Wednesday, September 7, 2011
Editorial
Dear Reader
We are happy to place before you the latest issue of Capsule. This issue portrays a clinical case review and other regular features: but, the highlight is a lucid article on Management of diabetes mellitus in acute coronary syndrome by Prof.Dr.H.S.Devaraj. The article delineates the pathophysiological aspects in ACS and the benefits bestowed by good glycemic control achieved by insulin therapy. The article places a clear management protocol before the reader which would be very handy in day to day practice. The message on the wall is clear - Insulin is the only option in clinical situations like ACS and other critically ill patients. However, the target of glycemic control, ensuing effect on the length of ICU stay, morbidity and mortality have been creating storms in the cup ever since the publication of first Leuven study, in 2001 by Van den Berghe et al. The study highlighted on Intensive Insulin Therapy (ITI) targeting blood glucose of 80 to 110 mg/dL. The subsequent NICE-SUGAR (Normoglycemia in Intensive Care Evaluation Survival Using Glucose Algorithm Regulation), VISEP (Volume Substitution and Insulin Therapy in Severe Sepsis ) - Glucontrol trials and also Leuven medical trial all of them land on the common recommendation of a less stringent glycemic control in mixed medical and surgical ICU patients -a more permissive blood glucose range of 140 to 180 mg/dL.
On the other hand, patients in the ambulant setting exhibit great resistance for initiation of Insulin. However, the reasons for insulinophobia are worth giving a proper consideration along with the less discussed but, more pondering issues which would make a big difference on the long run. These include progressive weight gain and its associated complications. Increased risk of neoplasms noted in long term insulin users has not received much attention amongst researchers! These considerations would tempt any conscientious clinician to explore the possibility of residual Beta cell activity in a diabetic elegantly demonstrated by the PioSwitch Study. The switch from insulin therapy resulting in a moderate HbA1c level, to oral treatment with pioglitazone was successful in a majority of patients with sufficient residual beta-cell function. It allows a simple and less expensive therapy with a better cardiovascular risk marker profile. These points would leave our elite reader with the practical issues of diabetes management on every occasion when the oft quoted phrase 'Insulin is the final option in progressive Type 2 Diabetics' is heard!
Hope you will have a great reading.
Dr. Sudharshana Murthy K.A.
Professor & Head, Dept of Medicine
JSSMC & Hospital, Mysore
An Ocular clue for Diagnosis of Tuberculosis
HISTORY
A 35 year old female presented with low grade fever of 20 days and painless reddish lesion in the right eye of 7 days. There was no cough, breathlessness, weight loss, chest pain, haemoptysis, burning micturition, loose stools or vomiting. General Physical examination revealed no abnormality. There was no pallor, icterus, clubbing, cyanosis or lymphadenopathy. Systemic Examination was unremarkable. Ocular Examination revealed a localized non tender nodule with hyperaemia at 70' clock position. Cornea was clear and there was no evidence of iritis. Fundus showed no evidence of choroid tubercles or roth spots.Blood routine showed a normocytic normochromic picture with Eosinophilia (20%), ESR being 30mm/1st hr. Haematological and biochemical parameters were within normal limits. HIV tridot was non reactive and stool microscopy showed no ova/cysts/parasitic forms. With a strong suspicion of Tuberculosis, Mantoux test was performed which showed positivity at 48 hours with 5cm induration. Further investigating with a chest Roentgenogram non homogenous infiltrates were seen involving the left upper zone. Abdominal sonography revealed few enlarged lymph nodes in the Right iliac fossa.
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With the above evidence, a diagnosis of Phlyctenular conjunctivitis right eye secondary to disseminated tuberculosis with helminthiasis was made.The patient was initiated on ATT and made a satisfactory recovery and the ocular lesion resolved completely in another 2 weeks time.
