Critical care oct dec 2012 by IJCP

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Volume 7, 8, Number 23

April-June 2012 2011 October-December

Antibiotic Prophylaxis to Prevent A View on Combination Antiplatelet Agents in Surgical Ischemic Site StrokeInfections Comparison of Manual Hyperinflation Corrosive Poisoning using Mapleson C and Laerdal Bag on Lung Compliance and Hemodynamics Therapy in the Intensive Care Unit inAntimicrobial Mechanically Ventilated Adults ARuptured Study on Pregnancy-induced Acute Pulmonary Hydatid Cyst: Renal Failure Sign The Camalote Acute Pancreatitis Complicating Cardiac Arrest Following Neostigmine in Patients Pregnancy on b-blockerwith Severe Thrombocytopenia Scorpion Bite causing Acute Severe Myocarditis:

Pleural Effusion and Ascites in A Rare Complication Celphos Poisoning: An Unusual Presentation

Initial Assessment and Evaluation of the Patient with Acute Chest Pain

Calcifications in the Upper Abdomen

Updated Guidelines on Management AAP Updates Guidelines for of Atrial Fibrillation from the ACCF/AHA/HRS Evaluating Simple Febrile

Seizures in Children More...

Happy New Year 2013

Asian Journal of

Critical Care Volume 8, Number 3, October-December 2012

An IJCP Group Publication Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor Padma Shri and Dr BC Roy National Awarde

Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD & Group Executive Editor

Contents Contents From the Desk of Group Editor-in-chief

Reflexology for Cancer Symptoms

KK Aggarwal

Critical Care Editorial Board Dr MM Pandit Rao Prof. Anesthesia, BJ Medical College, Pune Dr Vijay Langer Head, Dept. of Anesthesia, Moolchand Medcity, New Delhi Dr Rajesh Chauhan Sr. Anesthetist, Escorts Heart Institute, New Delhi Dr A Kale Prof. Anesthesia, AIIMS, New Delhi Dr Manju Mani Director-Critical Care, Delhi Heart and Lung Institute

review article

A View on Combination Antiplatelet Agents in Ischemic Stroke

Bhargava M Vyasa, RD Dave, PS Daniel, IS Anand, CN Patel

New Delhi Dr Tarlika Doctor Associate Professor Anesthesia, BJ Medical College, Ahmedabad

IJCP Editorial Board

Corrosive Poisoning

R Raghu Ramulu Naik, M Vadivelan

Obstetrics and Gynaecology Dr Alka Kriplani, Dr Thankam Verma Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr SK Parashar Paediatrics Dr Swati Y Bhave

Antimicrobial Therapy in the Intensive Care Unit

MS Krishna Sarin, M Vadivelan, Chanaveerappa Bammigatti

Diabetology Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty ENT Dr Jasveer Singh Dentistry Dr KMK Masthan, Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dermatology Dr Hasmukh J Shroff Neurology Dr V Nagarajan Journal of Applied Medicine & Surgery Dr SM Rajendran, Dr Jayakar Thomas Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies

Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry Advisory Body Asian Journal of Critical Care Vol. 8,ofNo. 3, October-December 2012 World Fellowship Religions

case report

Ruptured Pulmonary Hydatid Cyst: The Camalote Sign

Manjot Kaur, Rakendra Singh

Cardiac Arrest Following Neostigmine in Patients on b-blocker 26 Gunjan Chaudhry, V Kathuria, K Vashisht

Asian Journal of

Review Article

Critical Care Volume 8, Number 3, October-December 2012

Contents

Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com

case report

Scorpion Bite causing Acute Severe Myocarditis: A Rare Complication

Printed at Entire Printers Nampally, Hyderabad

Tarachand Saini, Shailendar Gupta, Maniram Kumhar

ÂŠ Copyright 2012 IJCP Publications Ltd. All rights reserved. The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

Clinical Algorithm

Initial Assessment and Evaluation of the Patient with Acute Chest Pain

Editorial Policies The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article. Note: Asian Journal of Critical Care does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

Practice Guidelines

Updated Guidelines on Management of Atrial Fibrillation from the ACCF/AHA/HRS

Lighter reading

Lighter Side of Medicine

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Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

From the desk of Group editor-in-chief

Reflexology for Cancer Symptoms Dr KK Aggarwal

Padma Shri and Dr BC Roy National Awardee Sr. Physician and Cardiologist, Moolchand Medcity, New Delhi President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Vice President, Elect IMA Chairman Ethical Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)

A study led by a Michigan State University researcher offers the strongest evidence yet that reflexology can help cancer patients manage their symptoms and perform daily tasks. Funded by the National Cancer Institute and published in the latest issue of Oncology Nursing Forum, it is the first large-scale, randomized study of reflexology as a complement to standard cancer treatment, according to lead author Gwen Wyatt, a professor in the College of Nursing. Reflexology is based on the idea that stimulating specific points on the feet can improve the functioning of corresponding organs, glands and other parts of the body. The study involved 385 women undergoing chemotherapy or hormonal therapy for advanced-stage breast cancer that had spread beyond the breast. The women were assigned randomly to three groups: Some received treatment by a certified reflexologist, others got a foot massage meant to act like a placebo, and the rest had only standard medical treatment and no foot manipulation. They found that those in the reflexology group experienced significantly less shortness of breath, a common symptom in breast cancer patients. Perhaps as a result of their improved breathing, they also were better able to perform daily tasks such as climbing a flight of stairs, getting dressed or going grocery shopping. Also unexpected was the reduced fatigue reported by those who received the ‘placebo’ foot massage, particularly since the reflexology group did not show similarly significant improvement. Wyatt is now researching whether massage similar to reflexology performed by cancer patients’ friends and family, as opposed to certified reflexologists, might be a simple and inexpensive treatment option.

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Review article clinical practice

A View on Combination Antiplatelet Agents in Ischemic Stroke Bhargava M Vyasa*, RD Dave*, PS Daniel*, IS Anand*, CN Patel*

Abstract The evaluation of antiplatelet agents for prevention of ischemic stroke is being focused as a strategy for stroke reduction. The aim of this analysis was to focus specifically on the necessity of combination antiplatelet agents for secondary prevention of ischemic strokes. Aspirin, clopidogrel, ticlopidine and the combination of aspirin plus extended-release dipyridamole are all effective in reducing the risk of recurrent ischemic strokes and transient ischemic attack. Furthermore, the combinations of all above drugs show some merits and demerits in one or more condition. National guideline endorses any of these antiplatelet agents as appropriate treatment options but more research into this strategy is needed. Choosing a single antiplatelet agent or the combination must be tailored according to patient characteristics, cost, disease condition and tolerability. Other classes of antiplatelet drugs should undergo clinical trials to optimize antiplatelet therapy. Key words: Aspirin, clopidogrel, dipyridamole, ticlopidine, combination antiplatelet therapy, ischemic stroke

troke is a leading cause of death and the primary cause of serious, long-term disability worldwide. Roughly, 90% of all strokes are ischemic in nature, with the remaining resulting from intracerebral hemorrhage or subarachnoid hemorrhage. Nearly, 25% of patients who experience a stroke have sustained a previous stroke, making secondary prevention of recurrent stroke an important target of pharmacotherapy. The high rates of mortality and disability associated with ischemic stroke, coupled with its prevalence, necessitate good, long-term preventive strategies. Patients suffering from a transient ischemic attack (TIA) or stroke are particularly vulnerable to secondary stroke. Available antiplatelet therapies include aspirin, clopidogrel, dipyridamole and ticlopidine. Of these options, aspirin monotherapy has been the mainstay of treatment for secondary prevention of ischemic stroke or TIA. It has been studied extensively and is relatively safe and inexpensive. Unfortunately, aspirin monotherapy has its limitations. It has been suggested that aspirin alone produces only a 10-15% relative risk (RR) reduction in

*Dept. of Pharmacology Shri Sarvajanik Pharmacy College, Mehsana, Gujarat Address for correspondence Dr Bhargava M Vyasa D/301, Ashutosh Apartments, B/h St. Xavierâ&#x20AC;&#x2122;s Loyola School Naranpura, Ahmedabad - 380 013 E-mail: bmvyasa_1986@yahoo.co.in

stroke recurrence compared with placebo. Aspirin can also cause significant gastrointestinal discomfort and bleeding, and certain patients may be resistant to its antiplatelet effects. These findings have led investigators to consider alternatives to aspirin monotherapy, most notably, combination antiplatelet treatment. Combination antiplatelet therapy seeks to block platelet aggregation through multiple mechanisms. Aspirin inhibits the enzyme cyclooxygenase, thus preventing production of prostaglandins and ultimately the production of thromboxane A2. Clopidogrel acts on platelets by irreversibly binding the adenosine diphosphate (ADP) receptor, blocking the ADP-dependent activation of the glycoprotein IIb-IIIa complex. This complex works as a receptor for fibrinogen on the surface of the platelet. Dipyridamole inhibits the uptake of adenosine into platelets, resulting in elevated local adenosine concentrations. Adenosine then acts on platelet A2 receptors, increasing the production of cyclic adenosine monophosphate. This mechanism prevents platelet-activating factor, collagen, ADP and other stimuli from activating platelet aggregation. By blocking platelet aggregation through multiple mechanisms, it is postulated that secondary ischemic stroke prevention can be enhanced. The American Heart Association (AHA) and the American Stroke Association (ASA) published joint guidelines in 2006 for treatment of patients with a history of stroke or TIA. Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article Randomized trials have established combination antiplatelet therapy as a cornerstone for secondary stroke prevention. Results from these trials enhance the recommendations from the AHA-ASA and provide the foundation for the updates in the 8th ACCP guideline. To identify pertinent combination antiplatelet trials, we performed a medline search of the literature from 1967-2007. We identified two trials Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management and Avoidance (CHARISMA) and the European-Australasian Stroke Prevention in Reversible Ischemia Trial (ESPRIT). Data from these two trials are important to current recommendations for secondary ischemic stroke and TIA prevention. Data from historic trials - the European Stroke Prevention Study (ESPS), the Second European Stroke Prevention Study (ESPS-2), the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events trial (CAPRIE) and the Management of AtheroThrombosis with Clopidogrel in High-risk Patients (MATCH) - are also important to consider, as they provided the background for the AHA-ASA and most recent ACCP guidelines (Table 1). In this article, we review the evidence from randomized trials for the effectiveness and safety of established combination antiplatelet therapies for secondary

prevention of ischemic stroke and TIA. We have focused on trials and meta-analysis that included patients with stroke, TIA or peripheral artery disease. Aspirin Aspirin, the most commonly used antiplatelet agent, inhibits the enzyme cyclooxygenase, reducing production of thromboxane A2, a stimulator of platelet aggregation. This interferes with the formation of thrombi, thereby reducing the risk of stroke. The dose of aspirin in secondary stroke prevention studies ranged between 20-1,300 mg. Most studies have found that 50-325 mg/day of aspirin is as effective as higher doses. Furthermore, lower doses within this range appear to provide the same benefit as higher doses. In the ESPS-2, 50 mg of aspirin daily reduced stroke risk by 18% compared with placebo (29 strokes prevented per 1,000 treated), an effect of comparable magnitude to the other trials cited above. This benefit seen with very low-dose aspirin is consistent with laboratory observations that 30 mg of aspirin per day results in complete suppression of thromboxane A2 production. In an analysis of data from 31 randomized, controlled trials, aspirin doses â&#x2030;¤200 mg/day were associated with a significantly lower rate of major bleeding events compared with higher doses. However, there was no

Table 1. Trial Characteristics for Six Randomized Controlled Trials Trial

Subjects

Treatment arms

ESPS-1

2,500

ASA 330 mg q.d. + IR-DP 75 mg Stroke or death t.i.d. vs placebo

Primary endpoints

33.5% reduction in stroke

Results (% RRR)

ESPS- 2

6,602

ASA 25 mg b.i.d. + ER-DP 200 mg b.i.d. or ASA 25 mg b.i.d., or ER-DP 200 mg b.i.d. vs placebo

Stroke

37% with aspirin-dipyridamole, by 18% with aspirin alone, and by 16% with dipyridamole alone vs placebo

CAPRIE

19,185

ASA 325 mg q.d. vs clopidogrel 75 mg q.i.d.

