iraqi journal of medical sciences jms - volume 5 (2) 2007/… · volume 5 (2) 2007 issn 1681-6579...

Volume 5 (2) 2007 ISSN 1681-6579

IRAQI JOURNALOF MEDICAL SCIENCES

CHAIRMAN OF THE EDITORIAL BOARD

Hikmat A.R. HATAM FRCS

CONSULTATORY EDITORIAL BOARD

Abdul Kareem H. Abd PhDAbdul Amer JASIM FICMSAbdul-Hussien M. AL-HADI PhDAlaa G. Hussien FICMSAli A.A. Al-Taii MBChB , PhDFaruk H. AL-JAWAD PhDGassan AL-Shamma, PhD

Amal S. Khudair FICMSHashim M. AL-kadimy FRCMIsraa F. AL-Samaraee PhDLamia A.K. AL-Saady CDH,CABPMaha M. AL-Bayati MBCh B CABOGNidhal Abdul-MUHYMEN PhD

Chief Editor

Nidhal ABDUL-MUHYMEN PhD

EXECUTIVE EDITORIAL BOARD

Ahmad Duraid ABDUL-MAJID FICMS Editor

Enas Talib ABDUL-KARIM DCH,PhD Editor

Hala S. Ail CABP Editor

Hasan Azeez AL-Hamadani FICMS Editor

JOURNAL SECRETARY

Esraa' S. NAJI Alia'a N.hatam

Iraqi Journal of Medical Sciences

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Copyright 2000

Advisory Board

Abdul-Elaah Al-Jawadi (Al-Mosul University)Adnan Anoze(Al-Nahrain University)Akram Jirjies (Al-Mosul University)Amira Shubb'ar (Al-Mustansiriya University)Amjad Dawood Niazi (Iraqi Board for Medical Specialization)Anam Rasheed AL-Salihi(Irf Institute of Embryo Research &Infertility Treatment / Al-Nahrain University)

Dawood Al-Thamiry (Al-Nahrain University)Dhafir Zuhdi El-Yassin (Baghdad University)Fawzan Al-Na’ib (Al-Mustansiriya University)Hasan Ahmad Hasan (Al-Nahrain University)Hikmat Al-Sha'rbaf (Baghdad University)Khalid Abdulla (Al-Nahrain University)Ilham Al-Taie (Al-Mustansiriya University)Mahmood Hayawi Hamash (Al-Nahrain University)Najim A. Al-Roznamachi (Iraqi Board for Medical Specialization)Nazar El-Hasani (Iraqi Board for Medical Specialization)Nazar Taha Makki (Al-Nahrain University)Rafi M. Al-Rawi (Al-Nahrain University)Raja Mustafa (Al-Mustansiriya University)Raji H. Al-Hadithi (Iraqi Board for Medical Specialization)Riyadh Al-Azzawi (Al-Mustansiriya University)Samira Abdul-Hussain (Tikrit University)Sarkis Krikour Sitrak (Al-Basra University)Sarmad Al-Fahad (Baghdad University)Sarmad Khunda (Baghdad University)Tahir Al-Dabbagh (Al-Mosul University)Thamir Hamdan (Al-Basra University)Usama N. Rifat (Iraqi Board for Medical Specialization)Zakariya Al-Habbal (Al-Mosul University)


Aims and Scope

Iraqi Journal of Medical Sciences is published by College of Medicine,

Al-Nahrain University. It is a quarterly multidisciplinary medical journal. High quality

papers written in English, dealing with aspects of clinical, academic or investigative

medicine or research will be welcomed. Emphasis is placed on matters relating to

medicine in Iraq in particular and the Middle East in general, though articles are

welcomed from anywhere in the world.

Iraqi Journal of Medical Sciences publishes original articles, case

reports, and letters to the editor, editorials, investigative medicine, and review

articles. They include forensic medicine, history of medicine, medical ethics, and

religious aspects of medicine, and other selected topics.

Iraqi JMS FORMATINSTRUCTION TO AUTHORS

Iraqi Journal of Medical Sciences (Iraqi JMS) is a periodic, peer-reviewed journalpublished quarterly by College of Medicine, Al-Nahrain University. Iraqi JMS publishesmanuscripts in all fields of health and medicine written in English.Types of Contributions: Original articles, review articles, case studies, editorials,medical education, history of medicine, ethics, practical points, medical quiz, conferences,meetings and letters to the Editor.Manuscripts: Submission of a manuscript implies that is not being considered for publicationanywhere.

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).ھدف الدراسة، طریقة العمل، النتائج و االستنتاج

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References: All references should be listed in consecutive numerical order by Englishnumerical, in the order of citation in the text. Once a reference is cited all subsequentcitations should be to the original number.Examples1. Standard Journal Article: use et al when the number of authors exceeds 6.Halliwell, B., Gutteridge, J.M.C.: Oxygen toxicity, Oxygen radicals, transition metals anddisease. Biochem J, 1984; 219: 1-14.2. Books: Mann, J.I., Pyorala, K., and Teuscher, A.: Diabetes in epidemiologicalperspective. London: Churchill Livingstone. 1983.3. Chapter in book: Phillips, S.J., and Whisnant, J.P.: Hypertension and strock. In: Laragh,J.H., and Brenner, B.M. editors. Hypertension: Pathophysiology, diagnosis, andmanagement. 2nd ed. NewYork: Raven Press; 1995. p. 465-78.Tables: Each table should be typed on a separate page double-spaced, including allheadings, number all tables with English numerals and include a short title. Vertical linesbetween columns are to be avoided.Figures: All figures must be suitable for reproduction without being retouched orredrawn. Figure number, name of senior author, and title of the work should be writtenlightly on the back with red pencil. Photographs must be supplied as glossy black andwhite prints. The top of the figures should be indicated clearly.Legends: Captions for figures must be typed; double spaced, and must not appear onthe figure.Proof Reading will be done by the secretarial office of the journal. The principal author willreceive a copy of the journal. The authors are responsible for accuracy of all statements,data, and references included in the manuscript. After the manuscript has been accepted for publication, authors are required tosupply the final version of the manuscript on 3.5” IBM-compatible floppy disk in MS wordversion 6 or later. All corresponding to be addressed to the Chief Editor on the address below:

Chief Editor:Iraqi Journal of Medical SciencesCollege of Medicine,Al-Nahrain University,P.O. Box 14222,Tel. 5231521,Al-Kadhiymia,Baghdad,IRAQ.


A Medical Journal Encompassing All MedicalSpecializations

Issued Quarterly

CONTENTS

Editorial

MASS CASUALTY MANAGEMENT AND EMERGENCY CARE SYSTEM (E M S)

Hikmat A.R.Hatam………………………. ………....……………………………….………..1- 6

ARTICLES

ONE-YEAR (PATIENT AND RENAL ALLOGRAFT) SURVIVAL FOLLOWING RENALTRANSPLANTATION

Ausama S. A. Muhsin, Usama S. Alnasiri, Usama N. Rifat…………………………..….7- 12

BACTERIAL INFECTIONS IN NEONATAL UNIT IN TRIPOLI MEDICAL CENTER, LIBYA

Jawad K. Al-Diwan ,Tariq S. Al-Hadithi Abdul Latif Shaban,Mohammed Dekna…...13-17

ELECTROCARDIOGRAPHIC STUDY ON THE SIGNIFICANCE OF CHEST PAIN INPATIENTS WITH ACUTE ASTHMATIC ATTACK

ZAIDAN K. AL-HERGANI …………………………………………………………………..…18-22

PLEURAL EFFUSION, ADENOSINE DEAMINASE (ADA) AND LACTATEDEHYDROGENASE (LDH) ENZYMES LEVEL, CORRELATED WITH CYTOLOGICALEVALUATION.

