1 MK e-Alerts in Primary CareDr Anselm Fliedner Renal Consultant

2 AKI Acute Kidney InjuryWhat is it ? Causes/Risk Factors/Consequences ? Why is it important ? Electronic alerts AKI Care bundle in primary care in MK

3 What is AKI ? Clinical and biochemical syndrome reflecting abrupt kidney dysfunction Is not a primary disease nor a diagnosis Various causes and outcomes - Important to find underlying cause

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5 AKI: causes and consequences>50% pre-renal: sepsis, hypovolaemia, cardiac failure, hypotension 30% renal: acute tubular injury (incl. prolonged pre-renal, rhabdomylisis, contrast, NSAIDs, gentamicin) tubulointerstitial nephritis, glomerulonephritis, myeloma, vasculitis <10% post-renal: stones, prostate, tumor Complications: hyperkalaemia, acidaemia, pulmonary oedema, uraemic pericarditis, uraemic encephalopathy

6 600 deaths coded w/ AKI from 2007Median age 83y, 90% emergency admissions Unacceptable delay in recognition of post-admission AKI 43% Post-admission AKI predictable and avoidable 21% 6

7 Up to 100,000 deaths each year in hospital are associated with AKIUp to 30% of those deaths could be prevented with the right treatment and care¹

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9 NPSA mandates reporting and actioning by all English NHS trustsIntegrate AKI algorithm into LIMS systems Result sent for national monitoring Inform primary care 9

10 continued work needed

11 AKI national e-ALERT algorithmCompare sCr current to previous: if previous within past 7 days else median of values -7 to -365 days Ratio ≥3.0 → AKI stage 3 Ratio ≥2.0, <3.0 → AKI stage 2 Ratio ≥1.5, <2.0 → AKI stage 1 If sCr >354 & ≥1.5x rise → AKI stage 3 If sCr rise >26 within 48 hrs → AKI stage 1 If no previous sCr within past 365 days, but current sCr abnormal – “abnormal high/low result; repeat if high” 11

12 Erroneous AKI e-ALERTsFalsely low baseline healthy pregnancy pt has a blood test post-partum in follow-up which is normal but flags as above baseline First Bloods taken from drip arm Falsely raised creatinine Reduced tubular secretion (Trimethoprim, Cimetidine) Interference with old assay (Flucytosine) Advanced CKD including dialysis patients Dialysis patients: Post/Pre bloods (KT/V) Most likely in primary care will be first one and last ones. Lin et al., Clin J Am Soc Nephrol (2015) 12

13 Electronic alerts/Storage/Data-analysis70% of laboratories have implemented the Algorithm and are sending the data to the Renal Registry MK Hospital sends AKI Alerts to the Renal Registry since March 2016 MK Data Analysis is done by the Oxford Academic Health and Science Network The Oxford AHSN is a partnership of NHS providers, commissioners, universities and life science in Bedfordshire, Berkshire, Buckinghamshire, Milton Keynes and Oxfordshire. There is a population of around 3 million within this region. The patient safety collaborative has 6 work streams Renal Registry71 adult and 13 paediatric renal centres.

14 Electronic alerts/Storage/Data-analysisdata until December 2016: - over 1,200,000 AKI warnings in 390,960 individuals

15 Why is AKI Treatment in Primary Care Important?- 65% of AKI starts in the community (Selby et alt. 2012) - Prevention of progress into more severe stages of AKI - Avoids hospital admissions

16 De novo AKI e-alerts in primary care in Oxfordshire91 practice locations, 1588 alerts over 124 days 12.8 alerts a day across primary care, i.e /month On average 1 alert per practice location every 7 days Wide variation based on practice size and location

17 Primary care Oxford: 13 e-alerts /day17

18 AKI Primary Care BundlesFour different bundles: AKI 1 AKI 2 AKI 3 No previous result

19 AKI Primary Care Bundle- all relatively similar - MK CCG ~ Oxford CCG a) bigger comparable data sets b) MK renal service/ Oxford Kidney Unit c) Renal Unit /Transplant Unit/ Renal Registrar in Oxford

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29 AKI e-ALERTs: summary AKI e-ALERT isa nationally mandated system, intent on reducing avoidable harm a test which needs interpretation (may be falsely positive/negative) Initial source of advice is the MKCCG care bundle Also: THINK KIDNEYS website Follow a step-wise approach to initial management of AKI: stage I review <48h, hydrate, stop NSAID’s, Rx infection stage II review <24h, stop NSAID’s, ACE, Metformin + drugs stage III refer to hospital 29