Ischemic stroke, MI or vascular death

8.7% RRR favored clopidogrel group

MATCH

7,599

ASA 325 mg q.d. + clopidogrel 75 mg q.d. vs clopidogrel 75 mg q.d.

Ischemic stroke, MI, vascular death or rehospitalization for an acute ischemic event

No significant difference; increased risk for bleeding in combination group

CHARISMA

15,603

Clopidogrel 75 mg q.d. + ASA 75-162 mg q.i.d. vs ASA 75-162 mg q.i.d.

MI, stroke or death

No significant difference; increased risk for bleeding in combination group

ESPRIT

2,763

ASA 30-325 mg q.i.d. + DP 200 mg b.i.d. vs ASA 30-325 mg q.i.d.

Death from vascular causes, nonfatal stroke or MI

20% RRR favored combination group

ASA = Aspirin; IR = Immediate release; ER = Extended-release; DP = Dipyridamole; MI = Myocardial infarction; RRR = Relative risk reduction.

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article difference in major bleeding when aspirin <100 mg/day was compared with 100-200 mg/day. Aspirin <100 mg/day was associated with a lower risk compared with the 100-200 mg/day and >200 mg/day groups when the overall rate of bleeding complications (including major, minor and insignificant events) was considered. A later meta-analysis of 22 randomized trials of lowdose aspirin (75-325 mg/day) versus placebo for cardiovascular prophylaxis reached similar conclusions within the low-dose range. Compared with placebo, aspirin increased the RR of any major bleeding, major gastrointestinal bleeding and intracranial bleeding by 1.7- to 2.1-fold. However, the absolute annual increase in risk for any major bleeding episode (mostly gastrointestinal) and for intracranial bleeding was 0.13 and 0.03%, respectively. Furthermore, there was no evidence of an increased risk of bleeding with ‘high’ low-dose aspirin (>162-325 mg/day) compared with ‘low’ low-dose aspirin (75-162 mg/ day) (Fig. 1). Clopidogrel Clopidogrel is a thienopyridine that inhibits ADPdependent platelet aggregation. The CAPRIE trial randomly assigned 19,000 patients with recent stroke, myocardial infarction (MI) or symptomatic peripheral arterial disease (divided roughly equally between these three enrolling diseases) to treatment with aspirin (325 mg) or clopidogrel (75 mg). The primary endpoint, a composite outcome of stroke, MI or vascular death, was significantly reduced with clopidogrel treatment compared with aspirin treatment (5.3 vs 5.8% annually, RR reduction 8.7%, 95% confidence interval [CI] 0.3-16.5%). The benefit of clopidogrel over aspirin in the CAPRIE trial varied based on enrolling disease. Most of the benefit was observed in patients with peripheral arterial disease, and the difference in composite outcome between clopidogrel and aspirin treatment in patients with recent stroke and MI was not significant. However, the strength of these observations are limited, since they are based on subgroup analyses. Dipyridamole Dipyridamole impairs platelet function by inhibiting the activity of adenosine deaminase and phosphodiesterase, which causes an accumulation of adenosine, adenine nucleotides and cyclic adenosine monophosphate. 8

Dipyridamole may also cause vasodilation. Dipyridamole is currently available in two forms: zz An immediate-release form, usually given as 50-100 mg three times per day. zz A proprietary formulation containing both extended-release dipyridamole (ER-DP) 200 mg and 25 mg aspirin, given two times per day. The effectiveness of dipyridamole monotherapy for secondary stroke prevention was established by the following studies: The ESPS-2 trial randomly assigned 6,602 patients with a recent TIA or ischemic stroke to one of 4 groups: 200 mg ER-DP alone given twice-daily; 25 mg aspirin alone given twice-daily; 25 mg aspirin plus 200 mg ER-DP given twice-daily and placebo. An independent and significant benefit for stroke risk reduction was observed for both ER-DP monotherapy (odds ratio [OR] 0.81, 95% CI 0.76-0.99) and aspirin monotherapy (OR 0.79, 95% CI 0.65-0.97) compared with placebo. The benefit of combination ER-DP plus aspirin was significantly greater still than the two components alone and significantly greater than placebo (OR 0.59, 95% CI 0.48-0.73). A subsequent meta-analysis of individual patient data from all available randomized trials found that dipyridamole alone was effective for reducing recurrent stroke compared with control (OR 0.82, 95% CI 0.68-1.0). Since, the ESPS-2 trial provided 57% of the data in this meta-analysis, it is possible that ESPS-2 was the primary driver behind the results. When ESPS-2 data were excluded, the effectiveness of dipyridamole alone compared with control did not achieve statistical significance. Whether this is related to the lower doses and immediate-release formulation used in trials other than ESPS-2 remains unclear. Ticlopidine Ticlopidine is a thienopyridine with a chemical structure and mechanism of action similar to clopidogrel. Its role in stroke prevention has been evaluated in two major trials. zz The CATS trial compared ticlopidine with placebo in patients who had suffered a significant stroke. At a mean of 24 months follow-up, the primary composite endpoint of stroke, MI and vascular death was significantly lower with ticlopidine compared with placebo (10.8 vs 15.3%, RR Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article Aspirin/ Dipyridamole Ticlopidine Clopidogrel

Relative risk reduction (%)

25 20 15

10 5 0

Stroke, MI, Vascular death

Stroke

Figure 1. Comparison of antiplatelet agents.

reduction 30%). Analysis by intention-to-treat gave a smaller estimate of RR reduction for stroke, MI or vascular death (23%). The TASS trial compared ticlopidine (500 mg/day) to aspirin (1,300 mg/day) in 3,069 patients with a recent TIA or mild stroke. At 3year follow-up, ticlopidine was associated with a significant reduction in the primary endpoint (nonfatal stroke or death) compared with aspirin (17 vs 19%). Ticlopidine treatment was also associated with a significant reduction in the rate of fatal and nonfatal stroke compared with aspirin (10 vs 13%, respectively; RR reduction 21% [95% CI, 4-38]).

Aspirin plus Clopidogrel The combined use of aspirin and clopidogrel does not offer greater benefit for stroke prevention than either agent alone but does substantially increase the risk of bleeding complications. This conclusion is supported by results from the MATCH trial. This study enrolled 7,599 patients with stroke or TIA who also had some additional â&#x20AC;&#x2DC;high-riskâ&#x20AC;&#x2122; feature, defined as prior MI, prior stroke (in addition to the index event), diabetes, angina or symptomatic peripheral artery disease (PAD). The primary endpoint was a composite of ischemic stroke, MI, vascular death or rehospitalization for acute ischemia. Patients were randomly assigned to the combination of clopidogrel (75 mg daily) plus aspirin (75 mg daily) versus clopidogrel (75 mg daily) alone. Follow-up was 18 months. The following observations were reported: Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Aspirin plus clopidogrel treatment did not reduce the risk of major vascular events compared with clopidogrel alone (RR reduction 6.4%, 95% CI -4.6 to 16.3%). Aspirin plus clopidogrel was associated with a significant increase in life-threatening bleeding complications, mainly intracranial and gastrointestinal, compared with clopidogrel alone. Over the 18-month trial period, there was an absolute excess of 1.3% for life-threatening hemorrhage (95% CI 0.6-1.9) and an additional 1.3% for major hemorrhage in patients assigned combination therapy. Overall, treatment with aspirin and clopidogrel compared with clopidogrel alone might prevent 10 ischemic events per 1,000 treated (not statistically significant) at the cost of 13 life-threatening hemorrhages per 1,000 treated.

Several authors have noted limitations of MATCH. For instance, 54% of MATCH subjects qualified for trial entry because of a lacunar stroke, a stroke subtype that has the lowest recurrence risk. Furthermore, data regarding interaction between treatment and stroke mechanism were not reported, raising the question of whether combination therapy might still play a role in particular stroke subtypes. The combination of aspirin and clopidogrel has been shown to have benefit over aspirin alone in patients with acute coronary syndromes. However, there are important differences between patients with coronary and cerebrovascular disease, and between short-term therapy initiated in the acute setting, and longer term preventative therapy. The results of the MATCH trial serve to emphasize these differences. In contrast to the MATCH trial, which evaluated aspirin plus clopidogrel versus clopidogrel alone in patients with stroke or TIA, the CHARISMA trial evaluated aspirin plus clopidogrel versus aspirin alone in patients with symptomatic cardiovascular disease or asymptomatic multiple cardiovascular risk factors. In this patient population, the combination of aspirin plus clopidogrel was not more effective than aspirin alone for reducing the rate of MI, stroke or death from cardiovascular causes. CHARISMA enrolled 15,603 patients with either documented cardiovascular disease (coronary, ischemic cerebrovascular or peripheral arterial) or, in 21% of patients, multiple atherothrombotic risk factors (e.g., diabetes, hypertension, primary hypercholesterolemia, current smoking, asymptomatic carotid stenosis â&#x2030;Ľ70%) and randomly assigned them to low-dose aspirin (75-162 mg/day) plus either clopidogrel (75 mg/day) or placebo. 9

review article The following observations were reported at a median of 28 months: zz Combined aspirin plus clopidogrel treatment did not reduce the risk of the composite primary endpoint (MI, stroke of any cause or death from cardiovascular causes) compared with aspirin alone (6.8 vs 7.3%, RR 0.93, 95% CI 0.83-1.05) zz Combination therapy compared with aspirin alone was associated with a significant increase in moderate bleeding (2.1 vs 1.3%) and a nonsignificant increase in severe bleeding (1.7 vs 1.3%).

Table 2. A Semi-quantitative Evaluation of Antiplatelets for the Prevention of Stroke and other Vascular Events ASA Clopidogrel Ticlopidine

ASA/ Dipyridamole

Efficacy

↑↑

↑↑↑

↑↑↑↑

Tolerability

↑↑↑

↑

↑↑

Routine monitoring

Yes

Dosing frequency

o.d.

b.i.d.

↑

↑↑↑↑

↑↑

↑↑↑

Cost

Aspirin plus Dipyridamole The beneficial effects of aspirin and dipyridamole for secondary stroke prevention appear to be additive such that the combination of aspirin and ER-DP is significantly more effective than aspirin alone for stroke prevention. The data supporting this conclusion come from the following randomized trials: zz In a meta-analysis of six randomized trials with 7,648 patients, stroke risk was significantly reduced with aspirin plus dipyridamole (including immediate and extended-release formulations) compared with aspirin alone (RR 0.77, 95% CI 0.67-0.89). Nearly 80% of the patients in this meta-analysis came from just two trials, ESPS-2 and ESPRIT. zz In the ESPS-2 trial, the stroke rate at 24 months of follow-up was significantly reduced in the aspirin plus ER-DP group compared with the aspirin alone group (9.9 vs 12.9%; RR reduction 23%, 95% CI 9.2-37.0). There was no significant difference in the risk of death between the two groups. The risk of bleeding complications was not significantly different between the aspirin plus ER-DP group and the aspirin monotherapy group, whereas both groups experienced a greater frequency of bleeding complications than the placebo group. zz In the later ESPRIT trial, 2,739 patients within six months of a TIA or minor stroke of presumed arterial origin were randomly assigned to openlabel treatment with aspirin (30-325 mg/day) alone or aspirin plus dipyridamole (200 mg twicedaily). The median aspirin dose was 75 mg/day in both treatment groups, and the dipyridamole formulation used by most patients (83%) was extended-release rather than immediate release. Over a mean follow-up of 3.5 years, the composite 10

primary outcome (death from all vascular causes, nonfatal stroke, nonfatal MI or major bleeding complication) was significantly less frequent in the aspirin plus dipyridamole group than the aspirin group (13 vs 16%, hazard ratio 0.80, 95% CI 0.660.98, absolute risk reduction 1.0% per year). ESPRIT included patients using aspirin doses ranging from 30 to 325 mg daily, allaying concerns that the very low aspirin dose (25 mg twice-daily) used in ESPS-2 was in part responsible for the benefit of combined aspirin plus ER-DP over aspirin alone. The specific dipyridamole preparation may be important. In the meta-analysis cited above, the combination of aspirin and immediate-release dipyridamole was nonsignificantly better than aspirin alone for secondary prevention of stroke (RR 0.83, 95% CI 0.59-1.15). In contrast, ER-DP was used in all or the vast majority of patients in the much larger ESPS-2 and ESPRIT trials, and aspirin plus ER-DP was associated with a significant reduction in stroke risk compared with aspirin alone (RR 0.76, 95% CI 0.65-0.89). Triple Therapy As we know that two antiplatelet agents are beneficial to single, then three agents with different modes of action might be better still, providing bleeding risk doesn’t become vulnerable. The efficacy of combining three antiplatelet drugs (aspirin, dipyridamole and clopidogrel) on inhibiting platelet aggregation, the formation of platelet-leukocyte conjugates and leukocyte activation has been demonstrated in vitro. However, in human beings, for prevention of secondary Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article ischemic stroke, short-term triple therapy was no more effective. Recurrent cerebrovascular events ceased with triple therapy over a period of 5-23 months follow-up and no episodes of intracranial hemorrhage or major extracranial bleeding have occurred to date.

