medical digest vol 2 version 6

18
Doctors learn from many sources: teachers, patients and the printed word. I shall always be grateful to my teachers, all of whom taught for no or negligible personal gain. Many doctors are proud to talk about the lineage of illustrious doctors they came from, with the obvious implication that the superior knowledge from their forebears has been transmitted to them. Here, I shall recollect a few instances in which a few words led to big leaps in my understanding. When I was a student, I recall learning from Dr Chan Tiong Beng that chest movement is always diminished on the affected side. To me, this is a mind-boggling piece of knowledge. Up till then, everything in the chest examination seemed relative to me. For instance, if one side of the chest is more resonant than the other, I’m not sure if that side is hyper- resonant or the other is dull. With this information, I can be absolutely be sure which side is abnormal, and if that side is hyper-resonant, it’s a pneumothorax, if dull, collapse or consolidation and if stony dull, effusion. Later on, I learnt to appreciate signs such as Roth’s spots, the stooped posture of Parkinson’s disease and nail-fold erythema of dermatomyositis. Though most aspects of Medicine are relative, there are a few anchors here and there that keep us on the right track. I recall a talk by Dr Michael Iseman, world-renown TB expert from National Jewish Health. He was talking about finding viable mycobacteria in the tubercles of properly treated patients. “If someone is run down by a truck, and I ground all the tubercles in his lungs, I am sure I can find a few live bacteria”. I suddenly realize that’s how it is for chronic infectious diseases like tuberculosis, hepatitis B, melioidosis and a host of others. We prescribe long-term medications to these patients (being careful to fulfil the guidelines), hoping to choke the life out of these organisms. The bugs simply retreat to their lair, lying in wait for the chance to make a re-entry. To my student clinical group, an obstetrician declared, “If I know the foetal age, I know what to do.” The foetal age is crucial to know because it helps him decide if the baby remains in the womb when conditions turn hostile, or it can be safely delivered. In almost all branches of Medicine, there is one piece of information that is more important than others for patient management. It may be sugar control for the Diabetologist, disease activity for the Rheumatologist or urine flow rate for the Urologist. I shall keep my eyes and ears open because no one knows where the next pearl will come from. Medical digest Vol. 2 2014 From The Editor Dr Leong Khai Pang EDITOR Medical Digest Dr Chong Yaw Khian Ms Angie Theonis S.H. Low

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Page 1: Medical Digest vol 2 version 6

Doctors learn from many sources: teachers, patients and the printed word. I shall always be grateful to my teachers, all of whom taught for no or negligible personal gain. Many doctors are proud to talk about the lineage of illustrious doctors they came from, with the obvious implication that the superior knowledge from their forebears has been transmitted to them. Here, I shall recollect a few instances in which a few words led to big leaps in my understanding.

When I was a student, I recall learning from Dr Chan Tiong Beng that chest movement is always diminished on the affected side. To me, this is a mind-boggling piece of knowledge. Up till then, everything in the chest examination seemed relative to me. For instance, if one side of the chest is more resonant than the other, I’m not sure if that side is hyper-resonant or the other is dull. With this information, I can be absolutely be sure which side is abnormal, and if that side is hyper-resonant, it’s a pneumothorax, if dull, collapse or consolidation and if stony dull, effusion. Later on, I learnt to appreciate signs such as Roth’s spots, the stooped posture of Parkinson’s disease and nail-fold erythema of dermatomyositis. Though most aspects of Medicine are relative, there are a few anchors here and there that keep us on the right track.

I recall a talk by Dr Michael Iseman, world-renown TB expert from National Jewish Health. He was talking about finding viable mycobacteria in the tubercles of properly treated patients. “If someone is run down by a truck, and I ground all the tubercles in his lungs, I am sure I can find a few live bacteria”. I suddenly realize that’s how it is for chronic infectious diseases like tuberculosis, hepatitis B, melioidosis and a host of others. We prescribe long-term medications to these patients (being careful to fulfil the guidelines), hoping to choke the life out of these organisms. The bugs simply retreat to their lair, lying in wait for the chance to make a re-entry.

To my student clinical group, an obstetrician declared, “If I know the foetal age, I know what to do.” The foetal age is crucial to know because it helps him decide if the baby remains in the womb when conditions turn hostile, or it can be safely delivered. In almost all branches of Medicine, there is one piece of information that is more important than others for patient management. It may be sugar control for the Diabetologist, disease activity for the Rheumatologist or urine flow rate for the Urologist.

I shall keep my eyes and ears open because no one knows where the next pearl will come from.

MedicaldigestVol. 2 2014

From The Editor

Dr Leong Khai PangEDITOR

Medical Digest

Dr Chong Yaw Khian

Ms Angie Theonis

S.H. Low

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Clinical Practice

CASE VIGNETTE Mr Tan is a 65-year-old Chinese male with type 2 diabetes, hypertension and anterior myocardial infarction two years ago. He presents to the emergency department with acute breathlessness and lower limb swelling. He had been non-compliant with his blood pressure medications. How would you approach this problem?

INTRODUCTIONHeart failure (HF) is a rapidly growing clinical problem that affects up to 10% of the population above 70 years of age. It is associated with significant mortality and morbidity. Many patients have recurrent hospitalization and poor quality of life. It presents to clinicians across many specialties, requiring any practicing clinician to have a clear understanding and approach to managing patients presenting with this multi-systemic clinical problem.

HF can be defined patho-physiologically as an abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolizing tissues, despite normal filling pressures (or only at the expense of increased filling pressures).1 HF is a syndrome in which patients have a constellation of typical symptoms (for example, reduced effort tolerance, breathlessness and ankle swelling) and signs (such as elevated jugular venous pressure, pulmonary crackles, and third heart sound) resulting from an abnormality of cardiac structure or function.

The top three causes of HF are coronary artery disease (60-70%), hypertension and valvular heart disease. Table 1 shows the other common ones.