FA Al-Rawi, NJ Metib, Z Talib………………………………………………………………...23-27

BLEEDING AND THROMBOSIS IN PATIENTS WITH CHRONIC MYELOGENOUSLEUKEMIA

Saad Sh Mansour, Raad J Musa,Wakas F Al-Sammerai………………………………...28-33

COMPARISON OF BLOOD LEVELS OF ANTICHLAMYDIA TRACHOMATISANTIBODIES AMONG MOTHERS AND THEIR NEWBORN BABIES FOLLOWINGNORMAL DELIVERIES VERSUS MOTHERS AND NEWBORN BABIES FOLLOWINGCESAREAN SECTION

Enas Talib Abdul- Karim, Nidhal Abdul-Muhymen , Tara S.Al Chrmawindi………..34-39

Serum Magnesium Level in Chronic Asthma In pediatrics

Najim Al-Ruznamaj, Hussam M. Al-Alwany,Ibtisam T Alobusi,Ammar Al-Shebl…...40-43

Causes of Neonatal Deaths In Al- Kadhymia Teaching Hospital

Lamia Abdul Karim Al- Saady ……………………………………………………………..… 44-48

Lactate Dehydrogenase Isoenzymes Pattern in Differential Diagnosis of PleuralEffusions.

Hussam H. Ali, Hammed , Zainab T. Al-Okab………………………………….................49-58

THE VALUE OF PANORAMIC RADIOGRAPHY IN THE DIAGNOSIS OF MAXILLARYSINUS DISEASES

Tahrir N. N. Aldelaim…………………………………………………………………………...59-64

ANEMIA IN WOMEN DURING REPRODUCTIVE YEARS IN RURAL AREA .

Maida Y. Shamdeen……………………………...…………………………..……….…65-70

Effects of AflatoxinB1 on Some Skeletal Muscle Resident Cells Using a NuclearDifferentiating Stain Technique

May F Al-Habib………………………………………………………………..…….………….71-77

IMATINIB MESYLATE IN IRAQI PATIENTS WITH CHRONIC MYELOID LEUKEMIA

Nabeel S. Murad, Ali M. Al Ameri……………………………………..………………….78-84

CASE REPORT

A RELAPSED ACUTE PROMYELOCYTIC LEUKEMIA TREATED WITH ARSENICTRIOXIDE ALONE

Liqaa R. AL-Khuzai………………………………………………………..……………..……85-86

Brugada Syndrome

Mohamaad Hashim ,Tahseen AL-Kinani , Kamil Namiq , Amar AL-Hamdi , Kais Al-Mudares……………………………………………………………………..…………………..87-90

ARABIC ABSTRACTS

Iraqi Journal of Medical Sciences 1

Editorial:

Mass Casualty Management and Emergency Care System (E M S)Hikmat A.R.Hatam, FRCS.

A characteristic of the EMS isthe mechanism by which suddenincreasing demands on one localsystem are met by shifting resourcesfrom less involved areas to the scene ofthe demand. A common term for theprocess by which resources aretemporarily loaned to the system beingtaxed by emergency demands is“mutual aid “. In this manner, peakemergency care demands are often metby use of shared facilities ortemporarily borrowed resources fromsystems in neighboring areas.

EMS systems are triggeredlocally several times a year andtherefore planning and operations arekept current through repeated use.

The plan for managing victimsof disasters should be built around anexisting EMS system. Since detection,notification and primary dispatch ofrescue teams and on-site early care areall part of the EMS, it is the pre-hospital component of EMS that willcommonly provide hospitals with theirinitial notification and assessment ofthe scope and nature of the disaster.

Experience in handling largenumbers of injured patients isrelatively limited only to those whoinvolved in Iraq, Iran conflict andmuch of the accumulated experiencehas been military rather than civilian. Itis unlikely that we will ever have muchcarefully controlled data on which tobase our management of this type ofproblem.

Primary care consists mainly ofbasic life support (BLS) measurestogether with such advanced life

Supports (ALS) measures as may benecessary. (These are usually devotedto airway and ventilation factors,control of hemorrhage, anti-shocktreatment and preparation fortransportation).Principles of Disaster ManagementAdvance Planning

The most important andgenerally agreed – upon principles thathave emerged from the experience ofthe medical profession in handlingdisasters is the need for realisticadvance planning. In spite of theimportance and wide acceptance of thisprinciples, there has been lessthoughtful planning for handling masscasualties than there should Shaft ansummarizes this well in stating thatmost description of civilian disastersare concerned with implementation ofhospital disaster plans and casualtycare after the patient reaches thehospital triage area .

In many cases central medicalauthority cannot be designatedeffectively in time for any importantdecisions to be made. Obviously,criteria for such decision makingshould have been discussed in planningsessions with representative of allinvolved personnel (fire and policedepartments, medical planners and thesupport and mutual aid agenciescommonly utilized, including nearbymilitary recourses).

Disasters may range fromepisodes of violence in an urbansetting, in which scope of theoccurrence is relatively easy to define,to the large acts of nature withdisruption of communication and


transportation over wide geographicalareas.

Disasters may be natural(floods, earth quakes, windstorms,large fires, volcano eruptions) or man –made (transportation explosion, fire,riot and civil unrest, war). There aremany proponents of planning andexercises designed to meet the needs ofthe hospital involved in a disaster. Somany organizations would be involvedin such an exercise that theundertaking would be difficult andexpensive.

It is obviously difficult todevelop plans that will be suitable forthe limitless type and magnitude ofdisasters that may occur. Somedisasters cause a general disruption ina community and others are localizedto a building or two. There are certainfeatures that are sufficiently commonto enough different types and sizes ofdisasters to justify the effort involvedin planning. By definition in masscasualty situations the demands alwaysexceed the capacities of the personneland facilities.

The purpose of advancedplanning is therefore to establish asystem that will assure the optimalutilization of personnel and facilitiesfor the particular situation.Casualty predictability

As previously stated, the key toeffective handling of disaster situationsis realistic advance planning.Use of effective maneuversA third principle is that certainmaneuvers that are economical ofpersonnel, facilities and time mayproduce a decrease in mortality, earlymorbidity and long-term functionalloss. More Sophisticated techniquesthat require the prolonged services ofhighly trained individuals usingcomplex equipment and many suppliesthough extremely valuable in ordinarypractice, may not be a wise investmentof resources in handling large numbers

of injured people in a brief period oftime.Treatment modifications

This principle is that the way inwhich we handle specific types ofinjuries in ordinary practice must oftenbe modified when we are dealing withcasualties from a disaster this shift inthinking and action is extremelydifficult for many physicians to makeunaware of the modifications that mustbe made in a mass casualty situationare likely to continue to utilizeconventional techniques in such asituation unless there is forcefuldirection from those in charge in amass casualty situation are likely tocontinue to utilize conventionaltechniques in such a situation unlessthere is forceful direction from those incharge.Teamwork

This brings us to a fourthprinciple of mass casualtymanagement: teamwork. In ordinarypractice each physician is accustomedto working in a more or lessindependent capacity. The effectivemanagement of large numbers ofcasualties in a short time demands atotally different or organizationalstructure. There must be someone incharge, in the person of the disasterplan director, who by experience andtraining is capable of giving orders,and other must be able and willing tohave control as close to absoluteauthority as is seen in medical practice.Philosophical Approach

Special attention should begiven to the readjustment of thinking-literally of philosophy- that isnecessary if the best possible resultsare to be obtained from the medicalcare of disaster victims. The physicianis ordinarily committed to the highestquality of care for his individualpatient. When a hospital is floodedwith tremendous numbers of seriouslyinjured individuals, an abrupt


modification of this philosophy isessential. For example, certainindividuals will arrive at the hospital insuch condition that, under the disastercircumstances, there is no hope ofsalvaging them, though had theyarrived in isolated circumstances,aggressive treatment might havepermitted their survival. In the disastersituation we have no reasonable choicebut to regard these individuals ashopelessly injured and to turn the bulkof our efforts to those less seriouslywounded.Disaster Planning for the Hospital

A key feature of the hospitalmanagement of disasters is theprovision of separate space for triage,stabilization, major surgery, minorsurgery and recovery. Specialprovision should be made forsupplying space for waiting families ofdisaster victims, for the handling of thedead and for accommodation ofrepresentative of communication ofrepresentatives of communicationsmedia. The integration of thesefacilities, the provision of adequateresources and staff and mobilization ofa disaster plan require finely tunedcoordination. Such coordination can beachieved only if the plan is exercised atregular intervals through disaster drills.

