therefore less blood flow in systole. Increased coronary demand due to hypertrophy + increased contractility required. Even with normal coronaries, can still get ischaemia and angina (30% of severe AS patients)

Answer 230

Syncope (3 year survival for 50% of patients) Dyspnoea (2 year survival for 50% of patients). Highest risk symptom Angina (5 year survival for 50% of patients.

Answer 231

End of bed - ?dyspnoea, increase WOB Hands - slow rising pulse, narrow pulse pressure Chest - aortic region, crescendo-decresendo ejection systolic murmur right sternal edge 2nd intercostal. Radiating to carotid Otherwise, look for evidence of CHF - APO, orthopnea

Answer 232

Maximum jet velocity >4m/s Mean pressure gradient >40mmHg. Mean gradient is pressure gradient across the valve in systole. AVA <1cm squared DI < 0.25. DI = dimensionless index = ratio of LVOT to aortic valve VTI. Removes need to measure aortic valve diameter (which can be tricky

Answer 233

"Slow and tight". Goals are to preserve coronary perfusion, improve supply and reduce demand on coronaries. Not worsen diastolic dysfunction. Minimal capability to increase CO with increasing SV due to fixed stenosis. 1) HR - Low- normal. 50-60BPM 2) SVR - high normal. MAP +/- 10% of normal MAP 3) Avoid tachyarrythmia, keep sinus rythym 4) Preserve contractility 5) Euvolaemia, maintain preload Ways to achieve this: 1) Metaraminol - will decrease HR and increase SVR 2) Remifentanil - will decrease HR and blunt SNS to avoid arrythmia / increased HR 3) Iv fluids 4) arterial line. consider CVL 5) Slowly titrated GA or avoid if possible (regional anaesthesia) 6) Caution with neuraxial (especially spinal) 7) Treat tachyarrythmias aggressively. DCCV if needed. Esmolol

Answer 234

Aortic leaflet problem - bicuspid valve, connective tissue disease, IE, rheumatic heart disease, degenerative changes Aortic annulus / root problem - Marfans, aortic dissection, other connective tissue disease (Ehler's Danlos) May be acute e.g. aortic dissection. Or chronic

Answer 235

Hands - Widened pulse pressure, waterhammer collapsing pulse, finger nail bed pulsation (Quinkes sign) Head / neck - Neck vein pulsation (corrigans sign), Head nodding (De Musset's sign) Chest - diastolic murmur, aortic region. Loudest at start of diastole

Answer 236

colour Dopplet Jet width >65% Regurgitant percent >50% Regurgitant volume >60ml Holodiastolic flow reversal in descending aorta Vena contract >6mm Pressure half time <200ms

Answer 237

Full fast and forward. Aim to reduce regurgitant fraction and promote ejection into aorta 1) HR - high normal (80-100BPM). Bradycardia is the real problem and should be main thing to avoid 2) SVR - Low normal, promote ejection 3) Increased preload 4) sinus rhythm 5) Contractility preserved Ketamine, ephedrine, adrenaline, GA, atropine, neuraxial all pretty well tolerated

Answer 238

Rheumatic heart disease most common. Rarely, SLE, congenital heart defects, malignant carcinoid syndrome

Answer 239

Stenosis of mitral valve prevents LA ejection into LV (fixed output, low CO state). LV small. LA enlarges and increases in pressure --> increased pulmonary artery pressures --> pHTN. Eventually get RV failure. Common to get AF from LA enlargement. And thrombosis

Answer 240

MVA <1cm squared Mean gradient >10mmHg MS with pulmonary systolic pressures >50mmHg Pressure half time >150ms Other things to look for on echo - - thrombus in atrial appendage - LA and LV size - RV size and function. Evidence of pulmonary hypertension

Answer 241

History - MS alone: dyspnoea, fatigue, palpitations, syncope - With pHTN +/- RV failure: haemoptysis, peripheal oedema, raised JVP, ascites, hepatosplenomegaly Exam - As above. Plus malar facies (malar flush on cheeks) - Peripheral cyanosis - Tapping, low pitched disatolic murmur in apex. end of disatole

Answer 242

Slow and tight. Promote LV filling. Avoid worsening of right ventricle function 1) HR - low normal. 50-60BPM 2) SVR - high normal 3) Euvolaemia 4) Sinus rythym at all costs. Avoid AF and tachy arrythmias 5) Maintain contractility 6) Avoid worsening of PVR. Avoid hypoxia, hypercapnoea, hypothermia, increased SNS, drugs (N2O), acidosis, high airway pressures / PEEP

Answer 243

Leaflet - rheumatic heart disease, IE, mycomatous degneration, leaflet prolapse Chordae tendinae - rupture often ischaemic, IE possible Papillary muscle - dysfunction from ischaemia Ventricle - dilation from cardiomyopathy, "fucntional" MR

Answer 244

Vena contracta >7mm Pressure half time <200ms Eccentric jet Obvious flail segment Regurgitant fraction >50% Regurgitant volume >60ml

Answer 245

Primary: Genetic - Hypertrophic obstructive cardiomyopathy, dialted cardiomyopathy Stress - Takatsubo Ischaemic Tachycardia induced Drug induced (chemo, alcohol) Secondary (part of systemic diseases) Genetic: Haemochromotosis, muscular dystrophy Endocrine: thyroid disease Other: sarcoidosis, amyloidosis

Answer 246

Diastolic dysfunction main issue. Restrictive CM often due to ventricular infiltration (sarcoidosis, amyloidosis, haemochromotosis). Similar goals to tamponade. Do not tolerate drops in preload (so neuraxial or heavy handed GA is bad) HR - high normal. Reduce time in diastole SVR - high normal, maintain afterload Preload- lots. Maintain LV filling Rhythm - sinus Contractility - maintain

Answer 247

Autosomal dominant mainly, genetic condition. 70% of HCM have obstruction (hence HOCM). Most common inherited cardiac condition (1:500 with variable penetrance) Any part of ventricle can undergo hypertrophy. But commonly septal. Causes dynamic obstruction of LVOT. Also get systolic anterior motion of mitral valve (SAM), further obstruction from Venturi effect. Symptoms: similar to AS, from LVOTO. Worse with increased SNS activity (as worsens LVOTO). Syncope, dyspnoea, angina, palpitations. Can get CHF too. Familiy history and history of suddent cardiac death also relevant

Answer 248

Medical management: beta blockers, CCBs (verapamil). aim to have decreased HR, negative inotropy, rate control - anticoagulation if AF Interventional: catheter ablation of septum ICD (may be primary or secondary)

Answer 249

Not too dissimilar to AS (as LVOT obstruction). But aiming to not worsen LVOTO too HR - low-normal HR, preserves LV filling SVR - high normal. Reduces LVOTO. Phenylephrien good choice as no beta activity Preload - well filled. Reduces LVOTO Inotropy - low (main difference with AS and HOCM. Increased inotropy will worsen LVOTO). Beta blockers good Rhythm - sinus

Answer 250

1) Altered physiology - denervated heart. Resting HR 90. Respond to circulating catecholamines. Unable to increase HR if hypovolaemia, sepsis, exercise. More preload dependent - Frank starling mechanism still intact - Occasionally get PPM inserted for heart block - Coronary allograft vasculopathy (increased risk of CAD, especially around 10 years) 2) Immunosuppression (including steroids) - increased risk of infection. Pancytopneia possible - Side effects include renal impairment (ciclosporin, tacrolimus), prolonged action NDMRs (ciclosporin) - Steroids - T2DM, secondary adrenal insufficiency, skin, bones 3) Pharmacology - exagerated response to adenosine - No response to atropine, glyco - Less response from indirect acting inotropess (ephedrine) - No reflex bradycardia from alpha 1 agonists - normla response from direct acting B1 agonists (noradrenaline, isoprenaline, adrenaline) - unpredictable response from neo/ glyco. due to partial reinervation of vagal nerves. Use sugammadex 4) Other things - Sometimes get lungs transplanted with heart - difficult IV access - Impaired cough frequent - Impaired lymphatics. At risk to APO

Answer 251

Right heart cath = gold standard. Based on mean PAP. Anything over 25mmHg is pHTN Mild = 25-40mmHg Moderate = 40-55mmHg Severe >55mmHg Can be estimated using echo and TR jet velocity. Detect jet velocity using Doppler. Then apply Bernouilli principle. Pressure = 4v(squared). Then add RA pressure estimate to get estimate of RVSP (=PASP if normal pulmonary valve, not accurate if RVOTO). Note this is the systolic pressure (not mean) Mild = 35-45mmHg Moderate = 45-60mmHg Severe = >60mmHg

Answer 252

Pre-capillary pHTN with PA occlusion pressure >15mmHg, PVR >3 wood units and abscence of other causes of pre-capillary pHTN Causes include: idopathic, drug induced, toxin induced, HIV associated, portal hypertension

Answer 253

1) Pulmonary arterial hypertension = precapillary pHTN. Idiopathic. Drug induced. Toxin induced. HIV associated. Portal hypertension associated 2) From left heart disease. HFrEF, valve disease, cardiomyopathies 3) From lung disease. OSA, OHS, COPD, restrictive lung disease 4) From obstructions (chronic PE, tumours) 5) Miscellenous causes. Connective tissue disease. Haematological disease

Answer 254

Usually somewhat non-specific - fatigue, SOBOE, orthopnea, angina, syncope. Worse with exertion - haemoptysis May have evidence RV failure - peripheral oedema, raised JVP, ascites, hepatosplenomegaly symptoms can be classified with the NYHA class, same as for heart failure

Answer 255

Phosphodiesterase inhibitors: sildenafil. Pulmonary vasodilation. Improves functional capacity Prostacycline analogous. Iloprost, epoprostenol. Improves survival in idiopathic PAH. Endothelin antaonists. Bosentan. Improves symptoms, may slow progression Anticoagulation (common diuretics (if RV failure and needing offloading) Double lung transplants if young person. Improves survival in young people

Answer 256

between 6-20% risk of mortality, high risk for non-cardiac surgery Increased risk if: - BNP >300 - NYHA 2 or more - 6MWT <300m - CPET VO2 max <35% predicted or VE/VCO2 >45 - emergency surgery - high risk surgery - surgery > 3 hours Need to continue usual pHTN treatment if able

Answer 257

Goals to not cause increase in PVR, or worsen RV function Avoid (for PVR) - Hypoxia - Hypercapnoa - acidosis - hypothermia - excess SNS - drugs that increase PVR - N2O, ketamine, ergometrine, carboprost - High inspiratory airway pressures / excess PEEP. Spont vent may be ideal Aim for euvolaemia (preload dependent but do not tolerate overload) Maintain MAP clsoe to normal sinus ryhthym Prepare for stages where large fluid shifts or haemodynamic changes may occur (e.g. bleeding, hip cementing, aortic cross clamp removal)

Answer 258

Right to left shunting, usually through large ASD or VSD. - Surgery in teritary centre with TOE, ICU, ECMO - Personnel - cardiac anaesthetist, experienced surgeon - Often associated with syndromes. Check for this. May be difficult airway - Goals are to maintain SVR and give PVR low (to avoid worsening of right to left shunting which can lead to vicious cycle of hypoxaemia, heart failure and demise) - Maintain SVR with vasopressors, euvolaemia, carefully titrated anaesthesia. Avoid spinal. Milrinone useful. Vasopressin useful. - reduce PVR with usual pHTN things - avoid hypoxaemia, hypercapnea, acidosis, hypothermia, raised insp pressures / PEEP, excess SNS - always arterial line - either SV or IPPV defendable, both have pros and cons. Best would be LA or regional. - Bubble precautions - avoid paradoxical stroke

Answer 259

Uses DC current, up to 360J through pads. Biphasic most common. Can be synchronised (shock at peak of R wave) Hazards to patient: - R on T --> VF, arrest (synchronise if you can) - Burns. Especially if poor contact pads, metal in between, alcohol prep, medication patches - Damage to electrical equipment - PPM, ICD, CSII. Ideally pads not over these - Pain - Jolting off the bed Hazards to staff: - Burns, fire - Electrocution

Answer 260

QT = Start of Q to end of T wave QTC = QT / square root of R-R interval = Bazett formula Prolonged QTc if 440ms (men) or 460ms (women)

Answer 261

Congenital - Romano Ward syndrome = 99% of congenital long QT. Due to abnormal k+ or Na+ channels. Autosomal dominant - Long QT 1-16 exist. 1 = potassium channel. 2= another potassium channel. 3 = sodium channel. - LQT2 can get prolonged QT from physiological stress Acquired - Drugs - Ondansetron, droperidol, antipsychotics, SSRIs, methadone, metoclopramide - Electrolytes - hypokalaemia, hypocalcaemia, hypomagnesium - Temperature - hypothermia - Ischaemia

Answer 262

- Determine type - acquired vs congenital. -Correct if acquired - withhold drugs that cause, correct electrolytes, avoid hypothermia, investigate ischaemia - Continue beta blockers if on - Avoid sympathetic stimulation, especially if LQT2 which increases with stress - Avoid QT prolonging drugs (ondanstreon, droperidol... use dex and propofol infusion) - Consider arterial line to determine if patient has cardiac output - Treat TdP with magnesium

Answer 263

Orthodromic means majority of conduction is going through the AV node and then re-entry is via the accessory pathway back to atria. Will have narrow complex tachycardia. Can treat as per usual SVT with vagal manouvers, adenosine which will block the AV node and cause a hard reset. Once SVT stopped, will have usual narrow complex QRS with shortened PR interval (<120ms) and delta wave. Antidromic (or antegrade) conduction is via the accessory pathway first, which then depolarises the AV node and causes retrograde conduction through this back to the atria and then back down the accessory pathway. QRS will appear prolonged as no bundle of His. Treatment is with DCCV. Risk of giving AV blocking drugs (adenosine, beta blockers, verapamil) is not if its antidromic reentry SVT, but if it's AF with conduction down accessory pathway. ECG will look funky AF - some irregular beats will go down AV node (and be narrow with a delta wave present) and some will go down accessory pathway and be broady complex. If you give AV node blocking drugs you'll get more conduction via accessory pathway and increase risk of VF and death

Answer 264

8000 patients at risk for MACE, had either metoprolol or placebo before non cardiac surgery. BB group had less MI and AF. But more strokes and deaths. Other finding was those with AF had 3x increased risk of stroke periop compared to those without AF

Answer 265

Patient factors - Electrolytes - endocrine - Advanced age - Male - Ischaemic heart disease - HTN -Renal disease - Alcohol - valvular lessions (especially if dilated atria) - OSA - Obesity - Sepsis Surgical - Cardiac - Bypass -Large fluid shifts - Open surgery Anaesthesia - High SNS - Withholding beta blockers - Adrenaline, aphedrine, atropine

Answer 266

- Call for help if unstable, ABC assessment - Confirm diagnosis with ECG - Determine if stable or unstable. Based on BP (<90mmHg) or evidence of cardiogenic shock (APO, renal failure, ischaemia on ECG / symptoms of ischaemia, heart failure. If unstable, give synchronised DCCV biphasic 150J. Then 200J. Then 360J When considering shocking, need to consider risk of thrombosis. If not anticoagulated for >48 hours and in AF, risk of causing stroke. Can do TOE to rule out thrombus - If stable, determine if rate or rythym control appropriate. AFFIRM trial found no difference in mortality if rate or rythym control in non-valvular AF. Aim for rates <100BPM. BB, digoxin, CCBs - Rhythm control would include DCCV, amiodarone - Anticoagulation consideration (if CHADSVASC 1 or more) - Correct underlying cause - electrolytes, anaemia, sepsis

Answer 267

Congestive heart disease HTN Age (65-75) = 1 Diabetes Sex (female = 1) Vascular disease Age again (>75 = 2) Stroke (=2) Maximum score = 9 = 12% annual stroke risk

Answer 268

ABCs, confirm if CO or not - Stop QT prolonging drugs - Magnesium push 2g. Then Infuse 1-4g / hour. Monitor Mg levels. Target 2-3mmol/L. May need re-dose of bolus if not working - Refractory TdP may need to be paced. To increase the HR and shorten QT interval Isoprenaline 0.5-10mcg/min (400mcg in 50ml = 8mcg/ml) External pacing - Do not give amiodarone - Weirdly, if long QT syndrome, the treatment in long term is giving a beta blocker

Answer 269

If unsure, always treat broad complex tachycardia as VT. If unstable, syncrhonised DCCV More likely VT than SVT if: - Prior ECG had no LBBB or RBBB - Very broad complex QRS (>160ms), expecially if first part of QRS is slow up sloping - Precordial lead concordance - if all R waves are positive or all R waves are negative - AV dissociation - if you can see p waves in between intermittently, then likely VT

Answer 270

Physiological - Hypokalaemia, hypocalcaemia - Hypothermia - acidosis - Vagal tone (pneumoperitonium, cervix, eyes) Pathological - Ischaemia - infiltrative conditions - sarcoid, amyloid - Valve surgery injury - Congenital - Pharmacological - BBs -CCBs - Neostigmine - Amiodarone

Answer 271

1mg vial, make up to 50ml in 5% dextrose. = 20mcg / ml Run at 0.5-10mcg/min around 1.5-30ml/hr

Answer 272

Usually for heart blocks and bradycardias, especially if associated low BP or signs of cardiogenic shock Pads on - AP or right sternal edge + left axilla ECG attached too ideally. Will need a way of determining electrical and mechanical capture (arterial line, SPO2 or pulse) Select pacing mode, start at 80mA and 80BPM (needs to be 20-30 BPm above intrinsic rate) Increase pacing by 10mA until getting electrical and then mechanical capture. Increase mA by 10mA more than threshold If not getting capture at 130mA, check pads positioning and start again Titrate HR to optimise BP - may be better with 90BPM. Or 70

Answer 273

Usually better tolerated in awake patients than external pacing. And more reliable pacing too. Need way to measure electrical (ECG) and mechanical (SpO2, art line, pulse) capture Insert sheath - usually right IJ Assemble kit. Test balloon and leave deflated. Connect to pacing box Insert wire into sheath, once passed sheath or at 20cm, inflate balloon. Start pacing box at 80BPM and 4mA Continue to feed wire until starting to get electrical capture, then mechanical capture. Then advance 5cm more. Then deflate balloon At this stage, could then decrease current until determine capture threshold. Then double this threshold CXr to confirm placement and no iatrogenic injury If you get to 50cm, likely coiling or going down subclavian. Pull back to 20cm and repeat Get cardio and get PPM

Answer 274

Mobitz type 1 = Wenkebach = progressively increasing PR interval until dropped beat. Less scary Mobitz type 2 = 2:1, 3:1, 4:1. More concerning. Higher the Atria: ventricle block rate, the slower the HR will be. If urgent surgery, place transvenous pacing wires

Answer 275

Bifascicular = RBBB + one fascicle of the LBBB blocked. Will have RBBB. Then check for axis deviation (should have a normal axis if just a RBBB). If LAD then it is RBBB + left anterior hemifascicle block. If RAD, then will be RBBB + left posterior hemifascicle block Trifascicular blocks are a term that should be thrown out. AHA agrees. Used to mean bifascicular block + 1st degree AV block. But could also mean complete heart block with RBBB and LBBB.