CLASSIFICATION OF HEART FAILUREHF can be classified in a number of ways. For example, it may be categoried according to aetiology, or by the dominant type of left ventricular dysfunction – systolic HF versus HF with preserved ejection fraction. The

New York Heart Association (NYHA) Classification separates the patients according to symptom severity (table 2). The American College of Cardiology (ACC) and American Heart Association (AHA) document the stage of HF.

A CLINICAL APPROACH TO HEART FAILUREThe most sensitive symptom of HF is reduced effort tolerance and the most specific symptom is paroxysmal nocturnal dyspnea. The other common symptoms of HF are due to volume overload (dyspnea at rest or on exertion, orthopnoea, bilateral lower limb oedema, ascites and scrotal oedema) and decreased cardiac output (easy fatigability, giddiness and decrease in exercise capacity).

For a patient with HF, a search for the underlying cause is important. For example, the patient may have a history of hypertension, valvular heart

disease, ischaemic heart disease (IHD), previous revascularization procedures (percutaneous coronary intervention or coronary artery bypass grafting), other cardiovascular risk factors (diabetes mellitus, dyslipidaemia, and chronic smoking), alcohol use, family history of IHD or cardiomyopathy, and endocrine diseases like thyrotoxicosis which can result in tachycardia-induced cardiomyopathy.

A methodical search for the precipitating factors may give us the reason for the patient’s hospital admission. Failure to address this is often the reason for patient’s re-hospitalizations. The most common causes are non-compliance to medications or salt and fluid restriction, acute coronary syndrome, new-onset cardiac arrhythmia like atrial fibrillation with rapid ventricular response, and sepsis.

Important signs in physical

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An Approach to Heart Failure

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examination can be divided into three mains groups: those related to decreased cardiac output; those of volume overload; and signs specific to a cardiac pathology.

Signs indicative of decreased cardiac output include hypotension, tachycardia at rest, cool peripheries due to peripheral vasoconstriction and a narrow pulse pressure below 25 mmHg. Signs of volume overload include peripheral oedema especially of the lower extremities, ascites, raised jugular venous pressure (JVP), lung crepitations (typically bilateral basal crepitations), hepatojugular reflux and occasionally generalized oedema or anasarca. Signs specific to a cardiac pathology include a third heart sound (this is the most specific sign of HF), pulsus alternans (defined as peripheral pulses alternating between strong and weak beats), laterally displaced apex beat and a cardiac murmur.

Investigations are ordered to confirm the diagnosis and rule out the

differential diagnoses, to assess severity and complications of HF, and to determine the underlying aetiology (table 4). Demonstration of an underlying cardiac cause is central to the diagnosis of HF and is also important for therapy as the precise pathology determines the specific treatment (eg. surgery for valvular disease and revascularization for IHD).

The treatment of HF consists of managing the acute HF, correction of precipitating factors, treatment of underlying cause, and optimising long-term HF therapy.

The management of acute HF consists of correction of hypoxemia using supplemental oxygen as required, titrated to patient comfort and an oxygen saturation of at least 90%. Non-invasive ventilation or endotracheal intubation for conventional mechanical ventilation (if the patient fails or has contraindications to non-invasive ventilation) may be necessary if

supplemental oxygen therapy is inadequate. Fluid management is also essential for acute HF: low salt diet, fluid restriction and diuresis. Intravenous frusemide bolus dosing usually achieves adequate diuresis in most patients; dosing is individualised and determined largely by renal function and prior diuretic exposure. Vasodilators should be used in hemodynamically stable patients as they reduce filling pressures, improve symptoms and facilitate diuresis. In some cases, patients who are hypotensive and have compromised vital organ perfusion require inotropic support and/or mechanical cardiac support, such as via an intra-aortic balloon counterpulsation.

It is important to identify and correct precipitating factors. Table 5 summarises the common precipitating factors of HF.

After an underlying cause of HF is found, an important area of management consists of treatment of the underlying cause. This may include coronary revascularisation (percutaneous coronary intervention or coronary artery bypass grafting) in ischemic cardiomyopathy, valve repair/replacement in valvular heart disease and optimisation of blood pressure control in hypertensive heart disease.

Medications used for the management of chronic HF include neurohormonal blockers like angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), beta-blockers, aldosterone antagonists (spironolactone or eplerenone), ivabradine and other medications that reduce the morbidity of HF as diuretics and digoxin (table 6).

In patients with end-stage HF who failed medical therapy, consideration should be given for cardiac resynchronization therapy (CRT) or left ventricular assist device (LVAD) as a bridge to cardiac transplantation or as destination therapy and referral to the palliative team for end-of-life care and support.

In summary, an approach to a patient with suspected HF involves the following:1. confirmation of the diagnosis of

HF and exclusion of differentials;

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Types of test Specific investigation Reason

Hematological Full blood count To detect anaemia, which may be an alternative cause of the patient’s symptoms or the reason for the exacerbation of HF. It is also a bad prognostic marker in patients with chronic HF.

B-type natriuretic peptide (BNP) A hormone that is secreted in increased amounts when heart contractility is diseased or the load on any chamber is increased (for example, by AF or pulmonary embolism). A normal BNP level (<100pg/ml) in an untreated patient presenting with acute onset or worsening of symptoms virtually excludes significant cardiac disease, making an echocardiogram unnecessary. It is elevated in some non-cardiovascular conditions eg. renal failure and may be reduced in obese patients.

Blood chemistry including serum These allow evaluation of other causes of sodium, potassium, calcium, urea, volume overload, assessment of patient creatinine (and estimated glomerular suitability for diuretic, renin–angiotensin– filtration rate), liver enzymes and aldosterone antagonist, and anticoagulant bilirubin, thyroid function and therapy, detection of reversible or treatable ferritin/TIBC causes of HF (such as hypocalcaemia and thyroid

dysfunction) and co-morbidities such as iron deficiency anaemia.

