Predicting medical students who will have difficulty during their clinical training.

BACKGROUND: We aimed to classify the difficulties students had passing their clinical attachments, and explore factors which might predict these problems. METHODS: We analysed data from regular student progress meetings 2008-2012. Problem categories were: medical knowledge, professional behaviour and clinical skills. For each category we then undertook a predictive risk analysis. RESULTS: Out of 561 students, 203 were found to have one or more problem category and so were defined as having difficulties. Prevalences of the categories were: clinical skills (67%), knowledge (59%) and professional behaviour (29%). A higher risk for all categories was associated with: male gender, international entry and failure in the first half of the course, but not with any of the minority ethnic groups. Professional and clinical skills problems were associated with lower marks in the Undergraduate Medical Admissions Test paper 2. Clinical skills problems were less likely in graduate students. CONCLUSIONS: In our students, difficulty with clinical skills was just as prevalent as medical knowledge deficit. International entry students were at highest risk for clinical skills problems probably because they were not selected by our usual criteria and had shorter time to become acculturated.

Adverse drug events are a major cause of acute medical admission.

BACKGROUND: Adverse drug events (ADE) contribute significantly to hospital admissions. Prospective New Zealand data are scant, and the ability of clinical coding to identify ADE associated admissions is uncertain. Outcomes after cessation of causative medications are unknown. AIMS: To assess the frequency, nature and causality of ADE associated with acute admissions to General Medicine at Christchurch Hospital. METHODS: Prospective observational study of patients admitted to our medical team over 20 weeks. RESULTS: Of 336 admissions, 96 (28.6%) were ADE related. Sixty-five (19.3%) were caused by an ADE, and 31 (9.2%) were contributed to by an ADE. The mean age of non-ADE patients was 64.3 years (range 16-91), which was similar to the mean age of ADE patients (65.9 years; 21-92). However, if intentional overdoses and recreational drug use were excluded, ADE patients were significantly older at 72.4 years (21-92) (P = 0.0007). ADE patients took more regular medications on admission (mean 6.6, range 0-22) than non-ADE patients (mean 5.0, 0-18), (P = 0.003). The average length of stay was similar. The commonest medications implicated were vasodilators, psychotropics and diuretics. The most common adverse effects were postural hypotension and/or vasovagal syncope (29% of ADE), intentional overdoses and recreational drug use (15%) and acute renal failure and/or clinical dehydration (10%). Seventy-six patients had culprit medications stopped or reduced, and this potentially contributed to six readmissions. Coding identified 61% of ADE associated admissions. CONCLUSION: ADE are a common cause of hospital admission. The most frequent problems are postural hypotension and vasovagal syncope, intentional drug misuse and dehydration.

At the heart of the arterial baroreflex: a physiological basis for a new classification of carotid sinus hypersensitivity.

The aim of this review is to provide an update of the current knowledge of the physiological mechanisms underlying reflex syncope. Carotid sinus syncope will be used as the classical example of an autonomic reflex with relatively well-established afferent, central and efferent pathways. These pathways, as well as the pathophysiology of carotid sinus hypersensitivity (CSH) and the haemodynamic effects of cardiac standstill and vasodilatation will be discussed. We will demonstrate that continuous recordings of arterial pressure provide a better understanding of the cardiovascular mechanisms mediating arterial hypotension and cerebral hypoperfusion in patients with reflex syncope. Finally we will demonstrate that the current criteria to diagnose CSH are too lenient and that the conventional classification of carotid sinus syncope as cardioinhibitory, mixed and vasodepressor subtypes should be revised because isolated cardioinhibitory CSH (asystole without a fall in arterial pressure) does not occur. Instead, we suggest that all patients with CSH should be thought of as being 'mixed', between cardioinhibition and vasodepression. The proposed stricter set of criteria for CSH should be evaluated in future studies.

Polypharmacy--we make it worse! A cross-sectional study from an acute admissions unit.

