Vol.12

Sinsgor rydi,REVISWARTICI,DSRecent Advaoces in Hoepital InformaticsSutg Cdr K BoseLong Bone Radiology Soreening fc Dysbaric &conecmsisSury Capt G Yarghese, Col R Rai Kutttar Swg Lt Cdr Rohit Yenu, furg LtCdr LW Rao

UPDATEARflCLESConcepts and Controversies in Post Traumatic EpilepsySlulg CqtKI Mathai, SwgCdr KBoseMedical Organisation During Submarine Operations&try Cdr CS SaxenaORIGINALARTICLESExperie,nce of Nimotuzumab with Concunent ChemoradiotherapySury Cdr Hari Muhtndan, Swg Capt Subhash Ranjan, van, Sury Cdr R ShankaranHyperbaric Oxygen Therapy in Non Healing WoundsSurE Lt Cdr Sourabh Bhunni, Sutg Lt Cdr Rohit YermaRespiratory Muscle Training for Enhanced EnduranceSurE Lt Cdr LV Visweswararao

Effect ofHyperbaric Oxygen Therapy on Pulnonary IndicesSurg Lt Cdr Rohit Yerma

QT Dispersion in Diabetic Patients on Hypcrbaric OxygenSurg Lt Cdr SS Dalowayi, Surg Cdr HBS ChaudhryDisabilites in Naval Aircrew ApplicantsSutg Cdr PD Ayengaa Gp Capt N TanejaTroxerutin in Management of HaemorrhoidsSurg Cdr Ashutosh Chauhan, Maj Sangeeta Ilwari, Col PK Bhatia, Brig AK GaptaCMEFear of Flying in Trained AircrewSurg Cdr RC Yerma (Retd)MCQSwg Lt Cdr Rohit Uerma

CASE REPORTSlnfant with Diabetic KetoacidosisSurg Cdr Ashok K Yadau Sury Capt KM Adhiluri, Sutg Cmde G Gupta, NMPleural Effiision in Extramedullary MyelomaSury Capt S Ranjan, vsu, Sutg Lt Cdr Haimuhtndan, Sury Cmde SR Gedela,Brig UK Sharma, Sutg Capt Naveen ChawlaFingertip Pain due to Glomus TumorSury Capt G Wshwanath, Maj Atul Sahai, Maj Raj Singh, Sutg Capt Naveen ChawlaL€tters to the EditorSubject InderAuthor IndexContents

No. 2 December 2010

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MARINE MEDICAL SOCIETY(Regd F-361 I )

PresidentSurgeon Vice Admiral G Ramdas, SM, VSM

Vice PresidentSurgeon Rear Admirat KK Singh, SM, VSM

Executive Committee

Surg Rear Adm (Mrs) M Jaiprakash Surg Rear Adm yp Monga, NM

Surg RearAdm S Kumar, VSM Surg Cmde N Kannan, VSM

Surg Cmde A Banerjee, SC Surg Cmde AA pawar

Surg Capt G Verghese

SecretarySurg Cdr SS Pundir

TreasurerSurg Cdr P Deshmukh

Address for CorrespondenceSecretary

Marine Medical SocietyINHSAsvini

Colaba, Mumbai 400 005. IndiaWebsite : http ://www. mmsindia. net

JOURNAL OF

MARINEMEDICALSOCIETY

PublishedBiannually

Editor-in-ChiefSurgeon RearAdmiral KK Singh, SM, VSM

EditorSurgeon Commodore VSSR Ryali

Addre s s for C o rre sponde nc eEditor

Journal of Marine Medical SocietyDepartrnent of Psychiafiry,

INHSAsviniColaba, Mumbai 400 005. India

Website : http://www.mmsindia.netemail : joumalofrnms @ yahoo.com

journalofrnms @ gmail.comTelefax :022-22166729

Printed, published and owned by Director General Medical Services (Navy), Sena Bhavan,New Delhi I I 0 0 I I . Printed on his behalf at Typo Graphics, Mumbai 400 I 03.

Editorial

Tbansforming T[aining in Marine Medicine

Surgeon Commodore VSSR Ryali., Surgeon Captain George Varghese#

Key Word : Thaining, Marine medicine, Hyperbaric oxygen therapy

Introduction

Th. Armed Forces Medical Services maintain aI huge med ica l and hea l th re la ted t ra in ing

establishment. The Armed Forces Medical College(AFMC) at Pune, the Army College of Medicine atDelhi and the Army Dental College at Secunderabadtrain competitively selected students in medicine anddentistry at the undergraduate level. Postgraduatetraining in a host of specialties (MD, MS and diplomas)are provided at the AFMC and the larger servicehospitals at Delhi, Bangalore, Kolkota and Mumbai.Training in Service specific subjects like MarineMedicine (Diploma in Marine Medicine) and AerospaceMedicine (MD) are provided at the Institute of NavalMedicine at Mumbai and the Institute of AerospaceMedicine at Bangalore respectively. The Medical (MCI)and Dental Councils of India (DCI) recognize almost allthe courses conducted at these institutions. In addition,nearly 20 Zonal and Command Hospitals offerpostgraduate courses (Diplomat National Board orDNB) in various subjects recognized by the NationalBoard of Examinations. Further, superspeciality ffaining(DM, DNB and MCh) for postgraduates is provided atthe Army Hospital (Research and Referral) at Delhiand Military Hospital (Cardio Thoracic Centre) at Pune.All these institutions function under the aegis of theregional health universities where they are located likethe Maharashtra University of Health Sciences (MUHS)at Nashik.

Nursing cadets are trained for a diploma at eightSchools of Nursing (SON) attached to Zonal andCommand hospitals. Besides, a graduate degree innursing is offered by the College of Nursing (CON) atPune. Currently, only the course at CON is recognizedby the Nursing Council of India (NCD and the MUHS.The paramedical staff comprising soldiers, sailors andairmen, train at the Armed Forces Medical College(AFMC), Pune, Army Medical Corps Centre and College

(AMC C&C), Lucknow, INHS Asvini, Mumbai and theInstitute of Aerospace Medicine (IAM), Bangalore in aplethora of military and civil medical subjects in coursesof varying duration. Most of these courses weredesigned within the Armed Forces and were not peerreviewed and are not supervised by the NCI or theregional health universities. In recent times an efforthas been mounted to modify these courses incollaboration with the regional health Universities andthe NCI so as not only to improve the course content byinvoking peer review, but also to offer soldiers, sailorsand airmen diplomas recognized by the regionaluniversities and the NCI. The Schools of Nursing atMumbai and Kolkata have received approval from theNursing Council of India and the regional healthuniversities to convert to Colleges of Nursing and thefirst batch of BSc (Nursing) graduate students areexpected to commence training in these two collegesfrom the academic year 2010-11 onwards.

In these changing times, is there a scope to improvethe quality of various courses offered at the Institute ofNaval Medicine (INM). Areview of the courses in diving,submarine and undersea medicine held in India andabroad would help us navigate the future.

Long Courses

Practically all Armed Forces of the world, by virtueof operating submarines and divers, have some sort oftraining program for their doctors who deal with thesepersonal. The US Navy imparts a 6 months training todoctors opting for submarine service [1]. Doctors in theRussian Naval submarine service are primarily surgeonsand are trained at the Kirov Military MedicalAcademyat Saint Petersburg which was earlier called Leningradin erstwhile USSR. With the introduction of submarinesin the Indian Navy, the frst batch of Indian doctors wastrained in Marine Medicine for a year at the KirovMilitarv Medical Academv.

'Consultant in Psychiatry, #Senior Advisor in Undersea Medicine, INHS Asvini, Mumbai.

Jour. Marine Medical Society,20l0, Vol. 12, No.2

Since 1 979, a O2-y ear postgraduate diploma course,DMM, is being offered to doctors at the Institute ofNaval Medicine. Mumbai. The course is conductedunder the aegis of Maharashtra University of HealthSciences (MUHS), Nasik. The Diploma in MarineMedicine has recently been recognized by the MCI.The course content consists of physiology and the effectsof altered atmospheric pressure on the body, conceptsof preventive and occupational medicine specific to themaritime milieu, management of medical and surgicalemergencies and hyperbaric medicine. The takers havebeen mainly Service officers and a few civiliancandidates. Doctors in uniform who specialize in thissubject are entrusted with the care of submariners anddivers onboard and are also posted to places wherehyperbaric chambers are available to assist physiciansand surgeons in treating certain disabilities withhyperbaric oxygen therapy (HBOT). The increasingawareness about the benefits of HBOT has led to aproliferation of hyperbaric chambers in the corporatehospitals. Another sector which seeks these speciallyqualified doctors is the burgeoning diving industry whichservices ships and the oil rigs.

The INM has also been conducting a preliminaryunder water medicine course (IIWM ll) of 24 weeksduration and an advanced under water medicine course(UWM I) of further 24 weeks duration for submarinequalified medical sailors. These courses have beendiscontinued for the Indian Naval medical sailors since2009 and are presently being offered only for medicalsailors of friendly international Navies.

Short Courses

A number of short courses in diving medicine areoffered to physicians and other professionals byorganizations that maintain high educational standards.Among the highly regarded are the Undersea andHyperbaric Medical Society (UHMS) [2),the DiversAlert Network (DAN) [3], the American Academy ofUnderwater Sciences (AAUS), the South PacificUndersea Medical Society (SPIIMS) [4] and the BritishSub aqua Club. Courses for doctors who work athyperbaric chambers vary in content and length.Examples of these courses are "Introduction toHyperbaric Medicine" (five days), "Clinical HyperbaricMedicine" (four or five days), "Clinical Applications ofHyperbaric Oxygen Therapy/Wound CareManagement", and "Primary Training in HyperbaricMedicine" (five days). Some courses are aimed at thephysician, who is also a diver and are therefore held atprime diving destinations. They are so scheduled that

Jour Marine Medical Society,2010, Vol. 12, No.2

the doctor can get in a couple of dives a day betweenlectures. These include those offered by "TempleUniversity Underwater Medicine Course" (eight days)and "DAN DivingAccidentand IIBO Medicine Course"(eight days).

The European Committee for Hyperbaric Medicine(ECHM) and European Diving Technology Committee(EDTC) together developed "Training Standards forDiving and Hyperbaric Medicine". The Diving MedicalAdvisory Committee (DMAC) [5] of UK assessesselected courses in diving medicine. The courses soselected are a Level I Medical assessment of divers(Medical Examiner of Divers) course comprising 25hours of theory lectures and 3 hours of practical trainingand the Level II (a) Medical management of divingaccidents and illnesses course (Competence in DivingMedicine) which comprises the Level I course andfurther 30 hours of theory lectures and 10 hours ofpractical training. In India today, barring a few retiredNaval Marine Medicine specialists and the odd civildoctor who has done his DMM, the bulk of physiciansworking in the field of diving and hyperbaric medicinehave acquired qualifications abroad, as these are notobtainable in the counby. The INM is eminently equippedto obtain the necessary certification to conduct coursescomparable to the best offered any where in the world.Such a move, besides getting visibility to the INM andthe Indian Navy, would also lessen the substantialfinancial burden of civilian and the odd service doctorabout to retire who currently goes abroad to get qualified.In addition, it will increase the number of this valuedtechnical manpower in this niche field and therebyincrease the country's competitiveness in diving andundersea related industries.

The Institute of Naval Medicine (tr\rM) conducts athree-month medical course for medical officers andmedical sailors undergoing the basic submarine course,where issues related to submarine and diving medicineand basic HBOT are dealt with. A one-week course forclearance diving officers and sailors on aspects ofdivingmedicine is also conducted. Among the other coursesconducted at INM are a four-week course for NavalMedical officers at the time of induction to Indian Navyand atwo-week course on Medicare for Merchant NavvMasters.

Recent Advances

Modernization and the scheduled induction oftechnologically advanced submarines have necessitatedaugmenting skills of the Marine Medicine specialist. Theinduction of a nuclear propelled vessel adds another

facet in the form of prolonged submergence and non-availability of hospital based facilities. The field ofmilitary diving too is growing exponentially due toequipment complexity, dive profile variations, complexdive techniques and extended stay in the hazardousenvironmeng allof which arepushing thelimits ofhumanendurance, in tenns of depth and duration. Great snideshave also been made in the field of clinical hyperbaricoxygen therapy (IIBOT) in diving related illnesses. Thismodality is also being used to treat a variety of medicaland surgical conditions. INHS Asvini has been providingthis service to both Service and civil patients. Inftoductionof this therapy at the naval hospitals in Visakhapatnamand Kochi would augment the modalities of treatmentprovided by these hospitals.

The Institute of Naval Medicine is currently at anadvanced stage in obtaining recognition for a three-yearpostgraduate degree (DNB) in Marine Medicine. Thiscourse architecture is so designed, that a doctorqualifying would be competent to handle medical,

surgical or radiation related emergencies onboard anuclear propelled vessel and would be capable ofproviding comprehensive medical cover to diving andhyperbaric chamber operations. It is envisaged to offerall submarine medical sailors the two-year diploma inAdvanced Nuning and Critical Care. These sailors willthen be capable assistants to the Marine Medicinespecialist onboard a nuclear submarine or diving vessel.

References

1. Courses offered in the United States Army Medical Corpsavailable at: http ://en.wikipedia.org/wiki/Medical_Corps_(United_States_Navy)

2. Courses and Exams at Undersea & Hyperbaric MedicineSociety available at: http://www.uhms.org/

3. Course offerings at divers alert network available at: http://www. diversalertnetwork. org/

4. Requirements for SPLJMS diploma in diving and hyperbaricmedicine available at: http://www.spums.org.au

5. Courses in diving medicine available at: http://www.dmac-diving.org/courses/

74 Joun Marine Medical Society,2010, Vol. 12, No. 2

Review Article

Recent Advances in Hospital Informatics

Surg Cdr K Bose*

Abstract

Biomedical informatics has applications in nursing, clinical medicine, dentistry, public health and medical nesearch.In 2006, 60Vo of residents in England and Wales had extensive clinical records and their prescriptions wenegenerated on 4000 installations of one system (EMIS). The other 40 % had records stored on assorted SQL or frle-based systems. Hong Kong has a computerized patient record system called the Clinical Management System (CMS)which is used by all 30,000 clinical staff on a daily basis. The comprehensive records of 7 million patients areavailable on-line in the Electronic Patient Record (ePR). Since 20M, radiology image viewing has been added to ePR.Health informatics law deals with privacy, ethical and operational issues. Despite contrary claims made by the ITcompanies, the recent CIIAOS rcport by the Sandish Gmup has estimated that around 40 % of all Eospital Informaticssystems fail. Further research is needed in data capture, data integration, decision support tools, dataftnowledgeaccess and substitutability. Avibrant and evolving healthcarc information technolog5l infrastructure requires to bebased less on monolithic products from singlevendors and mone on a general-purpose platform thatwould supportacollection of simple applications. Health Informatics in combat include data communication systemswhich are ableto transmit combatant's physiologic status through various echelons.

Key Words : Computers, Hospitals, Information technologr

Introduction

he aim of biomedical informatics is to optimizethe processes of Coding, storage, retrieval, and

transmission of data for patient-care, biomedicalresearch, decision making for therapeut ic andpreventive intervention, health service organization andmedical teaching. Biomedical informatics tools includecomputers, clinical guidelines, medical terminologies andinformation and communication systems. It hasapplications in nursing, clinical medicine, dentisty, publichealth and medical research I I ]. Biomedical Informaticsencompasses Anificial Intelligence, Cognitive Sciences,Coding, Classification Terminology, Clinical Guidelines,Telemedicine, Signal processing, Electronic PatientRecords, Information Retrieval, Imaging, Robotics,Virtual Reality, Clinical Decision Support Systems,Medical Language Processing such as the SystematizedNomenclature of Medicine for Cl inical Terms(SNOMED CT) and the Unified Medical LanguageSystem (UMLS) and Standards (e.9. DICOM, HL7)for accurate exchange of data 12,31.

History

Between 1940-1.950, Von Neuman and Morgerstern

developed the axiomatic foundations of formal DecisionMaking Theory. Between 1950-1970, Collen andcolleagues investigated use of computers to improveclinical practice and outcomes at Kaiser Permanenteand Warner and colleagues developed the first successfulcomputerized diagnostic application in congenital heartdisease. Lindberg and Engle developed criteria-baseddiagnostic system. During this period dedicated "legacy"systems, such as laboratory information systems andpharmacy information systems appeared, along withcommercial applications for admission/discharge/transfer, billing and inventory. NLM introducedMEDLINE, a comprehensive computerized researchliterature database and Technicon developed the frstHospital lnformation System (HIS) atEl Caminohospitalin California during this period.

B etween I 970- 1 980, large-scale clinical informationsystems, such as hospital information systems (e.g.,HELP at LDS Hospital in Utah) and elecftonic medicalrecord systems (e.g., PROMIS at the University ofVermont) began to appear at pioneering academicinstitutions, followed laterby commercial products withlimited capabilities. Several prototypical demonsfiationsystems employed symbolic artificial intelligence to

'Officer in Charge, Fleet Medical Centre, Western Fleet, Mumbai and Member,Management System.

Jour Marine Medical Society,2010, Vol. 12, No.2

Implementation Committee for Naval Health Information

/)

support diagnostic and therapeutic decision making. TheINTERMST:I system at the University of Pittsburghcovered the whole of internal medicine and was shownto diagnose difficult cases with an accuracy equal to orat times better than an experienced physician. TheMYCIN system for diagnosis and therapy ofbacteraemia and meningitis was developed and evaluatedat Stanford during this period. Between 1980-1994, theBayesian Network emerged as the predominant modelfor medical knowledge representation and reasoning.Machine learning, data mining and automated discoverymethods were used in biomedicine. Messaging standardsthrough Health level 7 (fil-7) were developed duringthis period.

Between 1995 and today, extensive network-basedapplications such as client-server clinical informationsystems developed. Widespread adopt ion ofmicrocomputer-based clinical applications in medium-to-large sized hospitals and clinics, like laboratory datadisplay and display of textual documents also occurred.Explosive growth of Internet, World-Wide-Web-basedapplications including telemedicine and distributeddatabases took place more recently.

Heatth Informatics Today

In 2001, U.S. Army Medical Research and MaterialCommand (USAMRMC) created a BiomedicalInformatics Roadmap devoted to four focus areas:Hospital and Clinical Informatics, E-Health, CombatHealth Informatics and Biomedical Computation [4]. In20O4, the US Department of Health and Human Services(HHS) formed the Office of the National Coordinatorfor Health Information Technology (ONCHIT) forwidespread adoption of interoperable electronic healthrecords (EHRs) in the US within 10 years. In July, 2006first list of 22 certifred ambulatory EIIR products havebeen released [5-8].

The European eHealth Act ion Plan plays afundamental role in European Union's sftategy of sharingtheir best practices for quality health care [9]. In 2006,60Vo of residents in England and Wales had extensiveclinical records and their prescriptions were generatedon 4000 installations of one system (EMIS). The other4OVo had records stored on assorted SQL or file-basedsystems. The NHS in England has contracted severalvendors for a National Medical Informatics system'NPFIT', that divides the country into five regions, tobe united by a central electronic medical record systemnicknamed "The Spine" [0].The project is howeverbehind schedule and its scope and design are beingrevised.

76

Hong Kong has a computerized patient record systemcalled the Clinical Management System (CMS) whichhas been developed by the HospitalAuthority (HA)since1994. This system has been deployed at all sites oftheAuthority (40 hospitals and 120 clinics), and is used byall 30,000 clinical staff on a daily basis, with a dailyfiansaction of up to 2 million items. The comprehensiverecords of 7 million patients are available on-line in theElectronic Patient Record (ePR) with data integratedfrom all sites. Since 2004, radiology image viewing hasbeen added to ePR, with radiography images from anyHA site being available as part of the ePR.

Health informatics law deals with privacy, ethical andoperational issues. It also deals with the circumstancesunder which data and records are shared with otherareas that support and enhance patient care. The corecomponents of a viable Hospital Informatics systeminclude Electronic Medical Records for billing, schedulingand research, Clinical Decision Support Systems,Standards like DICOM and HL7 to facilitate theexchange of data between healthcare systems,Controlled Medical Vocabularies (CMVs) such as theSystematized Nomenclature of Medicine for ClinicalTerms (SNOMED CT) and hand-held or portabledevices to assist data entry and retrieval.

Electronic Medical Records (EMR)

Two key features of a robust EMR are simplifieddata Entry and quick access to patient status. Data entryis the rate-limiting factor of most EMRs. What is neededis a point-and-click system that enables the clinician toindicate positive and negative findings and uses a lotless free-text. Preoccupation with the keyboard divertsattention from the patient when a doctor might misssomething significant. Rather than type at the keyboard,some clinicians prefer software that converts theirdictated orhand-written notes to digital format. However,this technology has yet to reach errorfree status. EMRsget high marks for speed in accessing patient information,efficiency in chart management and convenience inordering prescriptions. However, there are frequentcomplaints about the lengthy patient charts produced byEMRs. An EMR that generates a clinical summary fromexisting fields would improve physician productivity.There is no "one size fits all" solution to choosing theright EMR. Questions that need to be answered are:What do you want the EMR for? How ready is thenursing staff to adopt technology? How will it benefitthe patient? Realistic needs are to be matched to thecost. However, once hooked on to the right system, theconvenience of EMR is hard to beat.

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Research Needs for Clnical Informatics

Contrary to various claims made by the IT companieswho provide commercial solutions, the recent CHAOSreport by the Standish Group has estimated that around40Vo of all Hospital Informatics systems fail. Furtherresearch is needed in areas of Data Capture, DataIntegration, Decision Support Tools, Data Access andSubstitutability.(a) Data Capture - Analysis is needed of current

voice-activated transcription tools and pen-basednote-taking tools. Multi-modality input (pen+ speech+ keyboard) recovering needs investigation.Advanced natural language processing to extractinformation from clinical notes needs development.

(b) Data Integration - Standardization of existingclinical terminologies to support data integration isbeing undertaken at various cenfres [2]. Integratingclinical guidelines with patient elecftonic medicalrecords is necessary for automated decision-supportsystems.

(c) Decision Support Tools - There is a need todevelop, standardize and encode medical guidelines[3]. Precision of information retrieval from the Webneeds improvement.

(d) Data Access - There is need for better technologyto review medical records and medical literature,including meta analysis and evidenced based studies.

(e) Substitutability - A vibrant and evolvinghealthcare information technology infrastructurerequires to be based less on the present trend ofmonolithic products from single vendors and moreon general-purpose platforms that would support acollection of simple applications, each doing a singletask. There are now more than 20,000 applicationswhich are easily substitutable by the lay person. TheiPhone separates the platform from the functionalityprovided by the applications that consumers candownload and use with the iPhone. If the sameprinciple is applied to the development of platformsforhospital informatics, then, as one's needs evolve,one could substitute simple applications within aplatform. For example, a medication managementapplication could be sourced from one vendor and anotifiable disease reporting tool from another. Asalternative applications are developed by competitors,the existing ones may be upgraded.

Research Needs for Combat Health

Informatics

There are certain specific applications of HealthInformatics in combat.(a) Sensing Devices - Development is needed of

wearable biosensors to monitor physiologic state andinjuries of soldiers [7]. It is envisaged that non-invasive scanning with hand-held devices and sensorvalidation algorithms can be used for injuryassessment.

(b) Communication - Digital photography can be usedfor assessing battlefield casualties through interactivetelemedical communications systems. Datacommunication systems should be able to transmitthe combatant's physiologic status through variousechelons.

(c) Data Warehousing - Combat CommunicationsSystems should be capable of integrating, storingand retrieving patient's records from battlefield tothe hospital.

(d) Sinulator based Tbaining - There is a need todevelop flexible, portable and realistic simulators andtraining tools, as well as computer-based aids fortriage ofinjuries [8].

References

l Hoyt R[ Reifman J, CosterTS, Buller MJ. Combat medicalinformatics: present and future. Presented at the AMIA 2002Symposium, 9-13 November 2002, San Antonio, TX.

2. McCray AI, Miller RA. Making the conceptual connections:The unified medical language system (LJMLS) after a decadeof research and development. ./ Am Med InformAssoc 1998; 5:129-30. [PubMed]

3 . Boxwala AA, e/ al. Toward a representation format for sharableclinical guidelines. J Biomed Inform 2O0l;34 : 157-69.lPubMedl

4. Bzik KD, Bellamy RF. A note on combat casualty statistics.Mil Med 1984:'149 :229-30. [PubMed]

5. Bellamy RF. Death on the battlefield and the role of frst aid.Mil Med 1987; 152 :634-5. [PubMed]

6. Bellamy RF. The causes of death in conventional land warfare:Implications for combat casualty care research. Mil Med 1984;194:55-62.

7. Zajtchuk R, Sullivan GR. Battlefield trauma care: focus onadvanced technology. Mil Med 1995; 160 : l-7.

8. Satava RM. Virtual reality and telepresence for militarymedicine. Ann Acad Med Singapore 1997;26 : ll8-20.lPubMedl

9. Giustini D. How web 2.0 is changing medicine. BMJ 2O06;333:1283-4.

10. Stuart Maguire, Udechukwu Ojiako. Interventions forinformation systems introduction in the NHS. HealthInformatics Journal2007; 13 : 283.