Radiological Chest X-ray The radiological features of pulmonary alveolar edema can be remembered through an acronym ABCDE (alveolar oedema, Kerley B lines, cardiomegaly, upper lobe diversion and pleural effusion). It also aids in the diagnosis of pulmonary tuberculosis, malignancy and obstructive airway diseases as other potential causes of breathlessness.

Cardiovascular Electrocardiogram (ECG) The ECG is the most useful and inexpensive tool in the evaluation of patients with suspected HF. It aids in the diagnosis of the underlying aetiology of HF (Q waves of myocardial infarction or hypertrophic cardiomyopathy, low QRS voltages of amyloidosis, large QRS voltages of hypertensive heart disease and atrial fibrillation due to mitral stenosis) and helps in planning advanced therapy (eg electrical and mechanical dyssynchrony for biventricular pacemaker implantation).

Transthoracic echocardiogram This is an important investigation in HF as it can gives important information about the ejection fraction, chamber size, LV systolic or diastolic dysfunction, valve abnormalities, cardiac output and regional wall motion abnormalities. This will aid in the diagnosis of HF, assessing the severity and prognosis of HF, assist in planning and monitoring of treatment, and to obtain prognostic information.

Coronary angiography Recommended in patients with angina pectoris, who are considered suitable for coronary revascularization, to evaluate the coronary anatomy.

Myocardial perfusion/ischemia These should be considered in patients thought imaging (stress echocardiography, to have CAD, and who are considered suitable for myocardial perfusion imaging, coronary revascularization, to determine whether cardiac magnetic resonance imaging) there is reversible myocardial ischemia and viable

myocardium.

investigations

investigations

investigations

Table 4. Investigations in heart failure.

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2. evaluation and treatment of the underlying cause;

3. evaluation and treatment of the precipitating factors;

4. optimization of the long-term HF medications;

5. patient education; and6. enrolment of patient into a HF

Program (such as the one available in Tan Tock Seng Hospital).

Returning to the case vignette, Mr Tan was diagnosed to have acute decompensated HF precipitated by a hypertensive emergency. The acute HF was rapidly reversed with IV diuretics, supplemental oxygen therapy and IV glyceral trinitrate (GTN) infusion. The poorly controlled hypertension was managed with ACE-inhibitors and beta-blocker therapy and cardiac evaluation

Drugs which improve morbidity

Diuretics Diuretics are used in patients who have evidence of salt and fluid retention to improve symptoms, especially in patients with problems restricting their salt intake. Loop diuretics have emerged as the preferred diuretic agents for use in most patients with HF. Thiazide diuretics may be considered in hypertensive patients with HF and mild fluid retention because they confer more persistent antihypertensive effects.

Digoxin In patients with frequent re-hospitalizations, digoxin can be used to decrease hospitalisations for HF.2

ACE inhibitors ACE inhibitors are recommended in all patients with prior or current symptoms as they reduce mortality3; ARBs are recommended in patients who are ACE inhibitor intolerant.4

Beta blockers Beta blockers are recommended for all patients with prior or current symptoms.5

Ivabradine Ivabradine is a drug that inhibits the If channel in the sinus node to reduce the heart rate of patients in sinus rhythm. It has recently been approved to be used in HF patients in NYHA functional class II–IV, sinus rhythm with a rate of ≥70 bpm, and an EF ≤35% already optimized with ACE inhibitors, beta-blockers and aldosterone antagonists.

Drugs which improve mortality

ACE inhibitors As above

Beta blockers As above

Aldosterone Aldosterone antagonists: can be added to ACE inhibitor/ARB and beta blocker for NYHA functional class II-IV symptoms and an EF ≤30% (≤35% if the QRS duration was >130 ms), provided CrCl >30ml/min and K <5.0mmol/L.6

Ivabradine It was shown in the SHIFT (Systolic Heart failure treatment with the If inhibitor ivabradine Trial) to reduce the primary composite outcome of cardiovascular death or HF hospitalization was 18% (P <0.0001).7

Combination of Hydralazine/nitrate combination can be used for patients self-described as African Americans with NYHA class III–IV HF receiving optimal therapy with ACE inhibitors and beta blockers.8 This combination can also be used in patients with prior or current symptoms who cannot be given an ACE-inhibitor or ARB because of drug intolerance, hypotension or renal insufficiency.

or ARBs

(only bisoprolol, carvedilol, metoprolol)

antagonists (spironolactone or eplerenone)

hydralazine and nitrate (for patients in which ACE-I or ARBs are contraindicated)

or ARBs

(only bisoprolol, carvedilol or metoprolol)

Table 6. Drug treatment of heart failure.

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revealed triple vessel coronary artery disease resulting in severe underlying ischemic cardiomyopathy (LV ejection fraction 30%). He underwent a CABG and was put on long-term HF medications that include ACE-inhibitor (lisinopril 10 mg daily), beta-blocker (bisoprolol 2.5mg daily), aldosterone antagonist (spironolactone 25mg daily), diuretic (frusemide 40mg daily) in addition to anti-platelet (aspirin 100mg daily) and HMG-CoA reductase inhibitor (atorvastatin 40mg nightly) therapy. A repeat transthoracic echocardiogram six months post-CABG revealed a significant

improvement in LV systolic function, to 50%. He was enrolled into the TTSH HF program and is currently well (NYHA class I-II), requiring no repeat hospitalization.

PRACTICAL TIPS FOR MANAGING HEART FAILURE1) The most sensitive symptom of

HF is reduced effort tolerance whilst the most specific symptom is paroxysmal nocturnal dyspnea.

2) The most specific signs that point to a cardiac pathology in a patient with fluid overload are the presence of the third heart sound (the most specific sign of

HF), pulsus alternans, laterally displaced apex beat and a cardiac murmur.