6. Leonardi-Bee J, Bath PM, Bousser MG, Davalos A, Diener HC, Guiraud-Chaumeil B, et al; Dipyridamole in Stroke Collaboration (DISC). Dipyridamole for preventing recurrent ischemic stroke and other vascular events: a meta-analysis of individual patient data from randomized controlled trials. Stroke 2005;36(1):162-8.

Comparison of Antiplatelet Agents

7. O’Donnell MJ, Hankey GJ, Eikelboom JW. Antiplatelet therapy for secondary prevention of noncardioembolic ischemic stroke: a critical review. Stroke 2008;39(5): 1638-46.

A semi-quantitative evaluation of antiplatelets for the prevention of stroke and other vascular events based on selected criteria and available evidence is shown in Table 2. All the antiplatelet agents except for ticlopidine are acceptable for initial therapy but because of its efficacy, safety and cost, ASA should probably be used first in most circumstances for ischemic stroke prevention. Alternatives to ASA for second choice would include clopidogrel or the combination of ASA/dipyridamole. The combination of ASA and clopidogrel cannot be recommended for long-term stroke prevention both because of a lack of efficacy and increased risk of intracranial hemorrhage. Conclusion Antiplatelet therapy has major role in secondary prevention of ischemic stroke is undeniable. Effectiveness of single drug aspirin in contrast to combination with other antiplatelet agents is questionable according to various studies. Further, the potential of newer antiplatelets and their combination for reducing ischemic stroke is to be explored before arriving at decisive relative effectiveness of various combinations.

8. Côté R, David M, Deveber G, Teal P, Roussin A, Sharma M. Prevention of ischemic stroke. The Thrombosis Interest Group of Canada. February 19, 2007. 9. Antiplatelet chemoprevention of occlusive vascular events and death. Int Soc Drug Bull Therapeut Lett 2000; 37a-37b. 10. Hass WK, Easton JD, Adams HP Jr, Pryse-Phillips W, Molony BA, Anderson S, et al. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. Ticlopidine Aspirin Stroke Study Group. N Engl J Med 1989;321(8): 501-7. 11. Gent M, Blakely JA, Easton JD, Ellis DJ, Hachinski VC, Harbison JW, et al. The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke. Lancet 1989;1(8649):1215-20. 12. Fong JK. Update on Secondary Ischemic Stroke Prevention. Med Bull 2004;9:5-7.

Suggested Reading

13. Thijs V, Lemmens R, Fieuws S. Network meta-analysis: simultaneous meta-analysis of common antiplatelet regimens after transient ischaemic attack or stroke. Eur Heart J 2008;29(9):1086-92.

1. Vande Griend JP, Saseen JJ. Combination antiplatelet agents for secondary prevention of ischemic stroke. Pharmacotherapy 2008;28(10):1233-42.

14. Kirshner HS. Therapeutic interventions for prevention of recurrent ischemic stroke. Am J Manag Care 2008;14 (6 Suppl 2):S212-26.

2. Katzan IL. Antiplatelet agents in secondary stroke prevention. The Cleveland Clinic 2009. 3. Sprigg N, Gray LJ, England T, Willmot MR, Zhao L, Sare GM, et al. A randomised controlled trial of triple antiplatelet therapy (aspirin, clopidogrel and dipyridamole) in the secondary prevention of stroke: safety, tolerability and feasibility. PLoS One 2008;3(8): e2852. 4. Sacco RL, Elkind MS. Update on antiplatelet therapy for stroke prevention. Arch Intern Med 2000;160(11): 1579-82. 5. Cucchiara B, et al. Antiplatelet therapy for secondary prevention of stroke. Up To Date 2009.

15. Kirshner HS. Secondary stroke prevention, and the role of antiplatelet therapies. Clinical Medicine: Therapeutics 2009;1:601-12.

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

16. Zhao L, Heptinstall S, Bath PM.W. Antiplatelet therapy for stroke prevention. Br J Cardiol 2005;12(1):57-60. 17. McCabe DJ, Brown MM. Prevention of ischaemic stroke - antiplatelets. Br Med Bull 2000;56(2):510-25. 18. Cote R. Prevention of ischemic stroke. Canadian J CME 2001;193-8. 19. Flemming KD, Wiebers DO. Optimizing antiplatelet therapy to prevent ischemic stroke. Emerg Med 2002;34:28-37.

Review article clinical practice

Corrosive Poisoning R Raghu Ramulu Naik*, M Vadivelan**

Abstract Corrosive poisoning is a common emergency as corrosive agents are easily available for household use. Emetics and neutralizing agents should be avoided in treatment. Management of corrosive poisoning includes parenteral hydration and nutrition, H2-receptor antagonists or proton pump inhibitors. Upper gastrointestinal (GI) endoscopy should be done once the patient is hemodynamically stable and there are no signs of perforation. Urgent surgery is required in the event of perforation. Patients with Grade 0-1 injuries do not need hospitalization, while patients with Grade 2 and 3 injuries require intensive care unit (ICU) management.1 Key words: Corrosive agents, proton pump inhibitors, perforation

orrosives are a group of chemicals that have the capacity to cause tissue injury on contact by a chemical reaction. They most commonly affect the gastrointestinal tract (GIT), respiratory system and eyes. Corrosives and caustics are synonyms, both mean â&#x20AC;&#x2DC;something that eats awayâ&#x20AC;&#x2122;. Acids and alkalis are the two primary types of agents most often responsible for caustic exposures.2 Exposure to corrosive agents continues to be a leading toxicological source of injury for children and adults. An average home contains a dozen different cleaning products. These account for a large number of accidental and intentional poisonings. The estimated prevalence of corrosive poisoning is 2.5-5% while the morbidity is above 50% and the mortality is 13%. Eighty percent of corrosive poisoning occurs in children below five years. But, adult exposure has more morbidity and mortality due to significant volume of exposure and possible co-ingestion.

zz zz zz zz

Oxidizers (with neutral pH) Alkylating agents Dehydrating agents Halogens and organic halides Phenol

Acids zz zz zz zz

Car battery fluid (sulfuric acid) Descalers (hydrochloric acid) Metal cleaners (nitric acid) Rust removers (hydrogen fluoride)

Alkalis zz Bleach (hypochlorite) zz Sodium hydroxide (liquid lye) Uses of Common Caustic Agents3

Common Caustic Agents

The common caustic agents include: zz Strong acids and alkalis zz Concentrated weak acids and alkalis

*Junior Resident **Assistant Professor Dept. of Medicine Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry Address for correspondence Dr M Vadivelan No. E-2, JIPMER Quarters, JIPMER Campus, Dhanvantari Nagar Pondicherry - 605 006 E-mail: mevadivelan@hotmail.com

Hydrochloric acid-metal/toilet bowl cleaner Sulfuric acid-automobile batteries Sodium hydroxide-paint remover/drain cleaner Phenol-antiseptic

Factors Determining Corrosiveness

Factors that determine corrosiveness include:3 zz Physical form: Solid/liquid zz Duration of contact with tissue zz Concentration of agent zz Quantity of agent zz pH of agent: pH <2 and >11 are more corrosive zz Food: Presence or absence of food in stomach Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article zz

Titratable acid or alkali reserve (TAR): This quantifies the amount of neutralizing substance required to bring the pH of a caustic agent to physiological pH of the tissue.2

Mechanism of Action of Corrosive Agents zz Alkali ingestion: Causes liquefaction necrosis. This process includes protein dissolution, collagen destruction, fat saponification, cell membrane emulsification, submucosal vascular thrombosis and cell death.3 zz Acid ingestion: Causes coagulation necrosis. In this process, hydrogen (H+) ions desiccate epithelial cells producing an eschar. This process leads to edema, erythema, mucosal sloughing, ulceration and necrosis of tissues.3 Both acids and alkalis cause fibrosis and cicatrization (stricture formation). Consequences of Caustic Injury Caustic injury may cause the following:4 zz

zz zz zz

Necrosis: Occurs within seconds of exposure to caustic agent Ulceration and perforation: Occurs within 24-72 hours of exposure Fibrosis: Occurs within 14-21 days of exposure Stricture: Occurs after weeks to years of exposure Carcinoma formation: Occurs after decades of alkali exposure.

Clinical Presentation in Corrosive Poisoning GIT zz Severe pain of lips, mouth, throat, chest and abdomen zz Excessive salivation zz Dysphagia and odynophagia zz Epigastric pain and hematemesis zz Symptoms and signs of GI perforation

zz zz

Burns at the site of exposure Erythema and vesicle formation

Investigations Laboratory Tests zz

zz zz zz zz zz

Hemogram: WBC count >20,000/mm³ is an independent predictor of mortality in corrosive poisoning. Serum electrolytes: Hypocalcemia can occur with hydrogen fluoride poisoning. Blood grouping and cross-matching Renal function tests Liver function tests Coagulation profile Arterial blood gas analysis: Arterial blood pH and base deficit correlate with severity and adverse outcomes.

Radiology zz

Chest X-ray: The radiographic signs of early mediastinal leaks are usually subtle. However, chest X-ray helps in detection of pneumothorax, pneumomediastinum and pleural effusion. Air under the diaphragm is suggestive of visceral perforation. A lateral view is more sensitive than PA view for detecting intraperitoneal air.5 Abdominal X-ray: Can help in the detection of pneumoperitoneum. Contrast studies: Barium studies have low sensitivity in detecting perforation and high-risk of aspiration and inflammation. CT scan: CT scan of neck/chest/abdomen should be considered if there is a high-risk of suspicion for perforation despite negative plain X-rays. Contrastenhanced CT (CECT) is used to assess esophageal wall thickness, which can be used to predict the response to dilatation of stricture and the number of sessions required to achieve adequate dilatation. CT studies done with water-soluble contrast will allow localization of leak of air.

Respiratory system zz Cough zz Dyspnea zz Bronchoconstriction zz Pulmonary edema zz Chemical pneumonitis

Endoscopy

Eyes and skin zz Pain at the site of exposure

Indications for upper GI endoscopy zz Corrosive ingestion by small children

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Endoscopy has been called ‘sine qua non’ for evaluating patients with corrosive poisoning. Direct evaluation by endoscopy is useful in grading severity of tissue injury, planning for nutritional support and long-term management of strictures.6

review article zz zz zz zz zz

Symptomatic older children and adults Patients with altered mental status Patients with intentional ingestion Patients with ingestion of large volumes Patients with ingestion of concentrated products.

done if there is severe dysphagia. Endoscopy and dilatation of stricture (if present) should be done three weeks after ingestion. Late Admission

Contraindications for upper GI endoscopy Hemodynamic compromise zz Peritonitis and mediastinitis zz Mild ingestion (asymptomatic patients with normal oral/upper airway examination).

More than three weeks of ingestion: Requires endoscopy and dilatation of stricture. If the procedure is successful, then follow-up endoscopy should be done at one month. If the procedure is unsuccessful, then surgical gastrostomy is performed, which is followed by retrograde dilatation of stricture after 10 days of operation.

