ࡱ>  mbjbj~~ 4^aaaaauuuuu$uqheeeee@@@BqDqDqDqDqDqDqCsurDqQa@@@@DDql aaeeql l l HaeaeBql @Bql l jk aaqP8rehu66m<6q q0qmTWvl Wvxql aq@@@ ':   Notes for VAQ Q5 This was a difficult question to mark it was relatively easy to interpret, management a bit more involved. However it was difficult to know what the examiners would really be after so I have kept it quite general. My model answer may only get 8-9. I realised afterwards there are some minor omissions. Part A 70%, and Part B 30% - this means the amount of time and amount of writing for each part must reflect this as the marks will be weighted accordingly. you should be writing solidly for the whole 7.5 min it was clear some of you did not. There are no half marks for the question overall. I have marked each section individually to give you an idea of where you stand, but where there were half marks overall, the mark was rounded down. Read the question. it quite clearly states the patient was 75 from a full care nursing home. This raises significant issues such as advanced directives and rules out very aggressive management such as intubation a.nd ICU. There was too much description and not enough interpretation in part a I have read the question, do not just repeat the numbers back to me, I want additional information. It is mandatory that a pass required an anion gap calculation. This is a basic part of interpreting electrolytes, especially when you are given the bicarb, and should have been drummed into you by now. Osmo calculations were a bonus and not mandatory for a pass. All candidates without exception were obsessed about metabolic acidosis. Although this was likely, there was no pH to lead to this conclusion. An isolated low bicarb could be related to a partially compensated resp alkalosis, a possibility in this gentleman with renal failure and dehydration. Good answers had a differential Dx of hypernatraemia and renal failure specific to this patient. The main part of the part b was the specific management of hypernatraemia it was extreme and the most significant pathology in this patient and you could not pass part b without it. There was too much management of hyperkalaemia it was really only mild-mod and not life threatening. This was probably a case of going to town on something that was easy rather than tackling the real question of hypernatraemia and renal failure what would you really do for a K of 6.3 anything?? This patient had been triaged, placed in the ED and had a full assessment including investigations. I do not want to hear the words triage to acute care/resusc. You are also unlikely to manage this patient in resusc. Q5 (a) Na 172 ! severe ! K 6.3 ! mod ! ? expect ECG changes cl 142 ! severe ! excessive rise compared to Na ? HcO3  losses met acidosis with cl ref. HcO3 20 ! decreased need ABG for pH likely met acidosis Ur/Ls 42/360 ! elevated likely acute (? on chronic) RF G/c 5.6 (N) Alb 38 (N) ! probable haemoconcentrated will ! with rehydration AG ! (172 + 6)  (142 + 20) ! 16 (N) interpret = severe hypernatraemia severe acute (? on chronic) RF complicated by ! (N) AG metacidosis ! cl ! K+ possible ! Alb. ! Na ! dehydr ! sweating ! intake Gi losses. hyperaldosteranism renal losses of free fluid diabetes insipidis renal failure ! likely pre-renal (dehydration) met acidosis ! HcO3 losses with ! Cl and (N) amen gap GIT losses renal losses ! K+ ! due to acidosis and ARF Overall likely picture of ! Na and dehydr with ARF and ! K+ acidosis. Q5 (b) initial Rx note ! 75 y/o ? full cov NH key points ! gentle rehydration over 48 hrs keep comfortable ID and Rx any cause avoid  heroic measures ! ICU inotropes rehydration ! restore intravascular volume = (N) saline has had 1L Hartmann s likely 1L (N) Saline add is sufficient then ! calculate free water deficite replace with (N)/2 saline over 48hrs. supportive ! IDC and strict fluid balance sedation if particularly confused / agitated ? advanced directive from family repeat K+ measurements ! should correct with hydr consider resonium consider more acute Rx if ECG changes Trial Fellowship Exam 2010.1 Suggested answer VAQ 6 Describe XRay The Xray is an AP and lateral of the right hand and writst Mobile film dne in ICU Pulse oxymetry, arterial line seen No plaster or other form of immobilisation Positive findings: Lunate dislocation (not perilunate) - crowded carpus - split teacup sign Also fractured ulnar styloid well corticated and likely an old injury (b) Possible complications Acute complications Related to Lunate difficult closed reduction, may need open reduction (if diagnosed late may be difficult to reduce