3) Heart failure is a clinical diagnosis. BNP is not needed in the diagnosis of heart failure, but can be useful if the underlying cause of fluid overload is difficult to ascertain. A normal BNP level (<100pg/ml) in an untreated patient presenting with acute onset or worsening of symptoms virtually excludes significant cardiac disease, making an echocardiogram unnecessary.

4) Always remember to look for an underlying cause or precipitant of heart failure.

Mr Jeremy Hoe (left) and Sim Wemyuan (middle) are medical students from the Yong Yoo Lin School of Medicine. Dr Ooi Yau Wei is a consultant in the Department of Cardiology, Tan Tock Seng Hospital.

References

1) Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA, Stromberg A, van Veldhuisen DJ, Atar D, Hoes AW, Keren A, Mebazaa A, Nieminen M, Priori SG, Swedberg K. ESC guidelines for the diagnosis and treatment of acute and chronic HF 2008: the Task Force for the diagnosis and treatment of acute and chronic HF 2008 of the European Society of Cardiology. Developed in collaboration with the HF Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur J Heart Fail 2008; 10:933–89.

2) The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with HF. N Engl J Med 1997; 336:525–33.3) The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive HF. Results of the Cooperative North Scandinavian Enalapril

Survival Study (CONSENSUS). N Engl J Med 1987; 316:1429–35.4) Maggioni AP, Anand I, Gottlieb SO, Latini R, Tognoni G, Cohn JN. Effects of valsartan on morbidity and mortality in patients with HF not receiving

angiotensin-converting enzyme inhibitors. J Am Coll Cardiol 2002; 40:1414–21.5) The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial. Lancet 1999; 353:9–13.6) Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H, Vincent J, Pocock SJ, Pitt B. Eplerenone in patients with systolic HF and mild

symptoms. N Engl J Med 2011; 364:11–21.7) Swedberg K, Komajda M, Bohm M, Borer JS, Ford I, Dubost-Brama A, Lerebours G, Tavazzi L. Ivabradine and outcomes in chronic heart failure (SHIFT):

a randomised placebo-controlled study. Lancet 2010; 376:875–85.8) Cohn JN, Archibald DG, Ziesche S, Franciosa JA, Harston WE, Tristani FE, Dunkman WB, JacobsW, Francis GS, Flohr KH, for the Veterans Administration

Cooperative Study Group. Effect of vasodilator therapy on mortality in chronic congestive HF. Results of a Veterans Administration Cooperative Study. N Engl J Med 1986; 314:1547–52.

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Review

Metabolic Evaluation of Urinary StonesWhat can we do for a patient who been diagnosed with urinary stones?

Mark was sleeping when he had a sudden bout of severe pain in his left back. He was found to have a stone in his kidney and underwent shockwave lithotripsy which resolved the problem.

Urinary stone disease is relatively common and affects 15% of the population, with a slowly increasing trend likely due to increasing rates of diabetes and obesity. Even after treatment, there is a 25 to 50% chance of recurrence in five years. Thus, in many cases, urinary stone disease is a chronic condition, especially if a patient has risk factors of stone recurrence.

So what can be done to prevent a repeat episode?

EVALUATIONPatients with urinary stone disease should be carefully assessed. The baseline evaluation includes blood

tests to determine uric acid and calcium concentrations and kidney function. In patients with a high risk of recurrence (table 1) a 24-hour urine test should be ordered. In Tan Tock Seng Hospital, we found that up to 95% of patients at high risk of stone formation have abnormalities in the 24-hour urine analysis. Correction of these abnormal urine parameters can significantly reduce the recurrence of stones.

An added benefit of these metabolic evaluations is that underlying systemic diseases that manifest as stone diseases can be picked up, including hyperparathyroidism, renal tubular acidosis and hyperoxaluria.

MANAGEMENT STRATEGIESDietary managementThere are a number of dietary interventions that can be applied to reduce stone recurrence.

Basic dietary managementFirst and foremost, patients with stone disease should be encouraged to drink more fluid with a goal of producing at least 2 litres of urine a day unless contraindicated. A study by Borghi et al found that increasing fluid intake would half the risk of recurrent stone disease.1

Lemonade and orange juice should be encouraged as the citrate in these juices help to reduce stone recurrence. The citrate alkalizes urine and stops stone precipitation. Soft drinks should be avoided as they have been shown to be associated with increased stone episodes.2

Patients should also be on a salt-restricted diet. They should aim to consume not more than 3 gm per day which is equivalent to half a teaspoon of salt. This helps reduce urinary calcium excretion, which could precipitate as stones in the urinary system. Animal proteins can raise the uric acid concentration in

Onset of disease below 25 years of age

Multiple stones in kidney

Calcium phosphate stone

Solitary kidney

Presence of remnant stones

Previous history of stones

Previous weight loss surgery

Family history of stones

Table 1. Risk factors for recurrent urinary stone disease.

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the blood (via purine metabolism) and acidify the urine, which together can increase the incidence of calcium oxalate and uric acid stones. Animal proteins intake should be restricted to not more that 0.8 to 1 gm/kg body weight per day. For example, an egg contains 7 gm, a fillet of salmon 22 gm, and 100 gm of chicken is equivalent to 26 gm of protein. In a recent study it was found that fish and chicken actually caused as much uric acid issues as beef.3

Fibre and vegetables should be encouraged as thy raise pH and reduce incidence of stones by keeping the stones in their soluble state.

I am often asked about the effects of supplements and calcium on stone formation. Vitamin C consumption should be limited to 500 mg per day and unless otherwise specified. High doses of 1gm or more are associated with increased calcium oxalate stone formation as the excess ascorbic acid is converted to oxalate.4 An adequate calcium intake of 800 mg per day should be adhered to.5 When taken with high oxalate foods, calcium binds oxalate in the gut and prevents its absorption; so a low calcium diet could lead to excessive absorption of oxalate and subsequently increasing the incidence of calcium oxalate stones. I have advised patients to take a 300-mg tablet of calcium together with high-oxalate meals

to try and ameliorate the effects of oxalate.