Endoscopy done very early (<6 hours) may not reveal the full extent of injury. The commonest practice is to perform endoscopy on Day 1-2.6

Clinical Approach in Management of Corrosive Poisoning

The findings on upper GI endoscopy are based on Zargarâ&#x20AC;&#x2122;s modified endoscopic classification of burns due to corrosive ingestion.6 They are graded as below: Grade Description 0

Normal mucosa

1 Erythema/Hyperemia 2a

Superficial exudates

Findings in 2a + deep discrete/circumferential ulcers

Scattered necrosis (black/grey discoloration)

Extensive/circumferential necrosis of mucosa

ulcer/erosion/friability/hemorrhage/

Approach to the management of corrosive poisoning is based on the clinical features of the patient with caustic ingestion. 1. Asymptomatic patient: If there is history of minimal corrosive ingestion and no oropharyngeal burns on examination, then the patient requires only observation in the Emergency Room. 2. Symptomatic patient: If there is history of ingestion of large volume of corrosive along with signs like stridor, hoarseness of voice and respiratory distress, then the patient requires admission in intensive care unit (ICU) and management as detailed below. zz

Management Management is based on the presenting clinical features on admission to the hospital. This can be divided into emergency management, management of stable patient and long-term management. Early Admission

Within 48-72 hours of corrosive ingestion: Upper GI endoscopy should be performed on Day 1-2. (ideally between 12-24 hours of ingestion). If endoscopy reveals only mild lesions, then the patient can be discharged and clinical follow-up should be done at one month. If severe lesions are found on endoscopy, then surgical gastrostomy is indicated, which should be followed by repeat endoscopy and dilatation after three weeks. Delayed Admission

Within 72 hours to three weeks of corrosive ingestion: No endoscopy is indicated. Gastrostomy should be 14

Protection of airway: In the presence of respiratory distress and airway edema, urgent endotracheal intubation should be done as airway edema may rapidly progress over minutes to hours. Supraglottic edema leads to acute upper airway obstruction and cricothyrotomy or tracheostomy is needed in such a situation. Delay in prophylactic airway protection may make subsequent attempts at intubation or bag mask ventilation difficult or impossible. There is no clear role for systemic steroids in decreasing airway edema and of intravenous adrenaline or nebulization in reducing the need for endotracheal intubation. Hemodynamic status: Acute circulatory compromise usually occurs due to hypovolemia. The reasons for hypovolemia are hemorrhage, vomiting and third-space sequestration. Hemodynamic correction can be done by replacement with crystalloid fluids. Invasive hemodynamic monitoring is indicated in unstable patients. Decontamination: Any attempt at gastric emptying or dilution of compound is contraindicated in corrosive poisoning. Emetics should not be given as they increase the risk of mucosal injury and subsequent perforation. Nasogastric tube should not be inserted since it may cause esophageal perforation and increase the risk of aspiration. Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article

Exceptions to general rules of decontamination are zinc chloride and mercury chloride poisoning because both cause systemic toxicity. Dilution and neutralization: Dilution and neutralization of corrosive by nasogastric tube lavage generates heat and increases the risk of aspiration. Both have no proven benefit and hence are contraindicated.

3. Stabilized patient: Initial evaluation of a stabilized patient aims to identify the acute complications of corrosive ingestion and stratify the risk for acute and long-term complications mainly by endoscopic grading of corrosive lesions. zz

Corticosteroids: While there is no role of systemic steroids in the management of caustic ingestion, intralesional steroids can be given.7 Antibiotics: Tissue destruction from caustic injury increases the risk of infection by enteric organisms. Antibiotics are not recommended prophylactically in corrosive poisoning. They are recommended in GI perforation.8 Proton pump inhibitors (PPIs) and H2-blockers: Gastroenterologists routinely recommend PPIs and H2-blockers in caustic ingestion.8 Nutrition: Endoscopic grade of lesions needs to be assessed for planning nutritional support in patients with caustic ingestion. Patients with Grade 1/2a lesions on endoscopy can tolerate oral feeds, while those with Grade 2b/3a lesions will need nasoenteral feeding. Patients with Grade 3b lesions require gastrostomy for enteral feeding and rarely need total parenteral nutrition (TPN).

Complications Acute: Airway compromise; shock (due to hemorrhage, vomiting or third-space sequestration); GI perforation (can cause esophageal leak/rupture and mediastinitis or gastric leak/bleed leading to peritonitis). zz Late: Stricture; obstruction zz Remote: Carcinoma of esophagus.9 Patients who develop esopahageal strictures after alkali consumption have high-risk (1,000 times more risk than the general population) for the development of squamous cell carcinoma of esophagus. The mean latency period is 40 years after ingestion and in 84% of the patients, the malignancy is located in the area of the bifurcation of trachea. zz

Management of Complications Laparotomy

Laparotomy is indicated in patients with: zz Endoscopic or radiologic evidence of perforation Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

zz zz zz zz zz

Severe abdominal rigidity Persistent hypotension Respiratory distress Ascites or pleural effusion pH < 7.2 on arterial blood gas (ABG) analysis

Laparotomy permits tissue visualization, resection and repair of perforation. Stricture management

Stricture formation begins weeks to months after injury and is the most important consequence of corrosive poisoning. Procedures used for prevention and treatment of strictures are: zz Dilatation therapy: This is done 3-6 weeks after injury, progressively larger bougies are passed over endoscopically placed guide wires for dilatation. But, the risk of perforation, aspiration and dysphagia is high. zz Surgery: Esophageal strictures resistant to dilatation therapy may require surgery that includes resection of stricture surgically and esophageal bypass surgery. References 1. Lahoti D. Corrosive injury to upper gastrointestinal tract. In: Manual of Medical Emergencies. 3rd edition. 2. In: Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient. 1st edition, Brent, Wallace, Burkhart, Phillips, Donovan (Eds.) 2005:p. 1035-44. 3. Caustics. In: Goldfrankâ&#x20AC;&#x2122;s Toxicologic Emergencies. 8th edition. 4. Sleisenger and Fordtranâ&#x20AC;&#x2122;s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 8th edition, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt (Eds.) 2006:p.406-9. 5. Woodring JH, Heiser MJ. Detection of pneumoperitoneum on chest radiographs: comparison of upright lateral and posteroanterior projections. AJR Am J Roentgenol 1995;165(1):45-7. 6. Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 1991;37(2):165-9. 7. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990;323(10):637-40. 8. Acids and alkalis. The Poisoning and Toxicology Handbook. 4th edition, Jerrold B. Leikin, Frank P. Paloucek Informa Healthcare, USA 2007:p.713-9. 9. Alkali injury. In: Clinical Management of Poisoning and Drug Overdose. 3rd edition, Lester M. Haddad, Michael W. Shannon, and James F. Winchester (Eds.) 1998: p.817-20.

Review article clinical practice

Antimicrobial Therapy in the Intensive Care Unit MS Krishna Sarin*, M Vadivelan**, Chanaveerappa Bammigatti**

Abstract Severe sepsis and septic shock in the intensive care unit (ICU) needs emergent coverage with empirical broad-spectrum antibiotics, with a commitment to de-escalation once the organism and its susceptibility to a particular antibiotic becomes known. The dose and duration of antibiotic must be optimized according to standard guidelines to prevent emergence of resistant pathogens. Strategies of using Procalcitonin measurements in guiding the duration of antibiotic treatment and aerosolized antibiotics are helpful in optimizing antibiotic usage. Efforts are needed to prevent emergence of antibiotic resistance by pathogens, as the antibiotic pipeline is dwindling and the number of newly discovered multidrug-resistant (MDR) pathogens is increasing. Prevention of infection must be given top priority by strict adherence to asepsis measures. Key words: Septic shock, intensive care unit, Procalcitonin, aerosolized antibiotics, multidrug-resistant pathogens

he intensive care unit (ICU) is a place where patients with complex medical problems are crowded into a small area. The acute nature of critically ill patients necessitates the use of broadspectrum antibiotics frequently. Fever in a patient in the ICU must be considered significant when the body temperature is >38.3째C (101째F) and a detailed evaluation must be carried out to ascertain whether infection is present or not.1 A lower threshold of fever must be used in immunocompromised patients. However, as many as 50% of ICU patients with fever have no apparent infection. Fever is a sign of inflammation, not infection. Hence, noninfectious causes of fever must be ruled out before subjecting the patient to a number of costly and invasive diagnostic procedures.

Noninfectious causes of fever in ICU zz Postoperative fever: Fever on the first day following major surgery is reported in 15-40% of patients.2

*Junior Resident **Assistant Professor, Dept. of Medicine Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Pondicherry Address for correspondence Dr M Vadivelan Q.No.: E-2, JIPMER Quarters, JIPMER Campus, Dhanvantari Nagar Pondicherry - 605 006 E-mail: mevadivelan@hotmail.com

zz zz

Procedures: Hemodialysis, bronchoscopy, blood transfusions. Endocrine disorders: Thyrotoxicosis, adrenal crisis. Myocardial infarction, stroke and venous thromboembolism. Drug fever: Common offending drugs are cephalosporins, penicillins and amphotericin B and phenytoin.

Infectious causes of fever in ICU zz Sinusitis zz Catheter-related bloodstream infection (CRBSI) zz Ventilator-associated pneumonia (VAP) zz Catheter-associated urinary tract infection (UTI) zz Wound infections Sepsis without an Obvious Focus In critically ill patients, the source of infection may not be apparent at the time of admission to the ICU. In such patients, empirical antibiotics must be started intravenously as early as possible within the first hour of recognition of severe sepsis and septic shock. Each hour of delay will decrease the survival by 7.6% approximately.3 A rough guide to the choice of empirical antibiotics when the focus of infection is unknown is presented in Table 1.4 Empirical coverage for methicillin-resistant Staphylococcus aureus (MRSA) with vancomycin is required in the following situations: Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article Table 1. Empirical Therapy for Severe Sepsis with no Obvious Focus Clinical condition

Antimicrobial regimens (IV therapy)

Immunocompetent adult

Piperacillin-Tazobactam/Meropenem/ Cefepime ± Vancomycin

Neutropenia Piperacillin-Tazobactam/Meropenem/ (<500 neutrophils/µl) Cefepime + Aminoglycoside ± Vancomycin Splenectomy

Cefotaxime/Ceftriaxone

IV drug user

Vancomycin

zz zz zz

Patients with indwelling vascular catheters If patient has received quinolone prophylaxis If the institution has a high incidence of MRSA infections. If there is a high prevalence of MRSA isolates in the community.

Indications for empirical antifungal drugs are: zz If the septic patient has been neutropenic for five days or more zz If the patient has had a long-term central venous catheter zz If the patient has been hospitalized in an ICU and received broad-spectrum antibiotics for a prolonged period. Amphotericin B is the drug of choice for all lifethreatening fungal infections and as empirical therapy in neutropenic patients with persistent fever. Fluconazole is used for treatment of candidiasis in patients who are hemodynamically stable and are not immunocompromised. The echinocandins (e.g. caspofungin) can be used for invasive candidiasis as the drug provides improved coverage against all Candida species. A combination of antibiotics is usually chosen for neutropenic sepsis and in patients with suspected Pseudomonas infections. The drugs which can be used in combination are ceftazidime or piperacillintazobactam or meropenem with an aminoglycoside.5 Indications for administering combination therapy with two drugs active against Pseudomonas are: zz Neutropenic fever zz Severe sepsis and septic shock zz Presence of serious infections like pneumonia, endocarditis and meningitis. Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

All patients must receive the full loading dose of each antimicrobial irrespective of the renal function. Subsequently, renal-modified dose of the drug can be given. Sepsis with an Identified Focus of Infection Ventilator-associated Pneumonia

The diagnosis of VAP is made on the basis of a new infiltrate in the chest X-ray with two of the following: zz Fever zz Leukocytosis zz Purulent tracheal secretions VAP can be classified as: zz Early: If infection began within five days after hospital admission. zz Late: If infection began more than five days after admission. Empirical therapy for early VAP is recommended using a single agent which can be any one of the following drugs:6 zz Ceftriaxone zz Levofloxacin/Ciprofloxacin/Moxifloxacin zz Ampicillin + Sulbactam zz Ertapenem Combination therapy is advised for late VAP and when VAP is suspected to be due to a multidrug-resistant (MDR) pathogen.6 The drugs used are: zz Ceftazidime/Cefepime zz Imipenem/Meropenem zz Piperacillin-Tazobactam + an Aminoglycoside/ Fluoroquinolone + Vancomycin/Linezolid. Optimum duration of therapy for VAP is eight days. Catheter-related Bloodstream Infections