Joun Marine Medical Society,2010, VoL 12, No.2 77

Review Article

Long Bone Radiology Screening for DysbaricOsteonecrosis

Surg Capt GVarghese., ColRRaviKumar*, Surg Lt CdrRohitVerma#, Surg Lt CdrLWRao**

Abstract

Dysbaric osteonecrosis (DOl$ is a disabling illness of professional divers. Long bone plain radiology has been usedas a screening modalityfordetectingDON. Therc are inherent advantages and disadvantageswith the modality. Therecommendation is screeningwith long bone plain radiologr once 5 yearly and MRI screeningat 3 yearintervals forthose at increased risk.

Key Words: Dysbaric osteonecrrsis, Radiology, Scr.eening

Introduction

J\lsbaric Osteonecrosis (DON) is the ischemiclJ death of cellular constituents of bone and bonemarrow caused by exposure to p ressur izedenvironment [1]. It is seen in professional divers whodive deeper than 30 metres, use mixed gas or performdives longer than 4 hours [1]. Divers with increasedage, obesity, alcoholism, cigarette smoking, fatty liver,hyperlipidemia and impaired fibrinolysis with increasedProthrombin Activator Inhibitor (PAI-l) have greatersusceptibility for DON [2-4]. It mainly affects the lowerend of femur (40%o),humeral head (29Vo), femoral head(l6Vo) and upper tibia(l1%o).Its incidence ranges from2.5 Vo in US Navy divers to 50.5Vo in Japanese shellfishdivers [1]. It is generally considered to be a disease ofprofessional divers and caisson workers although itsincidence has occasionally been reported amongrecreational SCUBA divers and dive masters as well

[1,4]. However, its incidence is negligible among aviatorsand hyperbaric chamber attendants [1,4]. It manifestsas a progressive and persistent radiating pain withrestricted joint movement. It usually affects the hip orshoulder and is precipitated by lifting of heavy weights,over months and years [4]. Secondary degenerativeosteoarthritis follows collapse of the articular cartilage,further reducing joint movements.

Etiology is notknown though itis thought tobe alongterm effect of inadequate decompression. It is howeverknown to occur after a single exposure also. Not alld ivers who develop DON have a history of

decompression sickness (DCS); neitherdo all divers whosuffer DCS develop DON [4]. It is postulated thatinappropriate decompression may lead to fat emboliwhich may obstruct end arteries in rigid haversian canalsof bone, leading to osteonecrosis. These fat emboli mayoriginate from fatty liver, coalescence of plasma proteinsor disruption of the bone manow [4]. Another hypothesisis that fat in the bone marrow takes up nitrogen underpressure which expands during decompression. Thisleads to increase in the intramedullary pressure whichcompromises blood flow within non - compliant bonecavities and leads to ischaemia and necrosis [1]. Thearea of necrosis is more widespread than is radiologicallyevident. Revascularization occurs, which leads toformation of a zone of thickened trabeculae separatedfrom the necrotic bone by a line of dead collagen and isthe first sign seen radiologically. The necrotic frabeculae,not strengthened by the revascularization processeventually collapse under load and clinical symptomsmanifest at this stage [4].

Various screening modalities have been employed todetect DON at a stage where further damage can beprevented. Long bone plain radiology, computeizedtomography (CT scan), Magnetic Resonance Imaging(MRI), 99'technetium labeled bone scan and SinglePhoton Emission Computed Tomography (SPECT) havebeen utilized for screening and diagnosis ofthis illness.No modality is ideal and each modality has inherentadvantages, disadvantages, side effects, varying costsand availabilitv issues.

'Senior Advisor and Head of Department (Marine Medicine); *Senior Advisor (Radiodiagnosis and Interventional Radiology), INHS Asvini,Colaba, Mumbai 400 005. *PMO and Graded Spl (Marine Medicine), INS Nireekshak, C/o FMO, Kochi 682 004. *Graded Specialist(Marine Medicine), COMCOS (East), C/o FMO, Visakhapatnam - 530014.

Jour Marine Medical Society,20l0, Vol. 12, No.2

Long Bone Plain Radiology

Long bone plain radiology has been recommendedas a screening modality by various studies [,2,3]. Itinvolves plain radiology ofboth shoulders, hips and kneesby using special projection. These films are taken seriallyat fixed frequencies depending upon the risk stratificationof the diver. Early diagnosis is based on minor alterationsin the trabecular pattern of the bone resulting inabnormal densities or lucencies. Early detection ofasymptomatic lesions may only be verified by serialradiological examination, showing the progression of thelesion [4,5].

The lesions have been classified according to the sitewhere they appear as either Juxta articular lesion (JAlesion or A lesion) or head, neck and shaft lesion (HNSlesion or B lesion) by the Medical Research Council(MRC) of UK 11,6,71. The JA lesions are potentiallydisabling and have been used to disqualify professionaldivers from further diving. Howeveq the problem of whatto do when confronted with an asymptomatic HNS lesionis not yet solved. Some authors suggest restrictions inthose with asymptomatic HNS lesions like disallowingdecompression diving, limiting maximum depth (l8m)and ascent rate, using standard air or helium - oxygentables and disallowing safuration or experimental diving

12,41.A considerable skill is required in the assessment of

radiographs, as these lesions need to be differentiatedfrom similar lesions of bone islands, enchondroma,normal variants and osteoarthritis. Solitary lesions requirecareful assessment, whereas multiple lesions makediagnosis easier. The radiological changes are relativelylate manifestations. The first radiological sign may benoted not earlier than three months and upto an yearafter onset [4].

The radiation hazard associated with radiographicexamination must be kept at an acceptable level. Themean dose associated with long-bone survey is between1-2 milli Sieverts (mSv) [ 1]. The probability of developinga fatal malignancy after a single long bone radiologicalsurvey is 8 x 10s or I in 12,500 exposures []. Theselevels of radiation are equivalent to receiving about 6days ofnatural background radiation and is considerablylesser than some common radiological procedures suchas CT scan of abdomen which delivers radiationequivalent to 3 years of natural background radiation

[]. Attempts to further reduce the radiation hazardinclude omitting the knee radiographs as the lesions inthis region are rare and restricting radiography to thosewho dive deeper than 30 metres. The gonads of thediver must be protected with a lead shield during the

Jour. Marine Medical Society,2010, Vol. 12, No.2

procedure.

The frequency of long bone radiology depends onthe type and frequency ofdiving undertaken by the diver.Baseline X-ray should be taken of all divers who intendto dive deeper than 30 metres, for a duration more than4 hours or use breath mixtures. Repeat studies must bedone according to the diver's experience over thepreceding 3 years. Divers who dive more than 4 hours,dive deeper than 50 metres, saturation divers or thosewho have suffered symptomatic DCS should undergoyearly follow-up, whereas those who dive shallowerthan50 meters but deeper than 30 meters and not lasting 4hours are recommended to be followed up radiologicallyonce every 3 years [2]. Other guidelines [8] recommendscreening only for divers with more than 20 hours divingper week. Some recommend individualization of thefrequency according to clinical assessment [9]. Thefilms should be retrievable and stored for the lifetime ofthe diver t8-121.

Other Modalities of Long Bone Radiology

99'technetium labeled bone scan picks up silentlesions earlier than long bone plain radiology [4].However, it has a higher false positive rate and increasedradiation hazard, apart from being expensive and lesseasily available. The same is true for CT scan. Therehave been attempts to utilize MRI scan, which has bettersensitivity and presents no radiation hazard [13].However, it is more expensive and also has a high falsepositive rate.

Long Bone radiology is a highly sensitive modality(-l007a) for detection of DON [14,15]. Long boneradiology has possibly decreased incidence of DON inJapanese professional divers [21. I t has beenrecommended by var ious professional div ingorganizations and navies as a useful method of screeningfor DON [2,8- l0]. It is non invasive, inexpensive and iseasily available. However Long bone radiology has lowspec i f i c i t y ( -30Vo) fo r de tec t ion o f DON [5 ] .Considerable ski l l and experience is required inassessment of the radiological films. It has poor temporalrelationship with the development of the illness, doespoor demarcation of the lesion and the course of actionin case of asymptomatic HNS lesions is uncertain.

Conclusion

The ideal screening modal i ty for Dysbaricosteonecrosis remains unenunciated t161. In the absenceof an ideal modality, long bone plain radiology remains acost effective method of screening for DON. Hence,baseline long bone plain radiology should be done forevery diver at entry. The frequency of conducting the

79

follow up should be dictated by the risk profile of thediver. In case ofa diver who does not dive deeper than50 metres and the duration of each dive is less than 4hours and cumulative dive is less than 20 hours for aweek, the radiological study may be conducted once in5 years. For divers, who dive deeper than 50 metres, dosaturation or experimental diving or who have receivedrecompression therapy for any decompression illness,the follow up should be done using MRI at 3 year intervals.Those divers who are at increased risk of developingDON as a consequence of being obese, alcoholic, havinghyperlipidemia, smoking cigareftes and having increasedPAI- I levels should undergo MRI of long bones every 3years. On detection of JA lesions, the diver should bewithheld from all professional diving activity. Ondetection of a HNS lesion, the diver should be cautionedto perform only "no-decompression" dives. Themethodology of long bone radiology should be thorougtrlyreviewed and proper positioning of the diver should beobligatory. The radiological assessments should be doneby experts who have considerable skill and experiencein detection of the relevant lesions.

Conflicts of Interests

None Identified

l .

References

John Pau l Jones J r and Tom S Neumann. Dysbar icOsteonecrosis. In: Brubakk AO. Neumann Tom S. editors.Bennett and Elliott's Physiology and Medicine of Diving. 5thed. London: Saunders; 2003. p 659 -6'19.

Hickey DD. Outline of medical standards of divers. UnderseaBiomedRes 1984; l l (4) :407-32.

3. Miyanishi K., Kamo Y, Ihara H, Naka I Hirakawa M andSug ioka Y. R isk fac to rs fo r dysbar ic os teonecros is .Rheumatology 2006: 45 : 855-58.

Chris Lowry. Dysbaric Osteonecrosis. In: Carl Edmonds, ChrisLowry, John Pennefather, Robyn Walker, editors. Diving andSubaquatic Medicine.4h ed. London: Amold Publishers, 2002,167-82.

Kawash ima M. Tamura H. Osteonecros is in d ivers -

prevention and treatment.In: K Shiraki and S. Matsuoka,editors. Hyperbaric and underwater physiology. 1983.Proceedings of 3'd International Symposium of UOEH onHyperbaric Medicine and Underwater Physiology.

Laden GDM, Grout P. Aseptic bone necrosis in an amateurscubadiver. Br J Sports Med2004;38: el9.

Ozkan H, Uzun G Yildiz S, Sonmez G Mutlu H, Aktas S.MRI Screening of Dysbaric Osteonecrosis in Hyperbaric-chamber Inside Attendants. The Journal of InternationalM e di c al Re s e ar c h 20Q8; 36 : 222-26.

European Diving Technology Committee. Fitness to divestandards - Guidelines for medical assessment of workinedivers. March 2003.

Statens helseti lsyn. Norwegian guidel ines for medicalexamination of occupational divers.August 2000.

Carson WK, Mecklenburg B. The role of radiology in dive-related disorders. Mil Med 2006; l7l (l) : ii.

Decompression Sickness Central Registry and RadiologicalPanel Report. Aseptic necrosis in commercial divers. Lancet1980; 2 : 384-88.

Okkalides D, Fotakis M. Patient effective dose resulting fromradiographic examination. Brit J Radiol 1994:67 :564-'72.

Dennis N Walder. Aseptic Necrosis of Bone. In: Alfred Bove,editor. Bove and Davis'Diving Medicine. 3'd ed. Philadelphia:Saunders; 1997 ,227 -34.

Radiological Society of North America. Radiation Exposure inX-ray Examinations [Online]. 2009 Jan 16 [cited 2009 Feb201 Available from: http://www.radiologyinfo.org

Jiang C, Bing B, Yu C, Xiao L, Liu W Jiao S, er a/. DysbaricOsteonecrosis by X-ray and CT Scan in Chinese divers.Undersea Hyperb Med 2005; (32) 3 : 169-7 4.

Takoa K, Kawashima M, Tamura H, Nagayoshi I, YamguchiT. Dysbaric osteonecrosis in divers. UHMS meeting abstracts2005.

Jour Marine Medical Society,20I0, Vol. 12, No. 2

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t 2 .

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t5 .

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Update Article

Concepts and Controversies in Post Tlaumatic Epilepsy

Surg Capt KI Mathai*, Surg Cdr K Bose**

Abstract

Post traumatic epilepsy (PTE) provides us an opportunity to study the pathophysiology of trauma and seizures. Therole ofpharmacotherapy in the control and prevention ofseizures has been revisited. Future avenues ofmanagementinclude stem cell transplantation and focal intervention by ablation ofaberrant circuits.

Key Words : Post traumatic epilepsy, Pathophysiology

Introduction

\Jormal brain becomes seizure prone after trauma.I \ Seizures involve lateral spread of electr icaldepolar izat ion as a result of increased neuronalexcitabiliry, loss of inhibitory influence and establishmentof aberrant synapses and reentry circuits. The incidenceof post traumatic epilepsy after severe Traumatic BrainInjury (TBI) varies from ll-l5%o in adults to30-35Vo inchildren [1]. The incidence is up to 507o, in missile injuriesof the head. Less severe head injuries may be associatedwith a seizure incidence of |Va. Post Traumatic Seizures(PTE) occur immediately (within 24 hours), early (withina week) or in a delayed fashion after neurotrauma [2].The pathophysiology of post traumatic seizures varieswith the temporal profile.

Pathophysiology

Neurotrauma results in neuronal membrane failuremediated excitotoxicity, with a failure of the sodium andcalcium pumps and the aquaporin system. culminatingin cytotoxic brain swelling. Calcium mediated toxicityto the mi tochondr ia causes an energy fa i lu re .Inf lammatory cascades act ivate calpains whichbreakdown the cytoskeletal structure and caspaseswhich trigger the apoptotic gene. The astrocyte footprocesses guarding the endothelial tight junctions retractresulting in increased vascular porosity and vasogenicedema.

If the quantum of insult is severe, the cell goes on toeither necrotic or apoptotic death. In subthreshold injury,the cell recovers, restoring its membrane potential.Recovering neurons remain hyperexcitable for a periodof time. This hyper excitability and the functional or

structural loss of inhibitory interneurons facilitate thelateral spread of impulses which results in seizures inearly PTE [3].

Delayed PTE on the other hand is consequent to therestorative and repair process. Neurotrophins, releasedin response to neuronal loss, stimulate neosynaptogenesisas well as neuronal precursor proliferation [4]. Thenewly formed neurons migrate from the stem cell nichesin the dentate gyrus and the subventricular zone.Regu la to ry mechan isms wh ich f ine tune theestablishment of neuronal circuitry include Reelin [5]and the radial seaffolds. These controls are deficient inadulthood and aberrant communication and reentrycircuits result, which constitutes the substrate for delayedPTE [6,7].

Seizure Prophylaxis

There is an ongoing debate on the prophylactic roleof anticonvulsants (AED) after TBI. In the early phaseafter a severe TB[, the brain is swollen and relativelyhypoxemic. There is a failure of the Cerebral PerfusionPressure Head and loss of Cerebrovascular reactivity(auto regulat ion). Seizures in this sett ing wouldaccentuate neuronal damage. During this phase, theduration of which would vary with the insult quotient,seizure prophylaxis is recommended. Phenytoin,barbiturates like propofol or even benzodiazepines maybe used to decrease neuronal excitability [8]. Theseantiepileptics however are not antiepileptogenic [9]. Theydo no t p revent aber ran t synaptogenes is . Neosynaptogenesis and neurogenesis are the basic templatesof neuronal plasticity and recovery. It is thereforeconceptually difficult to inhibit aberrant synaptogenesiswith out impeding recovery.

*Senior Advisor, Surgery and Neurosurgery, INHS Asvini, Mumbai. +*Officer in Charge, Fleet Medical Centre, Western Fleet, Mumbai.

Jour. Marine Medical Sociefi'.2010, Vol. 12, No.2 8I

Evolving Horizons

Cell transplantation to restore depleted interneuronsusing Neuronal stem cells.has been tried in Temporallobe epilepsy [10,11]. The role of Reelin in regulatingneosynaptogenesis holds therapeutic promise. Accurateelectrophysiological identification of aberrant and reentrycircuits would facilitate their inhibition by AED eludingdevices. Inhibition ofthese epilepsy circuits is possiblewith responsive neurostimulators [2]. These devices,stereotactically implanted can detect seizure patternsand trigger an inhibitory impulse aborting the seizuret131.

References

l. Annergers JF, Hauser WA, Coan SP. A population based studyof seizues after traumatic brain Injuries. N Engl J Med 1998;338 ( l) : 20-4.

2. D'Ambrosio R, Perrucca E. Epilepsy after head lnjury. CurrOpn Neurol20O4: l7 (6):731-5.

3. Garga N, Lowensten DH. Post traumatic Epilepsy: a majorproblem in desperate need ofmajor advances. Epilepsy Curr2 0 0 6 ; 6 ( l ) : 1 - 5 .

4. Jessberger S, Zhao C, Toni N. Seizure associated aberrantneurogenesis in adult rats charaterised with retrovirus mediatedcell labeling. "/ Neurosci2007;27 :940Q-07.

5. Heinrich C, Nitta N, Flubacher A. Reelin deficiency anddisplacement ofmature neurons, but not neurogenesis, underlie

the formation of granule cel l dispersion in the epi leptichippocampus. J Neurosci 2006;26: 4701-13.

Cavazoz JE, Goss DJ. The role of synaptic reorganization inmedial temporal lobe epilepsy. Epilepsy Behav 2006;8 :483-93.

Fortscher M, Janas P, Sloviter RS. Synapses formed by normaland abnormal hippocampal mossy fibres. Cell tissue Res2O06;326 :361-67.

Young KD, Okada PJ, Sokolove PE, er c1. A Randomised doubleblinded placebo controlled trial ofPhenytoin for the preventionof early post traumatic seizures in children with moderate tosevere blunt head injury. Ann Emerg Med 2004;43 : 435-46.

Temkr NR, Dikmen SS, Anderson GD. Valporate therapy forprevention of post traumatic seizures: a randomized treat. JNeurosurg 1999;' 9l : 593-600.

Kempermann G. They are not too excited : the possible role ofadult born neurons in epilepsy. Neuron 2006;52 935-37.

Richrdson MR, Barbaro NM, Alvarez Boylla A. Developingcell transpfantation for temporal lobe epilepsy. NeurosurgeryFocus 2008:24(3) : 17.

Barkley GL, Smith B, Bergrey G, Worrel G Chabolla D,Draskowski J, et al. Safety and preliminary efficacy of theRNS respons ive neuros t imu la to r fo r the t rea tment o finctractable epilepsy in adults. Epilepsia 2006; 47 (4 Suppl) :A t2 .

Fountas KN, Smith JR, Murro AM, Politsky J, Park YD,Jenkins PD. Implantation of a closed loop stimulation in themanagement of medically refractory focal epilepsy: a technicalnote. Sterrotact Funct Neurosurg2005;83 : 153-58.

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82 Jour. Marine Medical Societv, 2010, Vol. 12, No. 2

Update Article

Medical Organisation During Submarine Operations

Surg Cdr CS Saxena*

Abstract

Subrnarines by virtue of their operations and design limitations present a challenge in case of distressed submarine(DISSUB) situation. This article updates planning and mobilization of resources to carry out rescue and escapeoperations for a distressed submarine. The medical resources available in a submarine base are limited and arerequired to be augmented to ensure proper functioning of medical organization.

Key Words : Distressed submarine, Decompression, Triage

Introduction

41 849 submarines have been lost at sea over the pastI century. Most of these losses were during war, but

over 336 submarines have been lost at sea as non warlosses. These losses have occurred in the US. France.UK and the erstwhile USSR, over a period of six decadesafter World War II. The most recent was the loss ofRussian submarine KURSK with all hands onboard.Submarines are liable to frequent accidents due to thenature of their operations and peculiar construction. TheBlack superstructure is difficult to detect whilst onsurface at night and collisions occur commonly.

Medical Organization

Medical organization for Indian Naval Submarineoperations are organized underthe Base Medical Officer(BMO)I. He heads the medical organization and advisesthe Commodore Commanding Submarines (COMCOS)on all medical matters. The Base Medical Officer(BMO) is assisted by the Squadron Medical Officers.Under Squadron Medical Officers are the submarineMedical Off icers (S/M MO). Each submarine isauthorized one dolphin qualified Medical Officer whobesides carrying out the job of a doctor also doubles upas advisor to Commanding Officer in atmosphericmonitoring and control of captive atmosphere on board.This involves monitoring of gases like O, CO,, oxidesof Sulphur and Nitrogen, Cl, and other pollutants. TheMedical Officer also works as advisor on escape relatedissues, monitors and maintains all escape and salvageequipment on board and is assisted by the medicalassistant in this arduous endeavor. The maintenance andupkeep of submarine escape suit ISP-60 is done by IDA

Maintenance Units funct ioning under the BMOs.Submiss/Subsunk operations are initiated if a submarinemisses a check report within a designated time and isdeemed missing.

Operationat (Ops) Issues

The chain of evacuation consists of evacuation to asurface platform during peace time by a Gemini(inflatable boat/RIB). During forward deployment,casualty holding may be required for as long as 4-6 daystill the submarine reaches the withdrawal area. Afterreaching the withdrawal area, the casevac would be toa ship or to shore by a helicopter.

Management of casualty is the most important partin a Distressed Submarine (DISSUB) and Submiss/Subsunk situation. Medical organization for rescue andescape from submarines (MORES) consists of ashoreand afloat component (Table I & Fig. l). Manpowerwill consist of Medical Officers and medical assistantsdrawn from command resources and augmented byMarine Medicine Special ist (MMS) from othercommands on required basis. MORES should be capableofbeing deployed at very short notice and is headed byCommand Search and Rescue (SAR) Medical Officer.

The senior most Marine Medicine specialist in thecommand will be OIC MORES and will be designatedCommand SAR Medical Officer. He will close up atMaritime Operation Centre (MOC) and will be theadvisor to command on medical aspects of the rescueeffort. In view of shortage of s/m MO's at SouthernNaval Command (SNC) additional s/m MO's will bedeputed from other commands to augment MORES inKochi. ForAndaman and Nicobar Command, MORES

*Classified specialist (Marine Medicine) and BMO, INS Virbahu, C/o FMO, Visakhapatnam 5300 014

Jour. Marine Medical Socien'.2010. Vol. 12. No.2 8J

Table I : Ashore organization

Whilst deploying MORES one MMS and one SA4 MO each will be deployed at Re Compression Chamber (RCC) and Submarine baserespectively.

W N C : M O C ( M B ) Senior most S/1\4 MO

Under Sea Medicine Department (USM) - INHS Asvini - Marine Medicine Specialist

Command Clearance Diving Team (CCDT), Mumbai - Marine Medicine Specialist

INS Vajrabahu - S/NI Medical Officer

Senior most S/M MO

INS Satavahana - Marine Medicine Specialist

INS Virbahu - S/I4 Medical Officer

Senior most SA4 MO (MMS)

Diving School - Marine Medicine Specialist

ENC :MOC (V)

SNC : MOC (K)

SMO to STF0

MEDICAL COiITROLLER OPS

Table 2 : Triage categories

Priority - Categories

P0 - Uninjured(notincludingDCS)Pl - Immediate (e.g. Tension Pneumothorax, H'gic shock)P2 - Urgent (e.9. <20Vo burns, open fractures)P3 - Delayed (e.g. Minor injuries)P4 - Expectant (serious/severe multiple injuries)

Compression - Categories

C0 - UnexposedCl - Immediate RecompressionC2 - Urgent RecompressionC3 - Delayed RecompressionC4 - Observation

Reference (INBR) 2806 should be used. He will ensurethat casevac by chopper is at altitude of less than 1000feet.

The medical set up on board SRV will consist of Triagearea, Primary treatment area, Secondary treatment area,Tertiary treatment area and Expectant area. The triagearea is manned by one MO, MA, writer and messengerand will cater for assessing atleast 05 casualties at atime. Triage area should have basic resuscitation andairway management equipment with adequate oxygensupply. An additional triage category is added fordecompression insult (Table 2). All Pl or Cl will go toprimary treatment area. All P2 or C2 will go tosecondary treatment area. All P3 except P3C 1 and P3C2will go to tertiary treatment and monitoring area(Table 3).

The primary treatment area manned by One MarineMedicine specialist, 02 MA's, writer and a messengershould have resuscitation and advanced life supportequipment including drugs, chest drains, IV fluids,Oxygen and space for 06 stretcher patients. It shouldcontain the Recompression chamber and adequatenumber of divers to man it. Secondary treatment area ismanned by one MO, 03 MA s, writer and messengerand has space for at least l0%o of submarine crew and

RECEP1ION P,ICI TRT&TRIAGE AREA

- 01 ti40 SPL -01 !r0 SPL"02 iliA'S .0? ttl0'S

{8JM}-01 SflilA- 03 lilA'S

P?f'zTATAREA

-01 mo($,fi'll

-01 Ir itA.0? titAs

p TRT P4TRTAREA AREA

.01 srMA

.02 mA's-W lrl0'$

(8rMl.01 Sr iilA.02 MA'S

.CHAMBER TEAII

Fig. I : Afloatorganistion

will be deployed tiom Eastern Naval Command (ENC).

Total manpower requirement for MORES will be 08Medical Officers and 15 medical assistants (MA)besides chamber attendants, stretcher bearers, recordkeepers and sanitary staff provided by SubmarineRescue Vessel (SRV). The Senior Medical Officer(SMO) will be the senior most Marine MedicineSpecialist (MMS) onboard SRV and will be the OIC ofmedical personnel on board the SRV. He will ensurecollection of Submiss/Subsunk stores from respectivebases. He will regularly brief Senior Officer PresentAfloat (SOPA) and Commanding Officer (CO) of SRVon aspects of DISSUB survival, escape and rescue andprovisioning of additional assets to support the triageand treatment of escapees. He will be helped byController Medical Operations (CMO) in this endeavor.