I have also been asked about certain diets and their effects on stone disease. The Atkins diet and ketogenic diets are more likely to cause stones whereas the DASH and vegetarian diets tend to reduce stone formation.

Directed dietary managementWith a proper dietary history and 24-hour urine test, we can tailor the dietary management to correct the abnormalities found in the urine test. These interventions may include reducing oxalate, raising citrate and reducing urate in the diet.

I do not routinely ask patients to take a low-oxalate diet unless the history is suggestive of excessive oxalate intake. This is because oxalate is found in many vegetables that have beneficial effects for prevention of stone formation and cardiovascular health. If I have to restrict oxalate, I will just target the main culprit (this is often spinach).

MedicationsIn situations where there are significant abnormalities in the 24-hour urinalysis that cannot be corrected by diet alone, medications can be started to help correct the abnormalities. These include potassium citrate, thiazide diuretics and allopurinol depending on the

abnormalities.

For Mark, he was also noted to have bilateral small stones and on his 24-hour urinalysis showed citrate deficit. As it was mild, apart from basic dietary advice, he was advised to increase his intake of citrate in the form of orange juice and lemonade. A repeat 24-hour urinalysis showed that this corrected his citrate deficit and five years on he has not had a recurrence of stone disease.

CONCLUSIONUrinary stone disease can be a chronic condition. Recurrent stone disease can be prevented if an appropriate approach is taken.

References

1. Borghi L, Meschi T, Amato F, Briganti A, Novarini A, Giannini A. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol 1996; 155:839-43.

2. Shuster J, Jenkins A, Logan C, Barnett T, Riehle R, Zackson D, et al. Soft drink consumption and urinary stone recurrence: a randomized prevention trial. J Clin Epidemiol 1992; 45:911-6.

3. Tracy CR, Best S, Bagrodia A, Poindexter JR, Adams-Huet B, Sakhaee K, et al. Animal Protein and the Risk of Kidney Stones: A Comparative Metabolic Study of Animal Protein Sources. J Urol 2014 Feb 8. pii: S0022-5347(14)00132-3. doi: 10.1016/j.juro.2014.01.093. [Epub ahead of print]

4. Thomas LD, Elinder CG, Tiselius HG, Wolk A, Akesson A. Ascorbic acid supplements and kidney stone incidence among men: a prospective study. JAMA Intern Med 2013; 173:386-8.

5. Candelas G, Martinez-Lopez JA, Rosario MP, Carmona L, Loza E. Calcium supplementation and kidney stone risk in osteoporosis: a systematic literature review. Clin Exp Rheumatol 2012; 30:954-61.

Dr Tan Yung Khan is a consultant in the Department of Urology, Tan Tock Seng Hospital.

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Early management of any arthritic joint involves rest and analgesia. This reduces the inflammation and pain that is crippling the patient.

As we are constantly utilizing our hands to interact with our environment, it is a challenge to convince the patient of the need to rest. The hand therapist is helpful in reinforcing this non-invasive form of management. The therapist may apply a splint to immobilize the affected joint, with subsequent patient education on activity modification to reduce the frequency of flare-ups.

Another modality of treatment often employed is intra-articular steroid injection. The patient usually starts to feel the effect of the injection a week later, offering pain relief that lasts about three months. The injection can be repeated. Although side effects are rare and the amount of steroid used is small, there is a very small risk of septic arthritis.

THE ROLE OF SMALL JOINT ARTHROPLASTYFor patients with intractable pain despite other forms of treatment, surgery can be offered. Traditionally, fusion has provided reliable pain relief for these patients, at the expense of joint mobility. An alternative in the recent years is finger joint replacement.

Joint replacement surgery involves replacing a damaged or destroyed joint with an artificial one. Although replacement surgery for joints in the fingers has existed for more than half a century, it has not really been mainstream surgery like knee and hip arthroplasty. With advancing knowledge of finger joint

biomechanics and newer technology, this form of treatment for trauma, osteoarthritis and rheumatoid arthritis is becoming commoner in the world of hand surgery.

The complex anatomy of the finger, with the delicate balance of the extensor and flexor tendons working in combination with the supporting ligaments of each joint, means that good soft tissue and bone stock must be present before a finger joint replacement is considered.

Current indications for implant joint replacement include rheumatoid arthritis, osteoarthritis and post-traumatic arthritis. The aims of joint replacement are to correct deformity, reduce pain and maintain some range of motion for the joint. Arthrodesis or fusion of the joint has been reliable in removing the pain element from arthritic finger joints, but it sacrifices

the motion completely.

OUTCOMES AND COMPLICATIONSLigament insufficiency, poor extensor or flexor tendon, septic arthritis, poor bone stock, gout, and continued manual labour are some of the contraindications for joint replacement. At present, there is little information about the longevity of the implants, but Murray and colleagues looked at their institution’s results over a 30-year period and found a cumulative implant failure incidence of of 3% at one year, 8% at three years, 11% at 5 years, and 16% at fifteen through twenty-five years.1

Three main types of replacement arthroplasty are used in the digits: titanium-polyethlene, pyrocarbon and silicone spacers. Silicone spacers (figure 1) have been used for the last half-century and are the

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Medical Advance

Small Joint Arthroplasty – Advances in Joint Replacement in the FingersDeformity, pain, instability. These are the issues faced by patients with small joint arthritis in the hand. Our fingers and hands are generally taken for granted until pain, instability or deformity limit our daily activities, which can be simple acts such as driving, typing or even holding a pen. The symptoms can result from trauma or from degenerative or inflammatory arthritides.