The diagnosis of CRBSI depends on the demonstration, by culture, of the same organism from the catheter tip and blood culture. A colony count at least 3-fold greater for blood obtained from the catheter hub or a differential time to positivity (DTP) of at least two hours at the catheter hub also indicates CRBSI.7 The catheter must be removed in severe sepsis, suppurative thrombophlebitis, endocarditis and 17

review article infections due to S. aureus, Pseudomonas aeruginosa, fungi or mycobacteria, and in a CRBSI that continues despite 72 hours of antimicrobial therapy to which the infecting microbes are susceptible. CRBSI is treated with the combination of a fourthgeneration cephalosporin/carbapenem plus vancomycin to cover MRSA. An aminoglycoside is added if Pseudomonas is suspected. The duration of therapy depends on the infecting pathogen. Complicated CRBSI (i.e., CRBSI-associated with suppurative thrombophlebitis, endocarditis) requires at least 28 days of antibiotic therapy. Catheter-associated UTIs

Catheter-associated UTIs are diagnosed when bacteriuria (10³ colony forming units/ml) is associated with symptoms compatible with UTI. Symptoms

include fever with rigors, flank pain, renal angle tenderness, hematuria or pelvic discomfort. These infections are often polymicrobial and are caused by MDR pathogens. Urine culture results are required to guide treatment. Catheter has to be replaced if it has been in place for more than two weeks and if its use cannot be discontinued. The recommended duration of antimicrobial treatment for patients with catheter-associated UTI who have rapid resolution of symptoms is 7 days and 10-14 days for those with a delayed response, regardless of whether the patient remains catheterized or not.8 Antibiotic Therapy Depending on the Site of Infection Once the source of sepsis is known, the antimicrobial therapy should be tailored according to the possible infecting pathogens and their relative antibiotic

Table 2. Antibiotic Therapy Depending on the Site of Infection Site of infection

Bacteria

Suggested treatment

UTI

E. coli

Ceftriaxone or Ceftazidime ± Aminoglycoside

Severe acute pyelonephritis

P. aeruginosa Enterococcus species Staphylococcus species

Intra-abdominal sepsis

E. coli

Ertapenem

P. aeruginosa

Piperacillin-Tazobactam

Enterococcus species

Third- or fourth-generation cephalosporin (active against P. aeruginosa) + Metronidazole

Bacteroides species Nosocomial pneumonia

Enterobacteriaceae P. aeruginosa

β-lactam (active against P. aeruginosa) ± Aminoglycoside ± Glycopeptide (vancomycin)

S. aureus S. pneumoniae H. influenzae Pneumonia without risk factors for MDR Pseudomonas

S. aureus

Third-generation Cephalosporin ± Macrolide

S. pneumoniae H. influenzae Other gram-negative bacilli

Skin infections

CRBSI

Streptococcus species

β-lactam + β-lactamase inhibitor

Staphylococcus species

Piperacillin-Tazobactam

Gram-negative bacilli

Carbapenem

Staphylococcus species

Vancomycin + β-lactam with activity against P. aeruginosa

Enterobacteriaceae P. aeruginosa

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article susceptibilities. A summary of the possible etiologic agents according to the site of infection and the drug that can be used is given in Table 2.9 Treatment of Mdr Pathogens MDR pathogens are a real and constant threat in the ICU environment. The six most common MDR pathogens encompassed in the eponymous ‘ESKAPE’ group are Enterococcus faecium, S. aureus, Klebsiella pneumoniae, Acinetobacter species, P. aeruginosa and the Enterobacter species. Tables 3 and 4 summarize the treatment options for various MDR pathogens. Newer Concepts in Antimicrobial Therapy Procalcitonin as a Biomarker in Sepsis

Procalcitonin is the best studied biomarker for guiding antibiotic treatment duration in the hospital setting.

Procalcitonin dynamics within 72 hours after onset of sepsis may be correlated both with appropriateness of the empirical antibiotic therapy and with overall survival.10 Procalcitonin measurements integrated in clinical algorithms have been shown to reduce the duration of antibiotic courses by 25-65% in hospitalized and more severely ill patients with CAP and sepsis.11 Pharmacokinetics in Drug-dosing Time/ Concentration-dependent Killing

Antibiotics like b-lactams, quinolones and vancomycin exert their microbicidal activity depending on the duration for which the plasma drug levels remain above the minimum inhibitory concentration (MIC). An appropriate strategy is to administer these antibiotics as a continuous infusion rather than as bolus doses.

Table 3. Treatment Options for Resistant Gram-positive Bacteria Drug

Route of Activity against MRSA administration

Activity against resistant S. pneumoniae

Activity against vancomycinresistant Enterococci

Vancomycin

IV only

Yes

Daptomycin

IV only

Skin infection/Bloodstream infection

Yes

Linezolid

IV or oral

Pneumonia/Skin infection

Yes

Quinupristin- IV only Dalfupristin

Yes

Yes, against E. faecium

Telavancin

IV only

Skin infection/Pneumonia

Yes

Tigecycline

IV only

Pneumonia/Skin infection

Yes

Ceftaroline

IV only

Pneumonia/Skin infection

Yes

Table 4. Treatment Options for Resistant Gram-negative Bacteria Organism Empirical therapy Monomicrobial infection

Polymicrobial infection

Directed therapy ESBL-producing Enterobacteriaceae

Carbapenemase-producing Enterobacteriaceae MDR P. aeruginosa

First-line therapy

Second-line therapy

Carbapenem

Piperacillin-Tazobactam

Tigecycline (not in UTIs) ± Antipseudomonal agent Carbapenem + Vancomycin

Colistin

Tigecycline (not in UTIs) ± Antipseudomonal agent

Colistin + Vancomycin

Carbapenem

Tigecycline (not in UTIs)

Piperacillin-Tazobactam

Fluoroquinolone

Tigecycline

Colistin Fosfomycin (parenteral formulation)

Colistin Meropenem

Colistin

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Piperacillin-Tazobactam + Vancomycin

review article On the other hand, aminoglycosides exert their action depending on the peak levels achieved in plasma. So, the appropriate strategy will be to give the entire daily dose as a single bolus injection. The pharmacokinetics of antibiotics is modified in ICU patients owing to the large daily fluid balance, acute changes in body weight, hypoalbuminemia, edema and low hematocrit values that lead to a marked change in elimination half-life, volume of distribution and clearance. Sepsis increases capillary permeability with third space sequestration resulting in higher antibacterial drug clearances. Multiple organ dysfunctions cause a decrease in antibacterial drug clearance. Hence, monitoring of plasma drug concentrations needs to be performed whenever possible because these concentrations are difficult to predict in critically ill patients. Aerosolized Antibiotics

Intermittent aerosolization of antibiotics into the respiratory tract has been used in patients with P. aeruginosa pneumonia, particularly in the setting of cystic fibrosis. Tobramycin and colistin have been used in pneumonia caused by MDR Pseudomonas. Recently, amikacin, nebulized with special devices has been used for MDR gram-negative pneumonia that was unresponsive to standard therapy. Antimicrobial Resistance and Its Implications MDR pathogens are most frequently encountered in the ICU. The prime reason for the development of antimicrobial resistance is antibiotic misuse. Irrational antibiotic prescription for nondocumented infections in stable patients, prolonged use of broad-spectrum antibiotics without de-escalation, incorrect dosages and dosing intervals and continuation of the antibiotic course beyond the optimally recommended duration contribute to the development of resistance. Practices that promote optimization of antibiotic use in the ICU are summarized in Table 5.12 The key point is to avoid antibiotic misuse by using them only in patients with documented infections except if the infections are life-threatening and avoiding the treatment of asymptomatic colonization. De-escalation of broad-spectrum antibiotics based on clinical response and microbiological findings is needed to avoid the emergence of MDR pathogens. 20

Table 5. Practices Promoting the Optimization of Antimicrobial Use in the ICU Setting Provide adequate initial treatment of serious infections (e.g. pneumonia, bloodstream infections) Awareness of predominant disease causing pathogens Up-to-date ICU-specific pathogen antibiograms Drainage of abscesses, empyema cavities, other infected fluid collections Removal of infected foreign bodies (e.g. central venous catheters) Monitor serum drug concentrations when appropriate to achieve therapeutic levels Avoid prolonged courses of empiric antibiotic therapy Consider de-escalation of antibiotics based on available microbiologic data and clinical course Use narrow-spectrum antibiotics when supported by clinical situation and culture data Establish appropriate thresholds for prescribing antibiotics Develop predetermined criteria for the discontinuation of antimicrobial therapy

Table 6. Predetermined duration of Antibiotic Therapy based on the IDSA Guidelines Site of infection

Duration of antibiotic therapy (days)

Lung infection CAP due to S. pneumoniae

VAP

VAP and immunodepression

Pneumonia due to Legionella pneumophila

Pneumonia with lung necrosis

â&#x2030;Ľ28

Intra-abdominal infections Community peritonitis

Postoperative peritonitis

CNS infections Meningococcemia Meningitis due to S. pneumoniae

5-8 10-14

Postoperative meningitis due to S. epidermidis or Enterobacteriaceae

Meningitis due to Listeria monocytogenes

Postoperative meningitis due to S. aureus or P. aeruginosa

Brain abscess

â&#x2030;Ľ28

Catheter-related bacteremia S. epidermidis or Enterobacteriaceae

S. aureus/Candida species (uncomplicated)

S. aureus (complicated)

â&#x2030;Ľ28

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

review article Optimizing the duration of antimicrobial therapy by following a protocol-guided discontinuation if appropriate cultures are negative after Day 3 and prescribing the antibiotic course for the optimum duration will help to reduce the emergence of resistance. The optimum duration of antibiotic therapy for the commonly encountered infections in the ICU, according to the Infectious Diseases Society of America (IDSA) guidelines is given in Table 6. Certain practices may be helpful in controlling antibiotic resistance. Scheduled Changes in Antibiotic Therapy

Periodic changes in the antibiotic preference in treating infections caused by the same pathogen (e.g. gramnegative infections treated with a cephalosporin for the first six months and a fluoroquinolone for the next 6 months) may help to reduce the emergence of resistance to either class.

zz zz

Consolidate insertion supplies (e.g., in an insertion kit or cart) Use a checklist to enhance adherence to the bundle. Empower nurses to halt insertion if asepsis is breached. Cleanse patients daily with chlorhexidine. Ask daily: Is the catheter needed? Remove catheter if not needed or used.

Prevention of VAP zz zz

Elevate head end of bed to 30-45°. Decontaminate chlorhexidine.

Use deep-vein thrombosis prophylaxis (unless contraindicated).

A class of antibiotic is withdrawn from use for a defined time period and reintroduced at a later point of time in an attempt to limit bacterial resistance to the antimicrobial agent.

Prevention of UTIs

Prevention of Infections in the ICU Simple measures to prevent infection and pathogen cross-transmission assume significance considering the huge expenses incurred in terms of patient morbidity and mortality as well as the indirect costs involved in treating a resistant infection. A summary of the recommendations made by the Centers for Disease Control is given below:13 Prevention of Central Venous Catheter Infections zz zz zz

Educate personnel about catheter insertion and care. Use chlorhexidine to prepare the insertion site. Use maximal barrier precautions during catheter insertion.

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

with

Use peptic ulcer disease prophylaxis.

For any ICU, written protocols must be developed based on the local ecology of microorganisms and their pattern of resistance. This is best done in consultation with the Dept. of Microbiology. An infectious disease specialist consultation helps in improving the accuracy of the prescription of antimicrobial drugs.

regularly

Give ‘sedation vacation’ and assess readiness to extubate daily.

Antibiotic Class Cycling

oropharynx

Place bladder catheters only when absolutely needed (e.g. to relieve obstruction), not solely for the provider’s convenience. Use aseptic technique for catheter insertion and urinary tract instrumentation. Minimize manipulation or opening of drainage systems. Ask daily: Is the catheter needed? Remove catheter if not needed.

Prevention of Surgical-site Infections zz zz

zz zz

Choose a surgeon wisely. Administer prophylactic antibiotics within one hour before surgery; discontinue within 24 hours. Limit any hair removal to the time of surgery; use clippers or do not remove hair at all. Prepare surgical site with chlorhexidine-alcohol. Maintain normal perioperative blood glucose levels (cardiac surgery patients). Maintain perioperative normothermia (colorectal surgery patients). 21

review article Prevention of Pathogen Cross-transmission

5. Kanj SS, Kanafani ZA. Current concepts in antimicrobial therapy against resistant gram-negative organisms: extended-spectrum beta-lactamaseproducing Enterobacteriaceae, carbapenem-resistant Enterobacteriaceae, and multidrug-resistant Pseudomonas aeruginosa. Mayo Clin Proc 2011;86(3):250-9.