Answer 276

Symmetrical, inflammatory, polyarthritis. Most commonly of MCP and PIP joints of hands. Can affect any artciular joint space. Rheumatoid factor (80% sensitivity) and anti CCP most common tests. Women 2-3x more likely than men. Most common age is in 60s. Has extra articular effects too Articular joints that have anaesthesia implications: - TMJ. Mouth opening - C spine. At risk atlantoaxial subluxation. 25% of patients have this, but only 25% of these patients will have symptoms. 80% are anterior with arch of atlas (C1) forward on odontoid peg (C2). >3mm is significant - Cricoaratenoids. Risk of stridor, stenosis, laryngeal obstruction even if minimal oedma - Other joints will make positioning tricky, IV lines, regional, pressure sores Extra articular effects - Resp - Risk of ILD. From connective tissue disease or from drugs (methotrexate). Prolonged immunosuppression --> risk infection - CVS - Increased coronary vasculitis risk, ischaemia. pHTN if lung disease, risk RV failure. Raynauds. Pericarditis or pericardial effusions - Haem - anaemia of chronic disease. Myelosuppression if MTX - CNS - subluxation may cause myelopathies - MSK - steroid induced fragile skin, osteoporosis - REnal - CKD. Autoimmune glomerulonephritis Consider PFTs if resp disease. ECG and Echo if CVS suspicion. Nasoendoscopy if cricoaratenoid suspected involvement - stridor Drugs: - Steroids. Effects are BGLs, infection, skin / wound healing, osteoporosis, steroid dependence - DMARDs - MTX (ILD, bone marrow suppression, liver impairment), cyclophosphamide, leflunamide, azathioprine. Often can cause renal impairment too. Continue though as no evidence to stop - NSAIDs - biologicals - immunosupressing. Usually have surgery end of cycle. Usually can recommence 14 days post op Discuss with rheum anything complex

Answer 277

Inflammatory arthritis of SI joints and spine. HLA B27 associated. Mostly in males, >20 years old. Causes "bamboo" spine on X ray, fusion of facet joints and between vertebral bodies Articular effects - Airway. Difficult. Historically a good reason for an AFOI. Use VL. May have poor MO (TMJ not often involved though). C spine often poor movement, risk of occlut fracture or subluxation. Careful positioning, no neck extension. May have severe kyphosis Cricoaratenoids can also be involved. Difficulty if any oedema --> stridor, upper airway obstruction - Resp - chest wall kyphosis, poor function. REstrictive lung disease. At risk of ILD (apical fibrosis - MSK - positioning difficult. Spinals may be challenging. Increased risk of epidural haematoma but not contraindications Extra articular - REsp - ILD risk - Cardiac - AR, amyloidosis - Haem - anaemia of chronic disease Medication effects. Same as RA. - Steroids, DMARDs, NSAIDs, biologicals

Answer 278

Chronic, multisystem autoimmune disease, more common in young females. ANA (anti nucleic acid) and ENA (anti extrable nuclear antigen) common. Anti double stranded DNA is a type of ANA, more sensitive for SLE (70%) and more specific too Airway - oral and pharyngeal mucosa involvement CVS - pericarditis, myocarditis (15%). Conduction abnormalities rare. Increase CAD risk Resp - infections, PEs common. Can get ILD. Immunosuppression increases infection risk Renal - glomerulonephritis. Nephrotic syndrome. CKD MSK - skin, joints invovled. Malar rash Haem - anaemia, thrombocytopenia, leuopenia. Can get coagulopathies (anti factor VIII) or hypercoaguloable (anti protein C, S). 30% will have antiphospholipid syndrome (VTE prophylaxis important) Medications - steroids, DMARDs, IVIG, monoclonal antibodies May not be able to have neuraxial if coagulopathy. Do coags and TEG

Answer 279

Inflammatory, autoimmune condition. Wide spread cutaenous and vascular dysfunction. 5x more common women. HLA types involved. Fibroblasts cause abnormal collagen deposition. ANA often positive. Anti-Scl70 and anticentromeere more specific. Localised scleroderma = more mild version, only cutaenous changes CREST = Calcium deposits, Raynauds, Esophageal dysfunction, scelrodactyly and telangectasia. 60% of systemic sclerosis. More mild form usually Airway - can be difficult with facial involvement. Poor mouth opening, poor neck movement. - Telangectasia can cause airway bleeding Resp - Pulmonary fibrosis, restrictive lung disease up to 40%. Risk of MTX ILD too - Recurrent lung infections if immunosuppression - OSA - pHTN CVS - Conduction defects, arrythmia - right heart failure - Raynauds, increased risk peripheral ischaemia and sensitivity to hypothermia - Increased thrombosis risk (3x VTE risk). Antiphospholipid syndrome common (50%) Renal - Sclerodermal renal crisis (up to 10%), from hypertension. Poorly understood. 1 year mortality is 30% if this happens. GI - Oesophageal dysfunction. ETT, RSI. May have malnutrition MSK - Difficulty IV access, positioning, pressure injuries. Unreliable NIBP Medications - steroids, DMARDs, biologicals

Answer 280

Most common cause for dwarfism. Autosomal dominant. Fibroblast growth factor receptor 3 (FGFR3). Average height 130cm. Premature ossification of bones. Airway - Large tongues, large heads. Difficult intubation, BMV, LMA insertion - Relatively small larynx Resp - High rates OSA, OHS. pHTN, right heart failure possible - Obesity common, increased risk restrictive lung pattern. High O2 consumption + decreased FRC. Increased risk desaturation with apnoea CVS - Higher rates ischaemic heart disease Neuro - Cognition normal - At risk of foreamen magnum stenosis. Avoid excess neck hyperextension Endocrine - Increased risk T2DM, monitor BGLs. Increases risk autonomic dysfunction, GI gastroparaesis, stroke, MI, renal nephropathy MSK - Smaller limb lengths with increased obesity --> difficult IV access, peripheral nerve blocks, monitoring, positioning - Challenging neuraxial due to small interspinous process spaces

Answer 281

Autosomal dominant due to fibrillin-1 defect on chromosome 15. Tall stature, slender patients. Alters connective tissue, particularly of blood vessels, more likely to get aneurysms Airway - high arched palate, elongated face. Kyphosis common --> may have difficult airway Respiratory - High risk for spontaneous pneumothorax. May have had previously. May have had pleurodesis. Always have chest drain available if PPV. Keep PPV pressures low as possible. Or SV if able. Pneumoperitoneum or Trendelenburg increases insp pressure requirements - Can get kyphosis related restrictive lung pattern CVS - Aortic root dilation (50% of patients). At risk of rupture or dissection if high shear wall stress. Determine size of root (>4cm = significant. Should get 6 monthly echos if >4.5cm and consider valve replacement) and rate of expansion. Aim to reduce BP (sys <120mmHg) and HR 60-80BPM. Avoid SNS excess e.g. laryngoscopy with lignocaine or remi. Use arterial line and VL - Often on BB to reduce shear stress. Continue this - May get aortic regurg with severe root dilation. Also at risk of TR, MR - Common to have Benthals, may have mechanical valve and be on anticoagulation MSK - Long limbs with usually lower BMI. At risk for peripheral nerve injuries, pressure injuries. Well padded - Scoliosis and kyphosis common. Difficult positioning + neuraxial CNS - eye lens dislocation, retinal detatchment Other - hernias common

Answer 282

1:10000. Large range of phenotypes with 6 major subtypes. Mainly autosomal dominant but occasionally recessive. Usually altered collagen production or post-translational modification. Features include: 1) Joint hypermobilitiy 2) Skin hyperextensibility 3) Delayed wound healing 4) Bleeding tendancy Airway - Increased risk of TMJ dislocation - Increased risk atlantoaxial subluxation - More likely to get airway bleeding Breathing - At risk for spont pneumothorax CVS - Some subtypes increased risk of valvular disease. Mitral valve prolapse. Aortic root dilation and dissection. (Ehlers Danlos types 3,4 and 6). Consideration for echo, valve + root replacement (Benthals), arterial line MSK - Scoliosis more common. Difficult neuraxial - At risk pressure injuries, nerve injuries - Poor wound healing. Vaginal delivery likely preferred over C section for wound healing Haem - Coagulopathies possible (vascular subtype EDS). high propensity for bleeding. Get bleeding history. TXA or DDAVP may be useful - may be best to avoid tourniquets, IM injections if high risk bleeding - Consult haem

Answer 283

Peptide molecule release from beta islet cells, binds to insulin receptor altering glucose, lipid and protein storage. Ultimately an anabolic hormone (promotes growth) Glucose: Promotes glucose uptake via GLUT transporters into liver, muscle, other cells. Promotes glycogen formation. Inhibits gluconeogenesis pathways. Lipid: promotes lipid uptake into liver, adipose cells, muscle. Promotes lipid storage. Inhibits lipolysis enzymes Protein: promotes amino acid uptake into muscle, promotes formation of proteins. Inhibits proterolysis

Answer 284

Lack of insulin (and excess glucagon) causes glucose to increase by glycogenolysis, gluconeogenesis. Causes increase in ketones by increase in lipolysis --> beta oxidation--> excess acetyl CoA --> increased ketone production. Ketones cause acidosis. Acidosis leads to negative inotropy, reduced cardiac output. Inhibits Na/K ATPase --> hyperkalaemia. Usually get HAGMA - bicarb will be low. Anion gap will be high (>12mmol/L) Glucose causes hyperosmolar serum. Leads to large volume diuresis --> hypovolaemia. May get further acidosis from tissue poor perfusion. May also lose lots of K+ so may end up with a normal serum potassium despite acidosis (but be K+ deplete) Lipolysis, proteolysis --> wasting.

Answer 285

CVS: - macrovascular complications. IHD, stroke, PVD. - Increased risk arrythmia (AF) - Increased risk thrombosis (CHADSVASc) - Autonomic dysfunction - highs and lows of BPs. Resp - Airway glycosylation, neck stiffness - difficult airway - Increased risk resp infections Renal - nephropathy GI - Gastroparesis, delayed gastric emptying CNS - retinopathy - Peripheral neuropathy. Neuropathic pains MSK - Poor skin / wound healing

Answer 286

Pregnancy - 4-6mmol/L (tighter control as risks to both mum and baby if hyperglycaemia) Poor control of diabetes having emergency surgery, inability to sense hypoglycaemia, over 75, autonomic neuropathy or if long QT syndrome - higher targets of 7.5-12.5mmol/L (= 10mmol/L +/- 2 mmol/L)

Answer 287

CSII usually assosciated with better glycaemic control for patients, more commonly used for T1DM. Combined with continuous glucose monitoring often. Usually get boluses on top of CSII. Need to balance risks of stopping vs starting alternative insulin therapy - DKA if inadequate insulin, hypoglycaemia if excess. Type of surgery will often dictate what to do. Short proceedure, under LA or regional, often patient can continue and self manage. Esepcially if no need for fasting. Needs to be removed for MRI or radiology (but often short procedures, so no worries). Need plan for if unexpected prolonged surgery, GA and patient unable to manage own device. If longer than 1 hour surgery under GA, likely best to cease CSII. No boluses while NBM. Determine usual insulin requirement basal rate. Program for 80% usual maintenance while NBM. Start VRII (make sure first on list), then cease CSII and remove leads Target BGLs in theatre - 6-10mmol/L. Add K+, glucose if needed. Post op, once eating >50% usual foods. Not vomiting. GCS 15. Ketones <1, able to manage own pump. Can restart CSII. After 2 hours, stop VRII

Answer 288

Biguinides. Metformin - continue. Unless major GI surgery, eGFR <60ml/min and Iv contrast to be used, eGFR <45ml/min. If TDS dosing, omit lunch time dose Sulphonylurea - Gliclazide - withhold any time NBM (including if 24 hour clear fasting for GLP1agonists) DPP4 inhibitors - Vildagliptan - continue Acarbose - withhold DOS SGLT2i - withhold 72 hours

Answer 289

Need to avoid giving short acting insulin while NBM, risk of hypoglycaemia Calculate long acting component of usual dose. E.g. if usually 10U of novomix 30, then 70% is long acting = 7 units. Then give 80% of the long acting component while NBM = about 5 units of protophane. If on >0.6U/kg of long acting insulin usually, consider giving only 2/3rds usual dose while NBM

Answer 290

Based on ANZCA ADS document 2023 Test BGLs and ketones If BGLs, ketones are normal then can carry on with day surgery, minor-intermediate surgery. Need availability of blood gas machine if continuing with more major surgery (e.g. cancer surgery). consider likelihood of eating and drinking afterwards If ketones >1.0, do blood gas. If base excess >-5, then no metabolic acidosis. Consider continuing non-urgent surgery with insulin-dextrose infusion. Endocrine involvement If base excess <-5, then acidosis present. Postpone non-urgent surgery. If urgent surgery, insulin + dextrose infusion + HDU input + guidance from endocrine.