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gold standard against which newer finger joint implants are compared, in terms of functional performance, revision rate and long term outcomes. Pyrocarbon (figure 2) is an inert

biomaterial with an elastic modulus similar to that of cortical bone that theoretically decreases implant-bone stress transfer. The implant is “press-fit” and osseointegration does not

occur. This differs from the titanium implants where osteointegration can occur. The titanium-polyethylene implants most closely resemble the knee implants commonly used (figure 3).

In a prospective, randomized, multi-centered trial conducted by Daecke et al., the three types of implants were compared. At mean final follow-up of 35 months, all implant types led to significant pain reduction at rest and at load, and with improved tip pinch strength. There were no significant improvements in range of motion for all three types of implants, though the titanium-polyethylene and pyrocarbon types showed superior joint mobility temporarily. However the explantation of implant was higher for the titanium-polyethlene (27%) and pyrocarbon types (39%) compared to the silicone type (11%).2

Complications of silicone spacers include implant fracture and silicone synovitis. Implant fracture usually requires revision surgery, unless the joint remains functional and pain-free. The latter also does not always require revision surgery. Septic loosening of implant has been reported to occur in 10% for the titanium-polyethylene type, and 12.5% for the pyrocarbon type of implants.Error! Reference source not found. They have been reported to be as high as 40% in radiological images, but this does not correlate to the patient’s outcome, function and need for revision surgery.Error! Reference source not found. Migration of the implant stem can lead to perforation through the cortex and usually requires additional surgery. Implant breakage has been known to happen to the stems of the pyrocarbon and titanium-polyethylene implants, though these are quite rare. Squeaking of the replaced pyrocarbon joint has been reported though this has no effect upon the function of the digit.

In the rheumatoid patients, silicone spacers are the preferred choice of implants as the patients are generally of lower demand in their activities of daily living. Pyrocarbon and titanium-polyethylene implants can also be utilized for them, though cost can become an issue when multiple joints in the hand require replacing. Of critical importance for the rheumatoid patients is the soft tissue balancing

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Figure 4. (A and B) AP and lateral X-rays of the left index finger showing a fracture of the proximal interphalangeal joint. (C) Pre-operative

photograph of the index finger showing loss of flexion of the proximal interphalangeal joint. (D) Volar approach to the proximal interphalangeal

joint. (E and F) Photographs showing recovery of good function of the left index finger. (G and H) X-ray of the finger with implant in situ.

during surgery to improve the cosmesis and function of the hand. The total range of motion is usually not changed, but the arc of motion is modified to be more functional.

CASE EXAMPLEA 41-year-old gentleman presented to our clinic with a neglected left index finger proximal interphalangeal joint (PIPJ) injury from a basketball game, sustained 3 months prior to consultation. X-rays (figures 4A and 4B) showed a healed pilon type fracture at the PIPJ with associated osteoarthritis. He had no motion in that joint (figure 4C). He was counseled for joint replacement of the affected joint. We used a volar approach to access the deranged PIPJ, which was excised (Fig 4D). A titanium-polyethylene implant

was “press-fit” into the phalanges. At two months he was achieving a very functional range of motion with therapy (figures 4E and 4F). X-rays at 6 months showed no subsidence or migration (figures 4G and 4H).

CONCLUSIONFinger joint replacement, regardless of the type of implant, has consistently shown to improve the pain and, to a certain extent, the grip strength of the patient, with little change in the range of motion. The alternative for these patients is joint fusion that sacrifices motion for a painless joint. Patients with post-traumatic, degenerative and inflammatory arthritides suffering from intractable pain, deformity or instability should benefit from early referral to a Hand Surgeon to assess if they are suitable for joint replacement

in the hand.

References

1. Murray PM, Linscheid RL, Cooney WP 3rd, Baker V, Heckman MG. Long-term outcomes of proximal interphalangeal joint surface replacement arthroplasty. J Bone Joint Surg Am 2012; 94:1120-8.

2. Daecke W, Kaszap B, Martini AK, Hagena FW, Rieck B, Jung M. A prospective, randomized comparison of 3 types of proximal interphalangeal joint arthroplasty. J Hand Surg Am 2012; 37:1770-9.

3. Adams J, Ryall C, Pandyan A, Metcalf C, Stokes M, Bradley S, Warwick DJ. Proximal interphalangeal joint replacement in patients with arthritis of the hand: a meta-analysis. J Bone Joint Surg Br 2012; 94:1305-12.

4. McGuire DT1, White CD, Carter SL, Solomons MW. Pyrocarbon proximal interphalangeal joint arthroplasty: outcomes of a cohort study. J Hand Surg Eur Vol 2012; 37:490-6.

Dr Yeo Chong Jin, consultant, is the Head of the Hand & Microsurgery Section, Department of Orthopaedic Surgery, Tan Tock Seng Hospital.

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Drug Subsidies and Financing Schemes in SingaporeThe established and better-known means of financing drug therapy are the 3Ms – Medisave, MediShield and Medifund - and subsidies for drugs found in the Ministry of Health Standard Drug List. In recent years, schemes such as Medication Assistance Fund (MAF), Community Health Assist Scheme (CHAS) and Pioneer Generation (PG) package have been introduced. This article serves to round up the available subsidies and schemes and provides a quick update on the newer schemes and how patients can benefit from them.

MEDISAVEMedisave was introduced in April 1984 and is a medical savings scheme. Working individuals put aside 7% to 9.5% of their monthly salaries into their personal Medisave accounts (depending on their age group), which reside with the Central Provident Fund (CPF) Board. These savings can be used to pay for their personal or immediate family’s hospitalization, day surgery and selected outpatient expenses.

Table 1 summarises the drug treatments which are eligible for Medisave claims as well as the corresponding withdrawal limits.

The charges for inpatient drug treatments are incorporated into the total bill for the hospital stay, which is entitled to Medisave claim but subject to a withdrawal limit of $450 per day for daily hospital charges.