30 The Road ahead 6 of June: Go live

31 Patients discharged after episode of AKIMonitor U&E, fluid status, BP weekly until at baseline Reintroduce nephrotoxic/stopped meds in stepwise fashion with serial U&E (only if meds still needed) Consider referral to nephrologist as per CKD guidelines (if eGFR persistently <30 mL/min/1.73m2 for ≥3mo) Even if fully recovered annual creatinine/dipstick check As previously stated, the diagnosis of AKI will be automatically added to the Problem List, which is where one should go if one needs to remove this diagnosis, for example a false positive e-alert in a haemodialysis patient who has blood tests taken outside of the kidney unit. Please also consider providing advice to primary care on the post-discharge management after an episode of AKI. This will probably include repeating blood tests and fluid assessment at least once after discharge and probably to continue to monitor these until the serum creatinine has returned to baseline. At this point a GP many need to reintroduce medications that were suspended because of the AKI, such as ACE inhibitors and Metformin. 31

32 Prevention of AKI in Primary CareRaise awareness patients/nursing homes: - “kidneys produce urine” - increase fluid intake when having temperature/ diarrhoea Check urine colour

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38 https://www.youtube.com/watch?v=sw9XfT2YTqw

39 By Dr Assad Hamid GPWSI in CardiologySyncope By Dr Assad Hamid GPWSI in Cardiology

40 Definition and Symptoms of SyncopeThe medical term for fainting is syncope. Syncope is a T-LOC due to transient global cerebral hypo perfusion characterized by rapid onset, short duration, and spontaneous complete recovery in usually less than 30 seconds Presyncope is a state of light-headedness, muscular weakness, blurred vision, and feeling faint (as opposed to a syncope, which is actually fainting). The following signs and symptoms may precede a fainting episode: A feeling of heaviness in the legs , Blurred vision, Confusion , Feeling warm or hot , Light-headedness, dizziness, a floating feeling, Nausea, Sweating, Vomiting Yawning.

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42 Causes of syncope Neurally‐mediated (reflex) Or Neuro-cardiogenicSyncope due to Orthostatic hypotension Vasovagal syncope (common faint) Mediated by emotional distress, fear, pain, instrumentation, blood phobia, Mediated by orthostatic stress Situational syncope Cough, sneeze or gastrointestinal stimulation (swallow, defecation, visceral pain) micturition (post‐micturition) post‐exercise post‐prandial others ( laugh, brass instrument playing, weightlifting) Carotid sinus syncope Atypical forms ( without apparent triggers and/or atypical presentation ) Primary autonomic failure Pure Autonomic failure, Multi system Atrophy, Parkinson's disease with autonomic failure, Lewy body dementia Secondary Autonomic Failure Diabetes, Amyloidosis, Uraemia, Spinal cord injuries Drug Induced Orthostatic Hypotension Diuretics, vasodilators, Alcohol, Phenothiazine's, Antidepressants ( TCA’s) Volume Depletion Haemorrhage, Diarrhoea, vomiting etc.

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45 Cont’d causes Structural cardiac or cardiopulmonary diseaseCardiac arrhythmias as primary cause Sinus node dysfunction (including bradycardia/tachycardia syndrome) Atrioventricular conduction system disease Paroxysmal supraventricular and ventricular tachycardias Inherited syndromes (eg, long QT syndrome, Brugada syndrome) Implanted device (pacemaker, implantable cardioverter‐defibrillator) malfunction Drug‐induced arrhythmias Obstructive cardiac valvular disease Acute myocardial infarction/ischaemia Obstructive cardiomyopathy Atrial myxoma Acute aortic dissection Pericardial disease/tamponade Pulmonary embolus/pulmonary hypertension Cerebrovascular Vascular Subclavian steal syndromes

46 Causes of non‐syncopal attacks (commonly misdiagnosed as syncope)Disorders without any impairment of consciousness Disorders with partial or complete loss of consciousness but without cerebral hypoperfusion Falls Cataplexy Drop attacks Psychogenic pseudo‐syncope Transient ischaemic attacks (TIA) of carotid origin Metabolic disorders, including hypoglycaemia, hypoxia, hyperventilation with hypocapnia Epilepsy Intoxications Vertebro‐basilar TIA

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48 Diagnosis of syncope The following questions should be answered:Was LOC complete? Was LOC transient with rapid onset and short duration? Did the patient recover spontaneously, completely and without sequelae? Did the patient lose postural tone? If the answers to these questions are positive, the episode has a high likelihood of being syncope. If the answer to one or more of these questions is negative, exclude other forms of LOC before proceeding with syncope evaluation.