Cleanse hands with alcohol hand rub before and after all contacts with patients or their environments. References 1. O’Grady NP, Barie PS, Bartlett JG, Bleck T, Carroll K, Kalil AC, et al; American College of Critical Care Medicine; Infectious Diseases Society of America. Guidelines for evaluation of new fever in critically ill adult patients: 2008 update from the American College of Critical Care Medicine and the Infectious Diseases Society of America. Crit Care Med 2008;36(4): 1330-49.

6. American Thoracic Society; Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcareassociated pneumonia. Am J Respir Crit Care Med 2005;171(4):388-416. 7. Mermel LA, Allon M, Bouza E, Craven DE, Flynn P, O’Grady NP, et al. Clinical practice guidelines for the diagnosis and management of intravascular catheterrelated infection: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis 2009;49(1):1-45.

2. Fry DE. Fever in the ICU. The ICU Book 2008; 39(3):716.

8. Hooton TM, Bradley SF, Cardenas DD, Colgan R, Geerlings SE, Rice JC, et al; Infectious Diseases Society of America. Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 International Clinical Practice Guidelines from the Infectious Diseases Society of America. Clin Infect Dis 2010;50(5):625-63.

3. Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al; International Surviving Sepsis Campaign Guidelines Committee; American Association of Critical-Care Nurses; American College of Chest Physicians; American College of Emergency Physicians; Canadian Critical Care Society; European Society of Clinical Microbiology and Infectious Diseases; European Society of Intensive Care Medicine; European Respiratory Society; International Sepsis Forum; Japanese Association for Acute Medicine; Japanese Society of Intensive Care Medicine; Society of Critical Care Medicine; Society of Hospital Medicine; Surgical Infection Society; World Federation of Societies of Intensive and Critical Care Medicine. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36(1):296-327.

9. Textoris J, Wiramus S, Martin C, Leone M. Overview of antimicrobial therapy in intensive care units. Expert Rev Anti Infect Ther 2011;9(1):97-109. 10. Schuetz P, Albrich W, Mueller B. Procalcitonin for diagnosis of infection and guide to antibiotic decisions: past, present and future. BMC Med 2011;9:107. 11. Harbarth S, Haustein T. Year in review 2009: Critical Care - infection. Crit Care 2010;14(6):240. 12. Kollef MH. Optimizing antibiotic therapy in the intensive care unit setting. Crit Care 2001;5(4):189-95. 13. Robert A. Weinstein. Health Care-Associated Infections. Harrison’s Principles of Internal Medicine (Volume 1); 131(18):1114.

4. Munford RS. Severe sepsis and septic shock. In: Harrison’s Principles of Internal Medicine. Volume 2, 2012;271(18):p.2229.

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

case report clinical practice

Ruptured Pulmonary Hydatid Cyst: The Camalote Sign Manjot Kaur*, Rakendra Singh**

Abstract Echinococcosis or hydatid disease is caused by larvae of the tapeworm Echinococcus. It remains an important health problem; especially in regions with inadequate hygienic environments and poor veterinarian control. Liver is the most common organ of involvement in adults and lung is commonly involved in younger people. The cysts are characteristically seen as solitary or multiple circumscribed or oval masses on imaging. The characteristic imaging appearance changes with rupture of cyst. Surgery is the recommended form of treatment. We present a case of pulmonary hydatid cyst with communicating rupture into the bronchus which is not very common. Key words: Hydatid cyst, rupture, computed tomography

ast majority of infestations in humans are caused by Echinococcus granulosus. E. granulosus causes cystic echinococcosis, which has a worldwide distribution.1 Humans are exposed less frequently to E. multilocularis, which causes alveolar echinococcosis. The hydatid tapeworm (E. granulosus) requires two hosts to complete its life cycle. Dogs (and other canines) are the definitive host and a variety of species of warm-blooded vertebrates (sheep, cattle, goats, horses, pigs, camels and humans) are the intermediate host. Humans are accidental hosts and do not play a role in the biological cycle. As two mammalian species are required for completion of the life cycle, direct transmission of echinococcosis from human-to-human does not occur.

stable and had mild respiratory distress. Patient was afebrile and had no cyanosis or pallor. A previous computed tomography (CT) scan, done about a month back at another center, showed a well-defined cystic lesion measuring 10.1 Ă&#x2014; 7.2 cm in size in posterior basal segment of left lower lobe (Fig. 1) and suspected diagnosis of intrapulmonary hydatid cyst was given. On presentation at our institute, a CT scan was planned. CT scanning of the lungs with CT/e scanner (GE; Milwaukee, USA) using 130 mA, 120 kV, 7-s scan time, 512 Ă&#x2014; 512 matrix and 7 mm section thickness was done. AP scout film of CT showed a well-defined

Case Report KL, a 70-year-old male came to the medicine department of our hospital with complaints of dyspnea, productive cough and pain chest following a mild chest trauma. He mentioned that his expectoration was salty in taste. On general examination, patient was hemodynamically

*Assistant Professor, Dept. of Radiodiagnosis **Assistant Professor, Dept. of Internal Medicine Adesh Institute of Medical Sciences and Research, Bathinda, Punjab Address for correspondence Dr Manjot Kaur 118/1 Gurjaipal Nagar, Jalandhar, 144 001, Punjab E-mail: drmanjot@hotmail.com

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Figure 1. Axial CT of chest (mediastinal window) showing well-defined cystic lesion in the posterior basal segment of left lung lower lobe.

case report

Figure 2. CT scout film showing a cavitating lesion in the left lower zone abutting the left dome of diaphragm.

Figure 3. Axial CT of chest (lung window) shows spherical cystic lesion (HC) with air-fluid level and surrounding consolidation in the posterior basal segment of left lung lower lobe.

Figure 4. Axial CT of chest (mediastinal window) shows a cystic lung lesion (HC) with dependent wavy contour consistent with germinative membranes (GM), the camalote or the water lily sign. Minimal left pleural effusion seen.

Figure 5. Axial CT of upper abdomen showing a well-defined cystic lesion in the gastrophrenic ligament proven to be hydatid cyst at surgery.

oval cavitating lesion with air-fluid level in the lower zone of left lung abutting the left dome of diaphragm (Fig. 2). On CT axial sections, a large spherical air-filled cavity with collapsed membranes was seen in the posterior basal segment of left lung (Figs. 3 and 4). It was surrounded by an area of consolidation. Left pleural effusion was noted.

Discussion

Well-defined cysts were also seen in the liver and gastrophrenic ligament on CT (Fig. 5). Diagnosis of findings suggestive of pulmonary hydatid cyst with communicating rupture into bronchus was given. The Casoni and indirect hemagglutination tests were found to be positive. Diagnosis was confirmed at surgery.

Pulmonary hydatid cyst may rupture into pleural cavity, pericardium or the bronchial tree leading to cough, chest pain and hemoptysis. The patients define this as a salty or peppery water expectoration, indicating spring-water expectoration and it may even be an expectoration of membrane particles.3

Hydatid disease is one of the most important helminthic diseases. The lung is the second most common involved organ, but in children it is the commonest site. The lung may be affected when the liver is bypassed via the lymphatic system.2

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

case report The most frequent complication of pulmonary hydatid disease is the rupture of the cyst into a bronchus, which is also regarded as a complicated cyst.4 The ruptured echinococcal cysts are of three types: Contained, communicating and direct. Contained rupture occurs when only the parasitic endocyst ruptures and the cyst contents are confined within the host-derived pericyst.

CT scan is useful to confirm the diagnosis and it is also able to demonstrate cysts not identified with plain radiographs.8 Apart from the classically described features of pulmonary hydatid disease, a crescentshaped rim of air at the lower end of the cyst (inverse crescent sign) and a bleb of air in the wall of as-yet unruptured cysts (signet ring sign) have also been described on CT scan.9

When cyst contents escape bronchial or biliary radicles that are incorporated in the pericyst, the rupture is communicating. Direct rupture occurs when both the endocyst and the pericyst tear, spilling cyst contents directly into the peritoneal or pleural cavities or occasionally into other structures. Communicating and direct forms have more serious clinical implications than contained rupture, but even contained rupture should have prompt surgical attention to prevent it from developing into one of the other forms.5

Conclusion

In our case, a cavity with air-fluid level and collapsed germinative layers consistent with direct rupture of hydatid cyst into left lower bronchus was seen. Surrounding consolidation and mild pleural effusion was likely due to inflammatory response to endobronchial spread of cyst contents as no larvae/membranes could be elucidated in the pleural fluid. Conventional chest radiography has been the mainstay investigation for diagnosis of hydatid disease of the lungs, often coupled with Casoni’s skin testing and serologic testing for antibodies. A variety of descriptive have been given to plain film findings if rupture of cyst occurs with the air around or within the endocyst, an air-fluid level and the collapsed, crumpled membranes floating in the fluid. The ‘camalote or water lily’ sign is described when endocyst membrane float on top of remaining fluid due to collapse of endocyst and partial evacuation of fluid. This was demonstrated in our case. The other signs named are the ‘meniscus/crescent’ sign, the sign of the ‘rising sun’, the ‘serpent’ sign, the ‘whirl’ sign, the ‘onion peel’ sign and the ‘cumbo’ sign.6-8 Sometimes, after rupture of a cyst into the bronchus, an inflammatory reaction may close the draining bronchus and imprison the membrane (incarcerated membrane). In these cases the definite regular outline is lost and there may be a blurred shadow that can easily be mistaken for tuberculous focus or carcinoma (Ivanissevich sign).3 Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

CT helps to elucidate the cystic nature of the lung mass, its accurate localization and evidence of any form of rupture so that surgical treatment can be planned at the first opportunity to avoid potentially fatal complications. References 1. Kurt Y, Sücüllü İ, Filiz Aİ, Urhan M, Akın ML. Pulmonary echinococcosis mimicking multiple lung metastasis of breast cancer: The role of fluoro-deoxyglucose positron emission tomography. World J Surg Oncol 2008;6:7. 2. Rebhandl W, Turnbull J, Felberbauer FX, Tasci E, Puig S, Auer H, et al. Pulmonary echinococcosis (hydatidosis) in children: results of surgical treatment. Pediatr Pulmonol 1999;27(5):336-40. 3. Xanthakis D, Efthimiadis M, Papadakis G, Primikirios N, Chassapakis G, Roussaki A, et al. Hydatid disease of the chest. Thorax 1972;27:517-28. 4. Doğan R, Yüksel M, Cetin G, Süzer K, Alp M, Kaya S, et al. Surgical treatment of hydatid cysts of the lung: report on 1055 patients. Thorax 1989;44(3):192-9. 5. Lewall DB, McCorkell SJ. Rupture of echinococcal cysts: diagnosis, classification, and clinical implications. AJR Am J Roentgenol 1986;146(2):391-4. 6. Pedrosa I, Saíz A, Arrazola J, Ferreirós J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics 2000;20(3):795-817. 7. Haliloglu M, Saatci I, Akhan O, Ozmen MN, Besim A. Spectrum of imaging findings in pediatric hydatid disease. AJR Am J Roentgenol 1997;169(6):1627-31. 8. Celik M, Senol C, Keles M, Halezeroglu S, Urek S, Haciibrahimoglu G, et al. Surgical treatment of pulmonary hydatid disease in children: report of 122 cases. J Pediatr Surg 2000;35(12):1710-3. 9. Koul PA, Koul AN, Wahid A, Mir FA. CT in pulmonary hydatid disease: unusual appearances. Chest 2000;118(6):1645-7.

case report clinical practice

Cardiac Arrest Following Neostigmine in Patients on b-blocker Gunjan Chaudhry*, V Kathuria*, K Vashisht*