Although polypharmacy is a major problem in the elderly, very few data have been published from Australasia. We retrospectively audited 68% of elderly patients admitted acutely to our medical unit (n= 424, mean age 80.3 ± 8 years) during a 30-day period (September, 2008). We found that long-term medications increased during hospital stay from 6.6 ± 4 to 7.7 ± 4 (P < 0.001). Adverse drug reactions were responsible for 24 admissions (5.7%). Polypharmacy is made worse by acute admission to hospital.

Prolonged post-faint hypotension can be reversed by dynamic tension.

A severe variant of vasovagal syncope, observed during tilt tests and blood donation has recently been termed "prolonged post-faint hypotension" (PPFH). A 49-year-old male with a life-long history of severe fainting attacks underwent head-up tilt for 20 min, and developed syncope 2 min after nitroglycerine spray. He was unconscious for 40 s and asystolic for 22 s. For the first 2 min of recovery, BP and HR remained low (65/45 mmHg and 40 beats/min) despite passive leg-raising. Blood pressure (and symptoms) only improved following active bilateral leg flexion and extension ("dynamic tension"). During PPFH, when vagal activity is extreme, patients may require central stimulation as well as correction of venous return.

Vagolysis.

We describe the case of a 75-year-old man presenting with labile hypertension and symptomatic postural hypotension 13 months following radiotherapy for squamous cell carcinoma of his external auditory canal. Magnetic resonance image (MRI) scan demonstrated scarring and a probable recurrence of his tumour. He underwent autonomic testing, including muscle sympathetic nerve activity (MSNA), heart rate (HR) and blood pressure (BP) responses to a variety of stimuli. Results were consistent with baroreflex failure. Urinary catecholamine levels were within the high normal range. We postulate that baroreflex failure was caused by vagal and glossopharyngeal nerve damage secondary to radiotherapy and tumour recurrence. This diagnosis is rare, but should be considered with pure autonomic failure and phaeochromocytoma in the presence of labile hypertension, especially in patients with a history of radiotherapy to the neck and high-normal catecholamine levels.

Tilt-test diagnosis of hypotensive transient ischaemic attacks.

Eight elderly patients with postural hypotension who presented with transient ischaemic attacks are reported. Six patients underwent head-up tilt testing with continuous blood pressure monitoring. During tilt, postural hypotension was found in five patients and in three patients transient ischaemic attacks were reproduced. Postural hypotension is probably a rare cause of transient ischaemic attacks, but may be underrecognized.

Adrenomedullin increases cardiac sympathetic nerve activity in normal conscious sheep.

The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.

Neurohormonal response to head-up tilt and its role in vasovagal syncope.

In a controlled study, 26 patients with a history of recurrent syncope were found to have increased arginine vasopressin, corticotrophin, and atrial natriuretic factor levels after 5 minutes of 60 degrees head-up tilt, long before they became hypotensive. The exaggerated neurohormonal response in these patients may indicate a greater sensitivity to central hypovolemia which may predispose to vasovagal syncope, mediated by the vasodilatory effects of atrial natriuretic factor or the sensitization of mechanoreceptors by arginine vasopressin.

Right atrial myxoma mistaken for recurrent pulmonary thromboembolism.

A 69 year old man was admitted for investigation of right sided pleuritic chest pain and dyspnoea, both of which began suddenly four days before admission. Acute pulmonary embolism was diagnosed. Six months after discharge while on warfarin he died. Necropsy found a 50 mm diameter myxoid tumour arising on the right atrial side of the interatrial septum. This lesion may have been discovered earlier by echocardiography although there were no clear indications for this investigation. Presentation was that of recurrent pulmonary embolism with no obvious source or cause of thrombosis. Patients who are thought to have idiopathic pulmonary embolism should undergo early echocardiography to exclude the rare but treatable diseases of the right heart that may be responsible.

Autonomic control of asystolic vasovagal syncope.