49 Clinical features suggestive of specific causes of syncopeNeurally‐mediated syncope Syncope caused by orthostatic hypotension Absence of cardiac disease Long history of syncope After sudden unexpected unpleasant sight, sound, smell or pain Prolonged standing or crowded, hot places Nausea, vomiting associated with syncope During or in the absorptive state after a meal With head rotation, pressure on carotid sinus (as in tumours, shaving, tight collars) After exertion After standing up Temporal relationship with start of medication leading to hypotension or changes of dosage Prolonged standing especially in crowded, hot places Presence of autonomic neuropathy or parkinsonism After exertion

50 Cont’d clinical featuresCardiac syncope Cerebrovascular syncope Presence of severe structural heart disease During exertion, or supine Preceded by palpitation or accompanied by chest pain Family history of sudden death With arm exercise Differences in blood pressure or pulse in the two arms

51 Suspected Epilepsy A bitten tongue.Head-turning to one side during TLoC. No memory of abnormal behaviour that was witnessed before, during or after TLoC by someone else. Unusual posturing. Prolonged limb-jerking (note that brief seizure-like activity can often occur during uncomplicated faints). Confusion following the event. Prodromal déjà vu, or jamais vu

52 DIAGNOSTIC YIELD AND PREVALENCE OF CAUSES OF SYNCOPEThe EGSYS study which is based on strict adherence to the Guidelines on Syncope of the European society of cardiology showed : A definite diagnosis was established in 98% (unexplained in 2%): Neurally‐mediated syncope accounted for 66% of diagnoses, orthostatic hypotension 10%, primary arrhythmias 11%, structural cardiac or cardiopulmonary disease 5%, and non‐syncopal attacks 6% . The initial evaluation established a diagnosis in 50% of cases

53 Evaluation of the patientCareful history taking including of any prodromal symptoms and preceding events also if there was any loss of sphincter control and tongue bite, palpitations, chest pains, association with food, exercise, alcohol intake Examination Detailed cardiovascular examination including Lying , Sitting and standing ( after 3 min) blood pressure with Systolic drop of >20 mm and Diastolic drop of > 10mm of Hg or reproduction of symptoms, listening for any heart murmurs, checking and comparing radial and femoral pulses, listening for any carotid bruits and infra/supra clavicular bruits, checking for any signs of dehydration, pallor, cyanosis. Complete neurological exam and checking for any signs of infection. ECG mainly looking for any arrhythmia, ischaemia, heart block, short PR interval, Prolonged QT interval. Blood test to look for Anaemia, electrolyte imbalance and renal and metabolic function including blood sugar levels.

54 ECG abnormalities suggesting cardiac causeConduction abnormality (for example, complete right or left bundle branch block or any degree of heart block) Inappropriate persistent bradycardia. Any ventricular arrhythmia (including ventricular ectopic beats). Long QT (corrected QT > 450 ms) and short QT (corrected QT < 350 ms) intervals. Brugada syndrome. Ventricular pre-excitation (part of Wolff-Parkinson-White syndrome) – Short PR interval less than 0.2 sec or Delta wave Left or right ventricular hypertrophy. any ST segment or T wave abnormalities. Pathological Q waves. Atrial arrhythmia (sustained) including atrial flutter, fibrillation, Atrial tachycardia Paced rhythm.

55 EGSYS Score and Urgent Cardiology referralPalpitations before syncope ( +4 ) Abnormal ECG and/or heart disease ( +3 ) Syncope during effort ( +3) Syncope while supine ( +2 ) Autonomic Prodrome ( -1) Predisposing/precipitating factors ( -1) Refer if score  ≥ 3

56 Referral and further testsNo need for referral if simple vasovagal faint with features suggestive of uncomplicated faint or Typical history with 3 P’s of Posture, provoking factors and Prodromal symptoms or typical history of situational syncope with normal examination, normal ECG and no alternative diagnosis If confirmed Orthostatic Hypotension with history and examination and no alternative diagnosis possibility then again no need for referral unless unsure of management and needs specialist input. Urgent Cardiology referral if An ECG abnormality as discussed earlier Heart failure (history or physical signs). TLoC during exertion. Family history of sudden cardiac death in people aged younger than 40 years and/or an inherited cardiac condition. New or unexplained breathlessness. A heart murmur. Consider referring within 24 hours for cardiovascular assessment, as above, anyone aged older than 65 years who has experienced TLoC without prodromal symptoms. Investigations can include Holter Monitoring , Echocardiogram, ETT, Cardiac MRI, Coronary angiogram, Implantable loop recorder ( ILR ) , Telemetery, tilt Table testing and carotid sinus Massage Neurology referral if Suspected Epilepsy, TIA/Stroke, History of head injury or concussion etc. Investigations may include CT/MRI brain, EEG ( has been shown to be of little benefit in diagnosing syncope ) Psychiatric referral – if after careful history, examination and tests Pseudo seizures are diagnosed especially if patient < 40 years of age with past history of some form of psychiatric illness and absence of cardiovascular disease . There are usually multiple episodes during the day/week with prolonged periods of LOC, do not be distracted with injuries as one study showed some form of injury in >50 % of patients with Pseudo Seizures.