Surgery in Most hospitals, themajor surgery area will be the main setof operating rooms in disasters. Amplenumbers of surgical staff, anesthesiastaff and nursing staff must beprovided and a plan must be at handfor orderly addition of staff as needed.A minor surgery area (and possibly aspecial fracture area) should beprovided so that patients need notremain for definitive care in thestabilization area and so that patients atthe same time will not overload themajor surgical area. The minor surgeryare must be supervised by anexperienced individual who canmaintain a steady flow of patients. It is

imperative to note that here, aselsewhere in the handling of disastersvictims, it may be necessary tocompromise the highest quality of carein the name of efficiency.

Recovery Area Plans mustprovide for the easy evacuation ofregular hospital patients from areasnormally used for recovery or forintensive care to provide large openareas for recovering disaster victims.

Intensive care unit personnelmust constantly be aware of patientswho could be moved out if a needshould arise suddenly.

It is particularly important thatan appropriate individual have theauthority to make decisions aboutpatient moving and that a crisis ofauthority not be allowed to arise thatwould be superimposed on the crisisimposed by the disaster itself.Logistics

The key feature in coordinationof hospital disaster efforts is successfulcommunication among thoseresponsible for resources. In order tocoordinate the various resources andfacilities, an information systemmanned by trained personnel mustprovide the communication sconnection. A single individual shouldbe in charge of coordinating disasterresources and facilities.

The disaster control centershould include representative of themedical staff, nursing staff,administration, materials management,security, public affairs and supportservices. Specific communicationsupport should be provided. Theindividual in the control center musthave the authority to call in staff fromoutside.Drills

As indicated earlier theeffective coordinating of facilities,resources and manpower requires bothplanning and practice. It iscommonplace that the requisite


disaster drills are given little attentionbeyond that necessary to comply withexternal standards. Complex problemsthat may arise to challenge keycoordinating staff in an actual disasterare not covered in many drills.TriageThe classification of patients intocategories is critical in determining thesuccess in handling a disaster. Thesecategories may include patients whoneed immediate stabilization, thosewho can proceed to definitive care andthose with relatively minor injuries.Physicians performing such triagemust be experienced in the care oftrauma patients and sensitive tounusual clinical problems. It isimperative that this task not berelegated to junior staff or houseofficers. The triage area must becapable of expansion to accommodateall patients that may be brought to agiven hospital. Since triage is bestperformed at the entry point to thehospital the emergency departmentshould have been planned to serve thispurpose. Ideally, the registration andwaiting areas should be capable ofconversion to triage.

The details of patient sortingwill, of course, depend upon theparticular circumstances. Patientsarriving at the hospital may beclassified into one of four majorcategories by the triage officer. Theseare:I.Patients with minimal injuries whowill do well on self-care or “buddy”care. Medicolegal responsibility makesit necessary not only to allow anypatient to register if he desires but alsoto provide “medically trained”personnel to render care. This holdstrue for the disaster situation and maymake the self-care or “buddy” systemnot feasible and force these patients tobe grouped with category II patientsII. Patients whose injuries are lesstrivial and will require medical

attention but are not of a seriousnature; these patients will not requireintensive care.III.Patients whose injuries will requiremajor medical attentions. This groupmay be subdivided into the following.A. Require early operation1- Immediate2- After an intervalB. Do not require operation oroperation will be performed only later intheir course.IV. Patients who are either dead onarrival or so hopelessly wounded thatunder the circumstances of disasterthere is no reasonable chance of savingthem.In some disaster situations , the patientflow may be so great that initiallytriage should be made according to themost basic classifications, i.e., (A)those who will live no matter what, (B)those who will die no matter what and(C) those whose survival depends uponearly critical care. It may be necessaryto have “tiered triage in whichcategory C patients are subdivided byanother team according to whether ornot there is need for surgery, and earlyoperation or delayed operation.

In Addition to sorting patientsinto categories, the triage officer mayor may not be assigned two additionalresponsibilities .The first is theestablishment of priorities amongCategory III patients. In other words,the triage officer may determine whichpatients most urgently need surgicalattention, blood transfusions and othercare. The other responsibilitysometimes as signed to triage officersis the institution of certain measures ofimmediate care such as the relief ofairway obstruction and the control ofhemorrhage. If it is elected to assign tothe triage officer the responsibility ofpriority of determination for CategoryIII patients or the responsibility forexecution of some immediate caremeasures.


Patient Identification and Record-Keeping

System that serves to identifypatients in a disaster situation shouldbe different from the hospital routinein several respects. A system such asD1, D2, D3, would identify the disastervictim as being such. Later permanenthospital numbers could be assigned sothat disaster numbers could be usedagain.Patient Care Categories

Patients in each categoryshould be cared for in a separatelocation. The segregation of patientson this basis, which in ordinaryhospital practice is called progressivepatient care, is properly the mostefficient means of handling largenumbers of causalities in a brief periodof time with limited resources.Category I – Minimal Care. Almostno medical personnel are necessary tohandle patients in this category.Category II- Light MedicalAttention. Again , very little medicalexpertise needs to be expended . Theprincipal duties to be carried out areperhaps the administration of tetanusshots, the application of light dressingand other chores that can safely beperformed by medical students.Category III-Major MedicalAttention. It is this category that willutilize most of the personnel,equipment and supplies. The specificorganizational structure of Category IIIcare is best determined by theindividual hospital on the basis of itsparticular resources. The designationof a senior person to supervise thislarge portion of the mass casualtymanagement is probably advisable inmost hospital.

Patients who require earlyoperation treatment must, if priorityhas not already been determined by thetriage officer, be sorted with respect tothe urgency of operative intervention.

The decision regarding the timing ofoperation will, of course, depend inlarge measure upon the nature and sizeof the disaster- several patients withmoderately severe head injuries mayrequire decompression quite early. Onthe other hand, in the event of a majorcatastrophe with hundreds of soft –tissue injuries to be cared for by a fewsurgeons, the talents may be muchbetter utilized in the performance of 30or 40 wound debridements than in theperformance of three or four cranialdecompressions. It is probablydesirable for a relatively high- rankingmember of the surgical staff to serve asa deputy disaster plan director inchange of Category III patients. Hismajor responsibility is to keep theworkload reasonably well distributedamong the personnel caring for thesepatients. Those with the greatestexpertise and leadership ability shouldbe utilized to fill the position ofdisaster plan director.Category IV- Hopelessly injured aD. O. A. The emotional difficulty –involved in classifying these patientsand the importances of assigning somepatients who arrive at the hospital aliveto this category have already beendiscussed. Patients in Category IVshould be made as comfortable aspossible with the facilities at hand. Afew nurses equipped with drugs canordinarily do this.

ConclusionOptimal medical care in

disasters of all sizes and types isdependent upon realistic advanceplanning by the community and itshospitals. The type of catastrophe thatwill occur in a particular communitycannot be anticipated, but planning canassure that when a disaster occurs,appropriate individuals will be in aposition to deal effectively with thespecific problems that arise. The factthat planning cannot be complete is no


justification for the absence ofpreparation. The integration of hospitaldisaster planning to the regional EMSplan is essential for realisticpreparedness in the event of a realdisaster.