Answer 291

4.5x increased OR for retained gastric contents if on GLP1 agonist in study on 200,000 endoscopy patients compared to control. But 0.25x decreased OR if had upper + lower GI endoscopy. Thought that clear fluid diet for 24 hours for colonoscopy reduced risk of retained gastric contents

Answer 292

Options include: - deferral. If risk unacceptable and non-urgent surgery that can be deferred. Informed patient. Re-present another time for elective surgery - Gastric ultrasound - if -ve, likely fine to proceed - Iv erythromycin. 3mg/kg, up to 250mg. Usually would expect stomach contents to go from 100% --> 58% without intervention from gastric emptying. with erythromycin, goes from 100% --> 6%. Useful in combination with gastric ultrasound - RSI, risk mitigation as per usual non-fasted patient - If endoscopy, could proceed with small 5mm ultrathin scope. And minimal sedation. Could be used to see if stomach empty too

Answer 293

Excess in growth hormone, most commonly from pituitary adenoma. May present for adenoma transphenoid resection or for unrelated surgery Diagnosis with GH suppression test with oral glucose. GH will be high and remain high despite glucose challenge. Then imaging of pituitary with MRi to confirm (in normal people, GH should drop to <1mcg/L CVS - Increased risk of IHD, HTN, cardiomyopathy, arrythmia. Particularly if T2DM. Consider arterial line, 5 lead ECG Airway - Difficult airway potentially. Large jaw, large tongue. Difficult with intubation, BMV, LMA insertion. - Can get hypertrophy of soft tissues. Concerning if voice changes or stridor. Consider VL or AFOI Resp - OSA risk high. STOPBANG screening. CPAP. May develop pHTN - Kyphosis possible. May get restrictive lung pattern Endocrine - Increased rates of T2DM, check BGLs. Increased risks of MI, strokes, PVD, nephropathy MSK - Enlarged feet, hands, skin thickness. difficulty with IV lines, monitoring, positioning Medications: -sometimes on octreotide (which can cause nausea, diarrhoea)

Answer 294

CVS: - Low cardiac output state with decreased systolic pressure, CO may be 50% of normal. Bradycardia, hypotension. - Increased risk of ischaemic heart disease - Increased pericardial effusions CNS: - coma (myxoedema coma) Resp: - Resp muscle weakness - OSA - Impaired hypoxic / hypercapnic drive GI: - Delayed GI emptying - increased ileus Haem: - Increased thrombosis risk - anaemia Renal: - Reduced GFR Metabolic: - hypoglycaemia - Hyponatraemia

Answer 295

Start treatment if clinical evidence for hypothyroidism. Low T3/ T4. Usually high TSH. Treatment is targeted to TSH. Aim is TSH between 0.5-1.5IU/ml. Thyroxine usually started at 25-50mcg / day. Long halflife so slowly uptitrated over weeks. If urgent surgery and hypothyroidism, can treat with liothyronine (T3). 10-50mcg IV slow push with ECG monitoring on. Probably at risk of angina, heart failure, ischaemia I'd guess

Answer 296

Myxoedema coma = medical emergency, has 25-50% mortality. Decompensation of hypothyroism. Commonly due to trigger (e.g. infection, malignancy). Especially in combination without being able to tolerate oral tabs for a while CNS: - Coma, reduced GCS CVS - Bradycardia, hypotension. Reduced cardiac output. Cardiac failure Resp - Resp muscle weakness, respirtatory failure - Poor resp drive response to hypoxia / hypercapnia. Metabolic: - Hypoglycaemia - Hyponatraemia - Hypothermia Management: - Admission to ICU - ABCs, may need intubation, ventilation, vasopressor support, Iv fluids (0.9% NaCl - do not raise Na too quickly) - DE - correct hypoglycaemia. Warm slowly (to avoid massive peripheral vasodilation) - Specific treatment: - 100mg Iv hydrocortisone Q6H. to treat concurrent adrenal insufficiency - T4 IV loading dose of 200-400mcg then 100mcg following day. Or can give 5-20mcg IV T3 (liothyrinone Q12H), particularly if urgent surgery needed) - Treat any underlying triggers e.g. sepsis

Answer 297

-No need to delay surgery if subclinical hypothyroism (e.g. asymptomatic, even if TSH abnormal). Long half life for thyroixine so missing single dose not a big deal - Give induction drugs slowly, titrate slwoly. Reduced CO will take time for delivery, at risk of hypotension. conversely, gas inductions will be speedier - Characteristically less responsive to catecholamines - At risk for hypothermia, warm patient - Reduced renal and hepatic metabolism. Dose accordingly. Monitor twitches for NDMRs - Better to have controlled ventilation as patients tend to hypoventilate while spont breathing

Answer 298

CVS: - Increased systolic BP, decreased diastolic BP, increased PP, increased MAP (HTN) - Increase SV, increased CO - Increased arrythmia (AF), cardiomyopathy, ischaemia, congestive heart failure (especially thyroid storm) Resp: - Increased RR, increased VO2 Metabolic - weight loss, hyperglycaemia CNS: - Anxiety, tremor - Exophthalmos

Answer 299

Most common causes are Graves (autoimmune, >50% of hyperthyroidism), multinodular goitre, excess iodine, pituitary adenoma, thyroid nodules - Carbimazole. Inhibits iodination of tryosine residues in thyroglubulin - Prophylthiouricail (PTU). 200-400mg daily, reduces release of thyroid hormones and reduces conversion of T4 to T3. PTU better than carbimazole if plans for pregnancy - Lugol's iodine - Propanolol for tremors, tachycardia, palpitations. 30-60mg PO TDS. B2 antagonism also reduces T4 --> T3 conversion - Thyroidectomy

Answer 300

Life threatening decompensation of one or more organs seystems, due to hyperthyroidism (thyrotoxicosis). Signs include: CVS - palpitations, arrythmia (AF), tachycardia (often >140BPM), HTN, congestive heart failure, APO, ischaemia CNS - coma REsp - tachypnoea, hypercapnia GI - nausea, comiting Metabolic - hyperthermia (often >40c) May be precipitated by illness or surgery, especially 6-24 hours post op Treatment: - ABCs, consider GTN infusion if hypertension driving APO - IV fluids, cooling to <38c. Supportive care in ICU - PAracetamol for fever. DO NOT GIVE aspirin or NSAIDs (as will compete for protein binding of T4 --> more unbound - Beta blockade - esmolol infusion probably best. 250-500mcg/kg loading followed by 50mcg/kg/min and uptitrated. Reduces conversion T4--> T3 too - Hydrocortisone 200mg IV Q6Hrly. Treat adrenal insufficiency and reduce conversion T4-->T3 - PTU 1g PO via NG tube. Reduces release of thyroid hormones + reduces conversion T4-->T3. then 200-300mg PO TDS

Answer 301

Ideally before surgery for hyperthyroism, should be free from arrythmia, HR <80BPM and no tremor. Airway - May be difficult with tracheal stenosis (especially if >50% and malignancy), tracheal deviation. consider AFOI Breathing - Potential for large anterior mediastinal mass (retrosternal extension), unable to ventilate post-induction. Ideal to keep spont ventilating until sure past lesion. Or just keep spont ventilating if able. Determine risk based on CT scan and symptoms for patient (orthopnea) - Risk of recurrent laryngeal nerve palsy - voice changes, stridor. If bilateral palsy post surgery --> complete obstruction Circulation - SVC obstruction possible - risk airway oedema, upper limb oedema, neck vein distension. IV line in lower limbs if this is the case - Risk cardiovascular collapse on induction if large anterior mediastinal mass, compression great vessels. Arterial line. Plan for lateral or prone position if issues - Possible to have IJV, CCA involvement with risk of stroke, raised ICP, massive haemorrhage if iatrogenic injury during surgery Disability - Anxiety - Tremors - difficult IV Exposure - risk of hyperthermia. May need cooling. Monitor temp - Exopthalmos may increase risk eye injury, pad eyes Medications - continue usual ones (PTU, carbimazole, beta blockers)

Answer 302

Goal is to increase calcium (hence why hyperparathyroism causes hypercalcaemia). Trigger for release is low Ca PTH also causes a decrease in PO4- Increases osteoclast activity Increases renal Ca absorption Increased vitamin D production (which also increased renal Ca absorption, increases Gi absorption

Answer 303

Primary = adenoma of parathyroid gland --> excess PTH. Adenoma associated with MEN1 - High PTH, high Ca, low PO4- - Often asymptomatic. Hypercalcaemia may cause: constipation, renal stones, GI pains, confusion / aggitation, depression, memory loss. Shortened QT interval on ECG Secondary = renal disease. Loss of calcium from chronic renal disease causing high PTH. - Hight PTH. Low Ca. High PO4- - Medical treament is with Calcium supplementation, Vitamin D and low PO4- diet - If fail medical management, parathyroidectomy (10%) Tertiary = renal disease but chronic, causes hyperplasia of parathyroid glands - High PTH, high Ca, high PO4- - May get calciphylaxis = skin, blood vessels and eventually heart deposition of calcium. May get "heart of stone", diastolic dysfunction

Answer 304

Usually caused by malignant processes (e.g. bone mets, myeloma), or undiagnosed hyperparathyroism. symptoms: Weakness, lethargy, renal stones, constipation, abdominal pains, mental changes (depression, anxiety), coma If Ca >4.5mmol/L = life threatening. Transiently lower with 500ml of 0.1M phosphate over 6 hours to transiently lower Typically can proceed with surgeries if <3mmol/L and asymptomatic. If >3mmol/L or ECG changes, renal impairment then needs treatment ECG changes - shortened QT interval. J waves. Rarely VT or VF -IV fluids. Aim for 4-6L. Plasmalyte has no calcium so good option - Bisphosphonates e.g. pamindronate 60mg over 4 hours. Inhibits osteoclasts, long duration of action - Calcitonin 3-4U/KG IV then 4U SC BD. Rapid but temporary decrease in Ca from bones - Sometimes give NaCl and frusemide to force diuresis. - Dialysis

Answer 305

Most commonly iatrogenic from removal of parathyroid glands in thyroid surgery, may also be idiopathic or post radiation. Calcium will drop around 20 hours mark. Often fixes itself at 3 day mark Features of hypocalcaemia: hypotension, tetany, muscle spasms, seizure, arrythmia, prolonged PR interval, prolonged QT interval. Rarely may get TdP Treatment: 10ml 10% calcium gluconate over 10 mins (10:10:10 rule)

Answer 306

Failure of the adrenal glands themselves. -75% due to autoimmune = Addisons Other causes: - Infection - TB - AIDS - Trauma - Iatrogenic (e.g. surgical injury or intentional bilateral adrenalectomy) - Malignancy, metastases - Sepsis Need to cover both glucocorticoid (cortisol) and mineralcorticoid (aldosterone) - Hydrocortisone 20mg PO mane, 10mg nocte - fludrocortisone 0.1mg PO daily

Answer 307

Most commonly due to ACTH suppresion from high dose steroids. At risk if >5mg per day prednisone equivalent for 4 weeks or more. Other causes are piuitary or hypothalamus tumours --> decreased CRH or ACTH Only need to replace glucocorticoids in these patients, mineralocorticoid cover is unnecessary

Answer 308

May be either primary adrenal insufficiency or secondary. Both have loss of glucocorticoid (cortisol). Primary has loss of mineralocorticoid too Signs / symptoms for both: Nausea, vomiting, fatigue, vomiting, diarrhoea, weightloss, joint pains Primary will have the following in addition: skin hyperpigmentation, salt craving, postural hypotension (90%) Diagnostic tests: - Early morning cortisol + ACTH level. Primary adrenal insufficiency if cortisol <165nmol/L and ACTH >22pmol/L. Secondary will have low ACTH and low cortisol - Short synacthen test. Synacthen = synthetic ACTH. Stimualtes adrenal gland to release cortisol. Check cortisol at 0 and 30 mins. If cortisol peak <500nmol/L at 30 mins, then has adrenal insufficiency (could be either primary or secondary though) - Insulin tolerance test = gold standard. Give insulin and check glucose + cortisol levels at 0, 15, 45, 60 and 90 mins. Need BGL <2.2mmol/L. If cortisol <500nmol/L, diagnostic for adrenal insufficiency Adrenal insufficiency common (50%) in septic ICU patients, probably why they respond to steroids. Consider synacthen testing, especially if on high vasopressor levels

Answer 309

Medical emergency due to lack of glucocorticoid activity. Importantly, glucocorticoids have permissive activity for catecholamines to function. May be due to lack of steroid cover in a patient with secondary adrenal insufficiency. Or a new presentation of adrenal insufficiency (e.g. first presentation of Addisons disease = autoimmune loss of adrenal glands) Signs / symptoms: - CNS. Weakness, presyncope, abdominal pains, coma - CVS- hypotension (in particularly, volume and vasopressor resistant), sweating, peripheral vasodilation, raised CO - GI - nausea, vomiting - Metabolic - hyponatraemia, hypoglycaemia, hyperkalaemia (lack of aldosterone = similar effect to spironolactone) Form of distributive shock. Very similar presentation to septic shock Management: - ABCs. Intubation, ventilation if needed. 100% FiO2 - Circulation - IV fluids, 0.9% NaCl at 1L / hour and glucose if hypoglycaemia. Likely to be vasopressor resistant until glucocortioid supplementation - Take baseline level cortisol + ACTH before giving steroids - Hydrocortisone 200mg IV loading then 100mg Q6Hrly thereafter - Treat hyperkalaemia with salbutamol (caution insulin-dextrose if hypoglycaemia) - ICU admission - Treat underlying cause (e.g. infection)

Answer 310

Need to ensure both mineralocorticoid + glucocorticoid supplementation in perioperative period. Will need increased levels of glucocorticoid to cover stress response for surgery (as unable to mount stress response themselves). -Ensure takes regular medications day of surgery (hydrocortisone + fludrocortisone) Major surgery - Give 100mg Iv hydrocortisone with induction. then 50mg Iv Q6-8hrly for 48H - 1 week depending on recovery. When oral route available, start on triple oral hydrocortisone dose for 48H then wean (Uk based association of anaesthetists suggests 100mg IV hydrocortione on induction then 200mg/24 hour infusion For labour: - Give 100mg Iv hydrocortisone with induction of labour then 50mg Q8Hrly until delivery. Then taper with 2x usual dose over 1-3 days then back to usual - AoA guideline suggests 100mg hydrocortisone with labour then 200mg/24 hours infusion until delivery then taper with 2x usual dose for 1-3 days then back to usual dose Monitor BGLs Q4Hrly or more frequently if diabetic. Give insulin if needed

Answer 311

If prednisone equivalent = or >5mg / day for 4 weeks. Only needs glucocorticoid replacement (dex is fine) Major surgery - 8mg IV dexamethasone, will provide 24 hours cover. Then can do 50mg PO or Iv hydrocortisone (or triple usual steroid dose PO) for next 48-72 hours Labour: - 100mg Iv hydrocortisone with labour then 50mg Q6hourly until birth. Then can taper with 2x usual steroid dose for next 1-3 days then back to usual. With high dose steroids, need to monitor glucose Q4hrly or more frequently if known diabetic. May need insulin

Answer 312

Excess of cortisol or glucocorticoids, most commonly driven by adenoma of pituitary causing increased released of ACTH (= Cushing's disease). Can also be from excess steroid use. Other causes are adrenal adenoma, adrenal cancer Diagnosis: based on cortisol levels + ACTH. If cortisol >700nmol/L. ACTH will be high if pituitary adenoma. Low if excess cortisol / glucocorticoids Signs and symptoms: - CVS - HTN (80% of patients), fluid overload - MSK - Buffalo hump, obesity (centrally). Osteoporosis. Moon shaped face. Easily bruised skin / thin skin. Proximal myopathy - Metabolic - hypernatraemia, hyperglycaemia, hyper bicarbonate. Hypokalaemia (cortisol has weak mineralocorticoid effect). Hypocalcaemia - Resp - OSA more common -GI - increased reflux May present for transphenoid pituitary surgery. Or adrenalectomy. Or other things Airway - May be difficult intubation, BMV with obesity, central adiposity around neck, OSA - increased reflux. Intubate Resp - May desat quickly due to obesity, reduced FRC Circulation - Hypertension common. consider invasive monitoring, echo - diabetes common. Monitor BGLs. Consdier consequences of diabetes (IHD, stroke, PVD, renal) MSK - thin fragile skin, more propensity to bleeding. Positioning important. Osteoporosis common - Difficult IV access if obese - Immune - Infection risk due to immunosuppresion. Poor wound healing. Maintain normothermia. give prophylactic antibiotics Medications - Ensure supplement steroids if on high doses preop

Answer 313

Excess aldosterone, most commonly from adrenal gland adenoma (= Conn's syndrome 60%), benign hyperplasia of the zona glomerulosa (35%). Rarely adrenal carcinoma. May also get secondary hyperaldosteronism from cirrhosis (inability to metabolise aldosterone) Causes: fluid overload, hypernatraemia, hypokalaemia, H+ excretion and Mg2+ excretion. Metabolic alkalosis Signs and symptoms: CVS - fluid overloaded, hypertensive often Resp - may have hypoxaemia from APO Renal - nephrogenic diabetes insipidus from renal tubular damage MSK - muscle weakness from hypokalaemia Metabolic - Impaired glucose tolerance, metabolic alkalosis Preop adrenalectomy - Spironolactone to block aldosterone. Up to 400mg / day - Aim for normal K+, HCO3-, pH before starting surgery. May need K+ supplementation - Spironolactone usually sufficient for HTN via diuresis. May need ACEi added (which will also aid in retaining K+) - Diagnosis with aldosterone:renin ratio (typically >400 for diagnosis). In primary hyperaldosteronism, aldosterone will be raised but low renin. Secondary will have raised aldosterone but appropriately raised renin. - BGLs important to check Intraoop: - Usually unilateral adrenalectomy will be laparoscopic - Airway - ETT. as laparoscopy - Standard ANZCA monitoring + art line (CVS swings in BP common). Plus allows for sampling blood - CVL only if complex or bilateral - Q1Hrly BGLs - May get some degree of BP surges with adrenal handling (but less than that of phaeo surgery). Use Mg2+, phentolamine. Or remi TCI Post op - HDU - Stop spironolactone and K+. check electrolytes and BGLs - Give 50mg IV hydrocortisone in post op period. Continue Q8Hrly - Do morning cortisol level 8am day after surgery. If unilateral adrenalectomy, then likely won't need steroids / fludrocortisone - If bilateral surgery, will need life long hydrocortisone + fludrocortisone. Can just use IV hydrocortisone 200mg/day until able to tolerate oral intake (will cover both glucocorticoid and mineralocorticoid. - Usual doses to end up on are 20mg mane, 10mg nocte of hydrocortisone. 0.1mg PO fludrocortisone

Answer 314

Increased losses - diarrhoea, NG losses, pyloric stenosis, hyperaldosteronism, Mg2+ depletion Intercompartmental shifting - alkalosis (each pH increase of 0.1, ket K+ decrease of 0.6mmol/L), insulin, beta 2 agonists, steroids decreased intake - malnutrition

Answer 315

Muscle weakness, tetany Encephalopathy Cardiac - dysrrythmia, decreased contractility, flattened T waves, prolonged PR, T wave inversion, U waves, ST depression