Casualty Management

CMO will be the second senior Marine MedicineSpecialist on board SRV and reports directly to SMO.He will establish Medical Headquarters on board andwill be assisted by one writer and messenger each andmaintain the master casualty state board. He willsupervise recompression of escapees if required. Onlyshallow oxygen tables 61 and62 of Indian Naval Book

84 Jour. Marine Medical Society,20l0, Vol. 12, No.2

Table 3 : Casualty expectation

(Average crew of submarine - 100)P lC l ' 20Vo

PZC2 -20Vo

P3 - 40VaP4 -20Vo

capable ofhandling at least l5 casualties for 6 hrs. TheTertiary treatment and monitoring area is manned by asenior medical assistant and he is assisted by 02 Jr MA s.The area should have sufficient space forhandling2}Voof the crew of DISSUB (Table 3) and have basic

resuscitation and first aid equipment and drugs. P4 areais manned by 02 MO's, 03 MA s, Topas and a messengerand should have adequate medical supply for palliativecare (Fig. l). The change in status of escapees isregularly updated to CMO.

The Submiss/Subsunk stores are ready to carry anduse stores maintained 24x7 at INS Vajrabahu (Mumbai),INS Virbahu (Vizag),INHS Sanjivani (Kochi) and INHSDhanvantari (Port Blair). With induction of AdvancedTechnical Vessel (ATV) and Scorpenes and likelyinduction of Deep Sea Rescue Vessel (DSRV) there isa need to have regular workup exercises at sea fordeployingMORES.

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Address for Correspondence

EDITORJOURNAL OF MARINE MEDICAL SOCIETY

INHS Asvini. Colaba. Mumbai 400 005.

Jour. Marine Medical Society,20l0, Vol. 12, No. 2 85

Original Article

Experience of Nimotuzumab with ConcurrentChemoradiotherapy

Surg Cdr llariMukundan., Surg Capt Subhash Ranjanrvsnr*, Surg CdrRShankaran#

Abstract

Background : The management of patients with head and neck cancer is complex. The treatment of squamous cellcarcinoma of the head and neck (SCCHN) varies according to clinical characteristics.

Material and Methods : We used Nimotuzumab in four patients with concurrent chemo radiotherapy used at outOncotherapy unit and recorded our observations.

Results : Our experience with Nimotuzumab is discussed and current literature reviewed.

Key Words : Ninotuzumab, Head and neck cancer, Chemoradiotherapy

Introduction

Th" treatment of squamous cell carcinoma of theI head and neck (SCCHN) varies according to clinical

characteristics. Comorbidies are quite frequent inSCCHN and can preclude aggressive therapy [1-4].Treatment may negatively affect basic physiologicalfunctions, sense organs, speech and physical appearance

[5]. Approximately 60Vo of SCCHN patients presentwith locally advanced (LA) disease [5]. A majority ofthese patients will require multimodal treatment.Standard treatment includes surgery, radiation (RT),chemotherapy (CT) and biological or targeted agents.We used anti-Epidermal Growth Factor Receptor(EGFR) agents in four of our patients to improveresponse to treatment.

Material and Method

We treated four patients with advanced cancers ofthe head and neck with a combinat ion ofchemoradiotherapy and an ant i-EGFR agent(Nimotuzumab). All these patients had stage III and IVasquamous cell carcinoma of the head and neck includingcervical oesophagus (Table 1). Radiotherapy wasdelivered by Linear Accelerator (LINAC) (Fig. 1).Inclusion criteria included age from 18 to 75 years, aKarnofsky's performance status of more than 70Vo,absolute neutrophil count more than 1500/mm3, plateletcount more than 100.000/mm3 and serum creatinine and

serum bilirubin less than 2 x normal. Exclusion criteriaincluded uncontrolled intercurrent infection, pregnancy,lactation, cardiac failure (NYHA-Class III or IV), otherconcurrent cancer or metastatic disease and history ofprior RT/chemotherapy. All patients under wentcomplete physical examination, hematologic andbiochemical evaluation, chest X-ray, USG of theabdomen and neck and contrast enhanced CT scan ofthe neck. Laboratory tests were repeated weekly whileon treatment and 06 weekly thereafter. Toxicity wasgraded according to National Cancerlnstitute's CommonToxicity Criteria (version 2.0) and the RTOG morbiditygrading system. Chemotherapy protocol involvedInjection Cisplatinum 35 mg/m2 weekly. They alsoreceived a fixed dose of Inj Nimotuzumab 200 mg/week.

'Graded Specialist (Radiotherapy); *SeniorAdvisor, Medicine and Oncology; "Classified Specialist, Surgery and Surgical Oncology, INHSAsvini, Mumbai

Fig. I : Patient with head and neck cancer receiving treatment onLinear Accelerator.

86 Jour. Marine Medical Society,20l0, Vol. 12, No.2

Results

All our patients (Table 1) tolerated the full course ofplanned radiotherapy (Table 2) with doses ranging from50 Gy to 70 Gy with only one patient requiring a breakin radiotherapy of more than 07 days. This was due to avasovagal episode which was possibly unrelated to thetreatment. One patient had mild eczematous dermatitiswhich responded to symptomatic treatment (Table 3).

Discussion

The epidermal growth factor receptor (EGFR) is aftansmembrane glycoprotein mediating mitogenic effects,which is over expressed in non small cell lung cancers,head and neck cancers. astrocytic tumors and ovarian,cervical, bladder and oesophageal cancers t6- I 0l . EGFRexpression has been correlated with alterations in cellcycle progression, increased invasive capacity, enhancedangiogenesis and decreased apoptosis of tumor cells andhas been associated with poor outcome[ I I - 14]. Severalstrategies have been developed to disrupt the EGFR -

associated signal transduction cascade and includemonoclonal antibodies directed against the extra cellulardomain of the receptor and small molecule tyrosinekinase inhibitors which act by interfering with ATPbinding to the receptor [5-16].

Table I : Depicting site and stage of disease with age andsex characteristics

Age Sex Diagnosis Site Stage

Cetuximab is an IgGl monoclonal antibody thattargets the epidermal growth factor receptor (EGFR)with high affinity. It binds to the epitope, promotesinternalization of the receptor and thereby preventsactivation by ligand binding. In addition, cetuximab maymediate antitumor immune effects such as antibody-dependent cell-mediated cytotoxicity I I 7]. Nimotuzumab(BIOMAb EGFR) is a humanized recombinant anti-EGFR monoclonal antibody which inhibits EGFR tyrosinekinase phosphorylation and is well tolerated by thepatients [8]. Nearly all SCCHN express EGFR andoverexpression is associated with poor prognosis, poorresponse to RT and higher risk for regional recurrence

l l9l . Ant i EGFR receptor ant ibody and RT havesynergist ic effects in precl inical models 120-221.Blockade of the nuclear influx of EGFR and subsequentformation of DNA-PK, Ku70/80 complexes which areinvolved in repairing DNA double-strand breaks inducedby inadiation was shown to be the mechanism by whichcetuximab sensitizes tumor cells to RT t231.

Results from a phase I study indicate that bothcetuximab and nimotuzumab can be safely given incombination with RT 124-26l.,{multinational phase IIIstudy compared RT plus cetuximab with RT alone inpatients with LA-SCCHN which showed that addingcetuximab to RT provides improvement in diseasecontrol and survival without increasing toxicity [27].Preliminary efficacy results of cetuximab plus CRT areencouraging with SCCHN and esophageal cancer [28-301.

Conflicts of Interests

None Identified

2.

l .

References

Piccirillo JF. Importance of co morbidity in head and neckcancer. Laryngoscope 2000; I l0: 593-602.

Chen AY, Matson LK, Roberts D, et al. The significance ofcomorbidity in advanced laryngeal cancer. Head Neck200l;23 :566-72.

Hall SF, Groome PA, Rothwell D. The impact of comorbidityon the survival of patients with squamous cell carcinoma ofthe head and neck. Head Neck 2000;22 '.317 -22.

Ribeiro KC, Kowalski LP, Latorre MR. Impact of comorbidity,symptoms, and patients' characteristics on the prognosis oforal carcinomas. Arch Otolaryngol Head Neck Surg2000;126: 1 0 7 9 - 8 5 .

Forastiere AA, Ang KK, Brizel DNY. Head and Neck Cancers.National Comprehensive Cancer Network. Clinical PracticeGuidelines in Oncology-v. 2.2008

Brabender J, Danenberg KD, Metzger R, et al. Epidermalgrowth factor receptor and HER2-neu mRNA expression innon-small cell lung cancer is correlated with survival. C/inCancer Res.2001: 7 : 1850-55.

50 male

3l female

58 male

54 male

Ca Oesophagus

Ca Larynx

Ca Oral Cavity

Ca Oesophagus

Mid-third

Right Vocal Cord

Buccal Mucosa

CervicalOesophagus

IIIIIIIVII

Table 2 : Depicting dose of radiation received, duration andskin tolerance

EBRT-dose Fractions Davs Break in davs Tolerance-skin

5040680070005040

28343528

3 8 065 t44 7 04 6 0

I

I I

I

I

Table 3 : Depicting hematological and other toxicities (FJ-Feeding jejunostomy)

Haematological Number of G-CSF Others-sp site

IIII

3l 000

Dysphagia

Dysphagia

Vasovagal

On FJ, dermatitis

4 .

5 .

6.

Jour. Marine Medical Society,20l0, Vol. 12, No. 2 87

20.7. Alper O, Bergmann-Leitner ES, Bennet TA, et al. Epidermalgrowth factor receptor signaling and the invasive phenotypeof ovarian carcinoma cells. ,I Natl Cancer Inst.200l'. 93 :1375-84.

Ngan Hl Cheung AN, Liu SS, et al. Abnormal expression ofepidermal growth factor receptor and c-erbB-2 in squamouscell carcinoma of the cervix:correlation with human papillomavirus and prognosis.Zunor Biol.2001;22 : 176-83.

Chow NH, Chan SH, Tzai TS, e/ a/. Expression profiles of c-erbB family receptors and prognosis in primaruy transitionalcell carcinomas of the urinary bladder. Clin Cancer Res 2001;7 :1957-62

Wang LS, Chow KC, Chi KH. Prognosis of esophagealsquamous cell carcinoma: analysis of clinicopathologic andbiologic factors. Am J Gastroenterol 1999;94 : 1933-40.

Giordano A, Rustum YM, Wenner CE. Cell cycle: moleculartargets for diagnosis and therapy: tumor suppressor genes andcell cycle progression in cancer. J Cell Biochem 1998;70 : l-'l .

Damstrup L, Rude Voldborg B, Spang-Thomsen M, et al.lnvitro invasion of small cell lung cancer cell lines correlates withexpression of epidermal growth factors receptor. Br J Cancer1998; 78 :631-40.

Kerbel RS, Viloria-PetitA, Okada R e/ a/. Establishing a linkbetween oncogenes and tumor angiogenesis . Mol Med 1998:4:286-95.

Gibson S, Tu S, Oyer R, et al. Epidermal growth factorspro tec ts ep i the l ia l ce l l s aga ins t Fas - inducedapoptosis.Requirement for Akt activation. J Biol Chem 1999:'274:17612-18.

Mendelsohn J, Baselga J. The EGF receptor family as targetsfor cancer therapy. Oncogene 2000; 19 : 6550-65.

Ciardiello R Totora G. A novel approach in the treatment ofcancers: targeting the epidermal growth factors receptor. ClinCancer Res 2001:7 :2958-'10.

Kawaguchi Y, Kono K, Mimura K, et al. Cetuximab induceantibody dependent cellular cytotoxicity against EGFR-expressing esophageal squamous cell carcinoma. Int J Cancer2007;120: 781-87.

Tania Crombet, Lionel Torres, El ia Neninger, et al.Pharmacological Evaluation of Humanized Anti-EpidermalGrowth Factor Receptor,Monoclonal Antibody h-R3,inpatients with advanced epithelial -derived cancet J Immunoth2003;26 (2): t39-48.

Ang KK, Berkey BA, Tu X, et al.lmpactof epidermal growthfactor receptor expression on survival and pattern of relapsein patients with advanced head a neck carcinoma. Cancer Res2QO2;62 :7350-56.

BonnerJA, Raisch KP, TrummellHQ,et al. Enhanced apoptosiswith combination C225hadiation treatment serves as theimpetus for clinical investigation in head and neck cancers. JClin Oncol 2000; 18 (21 suppl) :47s-53s.

Milas L, Mason K, Hunter N, et al.ln vivo enhancement oftumor radioresponse by C225 antiepidermal growth factorreceptor antibody. Clin Cancer Res 2000; 6 : 701-08.

Huang S-M, Harari PM. Modulation of radiation responseafter epidermal growth factor receptor blockade in squamouscell carcinomas: Inhibition of damage repair, cell cycle kinetics,and tumor angiogenesis. Clin Cancer Res 2000; 6 :2166-74.

Dittmann K, Mayer C, Fehrenbacher B, et a/. Radiation-induced epidermal growth factor receptor nuclear import islinked to activation of DNAdependent protein kinase. J BiolChem2005;280 : 31 182-89.

Robert F, Ezekiel MP, Spencer SA, et al. Phase I study ofanti- epidermal growth factor receptor antibody cetuximab incombination with radiation therapy in patients with advancedhead and neck cancer. J Clin Oncol 2OOl; 19 : 3234-43.

Tania Crombet, Marta Osorio, Teresa Cruz, Carlos Roca, et a/.Use of the humanized Anti-epidermal Growth Factor receptorMonoclonal Antibody h-R3 in combination with radiotherapyin the treatment of locally advanced head and neck cancerspatients. .J CIin Oncol 2004;22 (9) : 1646-53.

Kanaka Shet ty , Gov ind Babu. B IOMAb EGFRTM(Nimotizumab) in combination with the standard of care insquamous cell carcinoma of the head and neck (SCCHN)proceedings of the fourth International symposium onmalignancies of the chest and head and neck). J Thor Oncol2006; | (8) :920-2r.Bonner JA, Harari PM, Giralt J, et al. Radiotherapy pluscetuximab for squamous-cell carcinoma of the head and neck.N Engl J Med2006; 354 :561J8.

Pfister DG Su YB, Kraus DH, et al. Concunent cetuximab,c isp la t in , and concomi tan t boos t rad io therapy fo rlocoregionally advanced, squamous cell head and neck cancer:A pilot phase II study of a new combined modality paradigm.J Clin Oncol 2006;24 : 1072-78.

Merlano MC, Numico G Russi EG et al. Cetuximab (C-mab)and chemoradiation (CT-RT) for locally advanced squamouscell carcinoma of the head and neck (HNC): A phase II study.J CIin Oncol 2OO7; 25 (June 20 suppl) : 6043.

Suntharalingam M, Dipetrillo T, Wanebo H, et al. A phase IItrial evaluating the efficacy of weekly cetuximab, paclitaxel,carboplatin and daily RT in esophageal cancer. Int J RadiatOncol Biol Phvs 2006: 66:522-523.

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88 Jour. Marine Medical Societv,2010, Vol. 12, No.2

Original Article

llyperbaric Oxygen Therapy in Non Healing Wounds

Surg Lt Cdr Sourabh Bhutani., Surg Lt Cdr Rohit Verma#

Abstract

Background : Hyperbaric oxygen therapy (HBOT) is accepted as an adjunctive therapy for non-healing wounds.

Ischemia and infection are the common causes of non-healing.

l\{aterial and Methods : A retrospective analysis of 46 cases of non-healing wounds on HBOT was carried out. Theprimary end point was the appearance of healthy granulation tissue over 50 Vo of the surface area of the ulcer. Allpatients continued concurrent medical and surgical management.

Results : Out of 46 patients with non-healing ulcers of the lower limb, 39 (84.7 Eo) were due to diabetes. Forty threepatients completed the treatment and "Satisfactory Healing" was seen in 38 (88.37 7o ). Average sittings required forhealing were 14.2. Five patients (l l .63Vo) failed to respond despite the therapy being extended upto 20 sitt ings.Amputatiun ratewas6.9Vo. Three patients (6.5Vo\ did not conrplete the treatment and aural barotrauma was seen in12 cases Q6.08Vo\ .

Conclusion : HBOT improved healing in chronic wounds possibly by reducing ischemia and infection. Alternatinohypoxia and hyperoxia during I{BOT may optimise the healing process.

Key Words : Hyperbaric oxygen, Problem wounds, Hypoxic lvounds, Diabetic foot, Ttanscutaneous oximetry

Introduction

TJyperbaric oxygen therapy is the use of 1007oI loxygen at pressures -qreater than atmosphericp r e s s u r e . T h e p a t i e n t b r e a t h e s 1 0 0 7 a o x y g e nintermit tent ly whi le the pressure of the treatmentchamber is increased to greater than I atmosphereabsolute (ATA) [-5]. HBOT is an accepted adjunctivetherapy fbr a variety of inclications based on randontisedcontrol led tr ia ls and establ ished protocols (Table l )

[2,3.5]. It has also been useful fbr other indications fbrwhich firm evidence in the form of large multicentrerandomized controlled trials are stil l not available (Table

2) [3 .5 .6 ] .

Non-healing or chronic wounds are those that fail toheal rvithin 8 weeks rvith standard wound care. It mayalso be delinecl as a rvound that fails to proceed throughan orderly and t imely heal in-e process to produceanatomic and functi<tnal integrity 13.4,1l. This -qroupincludes diabetic lirot ulcers, arterial insufficiency ulcers.ulcers due to l'enous stasis, decubitus ulcers and fungalinfections of the fbot such as Madura fbot. Ischemiaand int'ection ale the lnost comlnon causes of non-healing

[81 . In fec t ion inc reases the in f lammatory p rocessthereby inducing wound hypoxia through lii-th oxygen

consumption and reduced local blood flow due to tissueoedema. Collagen deposition, epithelialisation and woundcontraction either do uot occur or occur only to a limitedextent t3.4,91. Although anaerobic metabolism is possible

Table l : Indications for HBOT

l. ' Ihermal

burns

2. C los t r id ia l rnyonecros is

3. Enhancer-nent of l-real irrs in selectecl problem wounds

o Diabetic fbot

o Fr"rngal int lct ions l ike Madura fbot

r Ulcelat ion due to arterial insufTiciency

o Venous stasis ulcer

r Decubitus ulcers

Neero t is inq so l t t i ssuc in fcc t ions

Comprorrisecl skin graf is and f laps

Refiactory osteonryel i t is

Crush injury' . conlpartr.nent synclrome. and other acutet l 'aumatic ischcnria

Late ladiat ion incluced t issue dama-rle. e.g. Procti t is. cyst i t is

Air/gas embolism

Decompression sickness

Carbon nronoxide poisoning and smoke inhalat ion

Exe ep t iona l b lo r rd loss aner r r iu

lntracranial abscess

4.

5 .6.7 .

6 .

r) ,

1 0 .I l .12.r 3 .

'Resiclent. Malint 'Medicine. lJndersel Medicine f)epartnrent. INHS Asvini, Murnbai 05. "PMO & Graded Speci l l ist, Marine Medicine. INS

Nireekshak. c/o Fleet Mail Ofl ' ice. Kochi 682004.

lour. Murirte Mcditul Soctelt ' , 2010, hl. 12. No. 2 89

Table 2 : Research indications

l. Post sternotomy mediastinitis

2. Stroke

3. Sickle cell disease

4. Malignant otitis externa

5. Acute myocardial infarction

6. Femoral head necrosis

7. Retinit ispigmentosa

8. Tinnitus

9. Interstitial cystitis

10. Facial (Bel l 's) palsy

I 1. Cerebral palsy

12. Mult iple sclerosis

13. Feto-placental insuff iciency

in a hypoxic wound, it cannot generate the vast quantityof energy required for normal healing [3,4, 10] . Hypoxialeads to impaired fibroblast production, failure ofmaturation of new capillary network and impairment ofbody's defence mechanisms against bacterial invasion

[ 1 I ]. However, hypoxia is a potent stimulus for secretionof angiogenic factors, migration of fibroblasts andinduction of pro-collagen synthesis 13,4,121. On the otherhand, a norrnal oxygen pressure is needed for formationof a capillary network, proliferation and maturation offibroblasts and formation of resilient collagen. Alternatinghypoxia and hyperoxia during HBOT optimises thehealing process by providing the stimulus of hypoxia andalso the needed oxygen substrate [3,4,13,14].

Material and Methods

A retrospective analysis of 46 cases of non-healingwounds referred to the Undersea Medicine Departmentfor HBOT between Jun 09 and Nov 09 was carriedout. Pre HBOT evaluation included clinical examinationwith emphasis on the respiratory system and a chestroentgenogram. Those with a past or concurrent historyof pulmonary Koch's, thoracic surgery, consolidation,pulrrronary fibrosis, pneumothorax, pleural effusion,spontancrous pneumothorax or a cavitary lesion wereexcluded due to the risk of pulmonary barotrauma.Further, any with history of ear surgery, tympanoplasty,otoscleiosis or otomycosis were excluded as thesepredispose tu barotrauma of the ear. A resting l2leadECG was taken to rule out arrhythmias which mayworsen in the liyperba.ric atmosphere.

All cases were initially given l0 sittings of HBOT at2.5 ATA pressure for 60 minutes each, six days a week.Wound evaluation was done clinically and photographsof the wound were taken on days 0, 5, and l0 forobjective wound analysis. Extension of treatment by 4-

90

l0 sittings was done depending on response to HBOT.No patient was administered more than 20 sittings at atime.

The pr imary end point of t reatment was theappearance of healthy granulation tissue over 50Vo ofthe surface area of the ulcer which was considered as"Satisfactory healing". "Failure of treatment" wasconsidered when granulation tissue covered less than507o of the surface area after 20 sittings or gangrene orpre gangrene necessitated urgent limb amputation.

All patients continued standard medical and surgicalmanagement apart from HBOT. Medical managementincluded strict glycemic control for diabetic patients andmedications for any other co-morbidity. Surgicalmanagement included wound debridement, dai lydressings, appropriate antibiotics and non-weight bearingmeasures.

Results

A total of 46 patients were seen with non-healingulcers of the lower limb (Table 3). An overwhelmingmajority (39 cases, 84.7Vo) were associated withdiabetes, the rest being arterial insufficiency ulcers (2cases,4Vo), venous ulcers (3 cases, 6Vo) and decubitusulcers (2 cases, 6Vo). Only one case (-2Vo) did not havea lower limb ulcer (Fournier's gangrene). Out of the 39diabetic patients, three cases (7 .7Vo of all diabetic cases)reported for treatment of non healing ulcers on theamputation stump (above knee in 2 cases and belowknee in l) and 5 cases (l2.8Vo) showed signs of pre-gangrene or gangrene of one or more digits of eitherfeet.

Three patients (6.5Vo) did not complete the treatmentas per the protocol. One (-2Vo of all cases) patient optedout due to intense claustrophobia during the secondsession, a second patient cited long distance travel anda third patient did not complete treatment due to auralbarotrauma. Aural barotrauma was seen in 12 cases(26.08Vo),ll (9l.l%o) of whom were Teed grade I, while

Table 3 : Number of cases as per indication

Diagnosis No of patients

l. Diabetic ulcer

o Post amputation stump ulcer

r Pre gangrene/Gangrene oftoes

r Fournier's gangrene

2. Decubitus ulcer

3. Venousulcer

4. Arterial insufficiency ulcers

3935l

232

Total

Jour. Marine Medical Societv, 2010, Vol. 12, No. 2

CouqrlaeHerlurg

SSoo

Fig. I : Treatnrentfailure and success rates.

the remaining one was Teed grade III who showedpersistent inability to equalize despite slow pressurizationand had to be discontinued HBOT. Rest of the l lpatients were managed conservatively for barotraumaand resumed HBOT after a break of 2 - 3 days. Nocases of pulmonary barotrauma or oxygen toxicity wereseen.

Of the 43 patients who completed treatment protocol(Fig. 1), "Sat isfactory Heal ing" was seen in 38(88.37Vo). Fourteen patients (32.5Vo of those whocompleted the protocol and 36.8Vo of those showing"satisfactory healing") responded well in l0 sittings but29 (67.4Vo of those who completed the protocol) had tobe given from 14 to 20 sittings for healing to occur.Average number of sittings required for healing were14.2 sittings. Five patients (Il.63Vo) failed to respond toHBOT despite therapy being extended upto 20 sittings.Of these 5,3 (6.9Vo) had to undergo amputation, 2 belowknee and 1 above knee.

Discussion

Hyperbaric oxygen increases tissue oxygen pressuresby increasing arterial oxygen pressure (PaOr). UsingKrogh's mathematical model, oxygen partial pressureat any point may be predicted in relation to the distancefrom a capillary and the oxygen pressure over the wholelength of the capillary [3,4,15]. By applying Krogh'smodel, when arterial oxygen pressure is increased from100 mmHg (with the patient breathing air at atmosphericpressure) to 2000 rnmHg (with the patient breathing pureoxygen at 3 ATA), there is a four-fold increase in theoxygen diffusion distance at the capillary arterial endand a twofold increase at the venous end [3, I 6] . Usingthe Krogh model, it is possible to predict the ability ofHBOT to increase tissue oxygen pressure in differentforms of hypoxia like (1) where there is an increase ininter-capillary distance due to edema; (2) with vasculardestruction due to infection, diabetes or radionecrosis,and (3) where the vascular flow is reduced due tovasculitis or arteriosclerosis.