closed, if > 1 week impossible) Avascular necrosis risk increased if need to perform open reduction Damage to surrounding structures; Median Nn injury common Vascular injury possible Chronic complications Pain / dysfunction of wrist common Reflex sympathetic dystrophy OA VAQ 7 65 year old male post LAD stent 2 days ago. INTERPRET (not describe and interpret) the ECG (50%). This ECG shows a run non sustained of ventricular tachycardia following 4 beats of normal sinus rhythm with a borderline first degree heart block. This appears to self terminate and the final rhythm is again sinus rhythm with a borderline first degree heart block. (<30 seconds so non sustained VT) and he goes back into sinus rhythm. Given his recent LAD stent, the most likely cause for this, is ischaemia although there is no ST elevation on this ECG. In more detail: The ECG report states there is a prolonged QTc at 538 ms but when calculated using Bazetts formula for the sinus rhythm part of the ECG the QTc = 330ms QTc = QT / square root of RR interval. Hence it is unlikely that this run of VT is due to prolonged QT (which would generally result in R on T and Torsades rather than monomorphic VT). The initial part of the ECG shows: Sinus rhythm at a rate of approximately 65 bmp with a normal axis. PR interval is borderline prolonged = borderline 1st degree HB (0.22 sec approx) QRS narrow with Qwave in lead III No acute ST changes in the initial part of the ECG T wave inversion in inferior leads seen The QTc is normal at 330 ms as above The ECG then progresses into VT. This is evidenced by a regular, wide complex tachycardia with a RBBB type pattern at a rate of approximately 180 bpm with left axis deviation (axis previously normal). There is not quite an RSr pattern in V1, although there does appear to be in leave V2 which is consistent with VT. The downstroke of the S wave in Lead V1 also appears slightly notched in V1 which supports the diagnosis of VT. The QS complex in V6 also supports the diagnosis of VT. The evidence of concordance. No capture or fusion beats seen within the run of VT although the run ends with a sinus beat and he remains in SR. There does appear to be AV dissociation which is difficult to see but most evident in lead V3. DDX: Ischaemia may have LAD stent reocclusion Arrhythmias related to scar tissue formation post AMI (may be maximal at 3 days)(evidence of prev AMI with T wave inversion in inferior leads (may be old or new inferior AMI usually RCA). Electrolyte abnormalities Medication related eg Class 1a 1c antiarrhythmics Mitral valve prolapse need to examine for MR murmur Prognosis: If a due to recurrent ischaemia may require revascularisation. Proarrhythmic medications contributing to this will need to be stopped Disposition admit for monitoring. May require AICD Outline immediate Management (Rx, supportive care, Disposition). Rx: If haemodynamically stable: Pt in resus room already Assemble resus team team approach PPE Apply O2 via NRB at 15L/min Attach non invasive monitoring: O2 sat / NIBP / ECG monitor / RR Attach defib pads and connect to defibrillator Ensure airway patent and breathing effective support as needed Insert 2 IV cannulae one at least proximal and 18g min Take bloods for: FBC infection / anaemia UEC electrolytes CMP- hypocalcaemia / Hypomagnaesaemia Troponin T and CK - ? NSTEMI (may be already elevated if recent AMI) Medication level eg Digoxin TFTs thyroid fx Coags (esp if on warfarin) Venous blood gas include urgent K, Hb CXR Repeat ECG Administer aspirin 300mg PO if no allergies (and has not had already today) Consider clopidogrel 600mg (no evidence STEMI on current ECG and pt likely to be on maintenance dose if so, do not give) Administer MgS04 10mmol in 100ml 0.9% saline IV over 30 mins (watch for hypotension) Administer bolus 250ml 0.9% saline if hypotensive and reassess repeat as needed Stop any medications which may be proarrhythmic If further episodes of VT with the patient haemodynamically stable, commence amiodarone bolus 150mg IV over 10 mins (if no underlying thyroid problems or other contraindications) can give a second dose of 150mg over 10-20 mins if no response. Follow this by infusion according to protocol. (e.g. 600mg over 24 hours) ** if pt stable, may not need amiodarone bolus consider infusion only to maintain SR Alternative to amiodarone = lignocaine 100mg bolus but less effective than amiodarone. More effective in ischaemic VT due to depression of automaticity but still only effective in 20% with initial bolus. Further bolus of 50mg is effective in anther 10%. (NB may also be