MEDISHIELDMediShield is a low-cost basic medical insurance scheme designed to help pay part of the expenses arising from the insured’s hospitalisations and certain outpatient treatments for serious illnesses at approved medical institutions. Introduced in 1990, it mainly serves to relieve large hospitalisation bills incurred in Class B2 or C wards, which cannot be sufficiently covered by Medisave balances. Premiums for MediShield can be paid for via Medisave. For patients who are more inclined to be admitted to Class B1 and higher ward classes or go to a private hospital, it is advisable to top up with another Medisave-approved private Integrated Shield Plan for a wider range of coverage.

The charges for inpatient drug

treatments are incorporated into the total bill for the hospital stay and coverage is not tagged to individual drugs. The deductible ($1500 to $3000) and co-insurance (10% to 20%) amounts will vary with the age of the insured and the bill size. For outpatient treatment, certain drug therapies are covered by MediShield and they are listed in Table 2.

MEDIFUNDMedifund is an endowment fund set up in April 1993 to help needy Singaporeans who are unable to pay for their medical expenses. It acts as a safety net for those who cannot afford the subsidized bill charges, despite Medisave and MediShield coverage.

To qualify for Medifund assistance, a person must fulfil all of the following criteria:1. is a Singapore citizen,2. is a subsidized patient,3. has received treatment from a

Medifund-approved institution,4. patient and family have difficulties

affording the medical bill despite heavy government subsidies, MediShield and Medisave.

Patients who fulfil these criteria or their doctors may approach the medical social workers (MSWs) of the Medifund-approved institution to apply for Medifund assistance. The actual amount of assistance provided will depend on the patient’s financial and social circumstances, as well as the size of the medical bill incurred. One hundred percent coverage of drug treatment costs is possible.

STANDARD DRUG LIST (SDL)The SDL was established by the Ministry of Health (MOH) in 1979

to ensure that essential drugs are available in public healthcare institutions at affordable prices. It is defined as a list of clinically relevant and cost-effective drugs considered as basic therapies that are essential for the management of common diseases afflicting the majority of the Singapore population.

The SDL is divided into SDL 1 and SDL 2. SDL 1 drugs are considered as essential and cost-effective first-line drugs required by many patients. SDL 2 category was introduced in 1992 with the initial aim to make some expensive first-line anti-cancer drugs partially subsidized by the government. In subsequent years, other expensive drugs for various medical conditions have been included. For any drug to be included into the SDL, it has to be recommended by the Drug Advisory Committee (DAC) based on cost-effectiveness analyses and approved by the MOH.

At polyclinics and restructured hospitals, subsidized class Singaporeans are charged the cost of the drug or $1.40 per item per week ($2.10 for permanent residents), whichever is lower. SDL 2 drugs are charged at 50% of cost (75% for permanent residents). The updated list can be viewed in the MOH website (Ministry of Health > Costs and Financing > Schemes & Subsidies > Drug Subsidies).

MEDICATION ASSISTANCE FUND (MAF)The MAF is a means-tested financial scheme which helps lower-to-middle-income patients who do not qualify for Medifund and have difficulty affording the costs of selected high-cost drugs.

Pharmaceutical Update

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Withdrawal limitsTypes of outpatient treatment

Approved vaccinations:1) Pneumococcal vaccinations for children under the age of 5 years

(for vaccinations received on or after 1 Nov 2009); Pneumococcal vaccinations for children under the age of 6 years (for vaccinations received on or after 1 Jan 2012)

2) Hepatitis B vaccination (for vaccinations received on or after 1 Nov 2009)

3) HPV vaccinations for females aged 9 to 26 years (for vaccinations received on or after 1 Nov 2010)

4) Measles, Mumps and Rubella (MMR), Tuberculosis (BCG), Diptheria, Pertussis & Tetanus (DTaP/Tdap), Poliomyelitis, Haemophilus Influenza Type B (Hib) (for vaccinations received on or after 1 June 2013)

5) Influenza and pneumococcal vaccinations for persons with higher risk of developing influenza-related complications and severe pneumococcal disease respectively (for vaccinations received on or after 1 Jan 2014)

Outpatient treatments of approved chronic conditions: diabetes, hypertension, lipids disorders, stroke, asthma, chronic obstructive pulmonary disease, major depression, schizophrenia, dementia, bipolar disorder

From 1 Jan 2014:Osteoarthritis, anxiety, benign prostatic hyperplasia, Parkinson’s disease, nephrosis/nephritis

Chemotherapy (includes analgesic medication and suppressive treatments such as neuroendocrine and nuclear medicine treatments)

HIV anti-retroviral drugs (includes drugs used to treat opportunistic infections)

Thalassaemia treatment (Desferral drug and blood transfusion)

Outpatient Intravenous antibiotic treatment

Immuno-suppressant drugs such as cyclosporin and tacrolimus

$400 per year per account on or after 1 Jan 2012

$400 per year per account Co-payment of 15% applies

$300 for 7-day treatment cycleS$1,200 for 21/28-day treatment cycle

$550 per month (only patient’s Medisave may be used. For patients aged 18 and below, the parent’s Medisave may be used.)

$350 per month

$600 per weekly cycle, up to S$2,400 a year

$300 per month

Table 1. Drugs eligible for outpatient Medisave claims and withdrawal limits.

To be eligible, the patient must:1. be a Singapore citizen,2. receive treatment as a subsidized

patient,3. require a drug for an approved

indication covered by MAF,4. face difficulty affording the drug

after subsidies for the overall bill, Medisave and/or MediShield.

Doctors can refer patients who

fulfil these criteria to the MSWs by applying for MAF assistance. The level of subsidy provided under MAF ranges from 50% to 75% depending on the financial assessments by MSWs. The approved drug list under MAF is found together with the SDL in the MOH website (Ministry of Health > Costs and Financing > Schemes & Subsidies > Drug Subsidies).