Abstract Neostigmine (anticholinesterases) is long been used to antagonize the effect of nondepolarizing muscle relaxants after surgery. Sinus bradycardia is the most common arrythmia associated with neostigmine. We report a 50-year-old female with diagnosis of fracture shaft humerus posted for open reduction and internal fixation. She was on b-blocker atenolol 50 mg once a day from two years prior to date of trauma. After completion of surgery reversal was planned when patient had adequate respiratory efforts. Injection neostigmine mixed with atropine was administered to the patient. She immediately developed severe bradycardia and heart rate dropped to 30 beats/minutes and further to 20 beats/minutes and near asystole. Immediately 1.2 mg of atropine was given and heart rate restored to 78 beats/minutes. All anesthetists should be familiar about the side effects of the drugs like neostigmine which can be life-threatening. Key words: Neostigmine, b-blocker, cardiac arrest

eostigmine (anticholinesterases) is long been used to antagonize the effect of nondepolarizing muscle relaxants after surgery. Cautious use of neostigmine is recommended in conditions like epilepsy, asthma, hyperthyroidism, cardiac arrythmias, bradycardia, etc. Sinus bradycardia is the most common arrythmia associated with neostigmine but rarely can result in atrioventricular (AV) block, nodal rhythms, nonspecific ECG changes and cardiac arrest.1

Case Report We report a 50-year-old female with diagnosis of fracture shaft humerus posted for open reduction and internal fixation. On preoperative examination, patient was found to be hypertensive and was on b-blocker atenolol 50 mg once a day from two years prior to date of trauma. Her preoperative blood pressure was 140/90 and pulse rate 68 beats/minute. All the investigations including ECG were within normal limits. After the standard induction patient was intubated and maintained on O2, N2O and isoflurane mixture and atracurium given as a nondepolarizing muscle relaxant. Surgery continued for one and a half

*Senior Resident Dept. of Anesthesiology and Critical Care Pt. BD Sharma, PGIMS, Rohtak, Haryana Address for correspondence Dr Gunjan Chaudhry Senior Resident House No. 424, Sector-14, Rohtak - 124 001, Haryana E-mail: gunjan26117@rediffmail.com

hour and intraoperative period showed no fluctuations in heart rate and blood pressure. After completion of surgery reversal was planned when patient had adequate respiratory efforts. Injection neostigmine mixed with atropine was administered to the patient. She immediately developed severe bradycardia and heart rate dropped to 30 beats/minutes and further to 20 beats/minutes and near asystole. Immediately 1.2 mg of atropine was given and heart rate restored to 78 beats/minutes. Discussion Neostigmine inhibits the enzyme cholinesterase, resulting in accumulation of acetylcholine at cholinergic receptors. As the concentration of muscle relaxant decreases at the neuromuscular junction due to hydrolysis and redistribution and accumulated acetylcholine competes with the relaxants to reverse the residual neuromuscular blockade.2 Cardiovascular effect of neostigmine depends on stimulation of muscuranic and nicotinic receptors.3 Arrythmias and cardiac arrest have been reported following the administration of neostigmine and atropine or glycopyrrolate.4-6 Injection of mixture of neostigmine and atropine impairs cardiac baroreflex sensitivity. Parasympathetic modulation of heart rate is said to be impaired for at least 120 minutes after administration of drug.3,7 When neostigmine and atropine are given in combination the vagolytic effect of atropine precedes the muscuranic effects of neostigmine by 1-2 minutes but when given in small doses produces significant decrease Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

case report in heart rate and large doses can result in dysrhythmias.3 Cautious use of neostigmine is recommended when patients are on drugs like b-blockers, calcium channel blockers and digoxin.1 Conclusion All anesthetists should be familiar about the side effects of the drugs like neostigmine which can be life-threatening. We recommend the slow administration of the drug over the period of five minutes and its cautious use in patients on b-blocker. Reversal in such patients can be alternatively tried with the newer drugs like ‘gamma cyclodextrin’. References 1. Payne JP, Hughes R, Al Azawi S. Neuromuscular blockade by neostigmine in anaesthetized man. Br J Anaesth 1980;52(1):69-76.

2. Calvey TN, Wareing M, Williams NE, Chan K. Pharmacokinetics and pharmacological effects of neostigmine in man. Br J Clin Pharmacol 1979;7(2): 149-55. 3. Ali L, Akhtar M. Cardiac arrest following the neuromuscular blockade reversal with neostigmine and atropine. Professional Med J 2004;11(2):228-31. 4. Lawson JI. Cardiac arrest following the administration of neostigmine. Br J Anaesth 1956;28(7):336-7. 5. Pooler HE. Atropine, neostigmine and sudden deaths. Anaesthesia 1957;12(2):198-202. 6. Lee YW, Lee YS, Park KW. A clinical comparative study of glycopyrrolate and atropine mixed to neostigmine. Korean J Anesthesiol 1982;15(3):274-80. 7. van Vlymen JM, Parlow JL. The effects of reversal of neuromuscular blockade on autonomic control in the perioperative period. Anesth Analg 1997;84(1): 148-54.

What Percentage of Medical Errors are Avoidable? According to a November 2010 study by the Office of Inspector General of the U.S. Department of Health and Human Services, about 1 in 7 Medicare patients in hospitals experience a serious medical error. Of these, 44% percent are preventable. –– U.S. Department of Health and Human Services, Office of the Inspector General, Adverse Events in Hospitals: National Incidence Among Medicare Beneficiaries (November 2010), pp. i–ii, found at http://oig. hhs.gov/oei/reports/oei–06–09–00090.pdf. No such data from India is available. —Prof. M C Gupta

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

case report clinical practice

Scorpion Bite causing Acute Severe Myocarditis: A Rare Complication Tarachand Saini*, Shailendar Gupta**, Maniram Kumhar†

Abstract Scorpion bites are common in India as well as in other countries. Usually, these bites are harmless but sometime have serious clinical sequelae, including death. We report herein a case of scorpion bite that presented with acute severe myocarditis - a rare complication. Key words: Scorpion bite, severe myocarditis, pulmonary edema

here are about 1,500 species of scorpions worldwide, out of these 50 are dangerous to human. Among 86 species in India, Mesobuthus tamulus and Palamnaeus swammerdami are of medical importance.1 Almost all lethal scorpions except Hemiscorpius species, belong to the scorpion family called Buthidae. The lethal member of Buthidae include genera Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus and Centruroides. Scorpions live in warm dry regions throughout India. They commonly inhabit the crevices of dwellings, underground burrows, under logs or debris, paddy husk, sugarcane fields, coconut and banana plantations. Their distribution is more in regions with abundant red soil.2 They hunt during night and hide in crevices and burrow during the day to avoid light. Scorpion stings increase dramatically in summer months and lower in winter. Scorpion stings causes a wide range of manifestation, from local skin reaction to neurological,

*2nd Year Resident **3rd Year Resident † Associate Professor Dept. of Medicine Jawaharlal Nehru Medical College, Ajmer Address for correspondence Dr Tarachand Saini 20, Gaurav Enclave, Near City Palace, Civil Line Ajmer, Rajasthan E-mail: drtcsaini20@gmail.com

respiratory and cardiovascular collapse. Cardiovascular effect are particularly prominent after stings by Indian red scorpion (M. tamulus).3 Case Report An 18-year-old girl was stung by a scorpion on the distal phalanx of the left index finger and presented with intense pain and swelling on the local site. She admitted with heart rate 140 beats/minute, and blood pressure 70/40 mmHg. Symptomatic treatment was given. But the patient’s condition continued to worsen, and she developed severe respiratory distress. Because of respiratory failure, she was immediately intubated and admitted to the intensive care unit. Bilateral basal rales were heard on auscultation, and cardiovascular examination revealed a loud S3 gallop at the apex. Laboratory results were as follows: Hemoglobin was 12.6 g/dl, white blood cell count was 24,380 cells/mm3, platelet count was 1,80,000 cells/mm3 and urine microscopy showed hematuria. Blood urea 71 mg/dl (17-43 mg/dl), serum creatinine 1.6 mg/dl (0.5-1.1 mg/ dl), aspartate transaminase 93 U/l (5-38 U/l), alanine transaminase 30 U/l (5-41 U/l), creatine kinase (CK) 743 U/l (26-190 U/l), CK-MB 52 U/l (0-24 U/l), Trop-I 0.02 ng/ml (0.00-0.04 ng/ml). An electrocardiogram (ECG) revealed sinus tachycardia and ST-T wave changes. Chest X-ray demonstrated bilateral fluffy shadows indicative of pulmonary edema (Fig. 1). Echocardiography reveal hypokinesia of the basal Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

case report Discussion Scorpion venom may contain multiple toxin-like neurotoxin, cardiotoxin, nephrotoxin and hemolytic toxin. The primary targets of scorpion venom are voltage-dependent ion channels. The long-chain polypeptide neurotoxin causes stabilization of voltagedependent sodium channels in the open state leading to continuous, prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic neurons results in autonomic and neuromuscular overexcitation symptoms due to release of excessive neurotransmitters such as epinephrine, norepinephrine, acetylcholine glutamate and aspartate. Meanwhile, the short polypeptide neurotoxin blocks the potassium channels.

Figure 1. Chest X-ray showing bilateral fluffy shadows.

Figure 2. Echocardiography.

two-third of the interventricular septum with reduced ejection fraction (Fig. 2). In accordance with these symptoms and findings, a diagnosis of acute heart failure with pulmonary edema was made. Dopamine, dobutamine, diuretics and steroids were given. With treatment, patientâ&#x20AC;&#x2122;s status improved. Repeat chest X-ray was clear within 24 hours of initiating this treatment. Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Scorpion bites usually have a good prognosis. However, occasionally potentially fatal complications such as myocarditis, pulmonary edema and shock occur.4 Among these, myocarditis and resultant pulmonary edema are important causes of death.5 Three possible mechanisms might explain cardiac dysfunction, including adrenergic myocarditis, toxics myocarditis and myocardial ischemia. a-receptor stimulation by toxins play a major role in development of tachycardia, myocardial dysfunction and pulmonary edema.6 Unopposed a-receptors stimulation lead to suppression of insulin secretion, hyerglycemia, hyperkalemia, free fatty acid and free radical accumulation that are injurious to myocardium. Bahloul et al4 examined the histopathology of two fatal myocarditis cases resulting from a scorpion bite. The pathologic conditions revealed a mixed picture of toxic myocarditis and coagulative myocytolysis, similar to catecholamineinduced cardiotoxicity.4 Myocardial ischemia is not only due to the release of catecholamines but also due to effect of cytokines and/or neuropeptide Y on coronary vessels. Cardiac damage might be enhanced by the depressive effect of cytokines upon myocardial cells. Hyperglycemia may also contribute to myocardial injury.7 Valdivia et al8 reported a series of 32 children with scorpion bites who developed cardiac complications. Among these, 50% exhibited myocarditis, 12.5% had subclinical disease, and 63% had observable ECG changes. We observed both ECG changes and myocarditis in this case. 29

case report Conclusion We report here the case of an 18-year-old girl who developed life-threatening, acute toxic myocarditis and pulmonary edema, after a scorpion bite. Aggressive medical treatment with inotropic agents, diuretics and parenteral corticosteroids resulted in rapid clinical resolution. References 1. Erfati P. Epidemiology, symptomatology and treatment of buthinae stings. In: Arthpod Venoms. Handbook of Experimental Pharmacology. Bettini S (Ed.), SpringerVerlag: New York 1978:p.312-5. 2. Bawaskar HS. Personal communication. 1998. 3. Bawaskar HS, Bawaskar PH. Indian red scorpion envenoming. Indian J Pediatr 1998;65(3):383-91.

4. Bahloul M, Kallel H, Rekik N, Ben Hamida C, Chelly H, Bouaziz M. Cardiovascular dysfunction following severe scorpion envenomation. Mechanisms and physiopathology. Presse Med 2005;34(2 Pt 1):115-20. 5. Gueron M, Yaron R. Cardiovascular manifestations of severe scorpion sting. Clinicopathologic correlations. Chest 1970;57(2):156-62. 6. Bawaskar HS, Bawaskar PH. Management of the cardiovascular manifestations of poisoning by the Indian red scorpion (Mesobuthus tamulus). Br Heart J 1992;68(5):478-80. 7. Garg AK, Pimparkar AB, Abraham P, Chikhalikar AA. Myocarditis and pulmonary edema following scorpion bite. (A case report). J Postgrad Med 1983;29(1):46-8. 8. Valdivia HH, Kirby MS, Lederer WJ, Coronado R. Scorpion toxins targeted against the sarcoplasmic reticulum Ca(2+)-release channel of skeletal and cardiac muscle. Proc Natl Acad Sci U S A 1992;89(24):12185-9.