arrhythmogenic) Commence heparin (bolus and infusion according to weight based protocol / enoxaparin (1mg / kg SC BD) if troponin is elevated (further if was elevated on previous admission) and if no contraindications If patient has sustained episode of VT and becomes haemodynamically unstable will require DC shock 50 100J synchronized. (with sedation) If loses output will need CPR and DC shock 150J and per ALS algorithm Obtain recent history, old notes ECGs and recent angiogram results In view of recent stent, discuss with cardiology team early as may require revascularisation / unblocking of stent Supportive Care Seek and treat evidence of hypoperfusion or heart failure Reassure pt Seek and treat electrolyte abnormalities Disposition Admit to CCU for monitoring Advise admitting cardiology team re recurrence VT and consider AICD implantation if does not settles This is obviously a fairly comprehensive answer for 7.5mins and in relative long hand for teaching purposes. However you can see there is quite a bit of info to cover. Overall: Examiners Report Interpret this ECG Most people got the non sustained VT part. This is more likely given the patients age and recent LAD stent! Agree DDx has to be SVT with aberrancy but this is really unlikely given part of the ECG is in SR and there are no delta waves there and the RP interval is long rather than short. The question was interpret this ECG not describe and interpret which means I was expecting a bit more than this is a run of non sustained VT Tell me why you thaink that and why in THIS patient! Some candidates justified their dx of VT really well mentioning concordance etc. Very few pointed out that the axis had changed from normal to LAD with the onset of the VT. Good to justify why you think that if you can I expected a DDX for causes in this ischaemia (most likely given his recent LAD stent. T wave inversion inferiorly on this ECG but no ST elevation or significant depression Medications / toxins Electrolyte abnormalities etc. Also there were a few numbers on the ECG which were there for a reason but very few people commented on them. The QTc was reported as 538 ms and the PR = 240ms. This was the average of the whole ECG and when you worked it out, the QTc was normal in the SR part and was only borderline prolonged. Better answers reflected this. Outline your management: Now according to the definitions, management is: Treatment Supportive Care Disposition So make it easy for the examiners use the headings!!!!! Rx: The patient is ALERADY in RESUS!!! You dont have to put him there! The better answers acknowledged that the patient is in SR now but has the potential to go back into VT. So they mentioned what they would do if the patient developed VT but was stable. Vs what they would do if he arrested with further CT. Supportive Care: See above Disposition CCU How I marked: I did mark hard! 3 you had too much that was way off the mark in your answer 4 bare bones but not enough 5 gave me non sustained VT but not much else. Bare essentials there for management but nothing more 6 Either some extra info re the ECG or in the management part 7 Good interpretation of ECG with some qualifying info (why is it VT) and DDx. Overall good description of management options based on haemodynamic status. I didnt mark you down re the borderline 1st degree HB as it was borderline. Better answers realised that the stated Qtc and PR intervals were incorrect. VAQ 8 The patient is fifty seven (57) years old and is the first time presenting with acute respiratory distress. His family report he is usually breathless and can walk only ten metres before getting profoundly worse. He smokes 30+ cigarettes a day since he was fourteen years old. You have the patient on BiPAP on an Fi02 of 0.6; IPAP = 15cm H20; EPAP = 7cm H2). The patient is becoming increasingly drowsy and no longer conversing with you. The following arterial blood gases have been obtained. pH 7.26 pC02 115mmHg p02 70mmol/L BE 22mmol/L HC03 50mmol/L 02 Sats 91% The overall pass rate for this question was 50% (12/24). In marking this it was expected that more than just a list of the abnormalities present in the blood gas were given. It was expected that further analysis of the blood gas be made and some comment made as to compensation. It was also expected that the significant (A-a) gradient be noted, and some thought as to the possible cause give. Interpretation required at least some consideration as to the possible causes for this mans condition and a focussed differential was expected. Failing answers did not address the points above, gave