DISCUSSION
Phlycten is a characteristic nodular affection of the eye as an allergic response by the conjunctival and corneal epithelium to some endogenous allergens to which they have become sensitised. It is a Type IV hypersensitivity reaction. Most common systemic association is Rosacea2
Causative allergens
? Tubercular proteins in developing countries
? Staphylococcal proteins in developed countries
? Proteins of moraxella axenfield
? Certain helminthic infestations
Stages1
? Stage of Nodule formation
? Stage of Ulceration
? Stage of Granulation
? Stage of Healing
Clinical features
Symptoms-Irritation,mild discomfort in the eye,reflex watering,may be associated with secondy infection
Phlyctenular conjunctivitis -Forms
1. Simple phlyctenular conjunctivitis
Typical pinkish white nodule surrounded by hyperaemia on the bulbar conjunctiva usually near the limbus
2. Necrotising phlyctenular conjunctivitis
Very large nodule with necrosis and ulceration leading to severe purulent conjunctivitis
3. Miliary phlyctenular conjunctivitis
Multiple phlyctens hapazardly arranged or in an annular form around the limbus and may form a ring ulcer
Phlyctenular keratitis
1. Ulcerative Phlyctenular keratitis
? Sacrofulous ulcer-shallow marginal ulcer due to breakdown of a limbal phlycten
? Fascicular ulcer-prominent parallel leash of blood vessels,leaving behind a band shaped opacity
? Miliary ulcer-multiple ulcers scattered over a portion or whole of cornea
2. Diffuse infiltrative Phlyctenular keratitis
Central infiltration of the cornea with characteristic rich vascularization all around the limbus
Differential Diagnosis
? Allergic conjunctivitis
? Episcleritis
? Scleritis
? Inflamed pterygium
? Foreign body Granuloma
COMPLICATIONS
? Secondary infection
? Severe thinning and perforation of globe
? Limbal phlycten can encroach upon the cornea
? Corneal ulcer and scar
TREATMENT
? Treatment of the underlying cause.
? Self limiting in 2-3 weeks
? A short course of topical steroids may accelerate healing
? Antibiotic drops to prevent secondary infection
REFERENCES
1. Kanski Jack J, Clinical ophthalmology, a systematic approach, Elsevier Butterworth Heinemann;2007:275
2. Khurana A K, Ophthalmology, New age international publications,4th Edition,2007:102-104
Management of Diabetes Mellitus in Acute Coronary Syndrome
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Diabetes is the fourth main cause of death in most countries.People with diabetes are three times more likely to require hospitalization than without this condition.Diabetes is the leading cause of death due to CVD and stroke.More than 3.2 million deaths worldwide are due to diabetes every year, i.e. more than 6 deaths every minute.
Nearly 65% of patients with diabetes die of cardiovascular/cerebrovascular disease.People with diabetes who walk two hours a day can lower their mortality risk as well as their risk of dying from CVD. Physical inactivity is estimated to cause about 16-20% cases of diabetes.One percent decrease in HbA1c results in 14% reduction in the incidence of ACS.Management of ACS with diabetes may be more difficult than management of ACS alone, since the complications associated with diabetes are difficult to treat. Mortality and morbidity due to ACS with diabetes is much more higher than ACS occuring alone.
The mortality and complications are much higher in patients continued on OADs with or without control than those treated with insulin when ACS ensues. IV insulin infusion should be commenced for acute management in first 24-48 hours. Patients with type 1 diabetes should continue their usual basal insulin daily to reduce the risk of diabetic ketoacidosis if IV insulin is interrupted.
Role of Insulin in ACS
Insulin reduces free radical generation and proinflammatory action and also decreases proinflammatory cytokines, TNF alpha concentration and increases anti-inflammatory cytokines and supresses Plasminogen activator inhibitor-1 (PAI-1) which facilitates clot dissolution in acute MI.
Insulin prevents adhesion circulating leucocytes by suppression of above mediators of inflammation and prevents apoptosis of myocardial tissue and improves lipid metabolism and thereby protects myocardium and improves its function.