HBOT corrects wound hypoxia by increasing blood

Jour. Marine Medical Society,2010, Vol. 12, No.2

oxygen content via dissolved oxygen [16]. HBOTenhances cell metabolism, preserves intracellular ATPand reduces oxidative injury to cells [13]. HBOTstimulates fibroblast proliferation, improves extracellularmatrix synthesis, increases collagen formation anddeposition and promotes rapid growth of capillaries andformation of functional microcirculatory network [7,18].HBOT reduces oedema and increases wound tensilestrength. HBOT reduces wound infection by direct effecton anaerobic bacteria and by enhancing the microbicidalcapability of polymorphonuclear leukocytes.

In our study, benefit was reported by 88Vo of thepatients whereas l2%o patients failed to respond toHBOT (Fig. 1). This correlates with other studies whichhave reported similar healing rates [4,5,19]. Poor efficacyof HBOT in some pat ien ts i s poss ib ly due tocompromised vascular supply which can only besubstantiated by transcutaneous oximetry $cPOr)[19-22]. TcPO, measurements have been usedsporadically in our centre and efforts are on to use themon a routine basis. Major lower limb amputation ratesranging from SVo to l2%o have been reported acrossvarious studies and our rates (7Vo) correlate well withthem (Fig.l) [21,22].

Conflicts of Interest

None ldentified

References

L Definition of HBOT. Available at http://www.uhms.org/De f au lt. aspx ?t abid=21 0

2. Approved indications for HBOT. Avai lable at http:/ /www. uhms.prg/Resourcelibrary/Indications/ProblemWounds

3. Mathieu D (ed); Handbook of Hyperbaric Medicine; Springer,2006.401-27.

4. Mathieu D. Role of Hyperbari'c Oxygen Therapy in theManagement of Lower Extremity Wounds. Int J Low ExtremWounds 2006; 5(4) : 233-35.

5. Boerema I, Meyne NG Brummelkamp WH. Life withoutblood: A study of the influence of high atmospheric pressureand hypothermia on dilution ofthe blood. J Cardiovasc Surg1960; I : 133-46.

6. Canadian Diabetes Association Technical Review: The DiabeticFoot and Hyperbaric Oxygen Therapy. Canadian Journal ofDiabetes 2006; 30 (4) : 411-21.

7 . Silver IA. Cellular microenvironment in healing and non-healingwounds, in: Hunt TK, Heppensstall RB, Pines E, Rovee D,eds. Soft and Hard Tissue Repair. New York: Prager, 1984:50-66.

8. Hunt TK, Linsey M, Grislis H, Sonne M, Iawetz E. Theeffect ofdiffering ambient oxygen tensions on wound infection.Ann Surg 1975; 181 ( l) : 35-9.

9. LaVan FB, Hunt TK. Oxygen and wound healing. Clin PlastSurg 1990; l ' l (3):463-72.

10. Niinikoski J. Effect ofoxygen supply on wound healing and

Patient Response

Tleat|lr€|rtFarltue

!d' Atltprrtatronstoo

Nol'esoltttrortofulcq

< o ̂

9t

formation of experimental granulation tissue. Acla PhysiolScand Suppl. 1969; 334 : l-72.

Knighton DR, Silver IA, Hunt TK, et c/. Regulation of wound-healing angiogenesis - effect ofoxygen gradients and inspiredoxygen concentration. Surge ry I 98 I ; 90 : 262-'7 0.

Bigfow WG. The microcirculation. Can J Surg 1964;7 : 23'7-9.

Boykin JV. Hyperbaric oxygen therapy: a physiologicalapproach to selected problem wound healing. Wounds I 996; 8( 6 ) : 1 8 3 - 9 8 .

Krogh A. The number and distribution of capillaries in musclewith calculations of the oxygen pressure head necessary forsupplying the tissue. J Physiol l9l9;52 (4) : 409-15.

Hunt TK, Twomey P, Zederfeldt B, Dunphy JE. Respiratorygas tensions and pH in healing wounds. Am J Surg 1967; ll4(2 ) :302- '1 .

Lazarus GS, Cooper DM, Knighton DR, et al. Definitions andguidelines for assessment of wounds and evaluation of healing.Arch Dermatol 1994:'130 :489-93.

Hunt TK, Pai MP. The effect of varying ambient oxygentensions on wound metabolism and collagen synthesis. SrrgGynecol Obstet 1972;135 : 561-7.

Silver IA. Cellular microenvironment in healing and non-healingwounds, In: Hunt TK, Heppensstall RB, Pines E, Rovee D,eds. Soft and Hard Tissue Repair. New York: Prager, 1984:50-66.

TcpO, predictive value for HBOT outcome; Available at http://www.ivhg.nUihgweb/referenc/ref4lp I 5.html

Wanell FE, Mathieu D, Neviere RR. Transcutaneous OxygenPressure Measurements. J of Hyperbaric Medicine l99l; 6( 4 ) : 2 8 1 - 9 0 .

Kranke P, Bennet t M, Roeck l -Wiedmann I , Debus S.Hyperbaric oxygen therapy for chronic wounds. CochraneDatabase of Systematic Reviews 2004, Issue L Art. No.:CD004 1 23. DOI : I 0. I 002/ I 465 I 858.CD 004123.pub2

Faglia E, er a/. Adjunctive systemic hyperbaric oxygen therapyin treatment of severe prevalently ischemic diabetic foot ulcer.Diabetes Care Yol 19, Issue 12 : 1338-43.

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16 .

CONTINUING MEDICAL EDUCATION (CME)

Continuing Medical Education (CME) consists of topics of common interest to ship borne medical officers

which are written by specialists in various fields of marine medical sciences. The topics selected should

be of relevance and should address day to day medical problems onboard ships. The topics should be

contemporary, should quote the latest references and should be written in a lucid style. The CME should

provide practical information on the diagnosis and management of commonly occuring medical problems

onboard ships with the help of algorithms, diagrams and photographs. The CME should not exceed 2500

words, should have less than 8 tables and figures and not more than 30 references. The editorial board

pruposes to continue the current practice of publishing at least one CME in each of the issues to make

eciucative reading to young naval medical officers.

92 Jour. Marine Medical Society,20l0, Vol. 12, No.2

Original Article

Respiratory Muscle Thaining for Enhanced Endurance

Surg Lt Cdr LV Visweswararao-

Abstract

Background : Respiratory muscle training improves pulmonary function but whether it improves whole'body enduranceremains controversial.

Material and Methods : Effects of respiratory muscle training (RMT) on endurance was evaluated in 20 sailors over10 weeks.

Result : Ibn weeks of daily respiratory muscle training (RMT) with an inspiratory muscle trainer, while marginallyimproving respiratory muscle strength and ventilatory capacity, significantly increased exercise endurance andperformance levels in twenty young naval ratees. The study did not show any improvement in basic pulmonaryfunctions.

Conclusion : We recommend introduction of respiratory muscle training in physical fitness regimen of Naval divers.

Key Words : Pulmonary function test, Respiratory muscle trainer, Exercise endurance

Introduction

fhough respiratory muscle training improvesI pulmonary function, it is to be seen whether it

improves whole-body endurance. Some studies reportenhancement of 50Va or more, while others report nochange at all. A number of studies show that whenbreathing muscles become fatigued, the body switchesto survival mode and "steals" blood flow and oxygenfrom the locomotor to the respiratory muscles. Deprivedof oxygen, the locomotor muscles become fatigued.Lowering of ventilation (Vr) during exercise afterrespiratory muscle training reduces respiratory muscleblood flow, which in turn benefits locomotor muscleswith increased blood availability and enables theindividual to sustain longer effort without tiring. Ourobjective was to test whether Respiratory MuscleTraining (RMT) significantly improves both pulmonaryfunction and exercise endurance.

Material and Methods

Sixty fit naval divers and submariners were recruitedfor the study on a voluntary basis and were randomlydivided into 3 groups, the RMT group (N-20), the shamRMT group (N-20) and the non-RMT group (N-20).Seven respiratory muscle trainers 'Powerbreathe' wereused to strengthen the respiratory muscles of the RMTgroup. Digital micro spirometer was used for spirometry,body plethysmograph for flow rates and tread mill

ergometer for endurance.

The study protocol was divided into five phases. Duringthe pre-training phase, subjects completed standard lungfunction tests like forced viral capacity (FVC), forcedexpiratory volume in f i rst second (FEV,), Peakinspiratory flow (PIF) and peak expiratory flow (PEF).A constant work-rate treadmill endurance test toexhaustion using modified Astrand & Rudahl Protocolwas used to determine work capacity as well as a timetrial test (2.5 km run).

During training phase, the RMT group performed 30dynamic breaths, twice daily at level 1 resistance forthree weeks, level 2 resistance for three weeks and atlevel 3 resistance for four weeks. The sham-RMT groupperformed 60 slow breaths once a day at level Iresistance for the entire period of l0 weeks while thenon RMT subjects did no RMT. All subjects wereinstructed to keep a constant level of physical trainingover this 10 week period and not to alter their exercisepattern.

During maintenance phase, all subjects continued thesame exercises but on alternate days. The RMT groupremained on level 3 resistance throughout this period offurther 10 weeks.

Two testin! phases were introduced in between theabove phases; one after the first 10 weeks of trainingand the other after 10 weeks maintenance phase. Allsubjects underwent the time trial test on day one, simple

'Graded Specialist (Marine Medicine), COMCOS (East), C/o FMO, Visakhapatnam 530 014

Jour. Marine Medical Socie\,2010, Vol. 12, No.2 93

Io

J

;

u

1 l

J

r

I

I

Pre Train ing Post Train ing Post Maintenance-t

IERMT Group nSham RMT Group *Non RMT Group l_.___ l

Fig I : Forced vital t'apacity.

4 . 5 i -I

I

l

Prer .a rn ins

- - " ; " ; ; ; ; - -

; ; ; ; ; . ; : ; : ; -

r - ' - - - - - - -| "+Rtr l r croup e sharn RMT 6roup . .* Norr RMT Group i*

;;,-r;;;;,;,n ,o,,u,,,,,.,:*,.* - -'

spirometry and body plethysmography on day two andthe constant work-rate exercise on day three.

Results

The study shows that RMT did not significantlyimprove the Forced Vital Capacity (FVC) in the studygroup. The RMT group had an average increase of 0.210Ls or 4.29Vo after l0 weeks of RMT and the samedecreased to an average gain of 0.180 Ls or 3.87Vo atthe end of another l0 weeks of maintenance RMT. Thesham-RMT group (0.99Vo) and non-RMT group (0.567o)

showed practically no gain in their FVC measurementsduring the study period (Fig. l).

The study shows that RMT significantly improvedthe Forced Expiratory Volume in l't second (FEV,).The RMT group had an average increase of 0.350 Lsor 8.27o after l0 weeks of RMT and the gain wasretained at an average of 0.320 Ls or 7.58Vo at the endof another 10 weeks of maintenance RMT. The sham-RMT group (4.68Vo) and non-RMT group (3.177o)showed insignificant improvement in their FEV, duringthe study period (Fig. 2). The study concludes that thereis mild improvement in the physical ventilating capacityof the lung as a result of respiratory muscle trainingwhich compares with some studies but contradicts others

94

P r c T f a i n i n g Post Trarr l rrg Post Maantenance

[:-v::Y " Shanr RMT Group - ' i * Non RMT Group

Fig 3 : Peak inspiruton flow (PIF).

ritl

t !lMr :role ,,r slam nmr Glo:e *:I"ll **t oi.,l_

Fig. 4 : Peak etpiratorv flo,,t (PEF).

who recorded much higher increases [ -3].

The parameters selected to study Respiratory MusclePower were Peak Inspiratory Flow (PIF) and PeakExpiratory Flow (PEF).The study shows that RMTmarginally improved both the PIF and PEF rates in thestudy group. The RMT group had an average increaseof PIF by 0.890 L/s or 9.l8Vo and PEF by 0.67 L/s or7.ZVo after l0 weeks of RMT. This gain in PIF wasretained at 0.830 L/s or 8.497o and in PEF at 0.630 L/sor 6.537o at the end of another l0 weeks of maintenanceRMT. The sham-RMT group (3.56Vo and 3.48Vo) andnon-RMT group ( I .927o & l.59Vo) showed insignificantimprovement in PIF and PEFrneasurements during thestudy period (Figs. 3 & 4).The study concludes that thereis definite improvement in the strength of the respiratorymuscles as a result of respiratory muscle training withPowerbreathe RMT device which compares withsome studies but contradicts others who found nochange [4-6].

In our study we used two performance tests, theConstant work rate treadmill endurance test' based onmodifiedAstrand & Rudahl Protocol which is consideredgold standard to demonstrate work capacity and the'Time trial 2.5 km running performance test' that hasthe advantage of a better reproducibility. The subjectsperformed the constant work-rate exercise on thetreadmill to the point of exhaustion. The treadmill was

Jour. Marine Medical Socie6',2010. Vol. 12, No.2

);u

$ szo

;F

Pre Training Post Training Post Maintenance

+RllT Group'-+-- Sham RMTGroup + Non RMf Group

Fip 5 : Constant work rate trademill endurance trest.

Pre Trainlng Post Training Po3l llaintonance

ERMT Group tr Sham RttiT Group I Non RilT Group

Fig 6 : Time trial 2.5 Km run.

set up to start with a speed of 8.05 km/hr (5 mph) and agrade slope of IVo. After 3 minutes, the grade wasincreased to2.5Vo (1.4") and then by 2.5Vo (1.4") every2 minutes. The test was stopped when the subject wasunable to continue. The RMT group had an averageincrease of endurance time of 2 min 34 sec or l4.04%oafter 10 weeks of RMT which was retained at 2 min 15sec or lZ.4IVo at the end of another 10 weeks ofmaintenance RMT. The sham-RMT group (6.48Vo) andnon-RMT group (4 . I IVo) showed ins ign i f i can timprovement in their endurance times during the studyperiod (Fig. 5).

In Time Tial2.5 km Running Performance Test, thesubjects were instructed to complete the required run(2.5 km) as quickly as possible while the time taken tocomplete the run was recorded. The RMT groupimproved their timings by an average of 1 min 41 sec orl5.32vo after 10 weeks of RMT which was retained atan average improvement of 1 min 34 sec or l4.29%o atthe end of another l0 weeks of maintenance RMT. Thesham-RMT group (7 .62Vo) and non-RMT group (3.88Vo)showed marginal and insignificant improvements in theirrun completion times during the study period (Fig. 6).

Approximately every 3 min throughout the constant

Jour. Marine Medical Society,2010, VoL 12, No.2

Pra Training Port Trainlng PoBt ilalntonancs

FIIiiliGIG-- str".nmrcroup +-nonnlticr*pl

Fig 7 : Preceived exertion rating (After 18 mins onTreadmill).

work-rate treadmill exercise test, the subjects were

asked to estimate their respiratory and leg effort usinga visual analogue scale which ranged from 0 - 20. TheRMT group showed marked decrease in dyspnoeic orleg effort sensation of average of l8.75%o after l0 weeksof RMT which was retained at an average improvemento f I7 . I8Vo a t the end o f another 10 weeks o fmaintenance RMT. The sham-RMT group and non-RMT group showed marginal and insignif icantimprovement in their perception of exertion during thestudy period (Fig. 7). In other words, the RMT subjectscould tolerate a greater ventilatory load without anincrease in dyspnoeic sensation after RMT, which maylead to enhanced exercise performance.

Discussion

Previous studies have examined the influence ofrespiratory muscle endurance or sfrength training on VO,max and found no significant improvement [7]. Morerecent studies have shown that respiratory muscletraining is associated with enhanced endurance whenthe exercise tests require the subjects to work at about70-80Vo of their maximal capacity [8]. Others haveexamined the effects of respiratory muscle training onthe ability to perform very intense endurance exerciseat85-95%o of maximal capacity and found no change inperformance [9].

Because of the more active nature of inspiration inthe breathing process, most research has focused onthe effects of inspiratory muscle training. Literaturesuggests that expiratory muscles may not contributesignificantly to the work of breathing while an individualis at rest. The trend to focus on inspiratory muscles ischanging because of recent research which shows thatexpiratory muscles become actively involved at highexercise intensities. Because high ventilation rates arerequired to maintain exercise intensity and airway flowduring this period becomes "turbulent", more effort isrequired of the muscles used in expiration. A principle

( )1 ' \ t r r - ng t l t t r a i n i ng i s t ha t I r i t i r t i n ! [ r o th ugo r t i s t un r l

at r t l tgotr is t gr( )ups rest t l ts i r t i nrp lo lcr l neur ( ) r rL lscrr lar co-o l t l inat ion ancl c f l ' ic icncv I I01. ' l 'h is has not unl i l rcccnt lvbeen appl iec l to thc rcspi la to lv nrusclcs. In a rcccnt s tuc l l .W c l l s . c / r r 1 . e v l l u a t c d t h c c f f c c t o f c o r . r c u l r c n tinspi l l torv ancl erp i la tor-1 ' r . t tusc le t ra i r r ing (CRM' l ' ) onpt t lnronary l 'unct ion ancl s t rcugth ancl enclurancc o l thclespi ratory nrusclcs.

Co t r c l us ion

Susta i necl Vent i la tory Capaci t r . a pul nro i rar '1 l i rnel ior rthat coulc l be extrcnre lV i rnpor tant in c lc terrn in ing thc

-ueneral er tc lu lance capabi l i ty o l 'ar r inc l iv ic luul . coLr lc l r r t l t

be saugccl in th is s tuc lv c lue to non-avi r i Iab i I i t t 'o l ' r 'cqui rcc l

equipt r icr t t and the sanre should l re inc lLrdecl in future

stuc l ics. This s tudy ' sussests thut re spi la tor l rnuscle

tlai n i rtg u'i th "Pou'ertrc'athe" r'eslt i r lrtor'\ ' nr u sc l e tlai ncr.

t hough c loes no t hc lp u ruch i n bu i l r l i ng pu lmonarv

e r tc lurar tce ls ev iderrced l ry pulnroni l rv l i l r . rc t ion: tkrcs

s igni l ' icant lv inrpr t lvc both corrstant \ \ 'ork rate ancl t inre-

t r i l t l e r c ' r c i se pe r l i r r n ta r t cc un r l hencc thc ge 'nc r u l

cnclutance. The re lat ive hypelvcnt i Ia t ion lv i th no c l ransc 'i tt respit 'a1ol') ' cl ' l i l l t stt qgests tltat 1cs1;i ritttttV t.t.tttsclc

t ra iu i t tg a l lor . 'u 's subiccts to to lcrate thc h ighe' r L ' \c le i \cv r - n t i l a t o r Y r c s p o n s c u ' i t h o u t c l t ' s p n o c a . I t i s

rcconrnrcnclecl to incorlrorate s()nrr- lbrrn ol ' respiralor'1

n lusc l c t l a i r t i r r g i n t hc phys i ca l t l a i n i ng l cg in rcn l i r r t hc

armerl f i lrccs. "Porverbreathe" onlY trains the in\l) irat(lr ' \

t . t tusc les. Cont l t le te or ' ( loncur le nt lespi rator ' \ ' rn t rse le

t ra in inc (Ct tN' lT) t lev iccs r reecl to l re s tuc l ie i l . Cul tLrnr l lysui table ancl cost-c l ' l 'ee t i r c lcspi rutor- r nrr rsc lc t l l r i r r ing

nrelhods such as "Kurtc la l i r t i vosu Plarurvrrnr l r le l r t l r ing

tcc l tn ic lues" uut l " l ' lu tha Yogu b lc l th i r r r : tcchnic l r rcs"

shou l t l u l s t l bc c r u l L r i r t c t l t ' o r i r t i ; l r t r v i r r u l r u l r uo r ta r rl ' r r r rc t ion urr r l cxc lc isc cnr l l l l ' l tncc.

Rel 'ercnc, :s

l . \ l a r k o r ( i . S P c r r r l l c r - ( ' \ 1 . K r r r r I l l i 1 . , ' n z i r t ( ' . S t r r c . : i ( .

[ ] o t r t e l l i c r L . [ l c s l t i t a t , r r r r r L t : c l c l l i t i t t i n g i r t c t u u : t . . r e l i t ] !

c n r i u r l i n c a $ i t h 0 u t l r I I e c l i n - r c l t t t l i r r r r i s c L r l l r t f ( ' \ | ( r i l \ ! ' \ l l )

e r . e t c i s r ' . L t u . l , \ 1 t 1 t l l ' l r : i r t l 1 0 1 ) l : S 5 l l . l l ( )

l . l . c t l t i r . l l . \ \ ' l l k u r t t l c r I ) l j . \ l , , , l l i e l r l r . I u n t l l r c n ( ' l : ( i . i S S l r l( ) p s ( ( ) n r n l r t t l I ) t r r . i c s t # [ S l . \ ] 1 0 0 ( 0 ( r 0 - l : I l . \ | i r r l ' r f \

l \ l r r s c l c f r ; r i n i n L i r r r p r , r r c r n r n n i r r s I r e r l o l r n . r n e e .

. 1 . \ \ . i l k : L r t t l c r D l : . i j r L r t h . \ l l . I - L r r r r l g i c r r ( - l : ( i . I r t i t t i t r 3 , r l t h t

r c s p i r . l r t o r r l l l u \ ! l e : c n l l u t t e s n i r \ \ ( l i \ e t s l i n s s i t t t r t r t n g

en r l u r i l n ! c r r l i c l t l s t L t t l r . { 11J l l i ) i ) l : l ( . ) : 1 . \ l r s t l l L c t I r o ( ) 9 .

l . I l r r r i r h t S . C ' l r ; r t l t . i t t t K . \ \ i r l : t c n l r o l r u c I { . - ' l

l r c c l l e e l o l l i r t ' t l

I o l r t l l e sp i l l r l o l r r r i use le t n r i n i ng i n l l r e c l i t u l r l h l , ' t c " ( i r l ) \ l l r ! t )

, \ n t ( t i r t r n . l r t t t t t t t t i ( ) l l l ( \ l ) i I ( t t t ) t - \ t r t t t l ( r i t i , , t l ( t t r L ' , l l t ' , l i r ' i n L l

l ( ) r ) 7 1 : l 9 : . l S L

5 . l r t b t i t ( ) . \ \ ' r i n r ' r l ' . . - \ z g l r l \ . 1 { o l s t c i r r . \ . \ \ ' c i n s t . ' i n \ . S 1 r g 1 j l i 1

i r t s l . l i l a l o l r r t t usc l e t r r L i r r i n -L i n u c l l t r a i t t e r l ( n ( l u l l nc t i l t l ) l ( l e \

X I ( r l . \ ( i . \ / , r , / 1 . \ h . \ ( ' / e l (X )0 . . l l : l l . i . l r 7 .

( r . \ \ ' i l l i a n r s . l S \ \ ' o n { r l L t l t r l i u n . l . I l l l n \ \ 1 . \ e . r r t l , r l : o

I n s I i | i r t o t r r ) l r l \ ( l c l n l i i l i n ! l : t i l : l r r i r r I r ' , i r r e r l ( [ u r . l i l \ 1 . ! . l i r i r ! r l \

i n l t l r l c l c s . J / r ' r l . \ ' r i . \ 1 r , , r 1 r l r l r ' , l 1 )01 : - l - i : I I i ) - l ' )S .

H i l n , ' l l l . S e e l r t r ' \ H . \ l r r r i r n l i l ( ) \ ) g c n L l I l l k r ' : r n ( l \ \ i r r k

c i r l ) i t e i t \ . t l l e r i t t : I i r i r t , , r ' \ l t i u \ ! l ( ' l l i U l l i l l L . : t ! L ) l l t l ( ) l l e , l \ l u r l \ .

. 1 . \ 1 t 1 t11v . ! , i I ( ) r ) 1 . t ) ' - f . i ' - r ) .

S . N l e \ l r i l r o n N I I : . I l o u l e l l r c r ' I i . S n r i t l r I { N 1 . S p c n u l c r ( ' i \ 1 .

H r p e r ' P r t , r e l r t r . r r r r i r t g a l l c r ) r . t u t e s P c r i l t l r e r ' ; i l c l r e r r r o s e r r r i l i r i l r

r t l t r l i l l t l ) r ( ) \ t 5 t \ t r l l t . r ' J l l r i t l i r u l c r . . l l . r l , B t r t i l { X ) , ' . l ( } - 5 ' l i ) . l l-l.r .

i ) F l L i r b l L r n \ { S . ( l L r l t . . I t ( ' l ) r i r t l r I i [ . \ l c K e r r z i r I ) ( l r r r | n , r e t l

r t s p i n i t o r t t l t L r s c l c c r t t l L r l l r r t e e r ' 1 l t i g l t l r t r . t i n c r l c r c l i s t s l t n t l

t l r c t l l c c t s o n n n i t t n t l L l r ' \ r r c i \ c P r ' t l i ) r ' , l l u l c a . ! r t t . l . \ l t t t t t s \ l L r l

l ( ) t . ) 1 . l l : ( ) 6 - 7 0 .

l { ) . S i r l c l ) ( i . l \ c L r r l r l i i r l i r I t i L t i l n t \ , r u \ r \ l i l n r r t r . r i n r r t l . . 1 1 t ' , 1 5 r r

. r , l t r t t t t I ' . r i ' r i i ( ) S S : l ( ) : S I l 5 - i : .