generic lists of differential without relating it back to the question and used compensation equations inappropriately or used wrong values in same. Hand writing was very poor for several candidates and this should be considered for the actual exam. Q8 pH = 7.26 = mildly acidaemic pC02 = 115mmHg = significant hyperabia p02 = 70mmHg = significant hypoxaemic BE = +22mmo1L-1 = significantly positive implying severe underlying chronic alkalosis HC03 = 50mmo1L-1 = significantly elevated * Primary disorder is a respiratory acidosis Now BE of +22 suggests a chronic condition and using the equation for metabolic compensation of respiratory acidosis: HC03 = 24 + 4 (pC02 40) 10 The expected pC02 for a HC03 of 50 is 50 = 24 + 4 (pC02 40) 10 pC02 = 105mmHg actual pC02 = 115mmHg Disorder is acute on chronic respiratory acidosis Additionally: PA02 Pa02 = (A a) gradient PA02 = 0.6 (760 47) 115 (assuming sca level) 0.8 = 0.6 x 713 115 x 1.25 = 280 (A a) = 210 # significantly elevated * Interpretation: Acute on chronic respiratory acidosis with hypoxemia and a dramatically elevate (A a) gradient Suggest an infectious exacerbation of chronic airways disease in a patient with very little respiratory reserve gases suggest failure of NIV and likely need to escalate therapy if indicated after discussion with pt and family and treating physician need to consider other (? reversible) causes of respiratory acidosis * Failure to initiate ? drugs ? pneumothorax related to NIV ? pulmonary oedema ? PE * Excess C02 - ? SAQ 3 Trial exam 2010.1 This is a very detailed question with a great deal of information provided. As the patient is multiply injured and presumably anti-coagulated, prioritisation of management options is the key to obtaining top marks. There are a number of variations to acceptable practice in this situation and some grey areas including response to the FAST finding. The following is how I see the essentials of answering this question. In analysing the information give; As A has been taken care of (but good to mention checking ETT for patency and position), we are left with B, C, D, to address complicated by presumed anticoagulation and likely requirement for massive BTX. High risk of C-Spine injury, but no immediate specific management required beyond spinal precautions Need for orogastric tube Flail chest and probable contusion already largely treated by intubation Intercostal drain required on right in view of #s, flail, relative hypoxia and low BP. Low threshold for left sided drain as well. Minimal findings on FAST scan-no immediate indication for laparotomy, opportunity to monitor by serial FAST while other issues are addressed. Good to mention that scoring systems for FAST exist Widened mediastinum on supine CXR of questionable significance, DDx projection, retrosternal, haematoma, great vessel injury, post surgical appearance. FAST already completed to exclude pericardial fluid. Shock refractory to fluid loading Requires limitation of pelvic blood loss through temporary stabilisation (binder), embolisation, optimisation of coagulation status and possible surgical fixation. MTP with aggressive factor replacement and Prothombinex 25-50 IU/kg plus IV Vitamin K. Good to mention activated factor VII at least in passing. Ideally make mention of rapid infuser/blood warmer usage, and comment on avoiding hypothermia. Investigation/management of potential neurosurgical lesion deferred until circulation stabilised. In view of probable major head injury, hypertensive resuscitation not advisable. If able to be stabilised a Pan-Scan would be highly desirable in view of wide mediastinum, probable significant head injury, and presence of small amount intra-abdominal free fluid. Young person with mechanical valve high suspicion of Hx IVDU, stringent use of universal precautions and avoidance of injury through needle stick, broken ribs etc. Consider possibility of drug/Etoh intoxication contributing to accident and reduced LOC Medico-legal-BAL +/- Urinary Drug Screen In order to pass a discussion of emergent warfarin reversal, principles of massive BTX protocols, and reasonable prioritisation management options (accepting that this a complex case where some variability of practice would be expected, and some aspects of management may be controversial) Blood sugar/IDC/OGT/Antibiotic cover/activated factor VII/avoidance of hypothermia are quick points to make, that were omitted in many answers The most significant shortcomings in candidates responses were; Failure to address probable warfarinisation Limited or even absent discussion of fluid