I have Received a Summon from the Magistrate’s Court to Appear as a Witness. It Contains no Details. The Police Man Informed that it Concerns a Case Filed by the Wife Against the Husband and I had Allegedly Treated the Wife as an OPD Patient in 2003 and that the Summon is Meant to Confirm my Outpatient Prescription. Should I Appear?? There is no question of your not appearing. If a court summons you, you must appear. Not doing so is a punishable offence. zz The police man is possibly right. When the woman produces your prescription to substantiate her allegation, the prescription itself must be “proved”, which means it must be authenticated as genuine by the one who wrote it. The prosecution lawyer (Public prosecutor) might ask you questions like the following: Was this prescription written by you? Is it in your handwriting and bears your signature? You may answer to these in the affirmative. No other questions may be asked from you. If they are asked, you may apply truthfully without any fear or anxiety. —Prof. M C Gupta

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Clinical Algorithm clinical practice

Initial Assessment and Evaluation of the Patient with Acute Chest Pain Chest pain consistent with coronary ischemia

Within 10 minutes l

Initial evaluation

12 lead ECG

Establish IV access

Establish continuous ECG monitoring

Aspirin 160-325 mg chewed

Blood for baseline serum cardiac markers

Therapeutic/Diagnostic tracking according to 12-lead ECG results

Nondiagnostic/ normal ECG

Continue evaluation/monitoring in emergency department

ECG suggestive of ischemia - T wave inversion or ST depression

Anti-ischemia therapy

ST segment elevation or new bundle branch block

Assess suitability for reperfusion l

? Contraindications for fibrinolysis

Serial serum cardiac marker levels - CK-MB subforms

Availability and appropriateness of primary angioplasty

Serial ECGs

Initiate anti-ischemia therapy

Consider noninvasive evaluation of ischemia

Consider alternative diagnoses

No evidence of MI or ischemia

l Analgesia

l Nitroglycerine

Analgesia

MI or demonstrable ischemia

Discharge with follow-up as appropriate (Goal: 8-12 hours)

b-blocker

Admission blood work

Admit to unit of appropriate intensity

Admission blood work l CBC l

Electrolytes, BUN, creatinine

Lipid profile

Initiate fibrinolysis if indicated. (Goal: 30 minutes from entry to ED)

ECG: Electrocardiogram; CK-MB: Creatine kinase-MB; MI: Myocardial infarction; CBC: Complete blood count; BUN: Blood urea nitrogen; PTCA: Percutaneous transluminal coronary angioplasty; ED: Emergency department; CCU: Coronary care unit.

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

Primary PTCA, if available and suitable. (Goal: PTCA within 90 Âą 30 minutes)

Admit-CCU Source: IJCP

Practice Guidelines clinical practice

Updated Guidelines on Management of Atrial Fibrillation from the ACCF/AHA/HRS

he American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the Heart Rhythm Society (HRS) have released updated guidelines for the management of atrial fibrillation. Since the previous guidelines were issued in 2006, new data have become available on strict versus lenient heart rate control, the combined use of antiplatelet and anticoagulation therapy, and the use of dronedarone. Table 1 summarizes the new and modified recommendations. Recommendations on the thrombotic agent dabigatran and the Watchman device for atrial appendage closure were not included in this update because neither was approved for clinical use by the U.S. Food and Drug Administration at the time of organizational approval of these guidelines. Rate Control Parameters for optimal rate control in patients with atrial fibrillation are controversial, and there is no standard method for assessing heart rate control to guide treatment. Generally accepted criteria for rate control include a ventricular rate between 60 and 80 beats per minute at rest and between 90 and 115 beats per minute during moderate exercise. The definition of adequate rate control has been based primarily on short-term hemodynamic benefits. This definition has not been well studied with respect to quality of life, symptoms, development of cardiomyopathy, and ventricular response to atrial fibrillation. Data have not demonstrated clinically relevant differences in outcomes between strict rate control (less than 80 beats per minute at rest and less than 110 beats per minute during moderate exercise) and lenient rate control (less than 110 beats per minute at rest). Lenient rate control requires fewer outpatient visits and examinations, and is generally more convenient for patients. Because it has not been proven inferior to strict rate control, lenient rate control is a reasonable strategy in patients with permanent atrial fibrillation. Data also have shown no benefit of rhythm control compared with rate control in patients with atrial fibrillation and systolic heart failure.

Source: Adapted from Am Fam Physician. 2011;84(11):1298-1306.

Combination Anticoagulant and Antiplatelet Therapy Studies have shown that oral anticoagulation therapy with warfarin is superior to the combination of aspirin and the antiplatelet agent clopidogrel for preventing vascular events in patients with atrial fibrillation. Treatment with clopidogrel and aspirin was associated with a risk of bleeding similar to that of treatment with warfarin. In patients with atrial fibrillation who are not suitable candidates for warfarin therapy, treatment with clopidogrel and aspirin was shown to reduce the risk of major vascular events, especially stroke, compared with patients taking aspirin plus placebo. However, the combination of aspirin and clopidogrel also increased the risk of major hemorrhage. Use of clopidogrel and aspirin plus warfarin (i.e., triple therapy) has been proposed for treating and preventing complications of two or more coexisting conditions (e.g., atrial fibrillation, mechanical valve prosthesis, presence of drug-eluting stent). This combination is associated with an increased risk of bleeding complications, and no randomized trials of this strategy have been reported. Dronedarone Therapy Dronedarone, which is similar to amiodarone, has been shown to reduce hospitalization for cardiovascular problems in patients with paroxysmal or persistent atrial fibrillation or atrial flutter and risk factors for thromboembolism. The recommended oral dosage of dronedarone is 400 mg twice per day with meals. Major adverse effects include bradycardia and QT prolongation. Dronedarone also has been shown to increase mortality in patients with a recent episode of decompensated heart failure and depressed left ventricular function. Sinus Rhythm Maintenance Catheter ablation has been shown to provide one year or more of freedom from recurrent atrial fibrillation; however, additional studies are needed to determine long-term effectiveness of sinus rhythm maintenance. Ablation has been studied in patients with symptomatic paroxysmal atrial fibrillation that has not responded to treatment with one or more antiarrhythmic drugs, with normal or mildly dilated atria, normal or mildly reduced ventricular function, and absence of severe pulmonary disease. Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

practice guidelines Table 1. 2011 Focused Update Recommendations on Managing Atrial Fibrillation Recommendation

Comments

Rate control Treatment to achieve strict control of heart rate (less than 80 beats per minute at rest or less New recommendation than 110 beats per minute during a six-minute walk) is not beneficial compared with achieving Class III (no benefit) a resting heart rate of less than 110 beats per minute in patients with persistent atrial Level of evidence: B fibrillation who have stable ventricular function (left ventricular ejection fraction greater than 40 percent) and no or acceptable symptoms related to the arrhythmia, although uncontrolled tachycardia may be associated over time with a reversible decline in ventricular performance. Combination anticoagulant and antiplatelet therapy The addition of clopidogrel to aspirin therapy to reduce the risk of major vascular events, including stroke, may be considered in patients with atrial fibrillation in whom oral anticoagulation with warfarin is unsuitable because of patient preference or the physicianâ&#x20AC;&#x2122;s assessment of the patientâ&#x20AC;&#x2122;s ability to safely sustain anticoagulation therapy.

New recommendation Class IIb Level of evidence: B

Dronedarone therapy Use of dronedarone is reasonable to decrease the need for hospitalization for cardiovascular events in patients with paroxysmal atrial fibrillation or after conversion of persistent atrial fibrillation. Dronedarone can be initiated during outpatient therapy.

New recommendation

Dronedarone should not be administered to patients with class IV heart failure or patients who have had an episode of decompensated heart failure in the past four weeks, especially if they have depressed left ventricular function (left ventricular ejection fraction of 35 percent or less).

New recommendation

Class IIa Level of evidence: B Class III (harm) Level of evidence: B

Sinus rhythm maintenance Catheter ablation performed in experienced centers is useful in maintaining sinus rhythm in select patients with significantly symptomatic, paroxysmal atrial fibrillation who have been unsuccessfully treated with an antiarrhythmic drug and have normal or mildly dilated left atria, normal or mildly reduced left ventricular function, and no severe pulmonary disease.

Modified recommendation (class of recommendation changed from IIa to I, wording revised, and level of evidence changed from C to A) Class I Level of evidence: A

In patients with atrial fibrillation without structural or coronary heart disease, initiation of propafenone or flecainide can be beneficial on an outpatient basis in those with paroxysmal atrial fibrillation who are in sinus rhythm at the time of drug initiation.

Modified recommendation (wording clarified) Class IIa Level of evidence: B

Catheter ablation is reasonable to treat symptomatic persistent atrial fibrillation.

New recommendation Class IIa Level of evidence: A

Catheter ablation may be reasonable to treat symptomatic paroxysmal atrial fibrillation in patients with significant left atrial dilatation or significant left ventricular dysfunction.

New recommendation Class IIb Level of evidence: A

Classes: I = Procedure/treatment should be performed/administered; IIa = It is reasonable to perform/administer treatment; IIb = Procedure/treatment may be considered; III (no benefit) = Treatment should not be performed/administered or is not useful; III (harm) = Treatment is harmful or potentially harmful and should not be performed/administered. Levels of evidence: A = Multiple populations evaluated (data from multiple randomized clinical trials or meta-analyses); B = Limited populations evaluated (data from a single randomized clinical trial or nonrandomized studies); C = Very limited populations evaluated (consensus opinion of experts, case studies, or standard of care).

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012

lighter reading clinical practice

As the distance between them continued to narrow, the man could see that the native was picking up starfish that had been washed upon the beach and, one at a time, was throwing them back into the water. Puzzled, the man approached the native and asked what he was doing. “I’m throwing these starfish back into the ocean. You see its low tide right now and all of these starfish have been washed up onto the shore. If I don’t throw them back into the sea, they’ll die up here from lack of oxygen.” “But there must be thousands of starfish on this beach,” the man replied. “You can’t possibly get to all of them. There are just too many. And this same thing is probably happening on hundreds of beaches all up and down this coast. Can’t you see that you can’t possibly make a difference?” The local native smiled, bent down and picked up another starfish, and as he threw it back into the sea he replied, “Made a difference to that one!” Each of us is but one person: limited, burdened with our own cares and responsibilities. We may feel there is so much to be done, and we have so little to give. We’re usually short of everything, especially time and money. When we leave this shore, there will still be millions of starfish stranded on the beach. Maybe we can’t change the whole world, but there isn’t one of us who can’t help change one person’s whole world. One at a time. We can make a difference. —Ms Ritu Sinha

Viruses Coming to a hard drive near you, the worst computer viruses yet: zz AT&T virus: Every three minutes it tells you what great service you’re getting. zz Government Economist virus: Nothing works, but all your diagnostic software says everything is fine. zz Politically correct virus: Never calls itself a “virus.” Instead, it’s an “electronic microorganism.” zz Government Spokesman virus: Nothing works but all your diagnostic software says everything is fine. zz Right to life virus: Won’t allow you to delete a file, regardless of how old it is. If you attempt to erase a file, it requires you to first see a counselor about possible alternatives. —Dr GM Singh

“Prayer is not a ‘spare wheel’ that you pull out when in trouble, but it is a ‘steering wheel’ that directs the right path throughout.”

Dr. Good & Dr. Bad Situation: A 36-year-old executive used to take 5 pegs

of alcohol once a week.

Continue it

Either stop it or just take one peg a day

©IJCP Academy

As a man walked a desolate beach one cold, gray morning he began to see another figure, far in the distance. Slowly the two approached each other, and he could make out a local native who kept leaning down, picking something up and throwing it out into the water. Time and again he hurled things into the ocean.

Laugh a While

How big is one?

QUOTE

An Inspirational Story

Lighter Side of Medicine

Lesson: The French habit of drinking wine almost daily

is less taxing to the heart than the Irish custom of downing an equivalent amount of beer on one or two nights a week, according to a study published in the British Medical Journal. Dr KK Aggarwal

Asian Journal of Critical Care Vol. 8, No. 3, October-December 2012