Effect of Hyperbaric Oxygen Therapy on Pulmonary

Surg Lt Cdr Rohit \ /entra'

Abstraet

BackgI . r l t r I r t | : \ \ ' i t I lpr .o | r l l rgcdl r ig | r l ) resst l I .eo\} 'gc l le \p()s t | re 'pu|nr t lnarr .ant ior idant t le tet rcesarel ' t , l l l 'he|Ior ic nrani lestat ions occul ' .

l l tthods: ( 'hest I lxaminatiun inclurl ing l iorcetl r ital capacitl (FVC). F'orcecl Expiratorr' \ 'olun.re in first second (FEVr)arrd l lar i r r ra l I I i t l l ' i rp i ratorr l - lou (F ' I tF, . r . ) r rereconcluctedun20sub. iectsbefbre,c lur ingandal lerHy'per l lar icOrr gen

'l'herap-,r' (H IIOT).

Rrsul ts : - [ ' l rc loc ls o1 'c lccrcrncnls in F\ ( ' ( -16.67o t 5 . ] ) , FEY, ( - l3 . t t7o + 7.1) and FEF,. r , ( -18.1%, t 9 . - l ) a l lerH I|O'f v e rc signifirantlv knver in out studl than that doculnentccl by other u'orkers.

L 'orrc l r rs iorr : The protocolof 20 s i t t ings of 60 nr inutes each at 2.J ATA is safe.

I{er' \\ irri ls : Hl pr:rbaric rx.yge nation, ()xl 'gen toricity, Pulmonar.v l irnction test

Original Art ic le

Indices

In t roduct iorr

f l rc t t ' . , ie c f tee ts o l ' [ ] r 'cut l t in i r purc Orygcr t urrc ler

I p l c \ \ i n -e h l r r c l r ecn c loc r rn ten tc r l i n t l r c l as t ccn l t r l v

by ' Puul LJer t ancl othcr s . ' l -hc scvcr i tv of or1 ' rcn tor ie i t1 'incrcuscs Lrot l r u i t l t t l rc r - isc t l l pa l t ia l l l ressLl rc o l ' r l r t 'ger t

l r td thc c lLr l i r t ion ot crposurc [ 1 . Stuc l ics I t l rvc ' s l toun

that nt l s ig l t i l ' ic i t r t l t t l r ic i t ) , \ \ / l ts l to tec l i l t t t ta t t breath ingo\ \ 'ncn l t ( ) . -5 , , \J 'A l i r r lJ duvs I I .3 l . r \ t par t ia l prcssure

ol ' l . \T\ pul r r ronl r rY tor : ic i t1 , oe cur ' \ in I l - I - l hours ancl

l l t l . \ t ' ' \ . lur tss gct r r l l 'eetcr l in l - ( r houts. sub. jcct to

i nd i r r c l u l l r u l i a t i on . ' l i l r i c e l l ' c c t s o f o r y ! cn u t h i ghpre\ \u lc ( ) r ) t l lc lun! \ r r rc sr r t - r t l i ! i r lcc l in to crr rc lat ivc anclp r o l i l e i u t i r c ; r l t u s c ' 1 1 . - 5 l . E l r l l ) ' s v n r p t o n l s a r c\ub\ tcnra l i r l i tu t ior r i rnc l c l r ' ,V e ough on c lcc l - r iuspi la t ior ru h ich r tur , r ' pr ( ) ! r 'e :s to r l r spt t t le l . pu in chcst ancl scvcrc

co i t u l r r i i t l t i n . r c l a r . l { c r l ue t i o r r o l ' r ' i t l l cap i r c i t y ' e i t r r l r e

obse t t c t l I rc totc t l ie sLr l l . jce t i r c s \ ' l l l l ] to l l ls c lc 'c l t l l l ar lc lr i tu l t r ip . rc i t t l 'e \ c l ts l r r rck to norr rur l a [ . rout 8 horr rs af icr

thr ' svnr l ) t ( )n ls h l rvc t l is rppcurcc l l ( r l .

lVlaterial antl lVlethods' [

h is : tudr ' \ \ ' l rs ur ] ( lcr tuke r r l ' r 'orn Dec l (X)7 to Dcc

l(X)fi rn l f l l-5 [,cclclecl te'r '1iur 1' carL- scr'\ ' ice hospital u' it lr

h rpe lh r r l i c o \ \ seu the lapv ( l lBOT) l ' ac i l i t 1 , . ' l r ven typrr t icnts reeciv in-u I r t per ' t - r . t r ic ( )x) 'ccn thera l r ; ' lor ' \ i - r r i ( )LrS

int l icut iorrs u c le sc lce ted. ' [ 'he

erc lLrs iorr cr i tc l i l r w crchis tor ' r o1 ' l ru l r l r ( )nal ' \ ' i l lncss. c( )nct t r rcr l t pu l t lonan i l lness

clernonstrable on chest X Ra\ , ( ) r anv acute i l lness.-fhe

hcight rrtt l r i,eiglrt nreusurenlent wlrs ckrne on

balc feet . A l l pat icnts rccc ivcd HBOT of l0 s i t t in-es of

60 rn inutes each at l . l A- fA. Chest X-Rays (PA r icw)wcle obta inecl l rc f i r re ancl af tc l HBO'f . Thc put ients

r , r ' c r e a s k e c l f o r s y ' m p t o u r s o f n a s a l c o r r g c \ t i ( ) n .r c t r o s t e n l u l b u r n i n g . 1 l a i n . i r l i t l r t i o r r , c o r , r g h a n dexpectorat ion bef i l re ancl af tc l cach HBOT scssion.

Bocly tcnrpe raturc. pulse. bloocl ; lressure. ENT and Chestexanr in i l f ion \verc repeatcdly conductcc l . Forccd Vi ta l

Capacitr ' ( FVC ). F-orced Expiratory Volunre in I ' ' seconcl(FBVr) rnc l Maxinra l [ \ ' l ic l E,xpi ratory F lorv (FEF.. . - . )

u as ekrnc lrcfirrc Hylterbaric Or1'gen Therapy ancl aftcr( )7. l+ ancl l0 s i t t ings ancl r ancl 5 hours af ter the last

s i t t ing.

Resu l t s( 'hest X-Ra1, PA v icn, be lore ' and af ter HBOT

exl )osure l i rund no changc. Thc f ind ings on FVC. FEV,anrl FEF , -r i l l 'e lecorclerl in Tables l. I ancl -1. Thesebrirtg or-rt not only the itnrtiurtt ancl rate ol 'declernent but

a lso the rate ( ) f rcc() \ 'erv.' l 'hc

HBOT protoeol proc lucecl nr in inra l t racheal

i r r i ta t icrn ancl bul r r ing sensat ion in 30( / r and mi lc l non-pror luct ivc cough in 50(2. No f 'e ler ' . i l lvc() lar atc lcctas is .

coi t rsc t 'a lcs. rhorrc l t i or bror tchra l breath sounds wcrcot- rscrvcc l in ( )ur \ tuch, . Hvncraent i t r c i f t l tc n i lsu l nrucosi r

[ ) \ lO r r n t l G l r L t l c r l Sp l { i \ l ; i l i r r c N le t l i e i r r c t . INS N i l c ckshak . C /o l r l c c t N Ia i l O l l i c c . Koe h i - 68 ] 00 -1

. l t t t t r . . \ l t r r i r t t , \ l t r l i t t t l . l r r t l r ' l r . l0 lO. \ ' r t l . /1, , \ / r , . l

ITable I : The Forced Vital Capacity (FVC) observations extracted from the spirometry records. Percentage decrements have

been calculated & shown

SrNo

Pre Day 7 Day 14Therapy

Day 20 Day 20 Day 20+ 2 h + 5 h

7o Decrementafter D 7

7o Decrement 7o Decrementafter D 14 after D 20

7a Decrement Vo Decrcmentafter D 20 + 2h after D 20 + 5h

I

z

J

A

56789l01 lt 2l 3l 415l6t 71 8l920

5.235 . 1 75.524.965 . l 5+ - t )

5 . 1 85.435.295.345 . 1 75.415.655.285 .315.495 . r 24.985.375.26

Mean

5.09 4.88 4.515.04 4.94 4.34s.29 5.09 4.M4.88 4.75 4.405.09 4.78 4.204.59 4.36 3.895.05 4.92 4.535.35 5.16 4.685.02 4.76 4. t25.2s 5.01 4.455.06 4.91 4.425.34 5.05 4.475.55 5.4t 4.805.03 5.01 4.205.18 5.09 4.495.43 5.18 4.555.05 5.00 4.394.80 4.55 4.005.28 5.04 4.475.08 4.78 4.20

5 .015.045 .18 5 .334.845.054.19 4.63s.055.284.40 4.865.275.035 .215.504.64 5.045 . r75.304.994.53 4.775.224.89 5.06

2 . 12.64.21 .7t . 22.92.5t . 45 . 11 .62 .11 .31 .84.82.4l . ll . J

3.71 .73.42.4

6.24.57.84.37.27.85 . 14.9l0 . l6 .15 . 16.74.25.24 .15 ; 7) 4

8.66 . 19.26.1

13.2l 6 . 119.511.218 .417.712.6r 3.922.116.7t4.6t7 .315 . I20.515.4r7.2t4.3r9.7t6.720.116.6

4.2

3.81.3

3.4

2 . 1

8.2

4.6

) - l

2.56 . 12.4r .97.22.62.816.9t .42.7

3.72.6t 2 . l2.63.42.69 .12.87 . 14.8

Table 2 : The forced expiratory volume in l't second (FEVr) observations extracted from the spirometry records. percentagedecrements have been calculated & shown

SrNo

Pre Day 7 Day 14Exposure

Day 20 Day 2O Day 20+ 2 h + 5 h

7o Decrementafter D 7

Vo Decrement Vo Decremenlafter D 14 after D 20

Vo Decrement 7o Decrementafter D 20 + 2h after D 20 + 5h

| 4.21 4.03 3.762 4.19 4.08 3.963 4.47 4.25 3.994 4.02 3.91 3.725 4.17 4.04 3.606 3.83 3.65 3.407 4.19 4.03 3.888 4.40 4.24 4.039 4.28 4.06 3.61l0 4.32 4.2r 3.87l l 4 .19 4.02 3.8612 4.38 4.26 3.9113 4.57 4.46 4.24t4 4.27 4.00 3.9315 4.30 4.13 4.0216 4.44 4.32 4. r5r7 4. r5 4.0r 3.9818 4.03 3.82 3.50t9 4.35 4.26 4.0320 4.26 4.r5 3.76

Mean

3.70 3.973.97 4.003.65 4.153.49 3.843.84 4.0r3. r2 3.523.74 4.003.89 4. r93.4r 3.563;10 4.263; t0 4.033.78 4.133.99 4.363.34 3.593.75 4.103.85 4.293.78 4.003.24 3.663.86 4.233.47 3.96

A l l

3.67

3.89

3.90

4.05

4.22.64.82.7

3 . 14.73.83.65 . t2.6

3.92.82.66.43.92.83.25.31 .92.53.6

t0;75.310.87.413 .6n .27.48.315;710.57.710 .87.28 .16.46.74 .1t3.27.4t t .79.2

t2 .25.218.41 3 . 17.918 .5r0.7I 1 .620.3t4.4I 1 . 6r 3.61 2 ; l21.8t2.8t3.4

8.919.7l 1 . 3l8 .613.8

5.74.57 . 14.43.98.24.64.816.91 . 45 . t

5.74.6t6. r4.63.43.69 .12.87 . 16.1

-'\ -z

4.81.5

4.4

4 .1

9.2

3.64 . t2

98 Jour. Marine Medical Socierv, 2010, Vol. 12. No. 2

lablc J : ' lhe uraxinral nl id expir l tor l ! ' lou Rate (t-E,F,.r.) observations exlracted from the spironretr. \ r 'ecords. Percentagetlecrernents have been calculated & shown

Sr P r . ' [ ) a r 7 l ) l r l - 1 Da l l 0

\ o l ; r p , r r t t r c

I ) l r l0 Dar l0 ' . , i Decrenrcnt

r - l h + - 5 h a l ' t c r D 7

r/r Decre nrcnt 'Z Decrcrncntaftc'r ' D lJ at ler D l0

% I)ccrenrcnt ( t i Decrenrenl

af ter D l0 + lh af te l D l0 + 5h

6 .5

u.9

I

l

-+.i

/J

1

s

l 0

l l

I ]

l . r

t l

l - r

l b

I ' i

l t i

I (./

l 0

l . e I J . l t l . l s-+.Si i J.(r(r l . f l

i . l i - 1 . 9 ( ) + + - l

l . ( rs l . i6 -1 .1 ( )

J .s r r - i .7 ( r + l7

J 1 1 - 1 . 1 5 l s l

+ S9 -1 .o7 + .+( )

5 . l . r 5 ( ) 0 - + . 6 1

J . ( )9 J . j J . t . , )6

5 .0-+ l .9 l l . l . l

l . s l t + 6s -1 . . t5

5 . 1 I 1 . 9 9 + - 1 ( .

. i . l . l 5 l q - 1 . 9 1 )

. l .r)9 -+.7.5 l . l3

5 01 J .19 l . ( r I

r 1s 5 . ( ) l J ( ) .1

l .S I -1 . , t t - -1 . ( r0

-1.70 +.5-l . i . ( .) l

5 0 ' i - i s s l 5 i

+ 97 +.S0 -+ l()

\ leu r r

+..1 | l.() I-+..iN -+ 6()i . 9 9 J . 1 )-1.07 l . l+

l . l + - + . 6 . 1

.r. .s I - l ()()

l . l 7 + . 6 0

I 1 7 l r ; I

.r 7 r J.o]-+.0(r - i .75

.r s r -1.61

.1.90 1.7()l t l 1 .9+.1.7-5 -l..ou

4 . t1 -+ .6e

l .J() J 90

l. l | -1.5(r

. r .51 -+ . l6

- t 19 f 11

i l i l 1.50

t s 7

+ t-+

L i l

+ . 1-1.(r

- t l

) . 1

t . l

J . 9

t . l

5 l

1 . 6

+ . I

l . . l

l 8-1.8

+.-+. 1 . I

L.l

.r.73 .7.r.l1 .5

l l . l J

8 .5I -+.lJ

lJ . i

t -+.1| -+.8t 0 . l9 .910.1| ] . II 0 . 3t ) . 18 . lI 0 . 1l i . I

lo.1-1. sI 6 . 61 0 . 6l -+.1

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was ()bsL ' r ' \ 'ec l i r t -5 c . tscs (25( / ( ) . which was s lat is t icr l ly

s icn i f lcar t t .

Out of thc s i r l l l t icnts \ \ 'ho cx l )cr iencc( l l )u lnronarysynrptonls. the f i ls t c le ve krpccl thcrr on thc I l ' r 'c lay, thc

next t \ \ 'o ( )n l l r r ' . anr l anothcr two on thc l5 ' r ' and the

last onc on thc l ( r ' r ' r la \ ' . Cough \ \ 'as not icc( l only af ter

thc l -5 ' r ' d i ry . Thc svnlptonrs c lcvc loped by cucl of thcsessi ( )n ln( l pers is tcc l l i r r not n lorc than two hours af ier

thc lap1, . No apprcc i r " rb lc changc \ \ 'as obscrvcd at the

cnd of thc t ' i rs t \ \cck. At thc cncl ( ) f the sccond wcck or

l t lcr l - l s i t t ings. nr i lc l c lccrcn)cnts wcre rccordcd wi th

rne an FV( ' a t -6. I ' ,4 + 2.5. Inean FEV I a l -L) .2% + 4.J

a r r c l r n c a n F E F . . . r t - l l . J ( / r ! 1 . 3 . A s i e n i f i c a n t

c lec lc lsc in nrearr FVC (-16.6( / r t 5 .3) . nrean F 'EVl ( -

l - 1 .87 l . 7 .1 ) an t l n r c i t n FEF- . r - . ( - 18 . - l% + 9 . J ) we re

obscr . r 'cc l by the ( - 'nd of 20 s i t t ings. Al l c lcc lcnrcnts in

F 'V ( ' ( - 1 .3 ) . F 'EVr ( - 1 .5 ) anc l FEF , , r . ( - 2 .6 ) r c tumed to

luon-s igni l ' icant lcve I r , i i th in 5 hout 's of the last se\s i ( )n(D l0) .

' fhcre u as no s igni f icant c l i f terencc bct \ \ 'een

pat ie l r ts u 'ho had sul ' f 'c rcc l sy l l l l l tonrs and those who

hacl not which corrobor i l tes lv i th Clark 's re pof t [ : l l .

D i scuss ion

Ox,ygerr tox ic i ty syndronre. a lso known as the "Paul

Bert e l ' l 'ect" is usual ly rnani l 'estatec l by exposure fbr

nrore than 1.1 houls to nonrrobal ic 100% oxvgen or to

. l t t u t . l l ( t i n ( l l ed i t t r l . t o . r r ' l r ' . 2 ( ) 10 . \ i ) 1 . I ) . No . 2

hyper baric oxysen in humans and experimental animals.The precise rnechanisnl of damage is not known. butl i r rrnat ion of react ive ()xygen species is l r rr intermediateevent in the proc luc t ion o f ox idant damage to ce l lrnembranes and constituents. The de-tree of darna-eeappears to be deterrninecl by the relative ri,rte at whichactir,e raclicals are fbrnred and rer.r.roved [4.51.

Rec luc t io r t o f mo lecu la r oxygen by ac ld i t ion o fc lec t rons one a t a t i l l re wou ld resu l t in scc luent ia lfirrtration of superoxicle. hydrogen peroxide. hydroxylradical ancl f inal ly water. There are indicat ions thatsuperoxidc radicals generated in mitochondda are rapidlycJismutatcd to hydrogen peroxide ancl that these productsinteract further in thc presence of catalyt ic amoulrts ofi lon. to generate highly react ive hydroxyl radicals andpossibly singlet oxygen. Ini t iat ion of l ip id peroxidat ionby ei ther of these highly react ive radicals could thengreatly inclease oxidant damage by propagation of chainreact ions with inact ivat ion of cr i t ical enzymes. ccl lularlnembranc clamage and possible oxidat ion of proteinsas we l l as l ip ids . Pnr te in c ross- l ink ing . fa t ty ac idoxidat ion ancl oxidat ion of arnino acids are al l potcnt ialr e s u l t s o f f r e e r a c l i c a l p r o c l u c t i o n i n h y p c r o x i cel lv ironment [51. Tl ic body's dcf 'cnce a-sainst sLlchdarnii-te con.l pri ses anti<lx idant en zy mes which i ncl r.rdesuperoxicle cl ismutasc. catalase. glutathione peroxidase.

99

glutathione reductase and the enzymes of the pentosemonophosphate shunt pathway. Other compounds, whichhave antioxidant activity include glutathione, selenium,vitamin E and vitamin C [7].

Acute changes in the lungs resulting from oxygentoxicity consist of alveolar and interstitial oedema,alveolar haemorrhage and proteinaceous exudate. Thisis followed by an inflammatory reaction. Furtherprolonged exposure to oxygen leads to proliferation oftype II epithelial cells and fibroblasts, followed bycollagen deposits. Distal airway epithelial cells, includingtype II alveolar and non-ciliated bronchiolar epithelialcells, are important targets for oxygen radicals underthe hyperoxic condition [5]. Healing may occur afterdiscontinuation ofoxygen exposure, but areas offibrosisand emphysema may remain.

The risk of pulmonary oxygen toxicity begins toincrease with exposure for over 16 hours to partialpressures of 0.5 bar or more [8]. Early symptoms ofbreathing l00%o oxygen are breathing difficulty andsubsternal pain, rarely seen before 24 hours ofexposure.Partial pressures between 0.2 bar (normal at sea level)and 0.5 har are usually considered non-toxic.

Oxygen toxicity is reversible in the early stages butrepeated exposure to HBO may lead to cumulativeeffects and irreversible lung damage [5]. Subjectivesymptoms such as substernal burning and pain, chesttightness, cough, and dyspnoea appear much beforevolume and flow changes become apparent. Withcont inued oxygen exposure, the pat ient developsprogressive impairment of pulmonary function andeventually, the adult respiratory disease. Initially, thereare indications of capillary endothelial damage, followedby pulmonary oedema, protein exudation and progressiverespiratory failure, which is seen over the course of daysto weeks at raised oxygen partial pressure [6].

To objectively measure and compare the ptrlmonary

damage caused by toxic doses of oxygen, ser ialspirometric pulmonary function studies are the goldstandard. The spirometer measures the amount (volume)and/or speed (flow) of air that can be inhaled and exhaledand generates a pneumotachograph to help assess /compare the pulmonary functions. Partial pressure ofoxygen used, length of daily sittings and breaks given inbetween the sittings currently are adequate to preventill effects ofoxygen in healthy lungs, as evidenced fromour study.

Conflict of Interest

None identified.

ReferencesL Clark JM. Oxygen toxicity. Bennett PB, El l ion DH (Eds.)

The Physiology and Medicine of Diving, 3rd Ed. London:Bail l iere, Tindal l and Cox. 1982; 200-38.

2. Clark JM. Pulmonary l imits of oxygen tolerance ln man.Experimental Lung Research 1988; l4: 897-910.

3. Clark JM, Gelfand R, Stevens WC, Lambertsen CJ. Extensionof pulmonary oxygen tolerance in man at 2.0 ATA byintermittent exposure on a 60: 15 oxygen : normoxic pattern inPredictive Studies VI. Undersea Biomed Res (Suppl) l99O; l7: 2 5 .

4 . C l a r k J M , G e l f a n d R , S t e v e n s W C , L a m b e r t s e n C J .Comparison of human visual and pulmonary responses tocontinuous and intermittent oxygen exposure at 2.0 AIA inPredictive Studies V and VI. Undersea Biomed Res (Suppl)l 9 9 l ; l 8 : 8 6 .

5. Balentine JD. Pathology of oxygen toxicity. New York:Academic Press. 1982.

6. Caldwell PRB, Lee WL Jr, Schildkraut HS, Archibald ER.Changes in lung volume, diffusing capacity, and blood gases inmen breathing oxygen. J Appl Phltsiol 1966;21 :1477-83.

7 . Allen JE, Goodman DB, Besarab A, Rasmussen H. Studies onthe biochemical basis of oxygen toxicity. Biochem BiophtsActa 1973:. 320:708-28.

8. Bardin H, Lambertsen CJ. A quantitative method for calculatingpulmonary toxicity. Use of the "Unit pulmonary toxicity dose"(UPTD) . Ins t i tu te fo r Env i ronmenta l Med ic ine Repor t .Philadelphia, University of Pennsylvania, 1970.

100 Jour. Marine Medical Socier,^,2010, Vol. 12. No.2

Original Article

QT Dispersion in Diabetic Patients on Hyperbaric Oxygen

Surg Lt Cdr SS Dalawayi., Surg Cdr HBS Chaudhry*

Abstract

Background: Increase in QT dispersion (QTd) is associated with malignant ventricular arrhythmias and suddencardiac death in patients with Diabetes mellitus. Diabetic patients receive hyperbaric oxygen therapy (HBOT) for nonhealing lower extremity ulcers.

Methods: TWenty patients receiving HBOT for non healing diabetic foot were randomly selected. Standard 12 LeadECG was used to measure QT interval manually and QTc and QTd dispersion was calculated using Bazetts formula.ECGs were taken before and after HBOT.

Results: Mean QTd decreased from 59.79 msto 52.24 ms after HBOT which was statistically significant.

Conclusion: HBOT by decreasing QTd in diabetes patients may reduce the risk of malignant ventricular arrhlthmiaand sudden cardiac death.

Key Words : Hyperbaric oxygenation, Diabetes mellitus, QT interval

Introduction

l^\T dispersion is the difference between the longest

\!and the shortest QT interval and is an index ofmyocardial electr ical act iv i ty. An increase in QTdispersion is associated with mal ignant ventr iculararrhythmias and sudden death in diabetic patients [].Diabetes mellitus is a systemic disease associated withcardiovascular complications such as coronary arterydisease, diabetic cardiomyopathy and cardiac autonomicneuropathy [2,3]. Myocardial ischemia can lead toelectrophysiological heterogeneity and asynchronism inventricular myocardium [4]. In addition, sympatho vagalimbalance due to cardiac autonomic neuropathy maycontribute to electrophysiological heterogeneity of themyocardium [5]. The abnormal i t ies in myocardialrepolarization are a risk factor for the occurrence ofrhythm disturbances and sudden death in diabet icpatients. Diabetic patients receive hyper baric oxygentherapy (HBOT) for non healing lower extremity ulcers.HBOT improves cardiac neuronal regulation in patientswith diabetic autonomic dysfunction [6]. This study aimsto evaluate the al terat ion of QT interval and QTdispersion in diabetic patients after ten sittings of HBOTat 2.5 ATA.

Material and Methods

The study was conducted from Jun 2007 to Dec 2008

in a 825 bedded, tertiary care multi-specialty servicehospital with hyperbaric oxygen therapy facility. Twentydiabetic patients in the age range of 45 to 60 yearsconsisted the study population. The inclusion criteriawere patients of diabetic foot with non healing ulcerselected for hyperbaric oxygen therapy with wel lcontrolled blood sugar levels. The exclusion criteria werepre existing cardiac illness, preexisting or concurrentpulmonary parenchymal disease and claustrophobia.

Standard 12 leadElectrocardiogram was taken beforecommencement of hyperbaric oxygen therapy and atthe conclusion of ten sessions. Hyperbaric oxygentherapy was given in the form of l00Vo oxygen at 2.5ATA pressure for 60 minutes delivered through built inbreathing system (BIBS) in the hyperbaric chamber onceevery day for ten consecutive working days. Pulse rateand blood pressure were recorded at the time of ECGrecording.