Answer 316

K+ >5.5mmol/L. Mild 5.5 - 6 Moderate 6-7 Severe >7 Increased intake - Oral / Iv K+ containing foods / solutions - blood transfusion Decreased excretion - Renal failure - Spironolactone - ACEis - Adrenocortical disease e.g. Addisons, lack of aldosterone Intercompartmental shifting - Acidosis (0.6mmol/L increase per 0.1 decrease in pH) - Haemolysis - Rhabdomyolysis - Trauma - crush syndrome, compartment syndrome - MH - Suxamethonium Pseudo hyperkalaemia - haemolysed sample

Answer 317

Cardiac - 6mmol/L - peaked T waves, prolonged PR - A bit more. Widened QRS, flattened P waves, St depression - around 8mmol/L. VF, TdP - Asystole MSK - Muscle weakness, especially >8mmol/L GI - Nausea, vomiting, diarrhoea

Answer 318

-Stop giving K+ or things causing hyperkaelamiea (sux) - usual ABCs - Iv line, monitoring with ECG and BP immediately - Give 10ml 10% calcium gluconate as slow push. Cardiac stabilisation - Insulin-dextrose. 50ml 50% with 10U actrapid. Over 20 mins - Salbutamol - neb 5mg. Get about 2 hours benefit - Sodium bicarb 8.4%, 1ml/kg. Give if acidotic - consider calcium resonium 5g PO. Binds to stomach K+. Slow to work. And now has full stomach. Only good in select circumstances - Dialysis if refractory hyperkalaemia - Cancel all but the most urgent of surgeries if hyperkalaemia until this is resolved

Answer 319

Hyperosmolar - Pseudohyponatraemia (hyperglycaemia) - Hypertonic solution excess (mannitol) Iso-osmolar - Pseudohyponatraemia here too. Hyperlipidaemia, hypertriglyceridaemia Hypo-osmolar (the main stuff): Hypovolaemic - Diuretics - Vomiting, diarrhoea, fistula losses, NG losses - Excess sweating, dehydration (although often hypernatraemia instead...) - Burns - Cerebral salt wasting - Bleeding - Primary adrenal insufficiency (lack of aldosterone) - Excess third spacing (pancreatitis) (can differentiate these based on urinary sodium. If urine sodium <20mmol/L, suggests pre-renal losses. If urine sodium >20mmol/L, suggests you are losing sodium through the kidneys (e.g. diuretics, adrenal insufficiency) Euvolaemia - SIADH - Hypothyroidism - Secondary adrenal insufficiency, excess steroids - Hypervolaemia - Excess oral intake - Excess hypotonic fluids (dextrose), TURP syndrome - Liver failure - Renal failure - Cardiac failure

Answer 320

Nausea, vomiting, weakness, lethargy, confusion/ delirium, headaches, seizures, respiratory depression, coma, death. Usually rate of decline of sodium concentration which is main indicator for if you actually get symptoms or not

Answer 321

Hypovolaemic - Diabetes insipidus - Burns - Intrinsic or obstructive renal disease - Vomiting, diarrhoea, GI losses - Sweating, dehydration - Osmotic diuretics (mannitol) Euvolaemia - insensible losses - Diabetes insipidus here too Hypervolaemia - Hyperaldosteronism (Conns) - Cushings syndrome (excess cortisol). Such as from pituitary adenoma (Cushings disease) - Iatrogenic (excess hypertonic solutions)

Answer 322

-Paralytic ileus (functional obstruction) - concentric narrowing (tumours, Crohns, diverticulitis) - Foreign body obstruction (large gallstones, ingested FBs) - Kinking - (adhesions, hernia) - Twisting (volvulus of caecum or sigmoid) - Intersussception (may be malignant or benign)

Answer 323

-Synthetic. Production of conjugated bilirubin, albumin, coagulation proteins, anticoagulation proteins - Metabolism. Degredation of endogenous + endogenous molecules (phase 1 and 2 metabolism) - Excretion. Of waste products in bile - Glucostat - storage of glycogen, fat. Responds to insulin + glucagon to maintain BGLs. gluconeogenesis - Immune - Kumfer cells. Production of compliment proteins - Storage - iron, fat soluble vitamins - Endocrine - EPO, thrombopoiten, angiotensinogen

Answer 324

Paracetamol Alcohol CMV Hepatitis A EBV Amanita phalloides (death cap mushrooms)

Answer 325

Alcohol Hepatitis B, C Medications: amiodarone, MTX Autoimmune Fatty liver disease

Answer 326

compensated = asymptomatic + preserved hepatic function. Decompensated = jaundice, encephalopathy, varices, ascites. Once decompensating, usually dead within 5 years

Answer 327

Portal hypertension - raised hydrostatic pressures drive fluid from splanchnic vessels into peritoneal space Hypoalbuminaemia - loss of oncotic pressure Secondary hyperaldosteronism - sodium and H2O retention. Fluid overload, including into peritoneal space

Answer 328

CVS - Fluid overload (e.g. from secondary hyperaldosteronism) - Hyperdynamic circulation with peripheral vasodilation and increased cardiac output - Hepatic cardiomyopathy Resp - Mechanical issues: massive ascites, hepatosplenomegaly, hydrothorax. All will decrease FRC - Hepatopulmonary syndrome. From increased NO synthesis, causes pulmonary vasodilation --> impaired V/Q matching. Orthodeoxia - Portopulmonary hypertension. Increased pulmonary pressures from increased PVR from increased CO through pulmonary vessels + raised CVP - increased risk resp infections GI - Impaired gastric emptying - Risk of massive GI bleeding CNS - Encephalopathy (West Haven classification of encephalopathy from 0-4) Renal -Hepatorenal syndrome Haem - Coagulopathy risk. Impaired platelets. Possible thrombocytopenia (splenomeagly + decrease thrombopoetin) - Thrombosis risk - Anaemia of chronic disease +/- bleeding from varices Immune - Impaired immune function, risk of post op infections Metabolic - Hypoglycaemia - Hyponatraemia - Malnutrition - Hypoalbuminaea

Answer 329

ABCDE Albumin Bilirubin Coagulation (INR) Decompensated ascites Encephalopathy 5 is the minimum score. 15 is the maximum. A = 5-6 points = least severe B = 7-9 points C = 10-15 points = most severe There is some subjectivity to it, with encephalopathy graded by West Haven classification. And ascites being either diuretic responsive or not Initially designed for predicting mortality in decompressive portal surgery A <5% mortality B 25% mortality C 50% or more mortality

Answer 330

Model for End Liver Disease Traditionally just 3 things. BIC Bilirubin INR Creatinine Uk uses Na-MELD which also includes sodium. MELD <10 approximates Child Pugh A MELD 10-15 = CP B Meld >15 = CP C Periop mortality for elective surgery: MELD <10, mortality 5-10% MELD 10-15, mortality 20-25% MELD >15, mortality 50%. Likely best to defer, find alternative management Emergency surgery likely 4-5x increased risk

Answer 331

VOCAL- Penn score Useful for both elective and emergency cases More inputs, includes type of surgery. Gives 30d, 90d, 180d mortality. And 90 day liver decompensation risk

Answer 332

Paracetamol ALF: - pH <7.25 after fluid resus and 24 horus or - Lactate >3.5 after 12 hours fluid resus or - Lactate >2.5 after 24 hours fluid resus + grade 3-4 encephalopathy, Cr >300, PT >100 (INR >6). Or another organ failure Non-paracetamol ALF: - INR >6 OR - Encephalopathy with any 3 of: (age <10 or over 40, INR >3.5, bilirubin >300, not from hepatitis A/B or drug reaction)

Answer 333

Atlanta criteria (need 2 of the 3): - pain in keeping with panc (epigastric, radiating to back) - Lipase / amylase >3x upper limit normal - Radiological evidence (CT with contrast) Atlanta criteria also classifies severity. Mild = no organ failure. Moderate = transient organ dysfunction / local complications. Severe = >48 hours organ failure Causes: - Obstruction (Gallstones, tumours, post-ERCP, cystic fibrosis) - Toxic (alcohol, drugs, hypercalcaemia, snake / scorpion venom, triglycerides) - Ischaemic - CPB, shock - Autoimmune - Hypothermia - Infection - CMV

Answer 334

Multi system genetic disorder. Can be autosomal recessive, dominant or X linked. Mainly collagen type 1 defect (Col1A1 and Col1A2 make up 90% of OI) Airway - Dentinogenesis imperfecta (highly unstable dentition) - Atlantoaxial instability possible Breathing - Usually kyphotic, scoliosis. Restrictive lung disease. May get pHTN Circulation - Mitral valve prolapse and regurg - ASDs, VSDs - Aortic root dilation CNS - Type 1 OI have blue sclera (usually more mild form of OI) - Adult onset sensoryneural hearing loss - Craniocervical junction abnormalities --> obstructive hydrocephalus MSK - Chest wall deformities, kyphosis, scoliosis Most commonly will present for orthopaedic surgeries from fractures

Answer 335

Airway (more difficult) - Large tongue, high arched palate, micrognanthia, retronganthia - Risk of atlantoaxial subluxation - Small larynx (subglottic stenosis, 1-3mm less diamete) relative to body size Resp - OSA very common, risk of pHTN CVS - High rates congenital heart disease. Tetrology of fallot, AVSDs (half of all AVSDs are from T21) - pHTN, RV failure especially if OSA or septal defect - Bradycardia with laryngoscopy, IV insertion - IHD Haem - High rates leukaemia Metabolic - High rates obesity, T2DM. Also increased risk of T1DM and Hashimoto's thyroiditis CNS - Intellectual disability, cooperation may be challenging - Autism - ADHD - Epilepsy more common GI - Higher rates of GORD, pyloric stenosis

Answer 336

Malignancy of uncontrolled plasma cell proliferation, abnormal bone marrow. MGUS = precursor = Monoclonal gammopathy of unclear signficance --> smouldering myeloma --> multiple myeloma Risk factors: age, obesity, previous radiation exposure, family history Symptoms may be from lytic lesions, antibody formation, anaemia, hypercalcaemia, renal impairment or VTE. CRAB = Calcium, Renal, Anaemia, Bone lesions Airway - May have C spine lytic lesions, could cause fracture if excess extension Haem - Anaemia common. risk from bleeding - Thrombosis risk from increased blood viscosity, especially if high protein counts (>120g/L). May need acute plasmaphoresis and plasma exchange with crystalloid / albumin - If had recent autologous stem cell, then will be severely immunosuppressed. At risk for GVHD Renal - At least 50% will get renal impairment. Multi factorial (from antibiodies, microemboli). Avoid nephrotoxics MSK - Lesions may be in any bones. May have chronic pain. At risk to intraop fracture

Answer 337

Hyperphosphataemia Hyperkalaemia Hyperuricaemia Hypocalcaemia Metabolic acidosis Raised creatinine, renal failure

Answer 338

Autosomal recessive, single nucleotide polymorphism (glutamate to valine, position 6) of beta globulin. HbS. May have sickle cell trait (virtually normal bloods and pretty much asymptomatic) or sickle cell disease Sickling can be triggered by hypoxia, acidosis, hypothermia, dehydration, fever, infection, sepsis. Which is key to providing anaesthesia to these patients. Sickling causes microthrombi --> painful, ischaemia to tissues. Renal impairment, haematuria. May also get ischaemic gut, stroke, PE, retinal clots, MI, limb ischaemia Hb often around 60-90g/L. Increased reticulocytes, film will have sickled cells. Howell-Holly bodies if spleen atrophy. No symptoms in first 4 months of life as foetal Hb more abundant than adult (which have no beta globulins) Usually have small, non-functioning spleen by adulthood --> at risk of sepsis Aplastic crisis = bone marrow failure due to rapid fall in Hb. Often triggered by infection e.g. parovirus Haemolytic crisis = rapid rise in bilirubin from haemolysis.

Answer 339

Key is to avoid sickling. Avoid hypoxia, acidosis, infection / sepsis, dehydrration, hypothermia Preop - Contineu hydroxyurea, increases HbF which reduces abnormal sickle beta globulin - continue prophylactic penicillin (splenic atrophy), ensure vaccines up to date - consult haem - Often have red cell antibodies, ensure group + screen done Intraop - Regional or Ga fine. - Ensure analgesia, multimodal to avoid excess opioids and possible resp acidosis - Sip til send + well hydrated IV - Warm patient, monitor temp - Treat any metabolic acidosis, infection - Best to avoid tourniquets Post op - Supplemental O2 - Keep warm - Treat sickle cell crisis with analgesia, O2, Iv fluids. Consider regional block if ischaemic limb - High risk for VTE, consider prophylaxis

Answer 340

Defect in haemo moiety synthesis. Causes accumulation of precursoer molecules which are oxidised to porphyrins. Can be divided into hepatic and erythropoetic sub types (8 different in total) 3 hepatic subtypes are autosomal dominant. - Acute, intermittent. Most common, most severe. Sweden = risk factor - Variegate porphyria. South African = risk factor - Hereditary coproporphyria More common in women in 20s or 30s. Can take 5 days to get crisis from trigger. Triggers include stress, medications, infection, alcohol, pregnancy, bleeding (including menstruation) Symptoms: abdo pain, vomiting, motor / sensory peripheral neuropathy, cranial nerve palsies, autonomic dysfunction, coma, seizures Definitely porphyrinogenic: thiopentone, halothane, hydralazine, methyldopa Probably or possibly porphyrinogenic: ketamine, etomidate, dexmed, dexamethasone, amiodarone, hydrocortisone Safe = Propofol, sux, roc, morphine, bupovacaine, adrenaline

Answer 341

Call for help Stop precipitating drugs A + B C - Treat with Iv fluids - Place A line as at risk of autonomic instability. HDU or ICU D - treat seizures with midaz, propofol (not thiopentone) - Analgesia Everything else - Withdraw precipitating drugs 3mg/kg haem arginate once daily for 4 days. Causes negative feedback on aminolaevulinic acid synthase

Answer 342

X linked, so mainly males affected (inheritence from mum). Haemophillia A = fVIII deficiency. Usually need <2% normal factor 8 to get spontaneous bleeding (severe haemophillia). If 5-30% normal, may just have increased bleeding with haemostasis challenges (trauma, menstruation, tonsilectomy / other surgeries). 1:10000 rates. Factor 8 part of the intrinsic pathway. combined with IXa, calcium to activiate X to Xa. Lack of X activiation --> less thrombin activation --> less fibrin formation from fibrinogen. Less clot formation Haemophillia B = factor IX deficiency.

Answer 343

Preop - Discuss with haematologist - Testing for fVIII levels. Severe haemophilia if <2% normal. Mild if 5-30%. Severe haemophilia often will have regular fVIII infusions pre-emptively to prevent complications from spontaneous bleeding. Some with mild disease might just get on demand fVIII infusions before surgery - Aim for surgery is to increase fVIII levels to 80-100% of normal, with troughs of 50%. Typical dose 50U/kg - Complications from bleeding history: Previous transfusions (get group + screen, red cell antibodies common) Iron deficient anaemia (from GI bleeding, epistaxis) May have had joint haemarthroses, joint replacements Psychological burden of chronic disease - best for surgery to be done in tertiary centre with access to large blood bank, haematologists on site Intra op - Have infusion complete prior to surgery incision start + test levels beforehand - DDAVP - increase fVIII, VWB factor. subcut 0.6mcg/kg - TXA - Avoid NSAIDs, IM injections, anticoagulation, antiplatelets (if mild haemophilia and minor-intermediate surgery, may be able to manage with just DDAVP and TXA. Get haem to make plan) - If emergency bleeding and no recombinant factor VIII available, cryo or FFP have fVIII in it Post op - Usually maintain fVIII levels between 50-100% for up to 7 days post op, depending on how major the surgery is - haem follow up + check levels regularly Differences with haem B: - It is factor IX not factor 8 - dose for fIX infusion is 80U/kg - Will not respond to cryo. Will respond to FFP - Also won't respond to DDAVP

Answer 344

Mum = carrier as X linked disease. Pre-labour: - May still have slight increased propensity for bleeding so still useful to check fVIII levels and discuss with haematologist. - Pre-pregnancy conseulling, genetic testing. If male, can get amniocentesis to confirm if +ve for haemophillia (ensure fVIII levels >50% for this) - If male baby, 50% chance of haemophilia so without genetic testing, assume it has the condition Labour -plan from haematologist - Check fVIII levels. If <50%, then top up with recombinant fVIII (50U/kg). Aim for peak of 80-100% with troughs of 50% throughout labour and delivery - Can have neuraxial, LSCS if fVIII levels >50%. Informed consent (but not shown to increase risk haematoma if above this) - Consider TXA and DDAVP, especially if bleeding - Cryo and FFP both have fVIII in them in an emergency - No assisted delivery (e.g. forceps, vacuum) as high risk intracranial bleeding. But if head stuck, may need forceps Post delivery - no heel prick tests - check newborn fVIII levels from umbillical cord (or APTT, if >40s then probably haemophillia) - monitor for bleeding, maintain fVIII levels >50% for 2-7 days post delivery