ONE-YEAR (PATIENT AND RENAL ALLOGRAFT) SURVIVALFOLLOWING RENAL TRANSPLANTATION

Ausama S. A. Muhsin1 FIBMS, Usama S. Alnasiri1 FRCS,Usama N. Rifat2 FRCS, FACS

AbstractBackground: Renal transplantation offers a realistictherapeutic option to patients with end-stage renaldisease (ESRD).

Objective: To evaluate one- year (patient and renalallograft) survival and comparing age and HLA-matching results as possible risk factors.

Methods: Fifty (50) patients underwent renaltransplantation in the renal transplantation unit ofSurgical Specialties Hospital-Baghdad from September2000 to October 2002. None had diabetes mellitus orclinical evidence of symptomatic cardiac disease. Allthe transplanted kidneys were from living donors.Direct matching between the serum of recipient andlymphocytes of the donor was negative. HLA class Imatching was performed. Recipients were followed forone year following renal transplantation clinically andby regular laboratory tests. Ultrasound and colorDoppler examinations were performed when there wasevidence of decreased urinary output, allograftdysfunction, or clinical suspicion of rejection. Graftnephrectomy, when needed, was done in the samecenter.Results: Thirty-nine patients (78%) continued theirlives one year following renal transplantation while

eleven patients (22%) died during the first yearfollowing renal transplantation, due to cardiovascularcomplications and sepsis. Death following renaltransplantation was compared with age and HLA-matching as possible risk factors. The comparison wasnot statistically significant. In thirty-eight patients(76%) the transplanted kidney was functioningnormally after one year from renal transplantation.Twelve (12) patients (24%) needed graft nephrectomyon the basis of clinical picture of acute rejection aidedby conventional sonographic and color Dopplerexaminations. Acute rejection was not confirmed byhistopathological examination prior to graftnephrectomy.

Conclusions: Cardiovascular disease is common inrenal transplant recipients and is a major cause ofmortality in this population followed by sepsis. Age ofrecipient and HLA- matching results were notcorrelated to the one-year recipient mortality.

Key words: Acute rejection, cardiovascular diseases, one-year survival, renal transplantation.

IRAQI J MED SCI, 2007; Vol. 5(2):7-12

1IntroductionRenal transplantation can restore

patients with end-stage renal disease (ESRD)to nearly normal health. Regardless ofwhether the treatment modality is dialysis or

1Dept. Surgeury-Section of Urology, College ofMedicine, Al-Nahrain University, 2 College ofMedicine, Baghdad University Chairman of IraqiCouncil for Urology.Address correspondence to Dr: Ausama S.A.Muhsin, Email: [email protected] 23rd March 2006: Accepted 29th May 2006.

transplantation, the major causes of death are,in order, heart disease, sepsis, and stroke1.

It has been known for some time thatcardiovascular mortality and morbidity arehigher in renal transplantation than in thegeneral population2. There is an approximate10-fold higher incidence of cardiovascularmortality in renal transplant recipients thanequivalent patients without renal disease. Incontrast, when one considers all patients withESRD, cardiovascular mortality is lower intransplant recipients than patients onmaintenance hemodialysis. Kasiske3

examined a large cohort of renal transplant

One-year survival following renal transplantation …. Muhsin et al


recipients and found that, in a broad sense,traditional factors such as lipids, HgbA1C,and diabetes mellitus were associated withcardiac morbidity and mortality in a similarquantitative manner as in the generalpopulation.

An often-overlooked phenomenon inrenal transplant recipients is cardiomyopathy,which in this population is thought to bemultifactorial. Once again, the incidence ofcardiomyopathy is significantly less in renaltransplant recipients (10%) compared withpatients on maintenance dialysis.Unfortunately, several commonly usedimmunosuppressive drugs interfere with thecardiovascular system.

One year graft survival rates arereported to be 80% for mismatched cadavericrenal grafts, 90% for non-identical livingrelated grafts and 95% for human lymphocyteantigen-identical grafts4. A variety of medicaland surgical catastrophes can occur followingrenal transplantation which compromise graftoutcome. Technical failures, infections, andrecurrence of the disease for which thetransplant was performed are among theproblems occasionally encountered in thesepatients. However, except for transplantsperformed between identical twins, transplantrejection continues to be the most importantcontributor to graft loss.

The aim of the study is to evaluateone- year (patient and renal allograft) survivaland comparing age and HLA-matching resultsas possible risk factors and under the difficultcircumstances of sanctions.

Patients & MethodsFrom September 2000 to October

2002, 50 patients underwent renaltransplantation in the renal transplant unit ofSurgical Specialties Hospital, Baghdad. Therecipients and their potential donors wereevaluated prior to transplantation. None wasshown to have diabetes mellitus or clinicalevidence of symptomatic cardiac disease. All

transplanted kidneys were from living donors(LDs).

Recipients and their potential donorswere ABO compatible. Direct matching wasnegative. HLA-matching class I only wasperformed as class II was not available. Panelreactive antibodies (PRA) test was performed.Recipients with less than 30 per cent reactionwere chosen.

The hot ischemia time was rangingbetween 4-14 minutes. The cold ischemiatime was ranging between 60-180 minutes. In(45) patients (90%) arterial anastomosis wasto the external iliac artery (according to thesurgeon's preference), while in (5) patients(10%) the anastomosis was to the internaliliac artery. The renal vein was anastomosedto the external iliac vein. The arterialanastomosis was done in an interruptedfashion, while the venous one wascontinuous. Extravesical technique forureteroneocystostomy was used. Tripleimmunosuppressive therapy that consisted ofcyclosporine, corticosteroids and azathioprinewas used. Newer agents were not available.

Data collectionThe recipients were followed for one

year clinically and biochemically. Renalallograft dysfunction was defined as apersistent/or progressive elevation of serumcreatinine. Conventional sonographic andcolor Doppler examinations were performedwhen there was clinical evidence of decreasedurinary output, and/or laboratory findings ofgraft dysfunction.Statistical analysis

Data were tabulated in a mean (±SD),number and percentage. Association betweendifferent variables was measured by usingFisher’s exact test. P value < 0.05 wasconsidered as statistically significant.Results

Fifty patients aged (15-62) years; witha mean age (34.46 ± 12.4) years underwentrenal transplantation. They were (35) males



(70%) and (15) females (30%). Thirty-ninepatients (78%) continued their lives one yearfollowing renal transplantation while elevenpatients (22%) died during the first yearfollowing renal transplantation, due tocardiovascular complications and sepsis.Cardiothoracic complications wereresponsible for death of (7) patients (63.63%).

Two of them died (they were 46 yearsand 25years) due to cardiac arrest in theimmediate 24-hour period. No autopsy couldbe performed so the real cause of death couldnot be verified. Two patients developed acuterejection and after failure of anti-rejectionmedical therapy, graft nephrectomy was doneand they were returned to hemodialysis but

later died due to acute pulmonary edema. Theremaining three patients died due torespiratory failure secondary to chestinfection. Sepsis was responsible for death in(4) patients (36.36% of cases). One developeddisseminated pulmonary tuberculosis. Theother three had septic shock leading to death.

Table (1) shows the causes of deathamong recipients of transplanted kidney.Death following renal transplantation wascompared with recipients' age and HLAmatching as possible risk factors. Thecomparison was not statistically significant.Table (2) and table (3) show the correlationbetween death and both HLA matching andrecipients' age respectively.