ECG recordings were analyzed by one individualblinded to the clinical data in a disorganized sequence.

QT interval was measured from the beginning of QRScomplex to the end of T wave. Corrected QT (QTc)intervals were calculated by using Bazett's formula (QTc= QT/\A.-R [seconds]). Minimum and maximum QTcwere calculated. QT dispersion was calculated as thedifference between the longest and the shortest QTcinterval.

.Graded Special ist (Marine Medicine), *Classif ied Special ist (Marine Medicine), Undersea Medicine Department. INM, INHS Asvini.

Mumbai 400 005.

Jour. Marine Medical Socien'.2010. hl. 12. No. 2 101

Results

The maximum QT dispersion was 87 .20m sec whilethe minimum was 42.40 milli sec with a mean of 59.79milli sec (Table l). Post HBOT (Table 2). the maximum

QT dispersion was 73.70 milli sec and the minimum was41.40 mi l l i sec w i th a mean o f 52 .24 mi l l i sec .Comparison of QT dispersion before and afterHyperbaric Oxygen Therapy showed a significant fallof 7.44 m sec. Significant lowering of QT dispersionmay reduce risk of ventricular tachyarrhythmia andSudden Death.

Discussion

Currently the most routinely used non-invasive methodto assess ventricular recovery time is the QT interval.The QT interval is measured from a single lead, withvery little standardization in dealing with low amplitudeT waves, lJ waves, P waves and small biphasic T waves.This lack of a standard measurement led to poorsensitivity and specificity in predicting susceptibility tolife threatening ventricular anhythm ias. 25 - 40Va of i nterand intra rater variability of manual measurement of

QT dispersion has been reported [18]. The maindifficulty in measuring QT dispersion is the unreliabledetermination of T wave offset both with manual andautomatic methods. Another is that QT dispersion is arelatively small value compared with the QT interval.Thus, a relatively small error in QT measurement

magnifies the error in QT dispersion. QT dispersion rs astrong predictor of cardiac death in patients with diabetesmellitus [7]. It was also suggested that QTc dispersionis a better predictor of mortality than microalbunuria indiabetes mellitus [8,9].

Ischemic myocardium forms an arrhythmic substratedue to intracardiac inhomogenieties of repolarisation [4].Asymptomatic myocardial ischemia is high in Diabeticpatients even in absence of significant coronary arterystenosis [0]. HBO therapy increases the oxygen contentof plasma and leads to hyperoxia even in poorly perfusedtissues. Improvement of silent ischemia by HBO therapymay be one of the probable mechanisms for improved

QT dispersion.

Addit ional ly, diabetes leads to increased pro-inflammatory response due to endothelial dysfunction,increased oxidat ive stress and aggravated plateletcoagulation I l]. QTc abnormality was suggested to bea surrogate indicator of sub clinical atherosclerosis,increased thickening of carot id int ima and mediathickness and predictor of future strokes in type IId iabetes [2 ] . D iabetes may a lso a f fec t card iacmicrovasculature negatively by inducing neutrophil andcellular adhesive molecules (ICAM- I and P selectin) incirculation [3,14]. HBO may improve endothelial cellfunct ion, prol i ferat ion and neo-vascular isat ion byinducing reactive oxygen species and these cardioprotective mechanisms may alleviate tissue ischemia

Table I : Pre HBOT Recording of QTd

Patient Heart rateNo. (sec)

Systol ic BP(mmHg)

Dias BP(mmHg)

Min QT( msec )

Max QT( msec l

Min QTc( msec )

Max QTc QTc dispersion(msec) (msec)

I23+

56789l 0ilt 2l 3I41 51 6T 7l 8l 920

85.982.874.783.984.479.476.780.373.384.8I i . z

79.980.475.483. I83.776.674.68 1 . 777.30

88.0062.0074.0070.0068.0084.0064.0082.0074.0078.0068.0074.0068.0072.0078.0080.0086.0072.0084.0062.00

3403403303003303203603303403303203403 1 03403303 1 03603s0300320

380380370360390360440380420370380400370390380350400390360340

140.00I10.00128.00l24.OO1r4 .00136.00118 .00146.00134.00130.00120.00128.00122.00112.00r08.00126.00130.00116 .00r44.00128.00

407.20399. l 0368.803s4.70394.90372 . t0412.30379.50386.30387.40358.4039'7.90362.30379.60384.80369.30403.30393.40356.90367.50

462.00454.404 r9 . r04 2 t . 1 0462.4042t .20499.50436.30458.70435.60,115 .80

461 .60424.20434.80446.504l L70449.20443. l0420.40453.90

5,1.8055.3050.3066.4067.5049. l087.2056.8072.1048.2057.4063.706 1 . 9 0-s5.206 r . 7 042.4045.9049.1063.5086.40

Average 380.5 38r.79 441.58 59.79

t02

79.6r r2s.70 74.40 330

Jour. Marine Medical Society.20l0. Vtl . 12. No.2

Table 2 : Post HBOT Recording of QTd

Patient No. Heart rate Systolic BP Dias BP Mininlum QT Maximum QT Minimum QTc MaximumQTc QTc dispersion

I2345678q

1 0l lt 2l - 1

14l 5l 6t t

1 8t920

84.68 r . 5I -).+

82.683 . l78. I'75.4

79.072.083.57 t . 478.6'79.1'74.1

8 1 . 882.475.3/ - ) . -1

80.476.0

3403403303003403203803303603203303483 1 63403303 1 03503603 1 0330

3803803703603903604403704t0360380400360390380350390400360390

142.00il6.00126.00126.00I r8 .00l32.00126.00144.00r32.00r34.00r 26.00l30.00t26.00r20.00r 10.00126.00r36.00t24.00142.00134.00

82.0064.0076.0072.0068.0082.0062.0078.0076.0072.0070.0074.0072.0074.0076.0078.0084.0070.0080.0064.00

409.00399. r 0371.60358.60399.80373.5042t .90379.60388.30382.00360.26398.20365.40380.60386.00365. r 0397.30393.50360.003'7',7.50

456.30446.90414.40417 .50157.304 1 5 . 1 0495.60428.90451.20428.70

4t4.840454.40417.80428.30440.20406.50441.10438.704r5.20447.70

4'7.3047.8042.8058.9057.5041.6073.7049.3062.9046.7054.5856.2052.4047;7054.2041.4043.8045.2055.2070.20

Average 78.31 128.50 73.70 52.24380.s0334.20 383.33 435.57

[15]. HBO treatment given prior and during the ischemicinsult increased survival of myocardium and ATPpreservation [5]. This is significant as integrity ofcellular structure and tissue was a prerequisite to benefitfrom HBOT t16,l7l. We propose that improvement in

QT dispersion may be associated with myocardialprotective effects induced by HBO therapy.

References

l. Rossing P, Breum L, Peterson A, Kastrup J & Parving HH.

QTc interval length and QT dispersion as predictors ofmortality in patients with NIDDM. Scand J Clin Lab Invest2000; 60 :323-32.

2. Ford ES, Giles WH &Dietz WH. Prevalence of the metabolicsyndrome among US adults: findings form the third NationalHealth and Nutrition Examination Survey. JAMA 2002:28'7:356-59.

3. Ali Raza J & Movahed A. Current concepts of cardiovasculardiseases in diabetic patients. Ittt J Cardiol 2003; 89 : 123-34.

4. Roukema J, Singh JP, Meijs M, Carvalho C & Hart G. Effectof exercise induced ischemia on QT interval dispersion. ArrHear J 1998'- 135 : 88-92.

5. Ewing DJ, Boland O, Neilson JM, Cho CG & Clarke BF.Autonomic neuropathy , QT in te rva l leng then ing , andunexpected death in male diabetic patients. Diabetologia l99l1,3 4 : 1 8 2 - 8 5 .

6. Sun TB, Yang CCH & Kuo TBJ. Effect ofhyperbaric oxygenon cardiac neural regulation in diabetic individuals with footcomplications. Diabetic Med 2006;23: 360-66.

7. Naas AAO, Davidson CN, Thompson C, et al. QT and QTcdispersion are accurate predictors of cardiac death in newlydiagnosed NIDDM: cohort study. BMJ 1998;316 :74546.

8. Darbar D, Luck J, Davidson N, er a1. Sensitivity and specificity

Jour. Marine Medical Sociery,2010, Vol. 12, No. 2

of QT dispersion for identification of risk of cardiac death inpatients with peripheral vascular disease. BMJ 1996:.312 :874-78.

Sawicki PT, Meinhold J, Kiwitt S & Bender R. QT intervaldispersion is an important predictor of mortality in NIDDMpatients. Diabetes 1996;45 (Suppl 2): 128 A.Koist inin MJ. Prevalence of asymptomatic myocardialischemia in diabetic subjects. BMJ 1990; 301: 92 - 95.Hink U, Li H, Mollnau H, Oelze M, et al. Mechanismsunderlying endothelial dysfunction in diabetes mellitus. CircRes 2001; 88 :14e-22e.

Cardoso CRL, Salles GF & Deccache W. QTc intervalprolongation is a predictor of future strokes in patients withtype 2 diabetes mellitus. Stroke 2003; 34 : 2187-94.Niwa Y, Ozaki Y, Kanoh T, Akamatsu H, Kurisaka M. Role ofcytokines, tyrosine kinase and protein kinase C on productionof superoxide and induction of scavenging enzymes in humanfeukocytes. CIin Immunol Immunopathol 1996:'19: 303-13.Buras JA, Stahl GL, Spoboda KK & Reenstra WR. Hyperbaricoxygen downregulates ICAM I expression induced by hypoxiaand hypoglycemia: the role of NOS. Am J Physiol Cell Physiol2000:278 : C292-C302.Yogaratnam JZ, Laden J, Madden LA, et a1. Hyperbaric oxygen:A new drug in myocardial revascularization and protection'?Cardiovasc Revasc Med 2006; 7 : 146-54.

Yamada T, Taguchi t Hirata Y, Suita S, Yagi H. Protectiveeffect of hyperabric oxygenation on the small intestine inischemia-reperfusion inj ury. ./ P e diat r Sur g I 995 ;30: 7 86- 90.Chen MF, Chen HM Ueng S[ Shyr MH. Hyperbaric oxygenpretreatment attenuates hepatic reperfusion injury. Liver 1998:l 8 : I l 0 - 1 6 .

Kautzner J, Yi G, Camm AJ, er a/. Short and long termreproducibility of QT, QTc and QT dispersion measurementin healthy subjects. PACE 1994: 17 :928-37.

9 .

10 .

1 1 .

t2 .

1 3 .

14.

1 5 .

16 .

t 7 .

t 8 .

t03

Original Article

Disabilites in Naval Aircrew Applicants

Surg Cdr PD Ayengar*, Gp Capt N Taneja..

Abstract

Background : All aircrew in the IndianArmed Forces undergo a stringent initial medical examination. Periodicanalysis of this data can provide insights into the nature of disabilities that lead to medical invalidation. While suchstudies on candidates for Indian Air Force have been carried out regularly, there was no such study on Indian NavalAircrew.

Material and Methods : Records of all Indian NavalAircrew undergoing initial medical examination from July 2003to October 2007 were studied.

Results : A total of 479 Naval aircrew underwent initial medical examination out of which 128 (26.72Vo) weredeclared medically unfit. The mean age of these aircrew was 22.93 t 1.86 years and the age range was from 20 to 33years. Of these, majority were pilots n=71 (55.4680). The leading cause for being declared unfit were spinalabnormalitie s (n= 63, 49.2 Vo) and substandard anthropometry (n=28, 21,9 Vo\.

Conclusion : The causes of medical rejection in Naval aviators are discussed.

Key Words: Navy aircrew, Medical examination, Fitness

Introduction

A pplicants from the Indian Navy for aircrew duties.flunderso their initial medical examination at Instituteof Aerospice Medicine (IAM) and Air Force CentralMedical Establ ishment (AFCME). The medicalstandards for the Indian Air Force are applicable to theIndian Navy [1]. Periodic analysis of disabilities leadingto rejection of aircrew in the Indian Air Force has beencarried out. However, no such study on the Indian Navalaircrew applicants has been done [2,3].

Material and Methods

Records of initial medical examination of Navalaircrew carried out at the IAM Medical EvaluationCentre (MEC) from July 2003 to October 2007 wereretrieved for analysis. In candidates with multiple medicaldisabilities, only those that were the cause for rejectionwere included for the studv.

Results

A total of 479 male Indian Naval aircrew candidatesunderwent their initial medical evaluation in this period.Out of these, 378 (78.9Vo) were for pilot duty and 101(26.7Vo) were for non pilot aircrew duty like observersand aircrew divers. A total of 128 (26.7Vo) candidateswere rejected on medical grounds. Of these 7l (55.5Vo)

were pilots and 57 (44.57o) were non pilot aircrewapplicants (Table 1). The mean age of the applicantswas 22.93 years with a SD of 1.86 years.

Spinal disabilities accounted for half the rejections(49 .ZVo) and were fo l lowed by incompat ib leanthropometr ic measurement (2l .9Vo) (Table 2).Spondylosis of the vertebra accounted for one third(n=20, 32.37o) followed by old healed compressionfractures in another 2l.5Va (Fig. l). Spondylolysis of

Table I : Proportion of rejection for various applicants

Non pilot aircrewPilot Diver Observer

Applicants

Rejected

Vo rejected

378 3371 2318.7 69.6

683450

Table 2 : Leading causes for medical unfitness

Disabi l i ty

SpineAnthropometryENTEyeOthers

6328t4l01 3

49.221.910.97.910 .1

Total 100128

-Graded Specialist in Aviation Medicine, INS Hansa, C/o FMO, Goa. ..Senior

Adviser in Aviation Medicine, AF Station, Bagdogra.

Jour Marine Medical Society,20l0, Vol. 12, No. 2

the spine and incomplete sacralisation were some of present study due to the lower age of the candidates intheir study [4].

Anthropometry is important for aircrew aircraftcompatibility and for flight safety. The four essentialmeasurements are standing stature, sitting height, thighlength and leg length. These measurements ensure anadequate clearance from the canopy and main instrumentpanel and good over the nose vision. No specificanthropometric standards exist for non pilot aircrew suchas observers and aircrew divers, since no ejection (thighlength) and no over the nose vision (sitting height) areapplicable for such duties. In this regard, a detailedevaluation of the waivers in anthropometric standardsfor observers was carried out at INS Hansa [5]. It wasrecommended in that study, that the waiver in respectto stature by 5.0 cms for males and 10.5 cms for thefemales may be allowed. The sitting height waiver was3.5 cms for both sexes in fixed wing fighter aircraft, 8.0

;;* "'

Fig. 3: Detailed causes for rejection due to ENT disability.

Eirr ! to! l Kl ! t

Fig. 4: Detailed causes for rejection due to Eye disability.

t05

cms for the fixed wing transport aircrafts and no waiverin Kamov 28 and 31.

Good visual acuity, ocular muscle balance andstereopsis are mandatory for pilots to have goodorientation during flying. In the present study the majorcause of rejection was high myopia and astigmatismwhich is consonant with other studies.

Conclusion

Almost a quarter of all applicants for aircrew dutiesin the Indian Navy are rejected on medical grounds asin the Indian Air force I2l. A significant number ofcandidates were asymptomatic. Degenerative conditionsof the spine were the most common cause for rejectionfollowed by anthropometry incompatibility. Unlike theIndian Air Force where majority of the candidates werein the age group of l6 to l8 years, the Naval candidateswere in the age group of 22 to 33 years. It is likely that

the increase in spinal disabilities may be the result ofthis age di f ference. The current anthropometr icstandards are essentially for pilots and need to bereviewed for the non pilot aircrew.

References

l. Manual of Medical Examinations and Medical Boards IAP4303 3"r Ed (revised) New Delhi, 2003.

2. Patil G Taneja N. Retrospective analysis of initial medicalexamination of aircrew applicants in the Indian Air Force. IndJ Aerospace Med 2006; 50 (l) : 44-49.

3 . Venkatesh S, Tane ja N. An ana lys is o f in i t ia l med ica lexamination of women cadets in the Indian Air Force. Ind JAerospace Med2006;50 ( l) : 50-53.

4. Hendriksen IJM, Holewijn M. Degenerative changes of thespine of fighter pilots of the Royal Netherlands Air Force(RNLAF).Avlat Space Environ Med 1999:70 ( l l ) : 1057-63.

5. Kapoor S, Ayengar PD, Yadav H, Singh AK, Soundrial V. Reporton waivers in anthropometric standards on entry for Observers.Report submitted to IHQ MoD (Navy).

PERSONAL VIGNETTE

Personal Vignette is a new inclusion in the Journal of Marine Medical Society to increase author and

readership interest. Authors can contribute their unique personal experiences onboard ships, submarines,

naval and military aircraft, military stations, military hospitals, field units or even those experienced in the

course of enjoying vacations or performance of staff duties which could be of scientific interest to the

marine medical community. The write up should not exceed 1000 words and may include up to 4 interesting

figures, photographs or tables. Very relevant references may be included but are not essential.

t06 Jour. Marine Medical Societt,2010, Vol. 12, No.2

Original Article

TFoxerutin in Management of Haemorrhoids

Surg CdrAshutosh Chauhan., Maj Sangeeta Tiwari*, Col PK Bhatia#, BrigAK Gupta..

Abstract

Background : Grade I and II haemorrhoids are managed conservatively with stool softeners, high fibre diet and oralor topical analgesics. TFoxerutin, a flavanoid, has been used in a variety of venous disorders and is found effective inhaemorrhoids too.

Material and Method : Seventy six cases of Grade I and II haemorrhoids were randomized into two groups of 38 each.Group I received standard conservative regime viz. liq paraflin, imago husk and topical lignocaine gel, while Group2 received troxerutin I gm daily. Both groups were followed up weekly for a maximum of 8 weeks.

Results : Thirty four cases of Group 1 and 37 cases of Group 2 were followed up for 8 weeks. There was statisticallysignificant reduction of bleeding after 05 weeks and of pain and pruritus after 8 weeks in the troxerutin group.

Conclusion : Troxerutin is a safe and efficacious management for Grade I and II haemorrhoids

Key Words : Haemorrhoids, Thoxerutin

Introduction

f femor rho ids . the most common cause o fI lhematochezia in adults, are varicosities of thehemorrhoidal venous plexus. Internal hemorrhoids areclassified by the degree oftissue prolapse into the analcanal as grades I , I I , I I I or IV. The most commonpresenting symptom of internal hemorrhoids is painlessrectal bleeding with defecation, which varies from a fewdrops to a brief stream. Grade I internal hemorrhoidsare usually asymptomatic, but at times may causemin ima l b leed ing . Grades I I , I I I o r IV in te rna lhemorrhoids usually present with painless bleeding, dullaching pain orpruritus []. Conservative medical therapyfor hemorrhoids includes stool softeners, topical andsystemic analgesics, high-fiber diet and adequate fluidintake. Medical treatment is considered to have failed ifsymptoms persist and then the patient is considered fornon-surgical modalities like banding, infrared coagulation,bipolar electro coagulation, sclerotherapy and lasertherapy or open surgery [2].

Troxerut in, an extract f rom Sophora Japonica(Japanese pagoda tree) has been widely used in Europesince the mid-1960s to manage a range of venousdisorders including hemonhoids [3]. There is no Indianstudy on troxerutin in Haemorrhoids.

Material and Methods

This prospective randomized study was conducted in

a large tertiary care service hospital in North India. Allcases of Grade I and II chronic haemorrhoids from Janto Dec 2005 were included in the study. Patients withconcomitant fissure, fistula-in-ano, acute haemorrhoidsand those who had taken some medication earlier wereexcluded.

Cases were randomized into two groups using arandom number generator. Group I controls weremanaged with standard conservative regime usinglaxative (Isabgol husk, I satchet HS and Syp Lactulose2 tsp TDS), stool softener (Liq Paraffin 4 tsp HS) andlocal Oint anovate TDS. Group 2 cases were treatedwith troxerutin (Cap Oxerute 500mg, Fourtis India Ltd,Tamilnadu. I capsule PO BD). Patients were followedup for 8 weeks at weekly interval by an independentobserver who was blinded to the initial randomizationand the treatment received. Symptomatic relief wasdocumented in terms of decreasing scores in amount ofbleeding, pain, pruritus and mucus discharge. MannWhitney U test and Chi square test were used tocompare mean scores in the two groups and p< 0.05was taken as significant.

Results

A total of 122 cases of Grade I and II were receivedduring the year 2005. Out of these, 23 were excludedas they expressed inability to come for follow upregularly. Another 17 were excluded as they had

.Classified Specialist (Surgery), Army Hospital (R&R) , Delhi Cantt. *Graded Specialist (Surgery). MH Sriganganagar. #Classfied Specialist(Surgery). Cornmand Hospital (WC), Chandimandir. ' .Commandant

, MH Jaipur.

Jour. Marine Medical Socie"r'.2010. Vol. 12. No.2 107

concomitant fissure and fistula. Six cases refused to bepart of study. Remaining 76 cases were randomized intotwo groups of 38 each using a random number generator.Four patients from Group 1 and one patient from Group2 withdrew from the study citing personal reasons.

Age, sex, mean duration of complaints and grade ofhemorrhoids in the two groups were evenly matched(Table l). There was significant reduction in amount ofbleed reported in group 2 compared to group I after 5weeks of treatment (Table 2). However, there was nostatistically significant reduction in pain and pruritus(Tables 3 and 4). Nine patients of group I reported analleakage of Liq Paraffin, significant enough to be sociallyembarrassing

Discussion

Hydroxyethylrutosides (HR) refer to a mixture ofsemi-synthetic derivatives of the flavonoid rutin. Rutinis a naturally occurring flavonoid glycoside comprisingf lavono id querce t in and d isacchar ide ru t inose.Hydroxyethy l ru tos ides are mono, d i , t r i andtetrahydroxyethyl derivatives of rutin and are preparedby hydroxyethylation of the phenolic groups of rutin.Formulations, consisting of the trihydroxyethyl derivativeof rutin are used in Europe, Mexico and other LatinAmerican countries for the treatment of varicose veinsand hemorrho ids . The gener ic name fo r theseformulations is troxerutin [4]. Because of it's antioxidantproperties, troxerutin is pharmacologically active on thevascular endothelium, reducing it's permeability. It showsa marked affinity for the venous wall. The highest uptakein the outer wall region is likely to result from transportthrough the vasa vasorum due to the rheologic propertiesof the drug. Troxerutin significantly inhibits plateletadhesion to the extra cellular matrix, yields an anti-erythrocyte aggregation effect and exerts a favorableaction on the blood fibrinolytic system [5,6].

A rnark-ed improvement of pain, bleeding, pruritus anddiscnarge were observed in early placebo controlledstudies of troxerutin at0.6-2 g/day for 3-4 weeks in atotal of 189 patients with mild to severe hemonhoids

[7,8]. Adouble-blind study enrolling 97 pregnant womenfounC oxerutins (.1,C100 mg daily) significantly betterthanplacebo in reducing pain, bleeding and inflammation ofhemonhoids [9].

This study may be criticized for not having done apower calculation to determine the number of cases tobe enrolled. This was a pilot study and the results arepreliminary.Ihe study may be criticized as it relies onsubjective reporting scores by the patient. The studywas also limited by the fact that a "per protocol" and

108

Table I : Age, Gender and Presentation profile

Group I : Control Group 2 : Test

N=34 N=37

Male :Female

Age(in years)+

Grd I haemonhoids

Grd Il haemorrhoids

Mean duration ofcomplaints

22 :1244.02 (t 17.8)

I 222

38 months(56- 08 months)

23:1441.7 (x .19. l )

t 225

43 months(61-07 months)

+ p >0.05; chi square test

Table 2 : Comaprision of "Bleed" scores

Post op week Group I : Control Group 2:n=34 n=37

Test p value +

Week IWeek 2Week 3Week4Week 5Week 6Week 7Week8

- l - J

-t- I

2.92.62 . 11 .91 . 81 . 6

3 .53.22.72.51 . 6t . 4t . 2l . l

0.890.910.620.320.04*0.03*0.03*0.02*

+ chi quare test; *p<0.05 significant

Table 3 : Test of Significance : Pain "score"

Post op week Group I : Control Group 2: Test p value +

n=34 n=37

Week IWeek 2Week 3Week4Week 5Week6Week 7Week8

0.890.910.620.760.930.'760.850 .81

t . 91 . 51 . 3t . 2t . 21 . 31

t . 2

1 . 81 . 61 . 21 . 3l l

l . l

l . l

I

+chi square test; p<0.05 significant

Table 4 : Test of Significance : "Pruritus" score

Post op week Group l : Control Group 2 : Test p value +

n=34 n=37

Week IWeek 2Week 3Week4Week5Week6WeekTWeek 8

0.890.910.620.760.920 .310.850.78

L . )

2 . 11 . 91 . 71 . 61 . 71 .5t . 4

2 . 12.01 . 81 . 5t ; 71 .41 . 4L Z

+ chi square test, p<0.05 significant

Jour Marine Medical Society,2010, Vol. 12, No.2

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not a "intent-to-treat (ITT) analysis was performed.

l .

References

Metcalf A. Anorectal disorders. Five common causes of pain,itching, and bleeding. Postgrad Med 1995; 98 : 8l-4,87 -9,92-

4.

Pfenninger JL, Surrell J. Nonsurgical treatment options forinternal hemorrhoids. Am Fam Physician 1995;52 821-34,839-41.