therapy including massive transfusion No acknowledgement of FAST findings or limited interpretation (eg free fluid = immediate laparotomy with no other options considered) Probability of serious head injury overlooked. Hypotensive resuscitation (the evidence for its use in blunt trauma is in my view rather flimsy) is very questionable with coexistant head injury. A number of candidates resorted to inotropes rather than concentrating on bleeding control and volume resuscitation Unclear description of management priorities Overall, this was a difficult question for candidates (and marker), with a pass rate of 64% PG QUESTION FIVE This is a bread & butter question so I have marked it reasonably hard. This is some of the things I was looking for in the marking: ASSESSMENT 2pts Triage to resuscitation area with ventilator/monitoring Team approach ABCDE approach Check and secure ETT Vitals adequate but borderline Focused clinical exam for signs heart failure, murmurs, trauma, focal neurology, drug use Member of team to obtain history from ambos, family, GP, Cardiologist AMPLE, prior cardiac status, investigations INVESTIGATIONS 2pts ECG ST elevation, new LBBB, electrolyte abnormalities, QT CXR tube, pulmonary congestion, PTX, infection, heart size & shape Bloods ABGs or VBGs, FBC, EUC, CMP, Troponin, coags, drug levels Bedside Echo wall motion, LV and RV function/dilation, valve function, effusion Head CT if suggested by history (fall with HI or sudden headache) or exam (focal neuro, head injury) THERAPY 3pts PPV settings CO judicious fluids to normovolemia, inotropes (which ones, doses), thrombolysis or PCI if indicated, aortic balloon pump when to use Rythmn amiodarone if further ventricular arrythmias; brady: drugs, pacing Anticoagulation, platelet inhibition Brain cooling ARC guidelines: 32-34 degC for 12-24 hrs; external (ice packs; devices) or internal methods (IV fluid: 30m/kg 4decC N/sal drops core by 1.5deg) Specific antidotes if required MONITORING/SUPPORT 2pts ECG, pulse oximetry, MAP; end-tidal CO2, glucose, core temperature discuss aim parameters Arterial line; central venous line IDC; N/G Sedation (? not Propofol) & ? paralysis to avoid shivering DISPOSITION 1pt Cardiology involve early to help decide on therapeutic options and echo ICu involve early may have cooling device Retrieval depending on situation Family discuss poor prognosis; involve social work The impaired doctor Obligations to report colleagues vary from time to time and place to place. At present obligations to report are based upon State legislation in Australia, although this may change in the future with national registration commencing in the years 2010-2012. In 2010 in NSW obligations are based upon 2 documents the Medical Practice Amendment Act 2008 and the NSW medical board code of conduct (see website) advisory only, not mandatory. The amendment act of 2008 obliges doctors to report colleagues who have practised medicine whilst under the influence of alcohol or drugs, practised medicine in a way that constitutes a flagrant departure from accepted standards and risks harm to some other person who have engaged in sexual misconduct in the practice of medicine. The medical board code of conduct recommends that advice be sought from the medical board and also that an appropriate person be contacted (eg hospital CEO in order to protect the safety of other persons. In regard to the question raised where a colleague of the treating doctor in the same public hospital has been found to be intoxicated with alcohol and or opiates, etc, there does not appear to be a mandatory requirement to report to the board as no medical treatment has been given by the impaired doctor. It seems correct, advisable and reasonable to consult the board regarding whether some form of notification is needed and/or if any restriction on practice should be imposed. As the patient may have taken s8 medications in non prescribed manner a restriction may be placed on his ability to prescribe such drugs. As any medical board tribunal meeting is now held in public in NSW it is strongly advised to the person to be reported that this will occur. Reports must be made in writing and cannot be made anonymously. Provided the medical board has been contacted for advice there seems no need for the reporting doctor to contact a medical defence body. The code of conduct recommends that a senior administrative person in the hospital be contacted. There does not seem to be an obligation to contact private areas the doctor may be employed in. 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