Table 1: Causes of death among recipients of transplanted kidney

Table 2: Donor- recipient HLA class I – matching and recipients' death

* P value not significant

Cause of death (n=11)Cardiopulmonary complication (s) 7 (63.63%)

Sepsis 4 (36.36%)

One-yearrecipients' fate *

Less than one haplotype(n=20)

One haplotype(n=30)

Total(n=50)

Death 4 7 11 (22%)

Survival 16 23 39 (78%)



0102030405060708090

100

%o

fd

ea

th&

gra

ft

ne

ph

rec

tom

y

1 2 3 4 5 6 7 8 9 10 11 12

Months

Dead patients

Graft nephrectomy

Table 3: Age and recipients' death *

Thirty-three patients (68.75%)developed renal allograft dysfunction, whichranged from mild reversible dysfunction tosevere deterioration that necessitated graftnephrectomy. After one year from renaltransplantation the transplanted kidney wasfunctioning normally in thirty-eight patients(76%) while twelve (12) patients (24%)needed graft nephrectomy on the basis of

clinical picture of acute rejection aided bylaboratory, conventional sonographic andcolor Doppler examinations. The diagnosis ofacute rejection was confirmed by biopsy intwo patients. Figure (1) illustrates the monthlypercentage of deaths and renal allograftnephrectomy during the first year followingrenal transplantation.

Figure 1: Monthly percentage of recipients' death and renal allograft nephrectomy

DiscussionTransplantation has revolutionized

treatment of end- stage renal disease (ESRD)by proving more cost effective thanhemodialysis, with a lower morbidity and

improved quality of life. Both patientmortality and graft loss were excessive priorto 1970, reflecting the limitations ofimmunosuppressive therapy available at thetime. As immunosuppressive therapy was

Age (years) Dead(n=11)

Survived(n=39)

Total(n=50)

10-1920-2930-3940-4950-5960-69

120611

41312550

5 (10%)15 (30%)12 (24%)11 (22%)6 (12%)1 (2%)



refined, patient survival improved. This wasdue to a decrease in the frequency of life-threatening infections. Currently, a 6-monthpatient survival of 95% is achievable at mostcenters, despite the fact that criteria forrecipient selection have been liberalized toinclude older individuals and patients withsystemic illnesses such as diabetes mellitus5.Other Registries now report 2-year patientsurvival exceeding 90% for HLA identicalmatches, and 85-90% for cadaveric andliving-related non-HLA identical transplants6-8.

Since cardiovascular disease (CVD) isthe main cause of death in renal transplantrecipients, optimal control of cardiovascularrisk factors is essential in the long-termmanagement of these patients9. Evidence isvery suggestive that pre-transplant screeningfor CVD, treatment of hypertension, the useof low-dose aspirin, and smoking cessationwill also help to reduce the incidence of post-transplant CVD. Less compelling are datasuggesting that intensive glucose control indiabetics will safely decrease the incidence ofCVD. Although there is little evidence thattreatment of erythrocytosis will reduce CVD,hematocrits above 55% to 60% shouldprobably be treated to prevent venousthrombosis. Vitamins for reducinghomocysteine, antioxidant vitamins, andprophylaxis for potentially atherogenicinfections are therapies that warrant additionalstudy3.

An attempt was made to evaluate theeffectiveness of the clinical history andcurrent screening techniques available inpredicting post-transplant coronary arterydisease and also to assess the role of coronaryangiography as a pre-transplant screeningtechnique. The conclusion was that clinicalhistory and electrocardiogram (ECG) resultsare good, practical and low-cost screeningmethods, and that exercise stress testing andechocardiography were found to be of limitedvalue. Coronary angiography is appropriate in

certain high-risk groups but not necessary aspart of screening in all potential renaltransplant recipients10.

The first renal transplantation in Iraqwas performed in 1973. Renal transplantationsurgery started in the Medical City in 1985.Several social and ethical issues of suchsurgical procedure were encountered.

In this study thirty-nine patients (78%)continued their lives one year following renaltransplantation while eleven patients (22%)died during the first year following renaltransplantation, due to cardiovascularcomplications and sepsis. Althoughrecipients did not have symptoms orotherwise clear clinical evidence of diabetesmellitus or active cardiac disease, two ofthem died due to cardiac arrest in theimmediate 24-hour period raising a questionof anesthetic protocol during surgery orwhether any further preoperative work up wasneeded. In our study Age of recipient andHLA-matching results were not proved to becorrelated to the one-year recipient mortality.

Cardiovascular disease is commonamong renal transplant recipients and is amajor cause of mortality in this population.Calcineurin inhibitors such as cyclosporin,although minimizing early acute rejection, areresponsible for considerable nephrotoxicity,leading to progressive renal dysfunction andgraft loss. The recent introduction of non-nephrotoxic immunosuppressants offers thepossibility of improved renal function post-transplantation.

After one year from renaltransplantation the transplanted kidney wasfunctioning normally in thirty-eight patients(76%) while twelve (12) patients (24%)needed graft nephrectomy on the basis ofclinical picture of acute rejection aided bylaboratory, conventional sonographic andcolor Doppler examinations. The diagnosis ofacute rejection was confirmed by biopsy intwo patients.



The indications for allograftnephrectomy are to remove a symptomaticirreversibly rejected kidney and, in the case ofa chronically rejected asymptomatic graft, towithdraw immunosuppression and to preventthe development of anti-HLA antibodies thatcould delay or prevent a subsequenttransplantation1.

In a previous study (42%) of non-functioning renal transplants required removalat some time. Graft failure due to acute orearly acute rejection invariably necessitatedremoval. The recommendation was thattransplant nephrectomy is reserved for thesymptomatic cases11.

Our figures of one-year patient andgraft survival are less than the standardinternational figures. This study wasundertaken while the country was undersanctions12, 13. We were short of manyappliances, anesthetic drugs, antibiotics, antisera, immunosuppressive drugs and kidneyperfusion solutions. HLA class II was and stillis not available. It was a hard decision tocontinue working with limited success or togive up. We hope that with a better supply ofrequired drugs and equipment the results willpick up.

References1. Walsh PC, Retik AB, Vaughan ED, et al.Campbell’s Urology. 8th ed. Vol. 1. Philadelphia, W.B.Saundres Company, 2003: p.p. 345-76.2. Foley RN, Parfrey PS, and Sarnak MJ.Epidemiology of cardiovascular disease in chronicrenal disease. J Am Soc Nephrol 1998; 9 (12 suppl):S16-S23.3. Kasiske BL. Cardiovascular disease after renaltransplantation. Semin Nephrol 2000; 20: 76-187.4. Brown ED, Chen MY, Wolfman NT, et al.Complications of renal transplantation: Evaluation withUS and radionuclide imaging. Radiographic 2000;20(3): 607-22.5. Kahan BD and Ghobrial R. Immunosuppressiveagents. Surgical clinics of North America 1994; 74:1029.6. United Network for Organ Sharing (UNOS),Division of Organ Transplantation USD. 1993 AnnualReport of the U.S. Scientific Registry for TransplantRecipients and the Organ Procurement and

Transplantation Network- Transplant Data 1988-1991.Richmond, VA: UNOS, 1993.7. Frei U, Brunkhorst R, Schindler R, et al. Presentstatus of kidney transplantation. Clinical Nephrology1992; 38 Suppl 1: S46-52.8. Aguilo J, Rodriguez O, Gaete J, et al. Vascularanastomosis techniques in renal transplants. InternatAngiolo 1991; 10: 39-43.9. Boots JM, Christiaans MH, and van Hooff JP. Effectof immunosuppressive agents on long-term survival ofrenal transplant recipients: focus on the cardiovascularrisk. Drugs 2004; 64 (18): 2047-73.10. Ali M, Giblin L, Farhad K, et al. Pretransplantcardiac investigations in the Irish renal transplantpopulation-the effectiveness of our current screeningtechniques in predicting cardiac events. Ren Fail 2004Jul; 26(4): 375-80.11. Aparicio FT, Lopez MB, Gomez FB, et al . Renaltransplantectomy. Arch Esp Urol 1996 Dec; 49 (10):1079-91.12. Rifat UN. Kidney transplantation and tissue typingin Arabic speaking countries of the Middle East.(Letter), BMJ Middle East 1995; May; 2 (16).13. Rifat UN. Kidney Transplantation in Iraq.Worldwide Kidney Section. J. Michael Cecka, InClinical Transplants 2000. University of California,Los Angeles. 2000; 365-6.