Answer 345

VWBF = glycoprotein, from megakaryocytes and endothelium. Binds to platelets, collagen via Gp1b receptor. VWBF also holds fVIII in circulation so test for this too. Autosomal dominant is most common, with variable penetrance. Type 3 autosomal recessive Type 1 = most common. Quantitative decrease in VWBF. If <30% normal, then VWD. Still have single functional gene (heterozygous). Responds well to DDAVP, VWBF concentrates or cryoprecipitate. DDAVP dose = 0.3mcg/kg subcut or infusion over 30 mins, give 60 mins before surgery Type 2. Qualitative. Subdivided into: 2A = loss of function, less binding to Gp1B (so still responds to DDAVP usually) 2B = gain of function. Increased binding to Gp1b --> increased clearance of platelets --> thrombocytopenia. DDAVP will cause worsening of this. TXA will work. Probably best not to give cryo, VWBF concentrate to these. Maybe platelets if thrombocytopenia. 2M and 2N are also loss of functions Type 3 = rare but most severe form, homozygous. Often complete loss of fVIII too. Also doesn't respond to DDAVP Platelet type (pseudo VWD) = Gp1b receptor defect. Does not respond to DDAVP or VWBF infusions Dose of VWBF infusion. 15-30U/kg if minor surgery, 40U/kg if major for all types, reducing bleeding risk with normothermia, normal calcium, avoiding acidosis

Answer 346

Pre labour -Determine subtype (type 1 most common) - haem plan - anaemia screening, iron if needed - antenatal planning, discussion around genetic testing Labour plan - VWBF will tend to rise in pregnancy so checking early in pregnany not usually useful. Check at 34 weeks (or earlier if risk preterm labour), if VWBF >50% and fVIII >50% then can have spinal, epidural as per usual (if not, then should be avoided) - Can give DDAVP 0.3mcg/kg sc once cord clamped (for types 1 and 2a). Risk of hyponatraemia and fluid overload with DDAVP and oxytocin - TXA always useful too - For more severe VWD (e.g. type 3. Or type 1 with <50% VWBF after DDAVP), give fVIII (50U/kg) and VWBF infusion (40U/kg). Give this to any haemorrhaging VWD patient (except for type 2b, which will worsen with DDAVP and VWBF) - Avoid other causes for bleeding. Treat bleeding promptly (e.g. uterotonics, surgery) Post labour - monitoring

Answer 347

Decreased production - bone marrow suppresion (drugs, radiotherapy, myelodysplasia, bone marrow infiltration) - platelet selective reduction (hereditary, drugs, alcohol) Increased consumption - Immune mediated (ITP, SLE, viral, lymphoproliferative) - Non immune (DIC, CPB, HELLP) diluttional - massive haemorrhage, pregnancy splenic pooling -Splenomegaly, liver failure

Answer 348

Dissemenated intravascular coagulation Where a pathological process disturbs coagulation homeostasis. Abnormal coagulation and fibrinolysis. Can be acute or chronic. Causes: Sepsis Trauma MH Anaphylaxis Malignancy Massive haemorrhage Amniotic fluid embolism Heat stroke ABO incompatible transfusion Type 1 - OVer activation of coagulation cascade (consumption coagulopathy) casues thrombi, platelet aggregation. MAcro and micro circulation thrombi and ischaemia Type 2 - Excess thrombi --> excess fibrinolysis and fibrin degradation products. Raised d dimer. Bleeding ++

Answer 349

Stasis, hypercoagulability and endothelium dysfunction. For increased risk fo thrombosis

Answer 350

Caprini screening tool gives risk for VTE, determines if intra op and post op VTE prophylaxis should be utilised Patient factors: - Hypercoagulable disorders (antiphospholipid, protein C or S, thrombophilia, polycythaemia) - PRevious VTE - Family history VTE - Female - Older - Smoker - Obesity - Hormones / contraceptive pill - Pregnancy - Immobility (casts, recent long haul travel) Malignancy (especially metastatic and active cancers) - Dehydration Surgical factors: - Major surgery, especially when less likely to mobilise post op - Duration >2 hours - tourniquet use - trauma - Emergency surgery

Answer 351

Preop - Identify high risk patients. Caprini screening tool - Set expectation to mobilise - Have haem plan for high risk of VTE (e.g. antiphospholipid) - Not excessively stopping anticoagulation. Bridging if needed - sip til send or avoiding excess fasting to avoid dehydration - Avoid purely elective surgery while pregnant - Ensure complete recovery from acute VTE Intraop - TEDS - SCDs - Foot pumps - Minimally invasive surgery, minimise surgery time - Avoid tourniquet - Ensure analgesia, antiemetics and avoid excess drains to promote post op mobilising (ERAS) - euvolaemia with Iv fluids Post op - Continue TEDs, SCDs, consider timing for chemical prophylaxis if inpatient (vs risk of bleeding) - Mobilise - recommence usual anticoagulation as soon as able - consider IVC filter if absolute contraindications to chemical prophylaxis and very high VTE risk (e.g. active DVT and current intracranial haemorrhage)

Answer 352

At risk for both venous AND arterial thrombosis (different to most other hypercoagulable sstates like polycythaemia) Presence of lupus anticoagulant. Increased APTT. Won't correct with mixing study Often on aspirin, unless thrombosis. then life long warfarin. Needs bridging for surgery with enoxaparin. Don't reverse without a bridging plan May have (due to micro / macrovascular thrombi) - recurrent miscarriage -stroke -migraine - visual changes - cardiac failure

Answer 353

CVS - bradycardia - QT prolongation - at risk of arrythmia, TdP (especially when combined with electrolyte abnormalities) - Heart failure from hypophosphataemia, hypocalcaemia, hypokalaemia Resp - Loss of elastin, reduced lung compliance GI - delayed gastric emptying - Risk of liver injury Haem - Anaemia from malnutrition (iron, B12, folate) - Relative immunosuppresion (most common cause of death is sepsis). May have pancytopenia MSK - osteopenia, fragile thin skin. No fat. At risk to pressure injuries. At risk for hypothermia as no insulation Metabolic - Hypoglycaemia - If bulaemia, similar effects to pyloric stenosis (hypochloraemia, hyponatraemia, hypokalaemia, metabolic alkalosis) Endocrine - Can get hypopituitism. Ammenhorrea, hypothyroidism

Answer 354

Malnutrition Universal Screening Tool. Scoring system with BMI, unanticipated weightloss, acute disease. Gives overall risk and when to get dietician involved

Answer 355

In severe malnutrition, relative lack of Ca, PO4-, K+, glucose, magnesium (but serum levels can be normal due to homeostatic mechanisms) With introduction of glucose, insulin release causes uptake of phosphate, K+, magnesium intracellularly along with glucose --> at risk of severe electrolyte abnormalities and hypoglycaemia Also tend to get hypernatraemia and fluid retention Effects: CVS - arrythmia, congestive heart failure Resp - muscle weakness, resp failure possible. OVerload --> APO MSK - muscle weakness, rhabdo possible Neuro - seizures, confusion, delirium GI - nausea, abdo pain Management: - ABCs, call for help. HDU / ICU admission if needed. Occassionally need intubation, ventilation or inotropes - Correct electrolytes - Vitamin replacement (DEKA, thiamine), micronutrients. dietician led - Glycaemia control - aim 6-10mmol/L (NICE SUGAR study from ICU), avoid tighter control - monitor for infections, at risk (interestingly, may avoid propofol infusions in those at risk of re-feeding as lipid load has a reasonable amount of calories. Each ml = 4kJ)

Answer 356

ASD have mortality age gap of between 15-30 years. 2x more likely to die once present to ED. More comorbid with obesity, T2DM, IHD. Less likely to seek medical attention Have planning in place for below. Consider pre med. Consider post op destination (home often best). Most have normal intelligence. Capacity for consent until proven otherwise Sensory - all senses could contribute to distress - Sight - aim for low lights, less people in OT - Sound. Reduce conversations, low noise environment, mute unnecessary alarms. USe noice cancelling headphones - Smell. Inform of smell of mask, sevo - Touch. Minimise touching and if doing so, do so with firm intent. Patient holding mask themselves - Taste - less relevant Predictability - relative intolerance to suprise. Have first on list Acceptance - of their behaviour. Use their monotropic (fixated interests) as way of developing rapport Communication - may need to use alternative communication styles e..g written Empathy - autistic people have empathy, just express it differently

Answer 357

Permanet movement and posture disorder which limit activity due to acquired pathology to the developing brain Antenatal causes (80%) - Maternal: (TORCH) = toxoplasmosis, Other, Rubella, CMV, HSV - Foetal: Genetic, metabolism disorders, prematurity - Social: lower SES Perinatal causes (10%) - Birth asphyxia, placental abruption, obstructed labour Post natal (10%) - Infection (meningitis, sepsis) - Trauma (TBI in first 2 years) - other - hyperbilirubinaemia, hypoglycaemia, intraventricular haemorrhage Classification can be: spastic, dyskinetic or ataxic Or can be from Gross Motor functional Classfication (GMFC): 1 = can run, jump but slightly less than normal child 5 = no means of independent mobility, unable to maintain antigravity head and trunk

Answer 358

Higher the spinal cord injury, higher the chances of AD. T6 or higher usually Usually develops 3 weeks or more after spinal injury, abnormal disorganisation of autonomic nerves below the level of injury. When noxious stimulus occurs, causes abnormal response with no decending inhibition. Increased vasoconstriction below level of injury --> increased SVR --> massive hypertension. May get reflex bradycardia as intact carotid sinus Hypertension can cause: stroke, aneurysm rupture, myocardial ischaemia, APO, AKI Triggers include constipation, urinary distension, trauma to lower limbs / abdomen Need to treat with GTN, phentolamine, remifentanil, MgSO4 (not beta blockers as BB on top of high alpha tone --> CHF)

Answer 359

Airway - May be more difficult as reduced C spine movement - Impaired gastric emptying if high c spine injury - May have trache in situ Breathing - If C3-5, at risk for phrenic nerve injury --> ventilator dependence - If thoracic, may still have impaired ventilation from loss of intercostal muscles. Restrictive lung pattern - Impaired cough, secretion clearance - OSA more common Circulation - Autonomic dysreflexia - Reduced effective circulating volume - Increased risk of IHD from inactivity. Unable to exert to get symptoms - Anaemia - Higher rates VTE Disability - Difficulty with positioning - Contractures common. Spasticity. - Maybe be on neuropathic / other pain meds. May be on baclofen - Depresion - Sensory and motor changes may impair ability to detect noxious stimuli or whether a regional anaesthetic is working Exposure - Increased risk hypothermia Medications - Avoid sux (hyperkalaemia risk)

Answer 360

Enflurane, TXA, alfentanil, tramadol, pethidine, etomidate, methohexital

Answer 361

Phenytoin and carbemazepine cause induction (so will cause increased clearance of warfarin for example) Valproate causes inhibition (so increased warfarin)

Answer 362

Some genetic, some have preceding infection. But mostly sporadic. Can be upper motor neuron (primary lateral sclerosis), lower motor neurons (progressive muscular atrophy), bulbar specific or mixed upper + lower (amyotrophic lateral sclerosis). ALS - peripheral --> proximal muscle weakness, ascending to bulbar and resp failure. 50% dead in 2 years. Some have cognitive deficit, some don't Avoid sux. Sesnsitive to NDMRs. Consider regional to avoid a GA if ventilation impairment. May get hypotension from autonomic dysfunction

Answer 363

Autoimmune disease of central nervous system, inflammatory plaques, demyelination and axonal damage. Brain and spinal cord. More common in women (3x rates compared to men), typically in their 30s Typically starts as relapsing- remiting form of MS. Most lead to secondary progressive MS with chronic effects seen. symptoms may include: visual disturbances, sensory / motor changes, spacticity, bulbar symptoms, respiratory failure. Treatment: -Steroids - Other immunosupressants (interferon) - Analgesics (e.g. TCAs for neuropathics_ - Antispasmodics (baclofen)

Answer 364

Pregnancy in multiple sclerosis, no risk of increased relapsing if patient had neuraxial (also confirmed in future systematic reviews) In 3rd trimester, MS often have less relapses (as with all autoimmune conditions). May have increased relapses first 3 months post partum

Answer 365

Temperature - nerves more sensitive, more likely to get relapse if hyperthermia. Monitor temp and avoid over heating Regional - local not contraindicated but nerves have increased sensitivity to toxicity. GA probably preferred. Unless bulbar symptoms (e.g. in secondary progressive MS), then regional may be preferred - use lowest dose. Neuraxial does not increase relapses Airway - if bulbar symptoms, intubate and extubate wide awake - Avoid sux (especially if pre-existing spacticity, hyperkaelamia risk) Steroids - skin, bones, stress dosing, BGLs

Answer 366

Most common acute, demyelinating polyneuropathy with progressive motor weakness affecting the peripheral nervous system. Autoimmune mediated, often following viral or bacterial infection (campylobacter, influenza, CMV, EBV common triggers) Weakness is ascending, symmetrical. Areflexia (peripheral nerves, not upper motor neurons). May have sensory component. May get bulbar and resp weakness Diagnosis is clinical + CSF testing (high protein, low WCC) and nerve conduction studies 25% require intubation. 10% will die from complications. 10% will have long term sequalae of GBS Variations include: - Miller fischer = ataxia + eye weakness + bulbar / facial weakness - Acute motor axonal neuropathy (AMAN) = motor weakness but no sensory - Acute motor-sensory axonal neuropathy (AMSAN) = motor + sensory, more severe

Answer 367

Airway and ventilation - Increased risk aspiration (especially if bulbar symptoms) - May have resp muscle weakness, more likely to be unable to get off ventilator and need ICU + trache Medications - Avoid sux - More sensitive to NDMRs Autonomic dysfunction - especially if IPPv, pneumoperitoneum, position changes - consider art line - higher rates of post op ileus and urinary retention

Answer 368

Autoimmune condition targeting nACHRs of neuromuscular junction. Can also be following monoclonal antibody drugs (e.g. pembrolizumab) Causes skeletal muscle weakness, particularly with repeated effort. Bimodal distribution with young women and older men. 15% have another autoimmune condition (e.g. Graves, SLE) Often starts with ptosis. Can be all the way to resp weakness, failure. Thymus gland hyperplasia thought to be implicated Diagnosis with: clinical examination, ice pack test, edrophonium test. nACHR antibodies Treatment: - Anticholinestase drugs. Pyridostigmine (30-120mg PO Q4-6Hrly). 30mg = 1mg neostigmine. Only available as PO. Less side effects than neo. Neostimine IV 1-2.5mg Q2-4Hrly. Has poor oral bioavailability so dose is 15-30mg PO Q2H. More GI side effects and shorter half life - Steroids - IVIG - Plasma exchange - Thymectomy

Answer 369

Myasthenia gravis = autoimmune condition for nACHRs. Thymus hyperplasia present in 7/10 MG patients, thymoma in 1/10 MGTX trial (NEJM 2016) found reduced amounts of immunosuppresion needed if thymectomy + reduced risk myasthenia crisis. Controversial to do thymectomy in non-thymomatous MG Thymectomy either via trans-sternal, trans-cervical or thoracoscopic surgery. DLT if thoracoscopic

Answer 370

- delivery in centre with NICU. 30% of MG patients will have babies with transient muscle weakness (especially if high antibody titre counts) - Neuraxial possible. But aim for lowest possible dose, may struggle if mid-thoracic spinal. CSE useful - Ensure they get their acetylcholinesterase inhibitors (pyridostigmine usually 30-120mg Q4-6Hrly). Have IV neostigmine available (1-2mg Q2-4hrly) if unable to take orally - Caution with MgSO4 (may precipitate muscle weakness), only give if high risk eclampsia. Similarly, don't use beta blockers or CCBs. Hydralazine or methyldopa for hypertension. If needed to give MgSO4, prepare to intubate - if needing GA, can use sux (2x usual dose) or NDMRs (10% normal dose). May need ICU if unable to wean off ventilation - steroid replacement if on >5mg/day prednisone for 4 weeks or more

Answer 371

Myasthenia crisis is from a lack of acetylcholinesterase inhibiting drugs, which causes: - respiratory weakness / failure, bronchospasm, muscle paralysis - Treatment is with giving acetylcholinesterase inhibitor. PO pyridostigmine or IV neostigmine Cholinergic crisis = excess ACh. Can be from excess acetylcholinesterase inhibitors (e.g. too much neostigmine) - Bronchorrhoea, bronchospasm, bradycardia. But also nausea, vomiting, diarrhoea, lacrimation, salivation. Respiratory failure / paralysis (same presentation as organophosphate poisoning) - Treatment is with atropine Differentiate the two with edrophonium test - short acting anticholinesterase - Will improve myasthenia crisis. But worsen cholinergic crisis

Answer 372

Autoimmune condition of voltage gated calcium channels pre-synaptically Proximal weakness, may get bulbar or resp weakness. Weakness often improves with exercise (unlike MG which has fatiguability) Associated with small cell lung cancers (and other malignancies) Treatment with amifampridine (not available in NZ but it enhances ACh release). IVIG or plasma exchange Sensitive to both sux and NDMRs.