Clyne MB, Freeling P, Ginsborg S. Troxerutin in the treatmentof haemorrhoi ds. P rac t ition e r 19 67'. 198 : 420 -3.

Wadworth AN, Faulds D. Hydroxyethylrutosides. A reviewof its pharmacology, and therapeutic efficacy in venousinsufficiency and related disorders. Drags 1992;44 : l0l3-32.

Boisseau MR, Taccoen A, Garreau C, et al. Fibrinolysis and

hemorheology in chronic venous insufficiency: Adouble blindstudy of troxerutin efficiency. J Cardiovasc Surg 1995;36 :369-74.

Janssens D, Michiels C, Arnould T, Remacle J. Effects ofhydroxyethylrutosides on hypoxia-induced activation ofhuman endothelial cells in vitro. Br J Pharmacol 1996: I l8 :599-604.

Thorp RH, Hughes ESR. A c l in ica l t r ia l o ftrihydroxyethylrutoside ("Varemoid") in the treatment ofhemorrhoids. Med J Aust 1998;2: 1076-8.

Sinnatamby CS. The treatment of hemorrhoids. Role ofhydroxyethy l ru tos ides , t roxeru t in (Paroven; Varmoid ;Venoruton). Clin Trials J 2002;2 : 45-50.

Wijayanegara H, Mose JC, Achmad L. A clinical trial ofhydroxyethylrutosides in the treatment of hemorrhoids ofpregnancy. J Int Med Res 2002;20: 54-60.

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Jour. Marine Medical Society, 2010, Vol. 12, No.2

CME

Fear of Flying in Trained Aircrew

Surg Cdr RC Verma (Retd).

Abstract

Fear of flying (FOF) is a specific phobia, one of several kinds of anxiety disorders. FOF in trained aircrew can bedefined as ttthe development of an unreasonable fear or anxiety in those who are free from other emotional disorders".The aetiology is varied and leads to diagnostic dilemma when the aviator presents with psychosomatic symptoms thatprevent him from flying. In addition, secondary gain can intensify the symptoms. FOF in trained military aircrewresults in financial loss to the state and loss of combat edge to the aviation arm. We draw attention to this aero-medicaldisorder that can challenge the treating medical officer and suggest the initial approach in evaluation and managementat station level.

Key Words : Anxiety, Aircrew, Somatization

Introduction

Th. term "Fear of Flying" (FOF) was coined duringI World War II to address fear and anxiety seen in

combat pilots. It is also referred to as aerophobia,aviatophobia, aviophobia or pteromechanophobia. Theterm connotes "unreasonable fear or anxiety whenundertaking flying" []. Anderson (1919) described aero-neuroses as the strain of learning to fly, consequent toinvolvement in an aircraft accident [2]. FOF in traineda i rc rew is de f ined as " the deve lopment o f anunreasonable fear or anxiety of flying in someone freefrom other emotional disorders" [3]. The incidence ofFOF is low.

Aetiology

Some authors have suggested that different criteriabe adopted for "f-lying phobia" in pilots because, itrepresents a change in a t ra ined a i rc rew [4 ] .Manifestation of fear in a trained pilot represents a lossof adaptation. Frequent precipitants of such anxiety aremarital disharmony, irregular lifestyle and familydisruption [5]. The pilot's wife may fear for his safetyand this may in turn have a corrosive effect on therelationship because declaring such fears openly is oftenregarded as unacceptable.

Aircrew motivation for flying stems from differentresources [6]. Bond (1952) reported that flying is basedon deep seated aggressive urges with aircraft beingperceived as a symbol of power and an extension ofself [7]. Grinker and Spiegel (1945) described flying as

a means to escape the limitations of time and space [6].An unhealthy motivation to overcome symbolically afather figure can later lead to FOF []. A fascinatingaccount is about a pilot who suddenly developed adisabling FOF whenever thunderstorms were forecastand became obsessive about gathering minute bits ofweather information. His flying history revealed that heliked to fly aerobatics. However, the birth of his daughterproduced a conflict with that part of him which wantedto be a good father struggling with the thrill-seeker partof his personality. He ended up obsessing over theweather to hide the real issue. The thunderstormssymbolised the "gathering stom" in his married life [ ].Another pilot became acutely fearful after experiencingspat ia l d isor ien ta t ion in - f l igh t [8 ] . Ann iversaryPhenomenon, family and work problems may contributeto apprehension about flying [9]. There may be soloflight training issues because we cannot feel confidentuntil we perform the task under our own authority.

Symptoms and Signs

The level of anxiety may be so high as to prevent onefrom flying or cause great distress to a person whencompelled to fly. Physiological reactions include muscletension, t remors, heavy and laboured breathing,hyperventilation, palpitation, chest pain, abdorninaldiscomfort , sweat ing, weakness, dizziness, pr icklysensat ion , d ry mouth and f lushed or pa le face .Psychological symptoms include impaired memory,narrowed perception, clouded judgement and negativeexpectancy.

-Classif ied Special ist (Aerospace Medicine) and Ex PMO, INS Shikra, Mumbai

l t 0 Jour. Marine Medical Socie^.2010. Vtl . 12. No.2

Diagnos is

The presenta t ion may be w i th psychos t ' rn ra t i csymptorrs when the pilot will ask fbr help witl-r syrnptomsthat prevent him f ionr f ly ing. He wi l l not have anyanxiety. He rnay siry that he 'uvants to f1y bLrt back painor headaches bother hinr in-11ight. I f exarninat ion doesnot reveal any abnormality. look firr some secclndary

_gain. Financial recompense and the chance to move frorni l y rn -e in to l ' i e lds o f enc leavour perce ived as moreat t rac t i ve n rav be a power l 'u l mot iva t ing l 'ac to r .According to Jones (1986). the invest igat ion int t ' r anycase of FOF mr.rst inclr .rde cnqr.r i ry into the pat ient 'sexpectat ions and aspirat ions at the t ime that he becamean aviatur and an atteurpt to tr i rce ancl explore anysubsequent change in these I l0 l .

) Ianagenrent

Evaluation

The approach to a case of FOF rnust include adetai led history including f ly ing history. Enquire aboutthe order of birth and reason fbl optin-e fbr t' lying. Seekf o r s i g n i f i c a n t i s s u e s i n t h e t r a i n i n g p e r i o d a n ddissat isfact ion with the al lot ted stream. Encruire aboutsignificant events during the trainin-q consolidation phase.whi le achieving prof ic iency in f ly in-r in IMC. deckoperations. tlyin-e over sea in difterent n-toon phases.flying with nighn'ision goggles and occun-ence of spatiitld isol ientat ion in-f- l i -sht. Enquire about apprehensionspertainin-u to the maintenance and serviceabi l i ty of thea i rc ra f t . recent a i rc ra f t acc idents . admin is t ra t i vereprimands. recent fatality or major lif-e change events.Seek addit ional information from the CommandingOfTrcer. Squadron Comrnander. Senior Pilot. Observer.Station Technical OfTicer. ATC Otficer ancl SquadronMedrcal Off lcer. Enquire about any nnusual tasking interms ol ' rnission. terrain or durat ion of outstat iondetachment. Check IN 7(X). sick report book and lo-9book.

Cary out a thorough clinical cxamination and relevantinvest i -sat ion. Seek evaluat ion by a psychiatr ist andpsycho log is t where ind ica tcd . Eva lua t ion in F l igh tSimulator ancl in-flrght will in"rprove assessmeut.

Important guidel ines include fbrming a therapeut icalliance with the fearful pilot and explorin-e possiblesolut ions. Consider re-f l ight ing whi lst administer ingtherapy. In case no disqual i fy ing physical or mentaldisease is present. return tlie pilot to the squadron as fitt o f l y w i t h a r e c o r n n l e n d a t i o n f o r a p p l o p r i a t eadministrative action.

Behavioural Therapies

C o - q n i t i v e b e h a v i o u r t h e r a p y i i n d s y s t e m a t i cdesensitisation rest on the theory that phobia is due tc-ran ini t ia l sensit is ing event ( ISE). I . P. Pavlov, a Russianphys io log is t . p ropounded the theory o f c lass ica lcondit ioning. A condit ioned st imulus (bel l ) when pairedconsistently with an unconditioned stimulus (food) leadsto a condit ioned response (sal ivat ion) simi lar to theunconditioned lesponse (sali vation ). Wolpe reported thatanxiety could be reduced or inhibi ted when anxietyprovocor was systematically paired with relaxation. Thisp r o c e s s c a l n e t o b e k n o w n a s " s y s t e m r t i c

desensitisation" I l I ]. Hypnotherapy generally involvesregression to the ISE. uncoverin-g the event and theenrotions around the event to help the person understandthe source of f'ear.

Virtual Reality Therapy fbr treatin-s FOF has beendisappointing. Wolpe et al (2007) reported virtual realitytherapy to be as effbctive as sitting on a parked airplaneand thinking about flying because. panic often developsrapidly through processes which the person has noawareness o f I l2 ] .

Object Relations Theory works on the premise ofthe need to control panic automatically when flyin-r. Thetheory aims at intervention intended to operate withoutconscious thought. I t establ ishes a sequence in theunconscious procedural memory through repeatedviewing on r, ideo of potent ial ly threatening in-f l ightsituations. Intense f'ear may be alleviated throu-eh theuse of imagery.

Medicat ion

For FOF. the prescription may be benzodiazepines orother relaxant drugs. Some individuals with FOF mayself-medicate with psychoactive substances. particularlyalcohol. They must be advised against consunrin-9 alcoholdue to the strong risk of dependency.

Disposal

Evaluation of recalcitrant FOF is carried out at Instituteof Aero Space Medicine (IAM), Ban-qalore. In variably.the aircrew is declared fully fit fbr flyin-e in medicalcate-qory A lG I and the matter is fbrwarded fbr disposalby the administrat ive authori t ies I l3] .

References

l . DeHal t RL. Fundament l l s o f Aerospace Med ic ine . f " " ed .Ok lahonra : Wi l l iams & Wi lk ins , Inc . , 1996.

l . Anderson HG. The rnedical antl surgical aspects of aviat ion.London: Oxford Un ivers i t l Prcss . l9 l9 (c / f l ) .

- 1 . C h r i s t v R L . P c r s o n a l i t v f a c t o r s i n s e l e c t i o n o f f l i s h t

Iour. I lur i t t t ' Mt 'd ical Soci c/ r ' . 2010. \ I t l . 12. No. 2

9.

10 .

I l .

t2 .

1 3 .

4.

5 .

proficiency. Aviat Space Environ Med 1975',46 : 309-l L

Aitken RCB, Lisrer JA, Main GJ. Identification of featuesassociated with flying phobia in aircrew. British Jountal ofPstchiatry l98l; 139 :38-42(clfErnsting J and King P. TextBook of Aviation Medicine. 2"d ed. London: Butterworths.I n c . . 1 9 8 8 ) .

Karlins M, Koh F, McCully L. The spousal factor in pilotstress. Ayidt Space Environ Med 1989',60 : I I l2-5.

6. Grinker RR, Spiegel JA. Men under stress. Philadelphia;

7.

Blakiston, 1945 (c/f l).

Bond DD. The love and fear of flying. New York:InternationalUniversities Press, Inc; 1952 (clf I).

Ernsting J, King P. Text Book of Aviation Medicine, 2"r ed.

London: Butterworths, Inc., 1988.

Marsh RW, Perry CJG. Anniversary reactions in mil i taryaviators. Aviat Space Environ Med 1977:.48:61-64.

Jones DR. Flying and danger,joy andfear. Aviat Space EnvironMed 1986:57 : l3l-6.

The practice ofbehavior therapy,2nd ed. New York : PergamonPress, Inc, 1973 (clf l ) .

Wolpe J, Krijn M, Emmelkamp PM, Olafsson RP, et al. Fearof f lying treatment methods: virtual real i ty exposure vs.cognitive behavioral therapy. Av iat Space Envi ron M ed 2007 :78(D:121-8 .

Indian Air Publication - 4303.

t 1 2 Jour. Marine Medical Sociery*,2010, Vol. 12, No.2

MCQContributed by Surg Lt Cdr Rohit Verma-

Choose the best answer for the following Multiple choice questions.

Ql Who discovered Carbon dioxide?(a) Boyle (b) Black (c) Priestley (d) Lavoisier

Q2 Toxic effect of oxygen on the nervous system is known as:(a) Lonain Smith effect (b) Paul Bert effect (c) Oxygen Window (d) OTU

Q3 Which of the following gases has the least density at STPD :(a) Carbon dioxide (b) Air (c) Oxygen (d) Nitrogen

Q4 The ideal gas law responsible for Decompression Sickness in diving is:(a) Boyle's Law (b) Dalton's Law (c) Henry's Law (d) Graham's Law

Q5 The ideal gas law responsible for Barotrauma in diving is :(a) Boyle's Law (b) Dalton's Law (c) Henry's Law (d) Graham's Law

Q6 The time needed for diffusion of a gas is dependent on the size of the molecules of the gas, allowing smallergas molecules like helium to diffuse faster than larger ones. This Law is :(a) Graham's Law (b) Bunsen's Solubility coefficient (c) Fick's first Law (d) Fick's second Law

Q7 Oxygen Window is :(a) the difference between total barometric pressure and venous total pressure.(b) the difference between the partial pressure of oxygen in alveoli and the panial pressure of oxygen in tlrc arteries.(c) the range of arterial partial pressure of oxygen in which there is no cerebral hypoxia or oxygen toxicity.(d) a device which increases the fraction of oxygen in the inspired air.

Q8 During Hyperbaric Oxygen Therapy, which of the following will not occur:(a) Increased PaOZ (b) Increased PaCO2 (c) Increased breathing resistance (d) Increased PEF

Q9 Which of the following is true about CO2 toxicity during hyperbaric oxygen therapy:(a) Can contribute towards oxygen toxicity.(b) Increased gas density and work of breathing can contribute to CO2 toxicity.(c) Inadequate flushing of the chamber can lead to CO2 toxicity (d) All of the above

Ql0 Which of the following does not occur during hyperbaric oxygen therapy:(a) Vasoconstriction (b) Decreased cardiac output (c) Decreased RBC deformability (d) All of the above

Ql I Which of the following submarine rescue vessels is air transportable:(a) DSRV (b) LR5 (c) Remora (d) All of the above

Ql2 Pulmonary barotrauma is a likely problem of(a) Submarine escape (b) Submarine rescue (c) Both A and B (d) None of the above

Q l3 In submarine escape, which of the following is true:(a) Risk of DCS is less while performing Compartment escape(b) Compartment escape is preferable to escape through conning tower(c) Both escape through conning tower and compartment escape are similar(d) Escape through conning tower is preferable to 'compartment escape'

Q l4 Which of the following can be used as a reversible scrubber of carbon dioxide:(a) Soda lime (b) Lithium hydroxide (c) Monoethanolamine (d) 03 chemical

Q15 Polaris missile effect refers to:(a) Chronic minor radiation injury by being in close proximity to nuclear weapons(b) Overinflation of buoyancy compensator during ascent leading to increased risk of pulmonary barotrauma(c) The negative G force felt by a fighter pilot while ejecting from the cockpit in an emergency(d) None of the above

Turn to page 115 for key to MCQs*PMO & Graded Specialist (Marine Medicine), INS Nireekshak, C/o FMO, Kochi 632 004.

Jour Marine Medical Societv.2010, Vol. 12, No.2 1 1 3

Case Report

Infant with Diabetic Ketoacidosis

Surg CdrAshok K Yadav., Surg Capt KM Adhikari., Surg Cmde G Gupta, Nu#

Key Words: TYpe I diabetes,Infant, Diabetic ketoacidosis, Hypoglycemia

Introduction

tTlhe incidence of type 1 diabetes increased by asI

I much as two to threefold in the younger age group,specif ical ly in those of 0 to 5 years [1,2]. Themanagement of diabetes in preschool children presentunique problems to parents and health care providers

[3]. Difficulty in achieving glycemic targets arefluctuations in physical activity, marked sensitivity toinsulin, very small insulin requirements, unpredictableeating habits, small but frequent meals, limited ability ofchildren to communicate, frequent intercurrent infectionsand increased family stress [4] . We report ourexperience w;th an infant with diabetic ketoacidosis whopresented with respiratory distress.

Case Report

Nine months old female infant presented to our casualty withfever and breathing difficulty. Clinically she had tachypnea,tachycardia and sunken eyes. A provisional diagnosis of acutebronchiolitis was made and infant was admitted for observation.No relief was noted ovemight with oral fluids and humidified oxygen.The infant was reviewed in the morning in view of persisting fever,signs of dehydration and respiratory distress. Her blood sugar was635 mg/dl and urine was positive for glucose and ketone bodies.The venous blood showed a pH of 7.015,PO2 of 162 mmHg,PCO2 of 8 mmHg and Base excess of - 30.3 suggestive of severemetabolic acidosis with partial correction. Infant was managed withsaline boluses and IV insulin till blood sugar came down to 250 mgldl when the infant was placed on subcutaneous insulin injection.Medical nutrion plan was made and parents were explained aboutthe nature of the disease, need for life long treatment, the risk ofhypoglycemia and its effect on cognitive functions ofthe child. Thechild thereafter was placed on daily pre meal bolus doses of shortacting insulin analog Lispro and long acting insulin Levimir alongwith blood glucose monitoring by parents. Infant's blood sugar hasbeen targeted at I I 0- I 80 mg/dl premeal and 1 I 0-200 mg/dl at bedtime/overnight.

Discussion

Three-quarters of all cases of type I diabetes arediagnosed before 18 years of age. Children with diabetes

differ from adults in many respects, including insulinsensitivity related to sexual maturity and physical growth,ability to self-care and unique neurologic vulnerabilityto hypoglycemia. Strict glycemic control is possible withcontinuous subcutaneous insulin infusion (CSII) but suchtherapy has not been tried in infants with diabetes. Aretrospective study of CSII done for children above 02yrs of age was found to be safe. Recurrent hypoglycemiais a barrier to achieving lower hemoglobin A1c (HbAlc)levels in this age group [5]. There is some evidence thathypoglycemia may predispose children younger than 6years to neurocognitive developmental defects [6]. Thefear of hypoglycemia has led health care providers toset higher target ranges in this age group [7]. On theother hand, chronic hyperglycemia may result in impairedintellectual function [8]. The Diabetes Control andComplications Trial (DCCT) demonstrated that intensiveinsulin therapy reduces complications of diabetes inadults [9]. Vascular complications may start a few yearsafter diagnosis, especially early nephropathy, retinopathyand even impairment in neurocognitive development [0].Intensive insulin therapy in young children may reducethe development of chronic complications of diabetes inlater life.

References

I . Green A, Patterson CC. Trends in the incidence of childhood-onset diabetes in Europe 1989-1999. Diabetologia 2001;44(suppl 3) : B3-B8.

2. Devendra D, Liu E, Eisenbarth GS. Type I diabetes: recentdevelopments. BMJ 2004; 328 :'7 50-54.

3. Hatton DL, Canam C, Thorne S, Hughes AM. Parents'perception of caring for an infant or toddler with diabetes. JAdv Nurs 1995:22 : 569-77.

4. Wilson DM, Buckingham BA, Kunselman EL, Sullivan MM,Paguntalan HU, Gitelman SE. A two-center randomizedcontrolled feasibility trial of insulin pump therapy in youngchildren with diabetes. Diabetes Care 2005;28 : 15-9.

5. Silverstein J, Malone IJ. Strict glycemic control is necessary

'Cfassified Specialist (Pediatrics), oCommanding Officer, INHS Sanjivani, Naval Base, Kochi-682 004. *Staff Surgeon, INHS Asvini,Mumbai-05.

t 14 Jour. Marine Medical Society, 2010, Vol. 12, No.2

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but not practical in most children with type I diabetes. "/ ClinEndocrinol Metab 2000 85 : 2518-22.

Rovet J, Ehrlich RM. The effect of hypoglycemic seizures oncogn i t i ve func t ion in ch i ld ren w i th d iabetes : a 7 -yearprospective study. ./ Pediarr 1999;134: 503-6.

Ryan CM, Becker DJ. Hypoglycemia in children with type 1diabetes mell i tus: r isk factors, cognit ive function, andmanagement. Endocrinol Metab Clin North Am 1999:28 : 883-900.

Schoenle EJ, Shoenle D, Molinari L, Largo RH. Improvedintel lectual development in chi ldren with type I diabetes:

association with HbAlc, age at diagnosis and sex. Dinbetologia2 0 0 2 ; 4 5 : 1 0 8 - 1 4 .

Diabetes Control and Complications Trial Research Group.The effect of intensive insulin treatment of diabetes on thedevelopment and progression of long term complications oninsulin dependent diabetes mellitus. N Engl J Med 1993;329 :977 -85.

Donaghue KC, Fung ATW, Hing S, et al. The effect ofprepubertal diabetes duration on diabetes: microvascularcomplications in early and late adolescence. Diabetes Care1997 : 20 :

'17 -80.

10 .

KEY TO MCQs*l. B - Page 2: Handbook of hyperbaric medicine. Boyle discovered the relationship between the volume and pressure

of an ideal gas. Priestley discovered Oxygen and Lavoisier discovered oxidative phenomena.

2. B - Page2: Handbook of hyperbaric medicine.

4. D - Page 22: Handbook of hyperbaric medicine.

6 . D -

8. D - Page 43: Handbook of hyperbaric medicine.

10. C - Page 60: Handbook of hyperbaric medicine.

12. A - Page 668: Diving and Subaquatic Medicine.

14. C - Page 666: Diving and Subaquatic Medicine.

3. D - Page 17: Handbook of hyperbaric medicine.

5. A - Page 20: Handbook of hyperbaric medicine.

1. A - Page 37: Handbookof hyperbaric medicine.

9. D - Page 46: Handbook of hyperbaric medicine.

I l. A - Page 670: Diving and Subaquatic Medicine.

13. D - Page 667 : Diving and Subaquatic Medicine.

15. B - Page 481: Diving and Subaquatic Medicine

* If your score is 13- 15 - Apply directly to become a Graded Specialist in USM

If your score is l0-I2 - You are eligible to be selected for the DMM Course

If your score is 7-9 - You are okay wherever you are

If your score is 6 and below - You should repeat your Basic Naval Orientation Course

Jour. Marine Medical Sociery,2010, Vol. 12, No.2 t I 5

Case Report

Pleural Effusion in Extramedullary Myeloma

Surg Capt S Ranjan, vsr,,r#, Surg Lt Cdr Harimukundan*, Surg Cmde SR Gedela*, Brig UK Sharma**,Surg Capt Naveen Chawla..

Key Words : Multiple myeloma, Pleural effusion, Extramedullary myeloma

Introduction

leural effusion (PE) in Multiple Myeloma (MM)is extremely rare and seen in less than l%o of

cases []. It may be a non-specific complication ofthe disease or due to direct malignant infiltration ofpleural space [2]. Involvement of serous cavities inmyeloma carr ies a poor prognosis.

Case Report

A 69 years old elderly male presented with dyspepsia anddyspnrrea of short duration. Comorbidities included hypertensionand CAD. On examination he was orthopnoeic, Karnofsky scorewas 50Vo and tace was suffused with tortuous neck and upperchest veins. Hb was 9.9 gm/dl-, TLC 5300/cumm, DLC N577o,L31Vo,E02o/o,M02Vo, Platelets were 273000lcumm and ESR was44 mm in Ist h. Blootl Urea was 60 mg/dl, Sr Creatinine was 2.2mg/dl and Sr Uric Acid was 10.3 mg/dl-. CXR revealed mediastinalw iden ing w i th b i la te ra l p leura l e f fus ion (Rt>Lt ) . 2DEchocardiography was normal with no pericardial effusion. Apigtailcatheter was placed into Rt pleural space and approximately 1300ml of straw colored fluid was aspirated. A femoral venous accesswas placed for intravenous fluids and drug administration.

CECT Chest, abdomen and pelvis revealed well defined masslesion in posterior mediastinum measuring 22.4 cm x 5.3 cm x 8.78cm and extending from DV3 to LV2 level. Anteriorly the lesion wascompressing heart, encasing the descending aorta and extendingthrough diaphragmatic hiatus into celiac axis. There was compressionof thoracic oesophagus anteriorly. The trachea, carina and bothbronchi were compressed anteriorly causing narrowing of lumen. Inaddition, an anterior mediastinal mass of I 1.5 cm x 5.08 cm x 3.14cm size was also noted predominantly on the Rt side, posterior tosternum and extending from DV3 to DV9 craniocaudally,compressing and stretching the SVC and causing distension ofbothbrachiocephalic veins. There was collapse and consolidation ofanterobasal, posterobasal and mediobasal segments of RLL.Osteolytic lesions were seen in DVl, head of Rt humerus andbilateral i l iac blades. Impression drawn was of an aggressivelymphoproliferative disease with SVC obstruction, bilateral pleuraleffusion, consolidation and collapse.

An ultrasound guided fine needle aspiration cytogy (FNAC) ofthe med ias t ina l mass revea led numerous b inuc lea ted andmult inucleated plasma cel ls and blasts. Pleural f luid cytology

revealed intense plasma cell (PC) and lymphocyte response. Bonemarrow examination revealed 457o-plasmablastic type of plasmacells (Fig. l) .