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58 Management and TreatmentThe principal goals of treatment for patients with syncope are to prolong survival, limit physical injuries, and prevent recurrences. Knowledge of the cause of syncope has a key role in selection of treatment. Reflex syncope Non-pharmacological ‘physical’ treatments and avoidance of trigger factors . Isometric physical counter pressure manoeuvres ( PCMs ) of the legs (leg crossing), or of the arms (hand grip and arm tensing), are able to induce a significant BP increase during the phase of impending reflex syncope that allows the patient to avoid or delay losing consciousness  Tilt training The prescription of progressively prolonged periods of enforced upright posture (so-called ‘tilt training’) may reduce syncope recurrence Pharmacological therapy Many drugs have been tested but with disappointing results for reflex syncope including β-blockers, disopyramide, scopolamine, theophylline, ephedrine, etilefrine, midodrine, clonidine, and serotonin reuptake inhibitors. Cardiac Pacing plays a small role in therapy for reflex syncope, unless severe spontaneous bradycardia is detected during prolonged monitoring. Vasovagal syncope All patients should be taught PCMs, which now form the cornerstone of therapy together with education and reassurance. Driving follow the DVLA guidance , advice all patients to stop driving until the cause of syncope has been ascertained and for non simple faints until after specialist assessment and advice or once treatment has started and patient has no further attacks or has reduced risk.

59 Cont’d Situational syncope Treatment strategies are similar to VVS and have been covered. Treatment of most forms of situational syncope relies heavily on avoiding or ameliorating the triggering event and may be attenuated by maintenance of central volume, protected posture, and slower changes in posture. Carotid sinus syndrome Dual chamber Cardiac pacing appears to be beneficial in CSS when bradycardia has been documented also avoiding tight collars, ties, electric shaver. Orthostatic hypotension and orthostatic intolerance syndromes The principal treatment strategy in drug-induced ANF is elimination of the offending agent Expansion of extracellular volume is an important goal to drink 2-3 litres of water daily, salt up to 10 grams NACL for non hypertensive patients . Rapid cool water ingestion for post-prandial hypotension. Sleeping with the head of the bed elevated (10°) prevents nocturnal polyuria, maintains a more favourable distribution of body fluids, and ameliorates nocturnal hypotension. Gravitational venous pooling in older patients can be treated with abdominal binders or compression stockings. In contrast to reflex syncope, the use of the α-agonist, midodrine, (5–20 mg, three times daily) is a useful addition to the first-line treatment in patients with chronic ANF. Fludrocortisone (0.1–0.3 mg once daily) less frequently used treatments, alone or in combination, include desmopressin in patients with nocturnal polyuria, octeotride in post-prandial hypotension, erythropoietin in anaemia, pyridostigmine, use of walking-sticks, frequent small meals, and judicious exercise of leg and abdominal muscles, especially swimming. Cardiac Syncope – Specific treatments as per diagnosis including antiarrhythmic medication, ICD, Pacemakers, radiofrequency ablation, surgery for Atrial Myxoma HOCM etc.

60 Summary and Questions Careful history taking including of the eye witness and detailed examination including CVS with sitting /standing Bp, ECG, blood test, leads to diagnosis in > 50 % of cases. If you suspect a cardiac cause like an arrhythmia or Structural heart disease then your can refer to a community cardiologist for most cases. But if serious ventricular arrhythmia suspected , or there is a history of Ischaemic heart disease /MI or family history of SCD then urgent hospital admission or referral to hospital cardiology department is recommended. If the history is suggestive of a neurological cause like Epilepsy or there is history of head injury /concussion then urgent neurology referral is recommended. For simple vasovagal fainting with clear trigger and no sinister findings on examination and tests no referral is required. Manage as discussed before. If the cause of syncope is not clear from history and examination then the patient will possibly need both cardiology and Neurology input and more extensive testing likely insertion of ILR. Consider referral to a Psychiatrist/Psychotherapist for confirmed and persistent Psuedoseziures.