Answer 373

X linked, genetic condition. Altered gene for dystrophin (which aids in stability of myofibril) --> abnormal sarcolemma --> myofibril atrophy, necrosis and fibrosis. Female carries may have a mild phenotype. Rapidly progressive. Weakness starts at 2-5 years old. Proximal weakness before peripheral (hence calf hypertrophy), waddling gait. Lower limbs before upper limbs. Often wheelchair bound by teenagers, death by resp failure in 20s. May get scoliosis, contractures

Answer 374

CVS - dilated cardiomyopathy (50% of those over 15 will have DCM), CHF - Conduction abnormalities Resp - Resp muscle weakness, impaired cough, bulbar symptoms (impaired swallow). High aspiration risk and hard to get off a ventilator - Recurrent chest infections. Common mortality cause - May get restrictive lung pattern from kyphosis, scoliosis Medication - anaesthesia induced rhabdomyolysis from volatiles, suxamethonium - May be on steroids, baclofen GI - Delayed gastric emptying Haem - Platelet dysfunction and impaired vascular smotth muscle. Increased bleeding risks MSK - Contractures, scoliosis, kyphosis makes positioning, IV lines, regional anaesthesia challenging

Answer 375

[Do not confuse this with Duchenne Muscular Dystrophy which is much more severe, presents as a toddler and kills people in their 20s] Autosomal dominant. Presents in 2nd or 3rd deade of life. Males and females. Typically from abnormal sodium or cholride channels. Two main subtypes (DM1 and DM2, DM2 less severe adult onset MD) Myotonia - repetitive discharging of muscle action potentials causing sustained contractions from stimulation Dystrophy - progressive, muscular atrophy Body systems affected: CVS - arrythmia (particularly heart blocks). Rare can get cardiomyopathy Resp - muscle weakness, impaired cough, restrictive lung pattern MSK - peripheral and facial muscle weakness. Can have uterine weakness too (may be unable to have vaginal delivery, need LCSS) GI - delayed gastric emptying, dysphagia

Answer 376

Avoid triggering myotonic reactions (sustained muscle contractions from repetitive action potentials). Which can lead to hyperkalaemia and rhabdo Airway - may need RSI, ETT due to delayed gastric emptying Resp / ventilation - More likely to have impaired cough, resp weakness. consider regional instead of GA. Opioid sparing. Extubate wide awake and reversed CVS - More likely to have arrythmia, conduction abnormalities. Consider art line + external pads. - May have PPM / ICD Medications - Avoid sux - may trigger myotonia from fasciculations - Do not use peripheral nerve stimulator. Reverse with sugammadex - May be better to run TIVA Thermo - Warming patient + monitoring temp. Avoid shivering as may trigger myotonia - Can get shivering from spinal anaesthesia / epidurals. Tramadol may help. Lowest dose spinal possible or CSE

Answer 377

Autosomal dominant chronic peripheral neurmuscular denervation. May get spinal degeneration and muscular atrophy difficult airways Restrictive lung disease Sux --> hyperkalaemia NDMRs --> exaggerated response, use less

Answer 378

Loss of dopaminergic cells of the substania nigra of basal ganglia causing inhibition of thalamus. Results in triad of tremor, bradykinesia and muscle rigidity. some develop cognitive impairment, bulbar impairment Incurable, progression cannot be slowed. Affects 1% of >65 year olds

Answer 379

Aim to increase dopamine. Or treat symptoms. None slow progression - Levodopa + decarboxylase inhibitor. Levodopa as precursor to dopamine, crosses BBB. Decarboxylase inhibitor to prevent peripheral adverse effects - MOAi - Selegiline = MAOb selective. Also increases serotonin, risk serotonin syndrome - Dopamine agonists - pramipaxole, bromocriptine, ropinerole. Useful if intolerant to levodopa - Apomorphine = subcut infusion, dopamine agonist - Rotigotine = dopamine agonist patch (no available in NZ) - Anticholinergics - Benztropine. Help with tremor (but may cause confusion, urinary retention) - Deep brain stimulators

Answer 380

Preop - Medications - ensure they get their levodopa. If they won't get a dose intraop, use NG. Or get plan for apomorphine (or rotigotine patch in Aus) - Check for: - Cognitive impairment - Bulbar symptoms, dysphagia, excess salivation - Chest wall rigidity - Autonomic dysfunction - turn off deep brain stimulators before surgery, use bipolar or have pads away from head Intraop: - Check for drug interactions - selegiline = MAOb inhbitor, increases risk serotonin syndrome - May get worsened chest wall rigidity if preexisting + remi - ETT or regional if bulbar symptoms. Regional or neuraxial may get patient back to levodopa sooner. But positioning may be more challenging - Metaraminol if autonomic instability expected. Art line - glyco as anti-saliva - PONV prophylaxis to allow for oral intake + absorption Post op - avoid haloperiodol, metoclopramide, droperidol (D2 antagonists, precipitate dopamine withdrawal crisis, similar to neuroleptic malignant syndrome --> fever, tachycardia, hypertension, autonomic instability, rigidity, confusion) - Restart levodopa ASAP. Have plan in place if unable to have oral intake - Consdier HDU - IDeally non-pharmacological management for post op delirium (high risk, approx 60%). Midazolam or quetiapine if needing

Answer 381

If emergency surgery, need to just do it and accept high risk. If within 3 days of stroke, may be good compared to 3-14 days as there is worsened impairment of autoregulation after 3 days For non-urgent surgery, risk plateaus around 9 months post stroke (never returns to normal, still 10x risk). Based on JAMA 2014 paper (Jorgensen et al). surgery within 3 months of stroke, 14x increased risk of MACE, 68x increased risk of stroke (following adjustment). 3-6 months after stroke, 24x increased risk of further stroke if surgery.

Answer 382

Warfarin for AF, bridging with enoxaparin vs not in elective setting. No difference in stroke rates in patients where warfarin stopped without bridging (0.3 vs 0.4%). Bridging patients had 3x increased risk of bleeding Importantly, mechanical valves, valvular AF and high risk thrombosis settings (recurrent VTE on anticoagulation or antiphospholipid syndrome) excluded from trial. Probably should be bridged

Answer 383

Prospective cohort study (RCT was thought to be unethical). Pausing DOAC before surgery (1 day for low risk bleeding, 2 days for higher risk. 3 days if renal impairment + dabi). VTE and stroke rates were low (0.2-0.5%), probably acceptable

Answer 384

Use of preop aspirin and clonidine Clonidine - no mortality benefit, no reduction in MI. Increased risk of hypotension Aspirin - did not reduce MI or mortality risk. Significantly increased bleeding. Even for patients already on aspirin, this did not reduce MI risk or stroke. Also no increased risk of stroke if aspirin stopped 3-7 days before surgery (not included in study are those on aspirin for cardiac stents, best to keep these people on some form of antiplatelet)

Answer 385

European Stroke Organisation (ESO) guideline 2023 suggests systolic BP <185mmHg during mechanical thrombectomy and 24 hours AHA guidelines seem to suggest BP between 140-180mmHg during and after thrombectomy. Previously, some nonsense around systolics up to 220mmHg pre thrombectomy if they haven't had IV thrombolysis (but this seems to be less of a thing now) - There is some evidence to suggest more tightened targets of 140-160mmHg may be better and reduce haemorrhagic complications but guideliens haven't incorporated this in yet

Answer 386

Direct - suicide (25%), amniotic fluid embolism (10%), hypertensive disorders (5%), other embolism (5%), haemorrhage (5%) Indirect - neurological (strokes, seizures) = 10%. Cardiac (10%)

Answer 387

Maternal progesterone --> increased insulin receptor resistance (thought to be adaptation to provide more glucose to foetus). Particularly in 2nd trimester Glucose transfer to foetus by GLUT1, does not need insulin. Increased BGLs foetus. Macrosomia, hyperplasia of foetal beta islet cells. Increased insulin --> more rapid growth (insulin = growth affecting hormone). Increased hypoglycaemia post birth

Answer 388

Foetus - Increased stillborn (5x) - Increased death at home for first few months - Increased premature birth - Macrosomia, increased risk C section, shoulder dystocia - Foetal hypoglycaemia - Increased risk of future diabetes as adult Maternal - Sepsis - Preeclampsia - Tears, trauma from delivery - More likely instrumental delivery

Answer 389

PRe labour - Discuss with endocrine, will need increased insulin requirements during pregnancy due to relative insulin resistance. Monitor BGLs and aim 5mmol/L +/- 1 - Determine L&D plan, C section vs vaginal delivery - Discuss plans with mother, see if they want to use CSII during labour. Or have option for not using - Know how to turn off and remove pump in situation where mother unable to manage. Know how much insulin given per hour. Labour - In hospital, midwife trained in knowing how to run an insulin infusion if needed - Safety includes hourly BGL monitoring, 50% dextrose available, having an IV line in situ - Can use CSII as long as GCS 15, able to manage (and willing to) pump. If frequent hypos (or BGLs >7mmol/L), suggest VRII and stop CSII - If commencing VRII, start infusion with 30 minute cross over with CSII then stop CSII Post delivery - No matter what form of insulin delviery, decrease to planned insulin rate from endocrine. If no plan available, decrease to 50% pre-delivery rate - Can restart CSII when eating and drinking at least 50% usual diet, GCS 15 able to manage pump by themselves, no PONV. Start pump and have 2 hours of overlap before stopping VRII

Answer 390

Low lying placenta that covers cervical os. Can be cause for antenatal haemorrhage. Women unable to have vaginal delivery. Risk factors: previous placenta praevia, prev C section, multiple gestation, other uterine surgery (e.g. fibroids). 1:200 pregnancies Management is wait until 36 weeks to see if placenta migrates. Needs to be >2cm clear on US. If not, LSCS higher risk for bleeding. If anterior, surgeon may have to pass through placenta to do LSCS. Can also have higher risks of placenta accretia spectrum (PAS) if overlying uterine scar

Answer 391

Accretia - placenta through endometrium, abutting myometrium (75% of PAS) Increta - into myometrium Percreta - through myometrium, serosa. Potentially invading local organs Usually placenta sheds from uterus, vessels contract. This is impaired with PAS --> massive haemorrhage risk 1:500 pregnancies. Risk increases with previous c section. 11% if 1x prev LSCS. 40% if 3x LSCS. Also increasing maternal age, previous fibroids or uterine ablation surgery Diagnosis commonly by US. Can be by MRI. Some are made intraop

Answer 392

Caesarean hysertectomy - most commonly performed. High midline hysterotomy away from placenta, baby removed and placenta kept in situ. Then hysterectomy. Sometimes delayed hysterectomy (e.g. in placenta percreta as allows for placenta outside of uterus to shrink) Hysterotomy + leave placenta in situ to reabsorb. Fertility spraring. 6% morbidity "triple P" - Placenta localisation (use US to map out placenta) - Pelvic devascularisation (IR guided balloons to reduce blood flow to uterus) - Placental non-separation with myomectomy (cut out placenta and myometrium in entirety). Fertility sparing

Answer 393

Relatively contraindicated, especially if the placenta is still in situ. Contraction may cause placental separation and worsening of bleeding. Only recommended if removal of placenta has taken place

Answer 394

90% of PAS need transfusion, mean blood loss 3-5L. Preop - optimise Hb, anaemia - Plan for surgery - caeseraen hysterectomy vs IR placed balloons in internal iliacs + myomectomy with placenta in situ vs keeping placenta in place to be reabsorped - Book for tertiary centre, access to ICU and blood bank - G+S and X match blood Intraop - SMO anaesthetist, obstetricans x2 + assistants - large bore (RIC lines) + arterial lines - TXA - Internal iliac balloons - REBOA - usual reducing bleeding of normothermia, avoiding acidosis, avoiding coagulopathy (including calcium, 1:1:1 transfusion, low threshold for cryo in obs) (DO NOT GIVE UTEROTONICS - contraindicated) Post op - Monitor for bleeding - HDU at minimum

Answer 395

Onset of hypertension after 20 weeks. With either - Proteinuria (1+ protein in urine or protein:creatinine ratio >30mg/mmol) - other maternal organ dysfunction (renal impairment, neurological (clonus), haem complications, foetal growth restriction Between 2-8% of pregnancies have PET

Answer 396

Advanced maternal age Obesity Previous PET Family history PET Multiple gestation Smoking Cocaine use Gestational diabetes / other diabetes SLE Antiphospholipid syndrome First baby Chronic hypertension

Answer 397

Abnormal placental implantation, localised ischaemia --> systemic effects. Immune complexes formed may cause abnormal uterine vasoconstriction (maternal-foetal antigen-antibody complexes) Endothelial dysfunction, due to failure of trophoblast invasion causing imbalance of TXA2 and PGI2. Genetics Platelet dysfunction Fatty acid metabolism, uptake into liver

Answer 398

Airway - More likely difficult due to airway oedema from increased capillary permeability + HTN. Have concerns if stridor Resp - Risk of pulmonary oedema from hypertension CVS - Hypertension from excess catecholamines. Can lead to myocardial ischaemia, APO - Fluid overload, increased total body water - Decreased total circulating volume due to high catecholamines Renal - acute kidney injury, doesn't respond to fluids. Oliguria Hepatic - Fatty acid uptake into liver, liver impairment possible. Coagulopathy, elevated liver enzymes part of HELLP CNS - Risk of eclamptic siezures. From cerebral oedema + cerebral vasoconstriction. Headaches. Visual changes. Clonus - Hypertension, risk of haemorrhagic stroke (most common cause of death in PET) Haem - Haemolysis - Low platelets + platelet dysfunction. From consumption of platelets Foetal - Growth restriction + Oligohydraminos. From reduced placental perfusion

Answer 399

Using 75-150mg daily aspirin from 12 weeks gestation til birth. If high risk for PET (T2DM, chronic HTN, previous PET) or 2 or more risk factors (BMI >35 and age >40). 1.5% risk of PET compared to 4.5%

Answer 400

ACTOMgSO4 = 2003 trial in NZ + AUs, improved gross motor scores if Mg given to mothers 24 hours before pre term delivery BEAM trial = 2008. Decreased rates of moderate-severe cerebral palsy if mother at risk delivery 24-32 weeks (e.g. PPROM)

Answer 401

Eclampsia from cerebral oedema and cerebral vasoconstriction from PET MAGPIE trial = 2002 multi national trial with n=10,000. 33 countries. RCT. Patients with PET. Reduction of eclampsia (40 vs 96 patients, relative risk of 0.42). Criticism is that for high income countries, NNT for all comers with PET was 127. If PET with severe features, NNT is 36.

Answer 402

Usual call for help, ABCs Based on MAGPIE study. 4g MgSO4 over 20 mins followed by 1g/hr infusion. Aim 2-4mmol/L serum level. Could give 10g IM if no IV access Further 2-4g IV boluses in refractory seizures If still seizing, may need to consider benzos, propofol or other AEDs. Could be non-eclamptic seizures (especialy if known seizure disorder) - NICE recommends against benzos if eclamptic seizures Should be stabilised from eclampsia before pursuing a LCSC

Answer 403

1/6th of HELLP diagnosed before 3rd trimester, 1/2 in 3rd trimester, 1/6th after delivery Haemolysis (least common symptom, sign of severe HELLP. 5% mortality Elevated liver enzymes (most commonly AST and ALT) Low platelets (severe HELLP if <50) Only definitive management is delivery of foetus and placenta - Need to consider location for this. ?transfer to tertiary obs centre with ICU + blood bank - Recovery usually within 24-48 hours once placenta out If LSCS, need to consider if platelet count and coags normal for neuraxial. Else GA If haemolysis + low platelets --> high risk for DIC, bleeding. Need arterial line, large bore IVs. TEG guided transfusion

Answer 404

Diagnosis: Idiopathic cardiomyopathy with systolic impairment (<45% LVEF). Towards end of 3rd trimester or in months after delivery (2/3rd are post delivery). On TTE, mean LVEF is <30%. BNP rises with PCM Usual CHF symptoms of oedema, SOBOE, orthopnea, PND, fatigue (hard to differentiate from pregnancy often). Typically present with NYHA 3 or 4 symptoms Risk factors: IVF, advanced maternal age, multiple gestation, obesity, diabetes, high gravidity. Genetics Pathogenesis. No well understood. Abnormal placenta thought to be involved, altered angiogenesis and vasoconstriction in systemic circulation --> axidative stress --> prolactin fragment production (unclear how this contributes but maybe due to endothelial dysfunction. Prolactin increases in 3rd trimester and bromocriptine, which decreases prolactin, may be protective)

Answer 405

Largely supportive, similar to other forms of cardiomyopathy and heart failure Cannot use traditional 4 pillars of heart failure. ACEi, entresto, spironolactone contraindicated in pregnancy (maybe post delivery fine) Fine to use: - beta blockers (except atenalol) - frusemide (although caution to not cause hypotension) - Nitrates - digoxin If needing anticoagulation, enoxaparin is a good options as short acting ICDs or CRT-Ds not inserted usually until persistent CHF demonstrated 6 months post delivery and on maximal CHF treatment Bromocriptine (= dopamine agonist) reduces prolactin levels. 1 multicentre trial found increased recovery from PPCM. European cardiac society says "consider it" No demonstrated evidence to suggest the increased levels of prolactin from breastfeeding worsens PPCM Occassionally need ECMO or a heart transplant. VA-ECMO often as heart failing. One study of pregnant patients on ECMO showed a 75% survival rate for the mum and 65% for foetus.