Serum Immunoelectrophoresis was abnormal with M bandConcentration of 6.0 gm/dl-, IgA (N 82-453 mg/dl) of 17.7 mgldL,IgM (N 46-304 mg/dL) of 87 mg/dl, IgG (751-1560 mg/dl) of625OmgldL, Kappa (N 629-1350 mg/dl-) of 9060 mg/dl andLambda(313-723 mg/dl) of 25.0 mg/dl. Urinary Bence Jones protein werepositive, Rate Kappa was 0.0602 gm,24h urine Volume was 4800ml, beta 2 microglobulin was 8.71 mg/L (N 0.83-1.15 mg/L), SrAlbumin was 3.2 gm/dl-, Sr Globulin was 8.6 gm/dl, Sr LDH was288UIL and HBsAg, antiHCV and HIV were non-reactive.

In view of above, he was diagnosed to be Multiple Myeloma(Stage IIIB) with extramedullary disease type IgG Kappa. He wasstarted on parenteral steroids under cover of Pantaprozole andAllopurinol. He was taken up for urgent mediastinal radiotherapywith 30 Gy/l0#s @ 150cGy + l50cGy=300 cGy on fields AP-PA.

The patient improved initially with regression in tumor massand SVC obstructive symptomatology but soon developed bilateralrecurrent pleural effusion requiring repeated therapeutic taps. Hedeveloped oral candidiasis and was put on antifungal therapy withFluconazole. He also developed features of multiorgan dysfunction.He was placed on positive inotropic and ventilator support butdespite best efforts succumbed.

Discussion

MM is an infrequent cause of PE. In a review basedon 958 patients with MM, 58 patients (6Vo)hadPE andonly 8 (0.8Vo) had PE due to myeloma infiltration [2].Other reports also focused on the rare occurrence ofthis extramedullary localization [3,4]. Pathogeneticmechanisms include invasion of myeloma cells fromadjacent skeletal lesions, extension from chest wallplasmacytomas and direct pleural disease infiltration [3].

For PE, thoracocentesis should be performed to relievethe symptoms and to obtain sample to differentiatetransudative from exudative effusion and to measurethe levels of protein and LDH [3,5].

Malignant Plasmacytoma (PC) should be identifiedin cytological examination of PF or in pleural biopsy.

#Senior Advisor (Medicine & Oncology), .Graded Specialist (Radiation Oncology), *Consultant & Head of Department of Medicine, ..Senior

Advisor (Pathology), INHS Asvini, Mumbai 400 005. **Consultant (Medicine & Nephrology), Army Hospital (R&R), N. Delhi.

t 16 Jour Marine Medical Society,20l0, Vol. 12, No.2

Fig. I : Photomicrograph bone maruow aspirate.

The monoclonality of the PC infiltrate can be establishedby immunoperoxidase staining for light chains and byimmunophenotype analysis of the PF [6]. Treatment ofmyelomatous PE has been disappointing, as it does notusual ly respond to several regimens, includingthalidomide. Most of these cases survive for less than 7months despite initial improvement [4].

A negative cytology does not rule out a malignantetiology. If no specific diagnosis was obtained afterthoracocentesis, pleural biopsy was previously the logicalnext step. Currently, thoracoscopic examination isemerging as a superiortechnique due to low complicationrate, comprehensive visualization and opportunity forsimultaneous treatment by pleurodesis or pleurectomy.Due to patient's limited life expectancy, efforts to palliate,eliminate dyspnoea, optimize function and reducehospitalization should be the aim of treatment [8].

Mal ignant pleural ef fusion is a rare and latecomplication in the course of malignant myeloma [9].Cytological ly these cases have a predominant lylymphocytic infiltrate with scattered plasma cellsshowing atypical nuclear features. Dif ferent ialdiagnoses on cytology include other non-myelomatouseffusions like NHL and acute and chronic lymphoid

leukemia [ 10]. High cellularity with a predominant plasmacell population in a hemorrhagic or necrotic backgroundfavors malignant effusion. Morphological features ofmalignant plasma cells are nuclear pleomorphism,prominent nucleoli, frequent mitosis and asynchronousmaturation of the nucleus in relation to the cytoplasm.Pleural fluid electrophoresis, flow cytometry andimmunocytochemistry aid in conf irming themonoclonality of the plasma cells [9].

Referencesl. Manley R, Montath J, Patton WN. Coincidental presentation

of Ig A lambda multiple Myeloma and pleural involvementwith Ig M kappa Non-Hodgkins lymphoma. CIin LabH a e m a t o l 1 9 9 9 ; 2 1 : 6 1 - 6 3 . d o i : 1 0 . 1 0 4 6 / i . 1 3 6 5 -2257.t999.0018t.

Kintzer JS Jr, Rosenow EC 3rd, Kyle RA. Thoracic andpulmonary abnormalities in multiple myeloma. A review of958 cases. Arch Intern Med 19'18: 138: 727 -30.

Rodriguez JN, Pereira A, Martinez lC, et al. Pleural effusionin multiple myeloma. Chest 1994;105 :622-24.

Meoli A, Willsie S, Fiorella R. Myelomatous pleural effusion.South Med J 1997; 90: 65-68.

Light RW. Useful tests on the pleural fluid in the managementof patients with pleural effusions. Curu Opin Pulm Med 1999;5 :245-49.

Palmer HE, Wilson CS, Bardales RH. Cytology and flowcytometry of malignant effusions of multiple myeloma. DiagnCytopathol 2000;22 : l4'l -51.

Kim YM, Lee KK, Oh HS et al. Myelomatous effusion withpoor response to chemotherapy. J Korean Med Sci 2000; 15 :243-46.

Antunes G Neville E, Duffy J, Ali N, Pleural Diseases Group,Standards of Care Committee, British Thoracic Society. BTSguidelines for the management of malignant pleural effusions.Thorax 2003; 58 (suppl. 2): ii29-38.

Palmer HE, Wilson CS, Bardales RH. Cytology and flowcytometry of malignant effusions of multiplemyeloma. DiagnCytopathol 2001, 22 : 147 -51 .

Deshpande A, Munshi MM. Pleural effusion as an initialmanifestation of multiple myeloma. Acra Cytol200O;44 (l) :103-4.

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Joun Marine Medical Society,20l0, VoL 12, No.2 117

Case Report

Fingertip Pain due to Glomus lhmor

Surg Capt GVishwanath., Maj Atul Sahai#, Maj Raj Singh#, Surg Capt Naveen Chawla.*

Key lVords : Glomus cell tumor, Finger tip pain

Introduction

ft lomus tumors are one of the most distinctive of the\Jcutaneous vascular neoplasms. They are benigntumors arising from the glomus body, a normalintradermal arteriovenous anastomosis [1]. The glomusbodies regulate skin temperature. They are present inthe tips of the digits, particularly in the subungual area[2]. The glomus apparatus contains an afferent vessel,a Sucquet-Hoyer canal and multiple shunts in theglabrous skin of the hand and beneath the nail bed. Itcomprises a narrow lumen lined by a single layer ofendothelium, surrounded by four to six layers of glomuscells, which can be regarded as smooth muscle cells.

Case Report

A 45 year old lady reported to the Surgery OPD with complaintsof pain in the tip of her left middle finger of six years durationwhich was triggered by pressure or contact. The patient also statedthat the pain increased by immersion in cold water. The patient

denied history ofinjury to the finger, swelling, discharge from thenail bed or similar swellings elsewhere in the body. General andsystemic examination was normal. Local examination revealed noswelling, deformity or color change and nails appeared normal. Apoint on the edge of the nail was exquisitely tender and Love's pintest was positive (Fig. l). Sphygmomanometer test was equivocal.Hand function and X-ray of the finger were normal.

Under regional anesthesia and tourniquet control an incisionwas made parallel to the edge of the nail and a 6 mm encapsulatedswelling was delivered. The wound was packed, the finger dressed,hand elevation provided and the patient sent home on oral antibioticsand painkillers. Gross examination ofthe excised lesion revealedgrayish white t issue of f i rm consistency and lobulari ty.Histopathology (Fig. 2) revealed multinodular appearance withintervening fibrocollagenous stroma, with surrounding epithelioidcells having moderate to abundant eosinophilic cytoplasm andinconspicuous nucleoli, consistent with Benign Glomus tumor.

Discussion

Glomus tumors present with a classic triad of severepain, point tenderness and cold sensitivity. Areddish orbrownishnodule and nail deformity maybe presentwhenthe lesion is sub orperiungual. Glomus tumors are mostcommon in the nail bed and subcutaneous tissues of thedistal phalanx. About 75Vo occur in the hand and 60Vo

'Senior Adviser (Surgery & Reconstructive Surgery); "Senior Adviser (Path & Oncopathology); *Resident (Pathology); INHS Asvini,Colaba. Mumbai - 400 001.

Fie . I :Love 'sP inks t Fig. 2 : H & E stained section (x400) of the tumor

1 1 8 Joun Martne M)dical Society, 2010, Vol. 12, No. 2

are subungual. Less frequent sites include the wrist,forearm and foot. Glomus tumors have rarely beenreported on the patella, tendons, bone, eyelid, stomach,colon, rectum, kidney and cervix. Glomus tumors aremore common in women between 30 to 50 years. Theyare usually solitary. Amultiple glomus tumor syndromehas been described that is transmitted as an autosomaldominant. Two clinical tests are helpful in diagnosis. InLove's pin test, localized severe tenderness can beelicited with the head of a pin or a toothpick (Fig. 1). InHildreth test, elevation and application of a tourniquetinflated to 250 mm Hs causes marked reduction intenderness.

Solitary and multiple glomus tumors have distincthistopathologic features. Solitary lesions appear as solidwell-circumscribed nodules surrounded by a rim off ibrous t issue. Mult ip le lesions are less wel lcircumscribed and less solid and have the overallappearance of a hemangioma. The vascular spaces arelarger than those in solitary glomus tumors. Multipleglomus tumors have focal aggregates of glomus cellsand account for their alternate name, glomangiomas. Amalignant version, glomangiosarcoma has more atypia,pleomorphism and mitotic figures. Differential diagnosisinclude nevi, enchondroma, osteoid osteoma, ingrownnail, chronic osteomyelitis, epidermal inclusion cyst,neurilemoma, neuroma, angioleiomyoma, angiolipoma,hemangioma, melanoma, arteriovenous malformations,hemangiopericytoma and entrapment neuropathy. If

lesions are multiple, Kaposi's sarcoma may meritconsideration [3]. The diagnosis of glomus tumor isessentially clinical. Ultrasound or angiography mayreveal high velocity flow in the swelling, being anarter iovenous anastomosis [4] . Glomus tumorsdemonstrate marked enhancement on MRI aftergadolinium injection.

Complete excision provides definitive treatment.Multiple tumors occur in 25 7o of cases. Additional tumorsshould be looked for carefully. In the case of multiplelesions, therapeutic alternatives to surgical excisioninclude sclerotherapy with sodium tetradecyl sulfate orlaser treatment with an argon or carbon dioxide laser.Intralesional injections of hypertonic sodium chloridesolution given in four sessions over six months have alsobeen tried [5]. The prognosis with solitary benign glomustumors is excellent. Excision of painful lesions most oftenresults in cure. with a low recurrence rate for solitarvlesions.

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5.

References

Sternberg's Diagnostic Surgical Pathology - Fifth Edition.

Carroll RE. Berman AT. Glomus tumors of the hand. J BoneJoint Surg 1972; 54A (4) : 691-703. (PubMed)

Robbin's and Cotran - Patholoeical basis of disease. - 8thedition.

Fornage BD. Glomus tumors in the fingers: Diagnosis withUS Radiology 1988; 167 ( l) : 183-185. (PubMed)

Freedberg, et al (2003). Fitzpatrick's Dermatology in GeneralMedicine. (6'h ed) McGraw-Hill.

Jour. Marine Medical Society,2010, Vol. 12, No.2 1 1 9

Letters to the EditorDear Editor,

J read with interest the excellent article'Aeromedical update for ship borne medical officers' []. The author has statedIrhat the duration for flying after diving to be l2 hours after a dive to l0 m and 24 hours for a dive deeper than l0 m. Thereis lack of unanimity on the Pre Flight Surface Interval (PFSI), which is defined as the duration for which an individual must beexposed to I ATApressure before exposure to decreased ambient pressure in flying. The UK Diving MedicalAdvisory Committee(DMAC) has recommended a PFSI of 12 hours for flights to 600 m (- 2000 f0 and 23 hours for flights to2438 m (-8000 ft) [2]. TheUndersea and Hyperbaric Medical Society (UHMS) has recommended a PFSI of 12 hours for no stop diving lasting less than 2hours in the past 48 hours and 48 hours for decompression dives [3]. However, some workers [4] have found the risk of DCS forflying after diving to be lesser for short and deep dives rather than long and shallow dives. The BR 2806 [5] recommends a 48hour interval to travel by air after undertaking any dive. In view of the vast disparities in opinion, the promulgated BRrecommendations should be followed.

The Pre Flight Medical Examination (PFME) of the air crew is conducted at different MI Rooms/Sick Bays on consecutivedays. This is because pilots keep moving from one location to another and also the PFME is generally conducted by the DMOof the nearest hospital on holidays. Due to this, there is little continuity in the medical examination conducted for the air crew.Consequently, the MO conducting the PFME is unaware about the past history of the air crew and is dependent on the historygiven by individual pilots. I am aware ofan instance where the crew had borderline hypertension and has not been allowed tofly thrice in the previous fortnight at three different locations! It is suggested, this sort ofinformation should be recorded in aconcise medical history record card, with the crew and should be compulsorily shown to the MO during PFME. Relevant medicaldetails including being not allowed to fly, and the reason, should be entered and signed by the MO, in the card. This will enablea naive MO, to have a quick reference to the past history of the air crew and make the PFME more meaningful and thus contributetowards flight safety.

References

1. Verma RC. Aeromedical update for ship borne medical officers. Journal of Marine Medical Society 2009; ll (2) :99-104.

2. Diving Medical Advisory Committee (DMAC). Recommendations for flying after diving. DMAC 07. London : Diving MedicalAdvisory Committee 2000.

3. Sheffield PJ, ed. Flying after diving. 77 (FLYDIV) l0ll/89. Bethesda, MD: Undersea and Hyperbaric Medical Society, 1989.

4. Gerth WA, Vann RD, Southerland DG. Quasi - physiological models for flying after diving guidelines. Final Report. Durham NC:Recreational Diving Research Foundation, duke University; 1993.

5. Para l2l8 (a), Royal Navy Book ofReference 2806.

Surg Lt Cdr Rohit VermaPMO and Graded Specialist (Marine Medicine), INS Nireekshak, C/o Fleet Mail Office, Koch 682004.

ReplybyAuthor

Dear Editor,

J thank Surg Lt Cdr Rohit Verma for his valuable inputs. On the matter of undertaking flying after diving, several case reviews,lretrospective as well as prospective animal and human investigations have resulted in a number of recommendations byvarious authors/agencies as to the sea level surface interval necessary to undertake safe flying after diving. Although the BR2806 recommends a period of 48 hour interval between diving and flying, the matter merits serious consideration in view ofmilitary requirements. For instance, a "stat" safe period of 48 hours following a no-decompression dive of less than two hoursdoes not merit a non flying period of 48 hours and can seriously affect military requirement. Thus, more specific guidelines arerequired on this matter.

On the matter of the Pre Flight Medical Examination (PFME), the practical concerns and suggestions of the reader are wellappreciated as the conduct and interpretation ofPFME raises several questions. Several Air Forces in developed countries haveabolished PFME due to the fact that if you can trust a pilot with a billion dollar aircraft, you should not doubt his honesty inreporting any matter that is not commensurate with safe flying. In my experience, I can confidently state that the aircrew can betrusted to volunteer any significant medical matter to the Medical Officer (MO) conducting the PFME and not hide anyinformation upon enquiry by the MO. Therefore, I am not in favour of the aircrew carrying a "concise medical history recordcard" as it will indirectly cast aspersions on the honesty and integrity of the aircrew and can affect their morale. The thumb ruleshould be to conduct the PFME as meticulously as possible.

SurgCdrRCVerma (Retd)Ex-PMO and Classified Specialist (Aerospace Medicine), INS Shikra, Colaba, Mumbai - 400 005.

Jour. Marine Medical Society,20l0, VoL 12, No.2

It20

Subject Index

AbdomenAircrewAmputationsAnxietyAsymmetric postureAvulsions

Bicornuate uterusBlunt TraumaBotulinum toxinBurns

CasevacChemical burnChemoradiotherapyChronic anal fissureComputers

DecompressionDiabetes mellitusDiabetic footDiabetic ketoacidosisDistressed submarineDysbaric osteonecrosis

Exercise enduranceExerciseExtramedullary MyelomaEye

FilariasisFinger tip painFitnessFractures

Glomus cell tumor

231 1 029

1 1 05329

6 1155738

83l0 l89

r148378

93< l

l 1 663

" Indian ocean region

1; Infant

;; Information technology

5j Injuries

75 Lateral internal spnicterotomy

HaemorrhoidsHead and neck cancerHemihaematocolposHospitalsHyperbaric oxygen therapyHyperbaric oxygenHyperbaric oxygenationHypoglycemiaHypoxiaHypoxic wounds

Localization of injuryLow back discomfortLumbar back supportLumbar lordosis

Marine medicineMaritime strategyMaxillofacial injuryMedevacMedical appreciationMedical examinationMedical support

Naval operationsNavy aircrewNavyNimotuzumab

Ocular traumaOnboard shipsOrbitOxygen toxicity

PathophysiologyPenetrating woundPleural effusionPost traumatic epilepsyProblem woundsPulmonary function test

QT interval

RadiologyRespiratory muscle trainer

ScreeningShipsSmoke inhalationSomatization

Thoracic InjuryTrainingTranscutaneous oximetryTraumatic brain injuryTreatmentTriageTroxerutinType I diabetes

107866 l757289

97,10rtt41 589

42t147523

57l0535353

72421 3

z

42104495 15 l

l l 63 l

49

42104

2,5,10,13,3r86

10386397

5,8115

l l 68 l89

93,97

l0 l

7893

7823,29

38l l 0

l 572895

l383

r071 1 4

MedicalO J

l l8 Mi l i tary

104 Multiple Ty."lo1u.

3l Musculoskeletalinjuries

l1g Naval landing operations

Author IndexSurg Capt KM AdhikariMaj S AkkiSurg Cdr PD Ayengar

Surg Commodore TKBandyopadhyay

Surg Capt Sundeep BhandariCol PK BhatiaSurg Lt Cdr Sourabh BhutaniSurg Cdr K Bose

Surg Cdr HBS ChaudhrySurg Cdr Ashutosh ChauhanSurg Capt Naveen Chawla

Surg Lt Cdr SS DalawayiSurg Cdr A Dutta

Surg Capt S GangulySurg Cmde SR GedelaBrig AK GuptaSurg Cmde G Gupta, Nu

5 I , l l 46r

104

t 349

5't,r0789

5,42,75,81

l0 l5710'l

l l 6 , l l 8

1015 ,15

t5l 1 6

57,107rt4

Surg Lt Cdr Harimukundan

Surg Capt A KapurBrig SK KathpaliaDr Mandeep KaurCol R Ravi KumarDrAnju Kumari

Surg Capt KI MathaiSurg Capt VK MohindraSurg Cdr Hari MukundanSurg Capt TVSR Murthy (Retd)

Surg Capt CS Naidu

Surg Cdr SS PundirDr Vani Puri

Surg Lt Cdr R Ranjan, vsuSurg Capt S Ranjan, vsuSurg Capt Subhash Ranjan, vsrvrSurg Lt Cdr LVV Rao

6l Maj Atul sahai6l Surg CdrMS Sahi63 SurgCdrCS Saxena'78 Surg Lt CdrAmit Sethi63 SurgCdrRShankaran

Brie UK Sharma' t x l

,;';; Surg Lt CdrA Sharma"';; Surg Lt Cdr Geetanjali Singh

A Maj Raj Singh

)7 Gp Capt N TanejaMaj Sangeeta Tiwari

l16 SurgeonCommodoreVSSRRyali 2,72

1 1 8l583l0

23,86l t 6l 563

l l 8

r0457,107

263

3rl l 68678

Surg Capt G Varghese 72,78Surg Cdr RC Verma (Retd) 53,1 l0Surg Lt Cdr Rohit Verma 78,89,97,ll3Surg Capt G Vishwanath 29,38,1l8Surg Lt Cdr LV Visweswararao 93

Surg CdrAshok K Yadav ll4

Jour. Marine Medical Society, 2010, VoL 12, No. 2 t21

ContentsVolume 12. June 2010

EDITORIAL

2 Surg Capt VSSR Ryali, Surg Cdr SS Pundir : Trauma Care at Sea, A Paradigm Shift from CASEVAC to MEDEVAC

UPDATEARTICLE

5 Surg Capt KI Mathai, Surg Cdr A Dutta, Surg Cdr K Bose : Evolving Paradigms in Neurotraumal0 Surg Lt Cdr Amit Sethi, Surg Capt VK Mohindra : Treatment Protocol for Eye Injuries Onboard Shipl3 Surg Commodore TK Bandyopadhyay : Treatment of Maxillofacial Injuries Onboard ShipI 5 Surg Cdr A Dutta, Surg Cdr MS Sahi, Surg Lt Cdr A Sharma, Surg Capt S Ganguly : Treatment Protocols for Thoracic Injuries Onboard Ships23 Surg Capt CS Naidu, Surg Cdr R Shankaran : Management of Abdominal Injuries During Naval Operations29 Surg Capt G Vishwanath : Management of Amputations and Avulsions at Sea3 I Surg Lt Cdr R Rajesh : Treatment of Musculoskeletal Injuries and Fractures Onboard Ships38 Surg Capt G Vishwanath : Protocol for Management of Burns, Smoke Inhalation and Chemical Injuries

CONTEMPORARY ISSUE

42 Surg Cdr K Bose : Medical Organization During Fleet Operation49 Surg Capt Sundeep Bhandari : Medical Organisation During Landing Operations

PERSONAL VIGNETTE

5 1 Surg Cdr KM Adhikar i : An Exercise. . . . . . . Par Excel lence!

ORIGINAL ARTICLE

5 3 Surg Cdr RC Verma : Aero-medical Evaluation of Lumbar Back Support in Chetak Helicopter57 Surg Cdr Ashutosh Chauhan, Maj Sangeeta Tiwari, Col PK Bhatia, Brig AK Gupta : Lateral Internal Sphincterotomy vs Botulinum Toxin in

, Chronic Anal Fissure

i cASE REPoRT61 Maj S Akki, Surg Capt A Kapur, Brig SK Kathpalia : A Rare Case of Hemihaematocolpos63 Surg Capt VK Mohindra, Surg Capt TVSR Murthy (Retd.), Surg Lt Cdr Geetanjali Singh, Dr Vani Puri, Dr Mandeep Kaur, Dr Anju Kumari : A

Case of Orbital Dirofilariasis

37 Book Review56 Jou rna l Scan65 Instruct ions to Authors

Volume 12, December 2010

EDITORIAL

72 Surgeon Commodore VSSR Ryali, Surgeon Captain George Varghese : Transforming Training in Marine Medicine

REVIEW ARTICLES

T 5 Srrrg Cdr K Bose : Recent Advances in Hospital Informatics78 Surg Capt G Varghese, Col R Ravi Kumar, Surg Lt Cdr Rohit Verma, Surg Lt Cdr LVV Rao : Long Bone Radiology Screening for Dysbaric

' Osteonecrosis

UPbATEARTICLES

81 Surg Capt KI Mathai, Surg Cdr K Bose : Concepts and Controversies in Post Traumatic Epilepsy83 Surg Cdr CS Saxena : Medical Organisation During Submarine Operations

ORIGINAL ARTICLES

8 6 Surg Cdr Hari Mukundan, Surg Capt Subhash Ranjan, vsrvt, Surg Cdr R Shankaran : Experience of Nimotuzumab with Concurrent Chemoradiotherapy89 Surg Lt Cdr Sourabh Bhutani, Surg Lt Cdr Rohit Verma : Hyperbaric Oxygen Therapy in Non Healing Wounds93 Surg Lt Cdr LV Visweswararao : Respiratory Muscle Training for Enhanced Endurance97 Surg Lt Cdr Rohit Verma : Effect of Hyperbaric Oxygen Therapy on Pulmonary Indices101 Surg Lt Cdr SS Dalawayi, Surg Cdr HBS Chaudhry : QT Dispersion in Diabetic Patients on Hyperbaric Oxygen104 Surg Cdr PD Ayengar, Gp Capt N Taneja : Disabilites in Naval Aircrew Applicants107 Surg Cdr Ashutosh Chauhan, Maj Sangeeta Tiwari, Col PK Bhatia, Brig AK Gupta : Troxerutin in Management of Haemorrhoids

CME

1 10 Surg Cdr RC Verma (Retd) : Fear of Flying in Trained Aircrew1 13 Surg Lt Cdr Rohit Verma : MCQ

CASE REPORTS

114 Surg CdrAshok KYadav, Surg Capt KM Adhikari, Surg Cmde G Gupta, Nlr: Infant with Diabetic KetoacidosisI I 6 Surg Capt S Ranjan, vstr.t, Surg Lt Cdr Harimukundan, Surg Cmde SR Gedela, Brig UK Sharma, Surg Capt Naveen Chawla : Pleural Effusion in

Extramedullary MyelomaI 18 Surg Capt G Vishwanath, Maj Atul Sahai, Maj Raj Singh, Surg Capt Naveen Chawla : Fingertip Pain due to Glomus Tumor

1 20 LETTERS TO THE EDITOR12I SUBJECTINDEX12I AUTHORINDEX122 CONTENTS

122 Jour Marine Medical Societv,2010, Vol. 12, No.2

December 2010 Registered with Registrar of news paperfor India Reg. No. 69828199