A 30 year old woman with a lifelong history of severe, recurrent, vasovagal syncope became asystolic for 30 seconds after 37 minutes of 60 degrees head-up tilt. During early tilt, sympathetic activity, heart rate, left ventricular contractility, and cardiac output increased. Mean blood pressure was initially maintained. Presyncope was associated with maximal contractility and bradycardia despite sustained sympathetic activity. Subsequently, asystole occurred associated with complete withdrawal of muscle nerve sympathetic activity. In asystolic vasovagal reactions, presyncope may be triggered by increased left ventricular contractility and is associated with increased levels of parasympathetic and sympathetic activity. Asystole and peripheral vasodilatation may be caused by sudden and complete withdrawal of the increased sympathetic activity.

Renal artery stenosis as a cause of heavy albuminuria.

We report three cases of heavy albuminuria occurring in hypertensive patients with unilateral or bilateral renal artery stenosis. In two of the patients the albuminuria and hypertension were corrected by removing the ischaemic kidney. The mechanism of the albuminuria, particularly in atheromatous renal artery stenosis, is probably multifactorial.

Vasovagal syncope: new physiologic insights.

This review deals with recent changes in understanding of physiologic mechanisms involved in vasovagal syncope. The approach is not comprehensive but attempts to integrate new findings with older studies. The major clinical presentations of the condition and recognized triggers are discussed first, followed by a summary of how new laboratory methods allow better understanding of the vasovagal reflex. A sequence of sympathohemodynamic events during tilt-induced syncope is suggested based on several different research approaches. The aim is to dissect out the different mechanisms for hypotension, then integrate current knowledge and clarify the sequence.

Sleep syncope: important clinical associations with phobia and vagotonia.

OBJECTIVES: To compare demographic and clinical data from patients with sleep syncope to those of patients with "classical" vasovagal syncope [VVS] collected over the last 8 years. DESIGN: Retrospective case-controlled study. SETTING: Syncope unit. PATIENTS AND METHODS: Fifty-four patients with a history suggestive of one or more episodes of sleep syncope (group SS) were matched for age and gender to 108 patients with VVS (control group). A syncope questionnaire was completed immediately before tilt-testing and included frequency, age-of-onset and severity of episodes; situations, postures and perceived triggers; lifetime prevalence of specific phobias; and symptoms during syncope. RESULTS: Group SS were mainly women (65%), mean age of 46±2.1 years, with a mean lifetime total of 5.4±0.83 episodes of sleep syncope. Compared to controls, SS episodes were more likely to start in childhood, 26.9% versus 50% (p=0.005), and more severe, score 2.40±0.11 versus 2.81±0.15 (p=0.03). In group SS: syncope onset whilst lying down was more frequent, 4.6% versus 32.7% (p=0.001); the lifelong prevalence of any specific phobia was higher, 32.4% versus 74.5% (p=0.001), in particular blood injection injury (BII) phobia, 19.4% versus 57.4% (p=0.001); and during attacks, distressing vagal symptoms were more frequent, e.g., abdominal discomfort, 13.9% versus 72.2% (p=0.001). CONCLUSION: Sleep syncope is not rare and is characterised by lifelong, intermittent but severe episodes of vasovagal syncope which may occur in the horizontal position, with distressing abdominal symptoms. BII phobia is strongly associated and may be a predisposing factor or a co-existent disorder in these patients.

The worm that turned.

When a patient presents with acute myelopathy in the developed world, helminthic infection is not routinely considered in the differential diagnosis. We report the case of a 34-year-old South African male who presented with acute urinary retention and lower leg paraesthesiae. Subsequently, myeloradiculopathy secondary to Schistosoma mansoni was diagnosed on the basis of typical magnetic resonance imaging changes in the conus medullaris and positive stool microscopy. Prior to this presentation the patient had lived in urban western South Africa and more recently in New Zealand, without exposure to infected water for 22 years. His symptoms and signs resolved following treatment with praziquantel and methylprednisolone. Spinal schistosomiasis is a rare but serious cause of myelopathy and should be considered in any patient who has ever visited or lived in an endemic area.