Answer 406

Prelabour - Plan for delivery in tertiary centre with obestretics, cardiac, ECMO, ICU available (if LVEF <30%) - Informed discussion of high risk nature of pregnancy, high risks to future pregnancies - Optimise for anaemia (Hb check, group and screen, iron studies), heart failure (maximal medical therapy) Labour and delivery - Ideally vaginal delivery, less bleeding than LSCS. In hospital from early labour - Large bore IV + arterial line. Consider CVL if likely to need inotropes - Experienced midwife - Early epidural with cautious slow top ups to achieve block (not dropping SVR). Minimise SNS from labour stages. If hypotension, treat with vasopressors (not fluids) - Avoid fluid loading, large volumes of fluids. Use concentrated solutions (e.g. oxytocin infusions) to reduce risk overload - assisted 2nd +3rd stage to minimise SNS response (if needing a LSCS) - aim for neuraxial as above, slow cautious titration of a CSE (1.5ml 0.5% bupi as spinal) - If GA, arterial line pre induction. Give 1.5mcg/kg remi to blunt sympathetic response to laryngoscopy. Consider ketamine induction Post delivery - High risk due to autotransfusion from uterus. May precipitate overload. Frusemide + CPAP O2 if APO - Slow IV oxytocin bolus + infusion (not wanting to drop SVR too quick) - TXA if PPH - Ergometrine (increases SVR ++) and carboprost (increases PVR++) relatively contraindicated - Remain in patient 48 hours, monitor in HDU - consider bromocriptine - VA-ECMO if persistent failure not responding to medical treatment - VTE prophylaxis post delivery

Answer 407

Ages 1-12 months use equation: (age in months / 2) + 4. For 6 months this will be 7kg Ages 1-5 years, use equation: (age x2) + 8. For 3 year old this will be 14kg Ages 6-12 years, use equation (agex3) + 7. For 7 year old this will be 28kg. (historically APLS stated could use (age+4) x2. But usually underestimates)

Answer 408

Neonate until 44 weeks post conception. So term baby born at 40 weeks gestation will ceased to be a neonate at 4 weeks old

Answer 409

= multinational european study assessing 5000 neonates and infants up to 60 weeks post menstrual age for 6000 proceedures. 1/3rd of kids had intraop critical event requiring intervention (cardiac instability the most common, then hypoxaemia and blood transfusion. 8 kids needed CPR. Events much more common in premature children (if under 32 weeks, 70% had critical event)

Answer 410

GAS trial = GA vs spinal. International multicentre RCT. Inguinal hernia in term and preterm infants. Randomised, not blinded (obviously). No diffierent in neuro outcomes (IQ, autism) at 2 and 5 years. Mostly only male patients. Only 1 hour GA - interestingly, neuraxial prem babies still had apnoeas PANDA = paediatric anaesthesia neuro developmental assessment. Observational trial. Sibling matched, one had GA for hernia repair before 3 years, the other didn't. No difference in IQ or neurodevelopment MASK = Mayo anaesthesia safety in kids. Obeservational stufdy comparing single GA vs multiple. IQ and neurodevelopment at 8-12 years. No difference IQ. Subtle but significant difference in worse fine motor skills and parental reported learning difficulties if multiple exposed. Animal studies - neuroapoptosis with repeat exposure

Answer 411

Machine Suction Monitoring Airways IV Drugs Special

Answer 412

Weight (estimation by (age+4) x 2) Energy = 4 joules / kg Tube = age/4 + 3.5 for cuffed tube FLuids = 10ml/kg bolus, usually plasmalyte or 0.9% NaCl Adrenaline = 10mcg/kg Glucose = 2ml/kg of 10% glucose

Answer 413

As per PS29, would expect a FANZCA to be able to look after a 2 year old, without significant comorbidity, for moderate complexity surgery. But there is also expectation if emergency, all FANZCAs should be able to provide care to children whose age, comorbidity or procedure falls outside usual scope of practice. Use available expert advice

Answer 414

Practitioner - my own level of skillset, expertise. also surgical expertise Procedure - complex or simple, urgency of surgery Place - facility have access to equipment, familiarity, post op destinations Patient - comorbidities, sick or not

Answer 415

As per ANZCA PS29 on paeds: If term, post menstrual age under 46 weeks If pre-term (<37 weeks delivery), then post menstrual age 54 weeks Basded on Cote et al study, found 35 week prem babies risk of apnoea fell to <1% by 54 weeks PMA

Answer 416

Obstructive - tamponade, tension PTX Cardiogenic - arrythmia, valvulopathy, ischaemia Distributive - sepsis, anaphylaxis, neurogenic, Addisonian Hypovolaemic - haemorrhage, dehydration

Answer 417

Inadequate delivery of O2 and metabolic substrates to meet meetabolic demands of tissues

Answer 418

APRICOT study showed 2.8x increased risk of periop resp adverse events (PRAE) if URTI. Back to baseline after 4 weeks of symptom resolution. PRAEs include laryngospasm, bronchospasm, apnoea and hypoxaemia

Answer 419

Patient factors: - timing and severity of URTI - 4 weeks post symptom resolution for back to baseline - Likely LRTI? (cough with sputum, fever, creps) - Asthma - Smoke exposed - Comorbidities - cardiac, respiratory, syndromic - Prematurity - Age - less than 3, but especially less than 1 (APRICOT study) - Social factors - location from hospital, difficulty getting to appointment Surgery - Higher risk if airway, ENT surgery. Risk of bleeding or debrid in airway - Major surgery vs CT scan - Length of surgery - Elective vs semi-elective vs emergency Anaesthesia - Paeds consultant anaesthetist - Airway deveice - Mask > LMA > ETT - TIVA There is a COLDS scoring system to show risk of continuing or not.

Answer 420

Most commonly refers to infectious croup = laryngotracheobronchitis. (sometimes may refer to any subglottic oedema e.g. from excessively high ETT cuff pressures) Usually viral, parainfluenza, influenza, rhino virus and humna coronavirus Most commonly in ages 6-24 months, more likely in winter. Most kids will only get croup once in their lifetime Non-specific viral symptoms --> barking like cough, inspiratory stridor and respiratory secretions. Stridor due to subglottic oedema Differentials for upper airway obstruction: - Foreign body - Epiglottitis - Bacterial tracheitis - Laryngomalacia - Peritonsilar abscess Westly Croup Score for mild, moderate, severe. Includes cyanosis, LoC, stridor, air entry and presence of retractions Treatment: Mostly conservative IV fluids, O2 if needed 0.25mg/kg Iv dex then 0.125mg/kg Q8hrly IV Neb adrenaline 0.5mg/kg up to 5mg Q1hrly 1% will need intubation. Tube same as epiglottitis - sit on parents lap, gas induction spont ventilation. Often laryngoscopy easy but need 1x smaller ETT size

Answer 421

Bacterial infection of epiglottitis - haemophillus influenzae B (mostly in unvaccinated kids). Rarely, Group A beta hyaemolytic strep. Can cause life threatening upper airway oedema of epiglottis and aryepiglottic folds Most common in 2-3 year olds Symptoms: Fever (>39c) Sitting forward, secretions ++ from mouth. Tongue pushed out Unable to swallow Stridor (if biphasic = insp + exp, late sign) Different to croup in that more febrile, more secretions and no cough Other differentials include: airway foreign body, bacterial tracheitis, retropharyngeal abscess, peritonsillar abscess, croup Treatment: - Medical emergency. ABCs. 60% will need intubation. O2 - 50mg/kg ceftriaxone - Keep child with parent, less anxiety. Any increased WOB with higher velocities will worsen turbulence - glycopyrolate may help with secretions - Dexamethasone to help with airway swelling. 0.3mg/kg IV then 0.1mg/kg IV Q8hrly

Answer 422

Upper airway infection causing stridor. Risk of airway collapse and CICO if given GA + muscle relaxant for intubation Need to weigh up risks of aspiration if going to do spont vent technique. But probably safer to still do gas induction with plan to mitigate risk if aspiration - IV + IM drugs for intubation (ketamine, sux) - Place - decide where you want to play. Likely best in theatre unless crashing emergency. Inform ICU or organise for PICU transfer - Personnel. Most expereienced paeds anaesthetist + assistant + ENT surgeon, scrubbed with trache kit if needed. Parent in OT with child on lap sitting upright - IV access with EMLA (historically suggested to intubate without IV to not distress child. But probably safer with IV) - Monitoring - SPO2 on for induction. etCO2 for ETT confirmation - Emergency drugs - adrenaline (draw up arrest dose (=10mcg/kg) into 10ml (=1mcg/kg)), sux (IV = 2mg/kg, IM=4mg/kg), atropine (20mcg/kg) - Induction agents (ketamine / propofol, rocuronium. aim to give once intubation confirmed) - Equipment - ETT (cuffed, likely 1-2 sizes smaller. Have multiple sizes available). VL as first option. DL as back up - rescue LMA, OPA, masks. Bougie, stylet. - suction - nasalprongs / HFNO for peroxygenation during intubation attempts - Pre-dose 10mcg/kg glyco for secretions - Gas induction with 8% sevoflurane + 100% FiO2. Keep spont breathing. T piece with CPAP likely ideal (Tom would like this). Then supine and have parent escorted out - intubate. If unable to recognise laryngeal inlet, light pressure on thorax from assistant may demonstrate bubble sign. - confirm placement with etCO2. Then can change to IV sedation (e.g. prop + remi +/- dexmed) - Transport to ICU

Answer 423

Triad of micrognathia (small mandible), glossoptosis (downward depression of tongue) and U / V shaped cleft palate Sequence (not syndrome) as it is a series of secondary abnormalities from a single anomaly May occur in isolation, but often a consequence of a syndrome (DiGeorge, Treacher-Collins, Patau) Pathophysiology theories: - Mechanical obstruction - intrauterine compression of mandible causing depressed tongue and cleft palate - Genetic - e.g. SOX9 or GAD1 genes. But often de novo mutations Implications: - Micrognanthia + glossoptsosis makes upper airway obstruction more likely. May need OPA. Some kids need tracheostomies, mandibular distraction or glosspexy after birth - Fibreoptic intubation likely gold standard for kids with PRS. But can use VL or intubate via LMA - Intubation improves with age. Very difficult in neonate with PRS - GORD common - Airway obstruction may improve with prone positioning

Answer 424

Neural crest abnormality due to genetic mutation on chromosome 5 (often TCOF1 gene). Autosomal dominant but 60% are de novo. 1:10,000 - 1:50,000 births Similar to Pierre Robin Sequence, often has micrognanthia, glossoptosis and cleft palate May also have zygomatic hypoplasia. Ear abnormalities (small, rotated or non-existent) Often present for mandible or cleft palate repair (around 6-24 months of age) Implications - Likely to have upper airway obstruction - Difficult intubation. One study found >50% had Cormack Lehane grade 3 or 4 direct. 5% failed intubation. But all rescuable with LMA - Small mouth aperture - Chonal atresia possible. May make mask ventilation challenging and nasal prongs ineffective. OPA or LMA will help - 60% have dental abnormalities - Unlike Pierre Robin Sequence, intubation often gets MORE difficult with age, due to mandible growth impairment

Answer 425

Lysosomal storage disorder, accumulation of mucopolysaccarides (like glycosaminoglycans) throughout body. Including in skeletal strctures, connective tissues, internal organs, airway Mainly autosomal recessive (Hurler syndrome) but can be x linked (Hunter syndrome) Treatment is with enzyme replacement therapy. Without this, often got cardiomyopathy and early death in childhood Implications - Difficult BMV, intubation. Due to coarse facial features (gargoylism), thickened oral and nasal mucosa, hypertrophy of tonsils, adenoids, larynx. One study had 25% of kids demonstrated "difficult intubation" - Shortened, thick walled trachea. May need smaller diameter ETT - At risk of atlanto-axial subluxation

Answer 426

Not well understood. Can be bacterial (E Coli, enterobacter, pseudomonas) or viral (corona, rota or entero), invasion into weakened preamture intestinal wall causing life threatning inflammation. After 26 weeks gestation, foetal gut develps secretory and absorption function. Secretion of chloride + H2O allows for washing away toxins. In premature gut, lack of goblet cells which secrete IgA --> more prone to toxins Symptoms: - Typically after first enteral feeding. - Blood diarrhoea -Lethargy -Respiratory distress -Shock -Hypothermia or hyperthermia Investigations: - Bloods - CRP, WCC, blood cultures - x rays (pneumoperitoneum, hepatic venous gas or dilated bowel loops) - US for mesenteric blood flow Mortality around 20-40%. Up to 50% if needing laparotomy historically.. Risk factors: - Prematurity (90% of NEC is in prem babies) - Not breast feeding (3-10x protective if breast feeding) - Maternal cocaine use - Perinatal asphyxia - Congenital heart disease - Umbilical artery cannulation - Low birth weight (<2.5kg) - Steroid use (although this may be due to it being used in premature babies for lung maturation, and these kids are living long enough to develop NEC and not die from respiratory failure)

Answer 427

Preop / conservative: - Consider futility in some circumstances (e.g. extreme prematurity) - Always managed in NICU by neonatologist - Bowel rest, decompression with NG aspirates - Broad spectrum IV antibiotics including cephalosporin, aminoglycoside and metronidazole - usual ABCs. IV fluids. TPN. Correct coagulopathy and thermoregulation dysfunction - If haemodynamic instability, coagulopathy / DIC, shock, pneumoperitonium --> laparotomy most likely Surgical - Laparotomy, removal of necrotic bowel and stoma - Need ETT if not already done in NICU - Occasionally will get surgery in NICU if very unwell e.g. on high frequency oscillatory ventilation - CVL and art line is best. May need to do CVL end of case as can take a while to do CVL - Induction with 5-10mcg/fentanyl to ablate surgical response. Maintenance with sevo or morphine / midaz - Do not use N2O (enlarges bowel) - Need large volume IV fluids usually. 20ml/kg/hour + 5% glucose supposedly. Due to third spacing - Warming is critical. Kids are poikilothermic, especially when prem and unwell. Post surgery - back to NICU

Answer 428

Diabetes (40%) Hypertension (25%) Glomerulonephritis (7%) Chronic pyelonephritis (5%) Polycystic kidneys Other (20%) - includes SLE, Goodpastures, neoplasms, toxins, vasculitis

Answer 429

History - Cause of CKD - diabetes, HTN, vasculitis, glomerulonephritis, SLE - ?produce urine - Dialysis - peritoneal vs haemo. Last done? Frequency? Vascular access or fistula? - Medications - EPO, calcium, vitamin D, BP, diabetes - Fluid status - dehydration, thirst, presyncope vs oedema, dyspnoea - Transplant status - ?previous ? on wait list ?on steroids or other immunosuppresion - Follow up status - known to renal Exam - OVerload - raised JVP, peripheral oedema, pulmonary oedema - Dehydration - Reduced cap refill, dry mucous membranes, low JVP Investigations - FBc (anaemia) - U+Es (K+, creatinine, calcium, phosphate) - blood gas - pH - ECG, especially for signs hyperkaelamia or IHD

Answer 430

AKI = creatinine increase >1.5x baseline within 7 days or >26micromol/L increase within 48 hours AKIN classification is based over 7 days(probably easier to remember than RIFLE): 1) >26micromol/L increase above baseline or >50% increase above baseline (25% for children) or urine output <0.5ml/kg/hr for 6 hours 2) Creatinine >2x baselines or urine output <0.5ml/kg/hr for 12 hours 3) Creatinine 3x baseline or >354micromol/L or RRT needed or anuria >12 hours

Answer 431

Mortality 10-20% for any AKI after abdominal surgery 40-50% mortality if needing RRT Higher creatinine, higher risk for death

Answer 432

Patient factors: - Age -Comorbidities - pre existing renal disease, diabetes, liver disease, cardiac disease - Pathology - sepsis, hypovolaemia, haemorrhage - Drugs - NSAIDs, ACEis, gent, chemo - Intrabadominal hypertension - ascites, hepatorenal syndrome Surgery factors: - emergency surgery, intraperitoneal, aortic cross clamping, CPB

Answer 433

Check urinary electrolytes. Renal hypoperfusion if Na+ <20mmol/L, urine osmolarity >500mOsmol/L (basically, kidneys are still able to reabsorb Na and concentrate urine well) Acute tubular necrosis if Na+ >20mmol/L and urine osmolarity <500mOsmol/L (kidneys have lost ability to properly concentrate urine) No use doing test if frusemide given Causes of acute tubular injury: CPB, sepsis, renal ischaemia, nephrotoxins (gentamicin, contrast)