Heart in Diabetes
Hyperglycemia increases circulating free fatty acids (FFAs), which are toxic to the myocardium and induce arrhythmias.It causes osmotic diuresis resulting in volume depletion and further compromise myocardial function.It increases blood viscosity and tendency for vascular thrombosis.
The myocardium depends on aerobic metabolism and, unlike skeletal muscle, must not develop an appreciable oxygen debt.The preferred fuel for the myocardium is free fatty acids (FFAs) during fasting, glucose postprandially, and lactate and FFAs during exercise.
If the myocardium switches to anaerobic metabolism, such as during ischaemia, the balance of substrate is disturbed, FFAs and their unoxidised products accumulate and may lead to myocardial cell death. Hence while treating ACS,Insulin is infused as a Dextrose-Normal Saline infusion unlike insulin-saline infusion in the treatment of hyperglycemic crisis.Insufficient insulin (qualitative/quantitative) with hyperglycemia reduces myocardial contractility, promotes cardiac failure and arryhthmias.
EFFECTS OF HYPERGLYCEMIA ON HEART
Management of Diabetes
Initial Management in first 24-48 hours
The protocol of insulin therapy is little different than in usual situations, otherwise in a patient who is already on insulin and develops ACS.
DIGAMI Protocol
INFUSION :
? 500ml 5% glucose with 80 IU of soluble insulin(1U/6ml).
? Start with 30ml/h.
? Check blood glucose after 1 hr.
? Adjust infusion rate according to the protocol and aim for a blood glucose level of 7-10mmol/litre (126- 180mg/dl)
? Blood glucose should be checked after 1hr if infusion rate has been changed, otherwise every 2hr.
If the initial decrease in blood glucose exceeds 30%, the infusion rate should be left unchanged if blood glucose is >11mmol/litre (198mg/dl).
BLOOD GLUCOSE LEVELS | ACTION |
1) > 15mmol/litre (> 270 mg/dl) | Give 8U of insulin as intravenous bolus injection and increase infusion rate by 6ml/hr. |
2) 11 to 14.9 mmol/litre (198-268.2 mg/dl) | Increase infusion rate by 3ml/hr. |
3) 7 to 10.9 mmol/litre (126-196.2 mg/dl) | Leave infusion rate unchanged. |
4) 4-6.9 mmol/litre (72-124.2mg/dl) | Decrease infusion rate by 6ml/hr. |
5) < 4mmol/litre (<72mg/dl) | Stop infusion for 15mins. Then test blood glucose and continue testing every 15 mins until blood glucose is more than 7 mmol/litre (126mg/dl). |
In the presence of symptoms of hypoglycemia, administer 20ml of 30% glucose intravenously. The infusion is restarted with infusion rate decreased by 6ml/hr when blood glucose is > 7mmol/litre (126mg/dl) |
Insulin should be continued for atleast 6 weeks before resuming to OAD s since the arrhythmias following myocardial infarction can be prevented if Insulin is used after discharge from CCU.
Insulin is always insulin and it always acts.Change over to insulin from OADs in ACS even though the blood glucose is within normal limits.
ACHIEVEMENTS
Echocardiography and exercise ECG testing in asymptomatic diabetics with CT Coronary Angiographic correlation. Subrahmanyam Karuturi, Basavana Gowdappa, H. Sudharshana Murthy, K. A
Best Paper Award in Free Paper Session in KAPICON 2011
Study of Nephrotic Syndrome in adults in with special reference renal histopathology and complications at presentation
Mihir,B.Shah, Sureshbabu,M,Manjunath S.Shetty, Sudharshana Murthy,K.A., Basavana Gowdappa,H
Dr M.Mahesh Associate Professor of Medicine delivered an interactive lecture with body donors and their relatives on "obesity" in Kannada on 12 th June 2011 at JSS Medical College Auditorium