Cardiac sympathetic nerve activity and ventricular fibrillation during acute myocardial infarction in a conscious sheep model.

The association between cardiac sympathetic nerve activity (CSNA) and ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been assessed in conscious animal models. During the first 60 min post-MI, mean blood pressure (MBP), heart rate (HR), and CSNA were recorded continuously in 20 conscious sheep. Resistant sheep (group A, n = 10) were compared with susceptible sheep (group B, n = 10) who developed fatal VF (n = 7) or sustained ventricular tachycardia (VT, n = 3). The mean time to VF/VT was 28.1 +/- 3.3 min. In group B, MBP, HR, and CSNA were averaged at each consecutive minute from baseline at 14 min before the onset of VF/VT and compared with time-matched values in group A. When compared with those of group A, indexes of CSNA burst size increased before the onset of VF/VT: burst area/minute (F(13,208) = 2.17, P = 0.01) and burst area/100 beats (F(13,208) = 1.86, P = 0.04). By contrast, burst frequency indexes were not significantly different: burst frequency (F(13,208) = 1.6, P = 0.09) and burst incidence (F(13,208) = 1.48, P = 0.13). In group A, CSNA burst area/min and burst area/100 beats did not change across this time period (F(13,117) = 0.97, P = 0.5, F(13,117) = 0.96, P = 0.7) but increased with time in group B (F(13,91) = 2.3, P = 0.01; and F(13,91) = 2.25, P = 0.01). Between-group comparisons demonstrated no differences in time of onset of ventricular ectopic beats: 18.5 (range 12-24) in group A versus 15.0 min (range 7-22) in group B (Mann-Whitney U-test, P = 0.09). Pre-MI baroreflex slopes were similar: R-R slopes were 11.8 +/- 2 and 15.6 +/- 1.1 ms/mmHg (t(18) = -1.6, P = 0.14). CSNA slopes were -1.8 +/- 0.3 and -2.3 +/- 0.2%/mmHg (t(18) = -1.4, P = 0.2). An early increase in CSNA burst size indexes (before 60 min post-MI), mediated by an excitatory sympathetic reflex, is important in the genesis of VF/VT.

Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model.

The time course of cardiac sympathetic nerve activity (CSNA) following acute myocardial infarction (MI) is unknown. We therefore undertook serial direct recordings of CSNA, arterial blood pressure (MAP) and heart rate (HR) in 11 conscious sheep before and after MI, and compared them with 10 controls. Conscious CSNA recordings were taken daily from electrodes glued into the thoracic cardiac nerves. Infarction was induced under pethidine and diazepam analgesia by applying tension to a coronary suture. MI size was assessed by left ventricular planimetry (%) at postmortem, peak troponin T and brain natriuretic peptide levels (BNP). Baroreflex slopes were assessed daily using phenylephrine-nitroprusside ramps. The mean infarcted area was 14.4 +/- 2.9%, troponin T 1.88 +/- 0.39 microg l(-1) and BNP 8.4 +/- 1.3 pmol l(-1). There were no differences in haemodynamic parameters or CSNA between groups at baseline. MAP and HR remained constant following MI. CSNA burst frequency increased from baseline levels of 55.8 +/- 7.1 bursts min(-1) to levels of 77.5 +/- 8.7 bursts min(-1) at 2 h post-MI, and remained elevated for 2 days (P < 0.001). CSNA burst area also increased and was sustained for 7 days following MI (P= 0.016). Baroreflex slopes for pulse interval and CSNA did not change. CSNA increases within 1 h of the onset of MI and is sustained for at least 7 days. The duration of this response may be longer because the recording fields decrease with time. This result is consistent with a sustained cardiac excitatory sympathetic reflex.