Answer 434

Myocyte damage or breakdown causing release of myoglobin and other intracellular components (creatine kinase, K+, phosphate) into blood stream. Results in glomerular dysfunction at kidneys --> AKI (which can worsen hyperkalaemia) Creatine kinase (CK) level >5x upper limit of normal. If >5000, then 50% chance of AKI. CK peaks at 24-72 hours Causes: - Trauma - direct injury to muscles (blunt force), crush syndrome - Medication induced - (especially those vulnerable, e.g. musculaar dystrophies) - volatile anaesthesia, malignant hyperthermia, serotonin syndrome, neurleptic malignant syndrome - Burns - electrocution, thermal injury - Exercise induced - marathons - Severe dehydration / heat stroke - Endocrine / metabolic - thyroid storm, phaeo, DKA - Seizures - autoimmune - myositis - infection - sepsis May present with myalgias (50% of cases), dark or coco cola urine, anuria or reduced urine output. Or consequences of renal failure (arrythmia, itch, lethergy, nausea) Treatment: - Identify cause and treat underlying cause if able (e.g. stop precipitating drugs) - ABCs with aggressive fluid resuscitation. Minimal K+ if able, start with 0.9% NaCl. Aim to haemodilute blood myoglobin reaching glomerulus - Treat consequences of AKI: - Hyperkalaemia - ECG, calcium gluconate, insulin-dextrose, salbutamol, sodium bicarb (especially if acidosis), RRT - Consider forced urinary alkalosis. Mannitol or frusemide. Increases tubular flow, increases pH and reduces precipitation of myoglobin so promotes excretion (sodium bicarb will also alkalise the urine) - RRT if refractory overload, hyperkalaemia, acidosis due to AKI

Answer 435

Grade 0 = unimpeded 1 = walk as far as they like, if they take their time 2 = street block limitation 3 = stop and rest between rooms 4 = dyspnoea at rest

Answer 436

GOLD = global initiation for chronic obstructive lung disease Based on FEV1% predicted. Mild >80%, moderate 50-80%, severe 30-50% and very severe under 30% (or less than 50% with respiratory failure = very severe too)

Answer 437

Based on exaccerbation history and mMRC. Used to determine therapy to start A = mMRC <10 and 0-1 moderate exacerbations (nil hospitalisations) B = mMRC 10 or more and 0-1 moderation exacerbations E = 1 or more admissions, or 2 or more moderate exacerbations. Regardless of mMRC A = start bronchodilator only B = LABA + LAMA. Pulmonary rehab E = LABA + LAMA + consider ICS if eosinophil count >300. Pulmonary rehab All should get vaccines, smoking cessation

Answer 438

2013, NEJM. TV or 6-8ml/kg IBW, PEEP 6-8cmH2O, recruitments every 30 mins --> less pulmonary events than 10-12ml/kg with no PEEP and no lung recruitments

Answer 439

Resp - dysfunctional mucociliary clearance - Increase sputum volume and thickness - Increase PRAE - 2.3x increased risk over all. 25x increased risk if young and asthmatic - Carbon monoxide - 5-15%, will reduce O2 carrying capacity - COPD, emphysema - 90% of lung adenocarcinomas CVS - IHD (increased risk 1.8x post op MI compared to non smokers) - Stroke (1.7x risk post op compared to non smokers) - Sympathomimetic effects nicotine --> increased HR, increase VO2 - increased thrombosis risk Other - Impaired wound healing - Increased GORD - Reduced PONV - Higher opioid requirements post op - Induction of CYP2E1

Answer 440

4 weeks. If cessation of smoking >8 weeks, then risk of PRAE similar to non-smokers Stopping for 12 hours will reeduce sympathetic effects nicotine and improve COHb levels Need to be off smoking for 10-15 years before MI and stroke risk reduces back to baseline

Answer 441

Non-pharma - quitlines, support groups Pharma - nicotine replacement (vaping included), nortriptyline, varenicline, clonidine, bupropion Varenicline = partial nicotine agonist. Can cause depression Bupropion = norad, dopamine reuptake inhibitor. Good if concurrent depression Cochrane review in 2021 concluded that vaping with nicotine was effective method for getting off smoking

Answer 442

Apnoea = cessation of airflow for >10 seconds. 85% due to mechanical obstruction upper airways. 5% are centrally driven. 10% are mixed. Causes SNS activation from hypoxaemia. Apnoeas for AHI score in PSG are scored if >2 breath cycles (even if <10 seconds) Hypopnoea = shallowed breathing, >30% airflow decrease for 10 seconds or more with resulting >3-4% desaturation in SpO2

Answer 443

Snoring (loud) Tired (excessively during the day) Observed apnoeas Pressure (HTN) BMI (>35) Age (>50) Neck circumference (>40cm) Gender (male) 5 or more = high risk for OSA Other risk factors not included: pregnancy, smoking, alcohol and being unemployed

Answer 444

AHI (apnoea-hyponoea index) and ODI (oxygen- sedaturation index). Same numerical values for severity Normal <5 Mild = 5-15 Moderate = 15-30 Severe = 30+ Different values in kids (anything more than 0 is abnormal for children, 10 or more is severe)

Answer 445

Society for Ambulatory Anaesthesia (SAMBA) 2012 guidelines. - Minor surgery - Minimal psot op opioid requirements - Other comorbidities well controlled - Sensible home set up (not too far from hospital, another adult at home) - Access to CPAP

Answer 446

Bronchial wall inflammation, hypersecretion of mucous and increased airways reactivity with lower airways obstruction Eosinophillia common. Multifactorial disease with genetics, environmental and patient factors Differentiated from COPD by: - Non-smoking history - Childhood history - Diurnal symptoms - Allergic triggers - Response to bronchodilators / inhaled corticosteroids

Answer 447

COPD = chronic obstructive pulmonary disease. Progressive, partially reversible airflow obstruction due to exposure of airways to noxious particles / gases (smoking most common risk factor). Includes chronic bronchitis and emphysema in diagnosis Emphysema = histological diagnosis (but most commonly based on CT). Permanently enlarged airspaces distal to terminal bronchioles. Loss of alveolar integretity and impaired gas transfer Chronic bronchitis = chronic, productive cough for >3 months for 2 successive years. Not due to other causes (e.g. bronchiectasis) Risk factors: - Smoking - alpha 1 antitripsin - Female - Atmospheric pollution - Smoke exposure - Maybe genetics - Lower socioeconomic status

Answer 448

Acquired, permanent bronchial wall thickening, dilation of bronchi or bronchioles on CT. Chronic cough, thick sputum 1) Infection - recurrent, especially in early childhood, pulmonary aspergilliosis 2) Congenital - cystic fibrosis, primary ciliary dyskinesoa 3) Persisting foreign bodies (e.g. inhaled) 4) Autoimmune / inflammatory - rheumatoid disease 5) Idiopathic Treatments - Non pharma = smoking cessation, vaccines, chest physio, airway clearance techniques - Pharma = steroids, azithromycin prophylaxis, longer courses of Abx (14 days usually), occasionally nebulised antibiotics (tobramycin). Bronchodilators less useful but some patietns get reversibility

Answer 449

FACED = FEV1 Age Colonisation (pseudomonas) Extension (number of lobes affected) Dyspnoea (mMRC score)

Answer 450

CFTR mutation causing abnormal chloride channel. On apical border of exocrine glands, disturbing balance of sodium and chloride. Results in high mucous viscosity. Autosomal recessive inheritence. Multisystem disease (with predominately respiratory effects) Respiratory - Thick mucous, difficulty clearing. Recurrent infections - Bronchiectasis - Chronic sinusitis - V/q mismatch and hypoxaemia - Risk of pHTN, RV failure Hepatobiliary - Biliary cirrhosis, portal hypertension from obstruction of biliary tree Endocrine - Obstruction of pancreatic ducts, type 3c CF induced diabetes mellitus - treat as type 1 MSK - Osteoporosis Metabolic - Malnutrition, vitamin deficiency Other - Psychosocial impact - Infertility

Answer 451

Non-pharma - pulmonary mucous clearance techniques - Chest physio - Hypertonic 7% saline nebulised - Psychological, regular resp physician visits - Lung transplantation Pharma - Trikafta = 3 drugs. Chloride channel opener + 2x chloride channel modulator - bronchodilators - Pulmozyme - Vitamins, nutritional support (particularly fat soluble, DEKA) - Pancreatic enzymes - Insulin (20% have CF diabetes)

Answer 452

Diverse group of lung conditions, grouped together due to simialr clinical, radiological, physiological similarities. Inflammation of alveoli --> collagen deposition, fibrosis of lung parenchyma --> intrinsic restrictive lung pattern with reduced DLCO Most common cause: idiopathic pulmonary fibrosis Secondary causes: - Occupational (from pneumoconiosis) - cotton, silica, asbestos, coal - Environmental - bird droppings, dust, fungi, mold - Medications - etanercept, infliximab, methotrexate, amiodarone - Auto immune - rheumatoid arthritis, SLE, sarcoidosis, systemic sclerosis - Chronic infection - Radiation exposure Treatment may include immunotherapy, steroids. Rarely lung transplant. Treating or removing underlying cause. Smoking cessation + vaccinations For idiopathic pulmonary fibrosis - pirfenidone (anti-fibrotic medication) or nintedanib (MAB anti-fibrotic) may be used. May slow down progression

Answer 453

Will have restrictive pattern on spirometry (normal FEV1/ FVC ratio but both FEV1 and FVC reduced). But should have normal DLCO when corrected for lung volumes (KLCO) Chest wall abnormalities - ankylosing spondyolitis, kyphosis, scoliosis, obesity, concentric burns / scar tissue, flail chest Abdominal pressure - obesity, pregnancy, ascites Neuromuscular weakness - muscular dystrophy, c spine injury, guillian barre, myasthenia gravis, MND

Answer 454

Non-caseating granulomatous formation, most commonly in the lungs (90% of patients with sarcoid have pulmonary involvement) but can be in any tissue (cardiac, brain, renal, MSK). Unclear cause. Typically presents in 20s-40s, potentially environmental trigger in genetically susceptible patients Granulomatas have epithelial core, macrophages, giant cells. Surrounded by fibroblasts, B cells and T cells. Heal by fibrosis. Airway - Pharyngeal, laryngeal, nasal, tonsillar airway involvement possible. Difficult airway. Beware if stridor Resp - granulomatas, fibrosis of bronchi, pleura, alveoli. Typically restrictive spirometry pattern with reduced DLCO - Perihilar lymphadenopathy --> bronchial obstruction, distal atelectasis - Mediastinal lymphadenopathy (lymph node excision from perihilum common method for diagnosis, 85% diagnostic) CVS - Cardiac invasion --> conduction abnormalities, SVT, VT, VF, sudden death. May have PPM (20% have known CVS involvement. One post mortem Japanese study suggested up to 50% have cardiac involvement) - pHTN, right heart failure possible from lung disease Renal - interstitial nephritis - Hyperclacaemia from excess vitamin D3 from macrophages. Kidney stones. CKD possible MSK - Bones, skin involvement (5-10%). Prone to pathological fractures CNS - Up to 25% have neural tissue involvement. But symptoms are rare

Answer 455

Steroids - often high dose, 20-40mg for 12 months. May be higher pulsed steroids if resp failure or cardiac involvement Other immunomodulation - Methotrexate (often second line) - Mycophenolate - Cyclophosphomide - Azothioprine - Infliximab Treatment for hypercalcaemia - bisphosphonates - Calcitonin infusion Usual non-pharma things for respiratory

Answer 456

Preop - Double lung (better survival odds) vs single lung vs double lung + heart transplant. Determine which one. Heart will obviously have implications too (e.g. denervated, higher coronary disease rates). - Immunosuppression - ensure they get their drugs - Steroids - effects may include secondary adrenal insufficiency, insulin resistance, obesity, skin / bone changes - Rejection - can present as cough, SOB. Hard to elucidate from infection - Get transplant team involved - consider reason for transplant - CF, sarcoid, alpha 1 antitripsin are multi system diseases that aren't cured by lung transplant. COPD may be froma long standing smoking history - Consider doing in transplant centre if time for transfer. Access to transplant team, ICU Intraop - Regional is ideal. Impaired cough, mucociliary clearance as denervated lungs. - If GA, LMA is reasonable. If ETT ensure cuff isn't on anastamosis (if double lung transplant) - If DLT, palce under direct vision and try keep cuff from bronchial or tracheal anastamosis. May need DLT if vastly different ventilation capabilities of each lung - Ventilation - aim for low inspiratory pressures, minimise FiO2 where able, small amount of PEEP - Asepsis is key - Steroid cover with 8mg dex - Minimise fluids - risk of APO. Lymphatics typically working 4 weeks post transplant but likely impaired compared to normal lungs - HPV is normal, as not neural mediated Post op - Extubate reversed, upright. Onto supplemental O2 - consider HDU - Ensure antirejection meds - Early chest PT

Answer 457

Sensitivity on the Y axis (True positive rate) 1-specificity on the X axis (False positive rate) AUROC = c statistic. >0.9 = excellent discrimination. 0.7-0.9 = acceptable. 0.5 = no better than random

Answer 458

National Surgical Quality Improvement Program From American college of surgeons (ACS). 21 variables. Includes BMI, ASA, surgery type, emergency or not, certain comorbidities Created in 2013, recalibrated in 2016 and 2021. From USA data, >1.4 million patients. Algorithm not publically available Gives outputs on mortality, nursing home placement, post op pnuemonia / VTE When used in USA, mortality AUROC of 0.94, morbidity 0.81 More variable when used in Aus / NZ. One study found mortaltiy predication 0.93 by morbidity 0.73

Answer 459

Surgical outcome risk tool (SORT). UK based. Only 10 variables SNAP2 study found clinical judgement alone had AUROC of 0.89. But improved when clinical judgement + SORT (0.92)

Answer 460

Subjective - Self resported ability to do activity (climb stairs). METS trial (2018) found no association with anaesthetist derived assessment and MACE - DASI - useful Objective - 6MWT - Stress echo / ECG - CPET - Cardiac biomarkers (troponin, BNP)

Answer 461

Association in COPD patients, if <200m then higher periop morbidity / mortality 6 minutes, 30m track, As many as possible laps Cheap, easy to perform

Answer 462

European society for cardiology and Canadian cardiac society suggest preop + daily post op troponins (48-72 hours) for those high risk for MACE (e.g. if RCRI >1 or BNP >92mg/L for Canadian guidelines) If raised troponin preop, increased risk of MACE. May consider 5 lead ECG, arterial line + monitor post op trops. Post op might have higher level of monitoring, HDU etc But hard to know what to do with positive result for post op troponin rises. Most are type 2 MIs. Unlikely to benefit from angiogram. Aspirin + statin if not on + refer to cardio

Answer 463

Raised BNP preop strongly correlates with MACE post op (more so than CPET or DASI based on the METS 2018 trial). May provide risk assessment information (informed consent), increased intraop + post op monitoring No obvious treatment plan for if BNP raised. BNP can be raised for numerous reasons (heart failure, renal failure, increases with age). Can also be normal with myocardial ischaemia (if no heart failure component especially)

Answer 464

Indications: - Prognostication for surgical outcomes - Identification of patients for prehab - Monitor effects of prehab / chemotherapy - Guide intraop, post op management - Identification of pathology Contraindications: - MI within 5 days - Unstable angina - Aortic dissection - Unexplained syncope - Uncontrolled asthma - Refusal Method - Equipment: 2 people needed, resus equipment, cycle ergometer, metabolic cart with ECG, gas analysis, SpO2, pneumotachygraph, NIBP - 3 mins of no exercise for baseline. 3 mins unloaded at 60BPM. then ramped exercise over 8-12 mins, with increasing Watts/min - based on age, height, gender, weight - Borg score for percieved effort (out of 10) - Recovery for 5 mins Variables - VO2 peak. Maximal O2 uptake in ml/kg/min (different to VO2 max which is a physiological end point). Peak is based on maximal effort. Based on predicted levels for patients age, gender. <50% predicted = poor (as is <10ml/kg/min VO2 peak) - Anaerobic threshold (AT) - point at which transition from oxidative phosphorylation to majority anaerobic metabolism, lactate production. AT < 11ml/kg/min suggests higher morbidity / mortality risk - Ventilatory equivalents for CO2. VE/CO2. Ratio of ventilation to CO2 output. indicator for ventilation efficiency. Higher value might suggest more physiological deadspace. >34 = increased periop complications - Other - ECG, NIBP, SpO2 during Evidence - Increased morbiditiy / mortality if outside of values mentioned above - As per METS 2018 study, did not out performed DASI score for predicting periop complications

Answer 465

Subjective questionaire with 12 items (yes or no), each associated with a score. Out of 58.2 total = 9.89 METS (1 MET = resting VO2 for 70kg male = 3.5ml/O2/min) Scores of <4 METS or DASI scores <34 are predictive of periop harms. In 2018 METS trial, it was the only functional assessment that correlated with postop death and MI. Questions include: walking indoors, walking around a level block, run short distance, do light housework, have sex, participate in strenuous sport Can convert DASI score to VO2 by: VO2 = (DASIx 0.43) + 9.5 And METS = VO2 / 3.5

Answer 466

Legal requirement. In NZ by HDC right 7 = right to informed consent - Informed - patient needs to know relevant risks, benefits, alternatives to make decisions - Without coercion - Capacity. Need to be able to retain information, weigh up pros and cons and make decision based on their preferences + communicate this decision. Should be consistency in their thinking and decision making. Patients are assumed competant until proven otherwise - Documentation. PS26 - Consent can be removed from patient at any point if still competent HDC right 5 = right to effective communication. Which includes having a qualified interpretter not a family member

Answer 467

Decreased phsyiological reserve with diminished resillience to a physiological insult (e.g. surgery). Associated with increased risk of periop complications. Domains include: physical, cognitive, psychological, nutritional and scoail, Association with increasing age, comorbidities and reliance on others for ADLs. But not mutually exclusive

Recall Flashcards

(500 cards)