BACTERIAL INFECTIONS IN NEONATAL UNIT IN TRIPOLIMEDICAL CENTER, LIBYA

Jawad K. Al-Diwan1 MSc, Tariq S. Al-Hadithi2 PhDAbdul Latif Shaban1 CABP, Mohammed Dekna1 PhD.

AbstractBackground: Infection is a frequent and importantcause of morbidity and mortality in the neonatalperiod.

Objective: This work was carried out to investigatethe prevalence of bacterial infection and thefrequency of different pathogens among newbornsadmitted to the Neonatal Intensive Care Unit (NICU)at Tripoli Medical Center (TMC), Libya.

Methods: The case records of all neonates admittedto the NICU of TMC, Libya for the period Sept.1996 through August 1997, inclusive, were reviewed.Blood and/or CSF cultures were used to establish thediagnosis of bacterial infection. The admissions werecategorized as sterile and unsterile.

Results: A total of 1123 newborns were admitted toNICU over the period of the study, 129 (11.5%) ofthem were proved to be bacterially infected, 10.6%and 24% of the sterile and unsterile admissions,respectively, had bacterial infection. Blood culture

was positive in 115 (10.2%) of the admittednewborns, while CSF culture was positive in 24(2.1%) of them. Gram-negative bacteria were thepredominantly isolated bacteria. Serratia spp. wasisolated from 38.3% and 50% of blood and CSFcultures, respectively. Klebsilla pneumoniae wasisolated from about 25% of both blood and CSFcultures. Coagulase negative staphylococcus (CONS)was isolated from 11.3% of blood cultures.

Conclusion: It can be concluded from this study thatneonatal infection is still a problem facing thecountry and there is a need for study of bacterialcolonization of anogenital tract of Libyan pregnantwomen and its relation to neonatal infections .

Key words: neonatal infection, gram-negative bacteria,Libya

IRAQI J MED SCI, 2007; VOL. 5 (2):13-17

1IntroductionInfection is a frequent and important

cause of morbidity and mortality in theneonatal period. Infections affect neonateseither through transplacentalhaematogenous vertical transmission orexposure to infectious diseases in thecommunity1, 2. The frequency of differentpathogens varies between geographicalareas and should be defined in each setting3-5.

This work was carried out toinvestigate the prevalence of bacterialinfection and the frequency of different

1Dept Paediatrics, College of Medicine, Al-FatehUniversity, Libya 2Dept. Community Medicine,College of Medicine, Baghdad University, Iraq.Address correspondence to Professor Tariq Al-Hadithi, e-mail: [email protected]\Received 26th July 2005: Accepted 22nd February2006

Pathogens among newborns admitted to theNeonatal Intensive Care Unit (NICU) atTripoli Medical Center (TMC), Libya.

Materials and MethodsThe case records of all neonates

admitted to the NICU of TMC, Libya forthe period Sept. 1996 through August 1997,inclusive, were reviewed. Data regardingdate of admission, gestational age, birthweight and laboratory results werecollected. Blood and/or CSF cultures wereused to establish the diagnosis of bacterialinfection.

The admissions were categorized assterile and unsterile. The sterile categoryrefers to neonates who delivered at TMCand admitted to the NICU, while unsterilecategory includes neonates who were

Bacterial infections in neonatal unit …. Al-Diwan et al


delivered at home or others hospitals andthen admitted to the NICU.

Data analysis was carried out usingscientific package for social sciencesprogram (SPSS) for windows version 11.Chi-square was used for comparison ofprevalence rates. P value less than 0.05 wasconsidered as statistically significant.

ResultsA total of 1123 newborns were

admitted to NICU over the period of thestudy, 129 (11.5%) of them were proved tobe bacterially infected, 10.6% and 24% ofthe sterile and unsterile admissions,respectively, had culture proven bacterialinfection. The difference between the tworates is statistically significant (p < 0.05)(Table 1).

Table 1 : Prevalence rates of neonatal bacterial infection

Type of admission Total Number Infected newborns*

No. %Sterile

Un SterileTotal

104875

1123

11118129

10.6.200624.011.5

* Blood and / or CSF culture positive (X 2 = 18.3, d.f. = 1, p < 0.05)

Blood culture was positive in 115(10.2%) of the admitted newborns, whileCSF culture was positive in 24 (2.1%) ofthem. Prematurity (gestational age less than37 weeks) was reported in 49.3% of

newborns, while low birth weight (LBW)was reported in 43% of newborns.Microorganisms isolated from bacteriallyinfected newborns are shown in Table 2.

Table 2: Microorganisms isolated from blood and CSF cultures

Blood culture CSF cultureMicroorganism No. % Microorganism No. %Serratia species

Klebsilla pneumoniaeEnterobacter speciesCoagulase negative

staphylococcus (CONS)Staph. Epidermidis

Others

44281513

15

38.324.313.011.3

13.0

Serratia speciesKlebsilla pneumoniae

E. ColiAcinetobacter species

Others

126222

50.025.08.38.38.3

Total 115 89.2 Total 24 18.6

Gram- negative bacteria were thepredominantly isolated bacteria. Serratiaspp. was isolated from 38.3% and 50% ofblood and CSF cultures, respectively.Klebsilla pneumoniae was isolated fromabout 25% of both blood and CSF cultures.Coagulase negative staphylococcus (CONS)

was isolated from 11.3% of blood cultures.Figure 1 showed the monthly variations ofprevalence of bacterially infection amongsterile and unsterile admissions to theNICU. Neonatal infection shows an increasein the prevalence with time in bothadmissions.



Figure 1: Monthly variations of prevalence of bacterial infections among sterile and unsterile admissions to NICU in TMC

DiscussionThe prevalence of neonatal sepsis

varies with considerable fluctuationovertime and geographical location, andeven from hospital to hospital. Thesevariations may be related to rates ofprematurely, low birth weight (LBW) 6, 7,prenatal care 8, conduct of labor 9, andenvironmental conditions 10.

This study revealed that 11.5% ofneonates admitted to the NICU had cultureproven bacterial sepsis of blood and / orCSF culture; 10.2% had bacteraemia only.Neonatal bacteraemia is estimated to occurin 1-8 infant per 1000 live births indeveloped countries 11. In developing worldneonatal sepsis is a greater problem, a rateof 5-10% was reported in Malaysia 12 and arate of 6% of neonatal septicaemia wasreported in Saudi Arabia13. The relativelyhigh prevalence rate of neonatal sepsisrevealed by this study may be attributed tothe finding of high prevalence ofprematurity and LBW which in turn couldbe due to the admission policy in TMC, as itwas a common practice to admit prematureand LBW neonates to the NICU. The risk ofinfection is inversely related to gestationalage and birth weight 6,7.

The finding that a significantlyhigher percent of unsterile admission thanthe sterile admission could be due to the factthat unsterile deliveries, whether homedeliveries which are largely in hands ofuntrained birth attendants or hospitaldeliveries which are mostly in hands ofnurses or midwives in the district andsubdistrict hospitals; these deliveriespresumably conducted in poor hygienicpractices with increased risk of neonatalinfection during delivery or thereafter.Nosocomial infection may account for largeproportion of both forms of neonatalinfections 7. Abdul Latif14, In Iraq reported asignificant association between neonatalinfection and type of delivery place andbirth attendant. A similar finding wasreported from India 15 and Bangladesh 16.