In 2011, there was an expansion of

MAF to provide financial assistance for clinically necessary non-standard medications beyond the list of MAF-approved drugs, i.e. MAF Plus. Similarly, the level of subsidy provided ranges from 50% to 75%.

COMMUNITY HEALTH ASSIST SCHEME (CHAS)The Community Health Assist Scheme (CHAS) is a scheme that enables Singapore Citizens from

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lower-to-middle-income households to receive subsidies for medical and dental care at participating general practitioner (GP) and dental clinics near their homes. Health Assist cardholders will also enjoy subsidized referrals to Specialist Outpatient Clinics (SOCs) located at restructured hospitals or National Dental Centre when required.

All Health Assist cardholders will be eligible for 75% subsidy for SDL 2 drugs covered under Chronic Disease Management Programme (CDMP). This is increased from the current 50% subsidy at restructured hospitals and polyclinics. The 75% subsidy is applicable for both inpatient and outpatient medical bills.

PIONEER GENERATION (PG) PACKAGEThe Pioneer Generation Package was introduced to honour and thank our pioneers for their hard work and dedication towards nation building. Eligible Singapore Citizens need to meet two criteria:1. aged 16 and above in 1965: a. born on or before 31 December

1949,b. aged 65 and above in 2014,

2. obtained citizenship on or before 31 December 1986.

With the Pioneer Generation (PG) card, all Pioneers will get an additional 50% off their bills for all subsidized drugs from 1 January 2015 at subsidized specialist outpatient clinics and polyclinics.

CONCLUSIONIn Singapore, the healthcare financing system is based on the twin philosophies of individual responsibility and affordable healthcare for all. The multitude of drug financing schemes available can occasionally be confusing to patients and new staff working in healthcare institutions. When there are queries about these schemes, they can be directed to the MSWs and pharmacists of the institutions.

Ms Lim Wan Peng is a principal pharmacist in the Department of Pharmacy, Tan Tock Seng Hospital.

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RADIOLOGY Quiz

Figure 1. AP and lateral plain radiographs of the right knee a 30-year-old man.

QUESTION 1What do these orthogonal knee radiographs show?

CASE PRESENTATIONA 30-year-old judoka presents with intermittent right knee pain. He recalls an episode of severe knee pain during a sparring session with team mate 4 weeks ago.

QUESTION 2He was treated symptomatically for knee pain. He re-presented 6 months later as he experienced only minimal improvement of his symptoms. He now complained intermittent locking of the knee and the occasional sensation of the joint ‘giving way’. He was referred to the Orthopaedic Surgeon for further management. An MRI was performed to exclude internal derangement of the knee. What abnormalities are seen on MRI?

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Figure 2. Black arrows showing the smooth lateral border of the mass arising from the anterior mediastinum.

ANSWER 1A small bone fragment is seen closely related to the lateral margin of the lateral tibial plateau (figure 3). This is due to an avulsion fracture involving the bony attachment of the lateral capsular ligament. This injury is known as a Segond fracture.

Diagnostic clues for a Segond fracture are small osseous fragment near the expected site of ligamentous insertion along lateral tibial plateau and an avulsion fracture of intercondylar eminence (indicating an anterior cruciate ligament (ACL) tear) may also be seen.

Figure 3. A small bone fragment is seen closely related to the lateral margin of the lateral tibial plateau. This is due to an avulsion fracture involving the bony attachment of the lateral capsular ligament.

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Further Reading1. Goldman AB, Pavlov H, Rubenstein D.

The Segond fracture of the proximal tibia: a small avulsion that reflects major ligamentous damage. AJR Am J Roentgenol 1988; 151:1163-7.

2. Gottsegen CJ, Eyer BA, White EA, Learch TJ, Forrester D. Avulsion fractures of the knee: imaging findings and clinical significance. Radiographics 2008; 28:1755-70

A Segond fracture is commonly seen in sports injuries such as basketball, soccer and skiing. The mechanism of injury is thought to be internal rotation and varus stress on the knee. There is a strong association with ACL tears and meniscal injuries.

Although the fracture itself is usually small, its association with internal derangement of the knee (ACL tear, meniscal injury, lateral collateral ligament sprain or tear) warrants an orthopaedic referral for management. Patients usually require surgical intervention to correct rotation instability of the knee.

Discussion

Dr Low Hsien Min is a resident in the Department of Diagnostic Radioolgoy, Tan Tock Seng Hospital

Figure 5. This sagittal section through the patient’s knee demonstrates a complete tear of the ACL.

Figure 6. There is an associated oblique tear of the medial meniscus, shown as a hyperintense (bright) line through the posterior horn.

Figure 4. The fracture has healed with the bone fragment seen fused to the lateral tibial plateau.

Figure 7. This coronal section reveals a radial tear through the lateral menicus, shown as an abrupt truncation of the normal triangular shape of the meniscus.

ANSWER 2The MRI findings are detailed with the following images (figures 4 to 7).

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Answer

Dr David Foo is the Head of the Department of Cardiology, Tan Tock Seng Hospital.

ECG QuizQuestionA 50-year-old presents with acute shortness of breath. His chest X-ray shows an enlarged heart shadow (figure 1) and ECG displays persistent changes (figure 2). Would you activate primary angioplasty?

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Figure 1. Chest X-ray of a man with acute breathlessness.

Figure 2. 12-lead ECG of a man with acute breathlessness.

No. The ECG findings are not typical of an ST segment elevation myocardial infarct (STEMI). Though there are deep Q waves and ST elevations in leads V2-V4, there are no reciprocal ST depressions in the inferior leads as expected of a STEMI. Coupled with the cardiomegaly and pulmonary edema shown on the CXR, the likely explanation of the persistent ST elevation is left ventricular apical aneurysm.