Several investigators reportedvariations in the frequency of differentpathogens between geographical areas; thebacterial pathogens affecting infant tend tobe those, which colonize the anogenital tractof the mother. In Western and developedcountries, group B streptococci (GBS) hasemerged as the leading cause of neonatalsepsis 3,17,18. The picture of neonatal

010

2030

4050

60

70

80

90

100

Sept

. 199

6

Oct

. 199

6

Nov

. 199

6

Dec

. 199

6

Jan.

1997

Feb.

1997

Mar

. 199

7

Apr

il .19

97

May

. 199

7

June

. 199

7

July

. 199

7

Aug

. 199

7

Months

Pre

va

len

ce

rate

(%)

sterile admissions

Unsterile admission



infection in the developing world is quitedifferent, gram- negative organisms stillpredominate, as revealed by this study withinsignificance of GBS as a pathogen. This isthe picture in India 19,20, Pakistan 21. SriLanka 22, Bangladesh 16 and Jordan 23. InSaudi Arabia, also, many workers reported arate of GBS neonatal infection, althoughsome of them found a high rate ofcolonization of anogenital tracts of pregnantwomen with GBS 13,24–27. Coagulasenegative staphylococcus (CONS) which wasisolated from 11.3% of blood culture in thisstudy, and staphylococcus aureus seem toemerge as important pathogens as thesedeveloping countries implement modernneonatal practices 13,20,25.

The increase in the prevalence rateof infection among neonates with time mayreflect just a simple increase in admissionrate due to increased referral to thisspecialized center, a relative deterioration inthe health services with time in the NICUafter its recent establishment in 1996, withsubsequent increase in nosocomialinfections.

It can be concluded from this studythat neonatal infection is still a problemfacing the country and there is a need forstudy of bacterial colonization of anogenitaltract of Libyan pregnant women and itsrelation to neonatal infections.

References1. Peter D. Infections in the newborn. In: Rennie JM,Roberton NRC, (editors). Textbook of Neonatology.3rd ed. Edinburgh, Churchill Livingstone. 1999: pp.1109-202.2. Gotoff SP. Infection in neonatal infant. In:Berhrman RE, Kliegman RM, Jenson HB, (editors),Nelsons Textbook of Paediatrics. 16th edition.Philadelphia, WB Sounders Co., 2000: pp. 938-52.3. Australian Study Group for Neonatal Infections.Early onset group B streptococcal infections inAboriginal and non-aboriginal infants. Med J Aust1995; 163: 302-6.4. Asindi AA, and Omene JA. Prolonged rupture ofmembranes and fetal outcome. East Afr Med J 1980;57: 707-11.5. Mander R, and Mikelsaar M. Transmission ofmother's microflora to the newborn at birth. BiolNeonate 1996; 69: 30-5.

6. Yancy M, Duff P, and Kubilis P. Risk factors forneonatal sepsis. Obstet Gynaecol, 1996; 87: 188-94.7. Baltimore R. Nosocomial infections. SeminPerinatol, 1998; 22: 25-32.8. Ernest JM. Neonatal consequences of pretermrupture of membrane. Clin Obst Gyne 1998; 41: 827-31.9. Haque KA. A scheme for better perinatal care inKingdom of Saudi Arabia. Saudi Med J 1988; 9:239-46.10. WHO. The state of child health in the EasternMediterranean Region, EMRO, 2nd ed. 1995.11. Klein J, and Marcy S. Bacterial sepsis andmeningitis. In: Remington J, Klein J, (editors),Infectious disease of fetus and the newborn.Philadelphia, WB Saunders Co., 1995: pp. 835-90.12. Boo N, and Chor C. Six years trend of neonatalsepticaemia in a large Malysian maternity hospital. JPeadiatr Child Health, 1994; 30: 23-7.13. Asindi A, Archibong EI, and Mannan NB.Mother-infant colonization and neonatal sepsis inprelabor rupture of membrane. Saudi Med J 2002;23: 1270-4.14. Abdul Latif BI. The pattern of morbidity andmortality of neonates admitted to neonatal intensivecare unit in Saddam maternity and pediatrics hospitalin Diyala governerate 1999-2000. MSc. Thesis,College of Medicine, Baghdad University, 2001.15. Mondial GP, Raghavan M, Bhat BV, et al.Neonatal septicaemia among inborn and outbornbabies in a referral hospital. Indian J Ped, 1991; 58:529-33.16. Nawshad Uddin Ahmed ASM, Azad ChowdhuryMAK, Hoque M, et al. Clinical and bacteriologicalprofile of neonatal septicaemia in a tertiary pediatrichospital in Bangladesh. Indian Pediatr, 2002; 39:1034-9.17. Kircher SM, Meyer Mp, and Jordan JA.Comparison of a modified DNA hybridization assaywith standard culture environment for detectinggroup B streptococci in obstetric patients. J ClinMicrobiol, 1996; 34: 342-4.18. Brumund TT, and White CB. An update on groupB streptococcal infection in newborn: prevention,evaluation and treatment. Pediatr Ann, 1998; 27:495-501.19. Sharma PP, Halder D, and Dutta A.Bacteriological profile of neonatal septicaemia.Indian Pediatr, 1987; 11: 1010-17.20. Mahapatra A, Ghosh SK, Mishra S, et al.Enterbacter cloacae: a predominant pathogen inneonatal septicaemia. Ind J Med Microbiol, 2002; 20:110-12.21. Bhutta ZA, Naqni SH, Muzzaffar T, et al.Neonatal sepsis in Pakistan: presentation andpathogen. Acta Pediatr Scan, 1991; 80: 596-601.22. DeSilva G, Perera J, and Seranyake M. Keepingtrack of microorganisms causing neonatal sepsis andtheir antibiotics sensitivity patterns . In annual



academic session of Seri Lanka College ofPediatritians, 1998.23. Saoud AS, Abuckteish F, Obeidal A, et al. Thechanging face of neonatal septicaemia. Ann TropPediatr, 1995; 15: 93-6.24. Aguis E, Bergqrist G, Smallbuck D, et al. GroupB streptococcal infection and colonization innewborn infants in Asir Province, Saudi Arabia. AnnSaudi Med, 1987; 7: 192-5.25. Haque K, Chagia A, and Shabad M. Half adecade of neonatal sepsis, Riyadh, Saudi Arabia. JTropic Pediatr, 1990, 36: 20-3.26. Asindi AA, Bilal NE, Fatinni YA, et al. Neonatalsepticaemia. Saudi Med J 1999; 20: 942-6.27. El-Kerch TA, Al-Nuaim LA, Kharfy TA, et al.Detection of genital colonization of group Bstreptococci during late pregnancy. Saudi Med J2002; 23: 56-61.


ELECTROCARDIOGRAPHIC STUDY ON THE SIGNIFICANCE OFCHEST PAIN IN PATIENTS WITH ACUTE ASTHMATIC ATTACK

ZAIDAN K. AL-HERGANI FRCPI, FRCPG.

AbstractBackground: Patients with acute asthma areusually presented with dyspnoea, wheezing andcough, but some are presented with chest pain,which is usually overlooked. The pain may be partof the clinical features or due to associatedischaemic heart disease.

Objective: To assess the origin of chest pain inacute asthmatic patients.

Methods: Tow hundred patients with acuteasthmatic attacks were studied for their symptomsand those with chest pain were especially selectedand studied by ECG with other investigations. ECGwas done on admission and repeated 48 hours later.

Results: Thirty cases out of the total 200 withacute asthma were found to have chest pain [15%]as alone or part of the clinical features. The caseswith chest pain were commoner in patients older

Than 50 years [80%]. ST depression and T waveinversion were the most common abnormalities to befound in cases with chest pain [67%]. After 48 hourssome of the ECG changes return back to normal andthe remaining cases with ECG changes were [40%]which was considered as a substantial ischaemia.

Conclusion: It appears that chest pain occurring insome of the acute asthmatic cases may be due toischaemia rather than only as a apart of the clinicalpresentation and it is recommended to be investigatedby repeated ECG in all cases.

Key words: Asthma, Chest pain ,Ischaemic heart disease

IRAQI J MED SCI, 2007; VOL. 5 (2):18-22

1Introduction

Bronchial asthma is presentedusually with various clinical featuresincluding dyspnoea, wheezing, chesttightness, and cough and diagnosis can oftenmade quickly and accurately from thepatient description and complaints, butsometimes difficulty arises to differentiatebetween pain and tightness. Peak expiratoryflow rate measurement may be needed withother investigations including eosinophilscount, chest x-ray, electrocardiography[ECG], and specific mediators to confirmthe diagnosis and complications1.

Doctors cared for the managementof acute asthmatic patients have often faced

Dept. Medicine, Al-kindy Medical College,Baghdad UniversityEmail: [email protected] 25th December 2005: Accepted 10th May2006.

Patients who complain of chest or epigastricpain alone or with the association of other

Symptoms, which occur during orafter cessation of acute attack2.

The chest pain in acute asthmaticattack is usually overlooked, because theseverity of other symptoms masks it3,however chest pain as the presentingsymptom is seldom noted. Non-cardiac painis a common clinical problem in patientswith various respiratory diseases, but someof these pains could be cardiac rather thanrespiratory in origin4.

In this study of patients with acuteasthmatic attacks, a repeated ECG withother investigations have been performed inorder to know the significance of chest painassociated with, and whether it is part of theclinical feature or an ischaemic anginalpain.

Chest pain in acute asthmatic attack …. Al-Hergani ZK


Patients and MethodsTow hundred cases with acute

asthma were studied at casualty and asinpatients regarding various symptomsanalysis during the period between 1998-2005 at Al-Karama Teaching Hospital, andAl-Kindy Teaching Hospital in Baghdadcity. They were 110 female and 90 malepatients. Their age ranges between 15-70year.

All patients had an ECGexamination on admission and another ECGafter 48 hours. Chest pain, dyspnoea, and

Tightness was recorded in studiedpatients with other symptoms of asthma.The chest pain varies in duration betweenfew minutes to many hours and was acuteand not recorded by the patients previously.

ResultsOf the total 200 cases with acute

asthma, only 30 cases found to have chestpain [15%] while most of them [85%] hadother symptoms but without chest pain.Wheezing and tight chest were the mostpredominant symptoms as shown in table 1.

Table 1: Clinical presentation of acute asthma causes (200cases)

Symptom No. /cases PercentageWheezingTightness

CoughDyspneoaChest pain

1901901206030

9595603015

There was no difference in theclinical presentation between male andfemale patients, but the cases with chest

pain were seen in patients older than 504year [80%] compared to younger age group[20%] as seen in table 2.

Table 2: Age related chest pain in asthmatic patients

Age in years No./chest pain cases Percentage> 50



between male and female patients with acute asthmatic attacks and chest pain.

Table 3: The site of chest pain in acute asthmatic patients

Site No./ cases PercentageRetrosternalLeft sidedEpigastric

Right sided

15843

50271310

Total 30 cases 100

Table 4: ECC changes in asthmatics with chest pain (30 cases )

ECG changes No. of cases Percentage

T inversionST depression

Ventricular ectopic beatsMyocardial infarction

Normal ECG

128415

402713317

Total 30 cases 100

DiscussionAsthma is an extremely common

disorder and though most common beforethe age of 25 years, it may develop at anytime throughout life. The worldwideprevalence of asthma has increased morethan 40% since the late 1970. It is amongthe most common reason to seek medicaltreatment5.

The symptoms of asthma consist of atriad of dyspnoea, cough and wheezing, thelast often being regarded as the sine quanon. In its most typical form all thesesymptoms coexist6.

Asthma is not a uniform disease butrather abroad spectrum dynamic clinicalsyndrome and the variable nature ofsymptoms is a characteristic feature7. In thisstudy acute asthmatic patients with chestpain were selected and studied for thesignificance of their pain. The chest painwas in 50% retrosternal. The other 50%recorded sites of pain, were left sided,epigastic and right sided. ECG on admissionrevealed that 67% of abnormalities included

T and ST segment but the repeatECG after 48 hours showed only 15% ofthem persist and considered. Unfortunatelyit was not possible to compare our ECGchanges to previous patients ECG becausethey were unavailable.

As a substantial ischaemia whichwere more evident in elder population. Astudy was done by Karwat k. in 2002 onasthmatic patients with and without chestpain showed 18.9% of patients had ST-Tchanges8. In comparison to this study whichshowed only 10% ST-T changes in allpatients with and without pain and whichrises up to 67% in those specifically withchest pain.

Out of the 30 cases with chest painin this study, one was found to havemyocardial infarction, which wasconfirmed, by ECG and cardiac enzymes. Asimilar report by Rubinsztajn et al waspublished on a 39 year old woman withoutany previous history of heart disease9.



Various studies regarding the causeof death in asthma agreed that the top causesof death were acute myocardial infarction,ischaemic heart disease and heart failure andthis is explained by hypoxia and the adverseeffect of beta-agonist drugs with tachycardiaand hypokalaemia10, 11.

It is also reported that the use ofinhaled beta-agonists were associated with atow fold increased risk of primary cardiacarrest among patients with asthmaespecially when inhaled steroids were notused12. In various studies of ECG in acuteasthma, many of the ECG changes havebeen observed to disappear within hoursafter initiation of effective asthma therapy,but return of ECG to normal may be delayedfor up to 9 days13, 14.

The effect of asthma oncardiovascular system has been appreciatedfor decades. During normal inspiration thereis an increased venous return to the rightheart as intrathoracic pressure becomesmore negative15-17. In contrast maneuversthat increase intrathoracic pressure such asValsalva may decrease venous return thattransiently decrease cardiac output andsystemic blood pressure and during acuteasthmatic exacerbation the interrelationbetween ventilation and cardiovascularfunction becomes much more complex withflattening of the interventricular septuminterfering with ventricular systolicfunction18-20.

There are several factors thatpredispose to myocardial damage includinghypoxia,vasospasm related to mediatorsrelease and electrolytes disturbances anddysarrhythmia associated with medicationsused to treat asthma21,22.

Hypovolaemia may be acomplication of asthma reflecting increasedinsensible fluid losses from excessivesweating or hyperventilation with decreasedfluid intake in severely dyspnoec patient andthe patient may become hypotensive duringacute exacerbation23. It is postulated thatdyspnoea associated with severe asthmamay mask the pain of myocardial ischaemia.Other complications associated with acute

asthma including metabolic acidosis,hypoxaemia, vasospasm which may lead tomyocardial contraction band-necrosis,circadian fluctuation in epinephrineand cortisol level ,pulmonary hypertention,increased intrathoracic pressure and leftventricular afterload which may lead topulmonary oedema24.

It is concluded from all above thatchest pain associated with acute asthmaattacks may signify underlying ischaemicepisode which is usually missed and it isrecommended to consider chest pain inacute asthmatic attack as an importantassociation and to be investigated carefullyto avoid cardiac complications in addition tothe complications of underlying acuteasthmatic episode.

References1. Williams HM, and Shim C. Clinical Evaluation.In: Weiss EB, and Stein M [editors]. BronchialAsthma, mechanisms and therapeutics, 3rd edition.Little, Brown and Company, 1993: p.p. 447-8.2. Norman PS. Clinical aspects of asthma. In:Michele FB, Bousquel J, Godord PH [editors].Highlights in asthmalogy. Berlin: Springer Verlag,1987: p.p. 373-5.3. Selbst SM. Consultation with the specialist, chestpain in children. Pediat Rev 1997; 18: 169-73.4. Saussez S, Richez M, and Roience YJ. Asthmaand thoracic pain. Rev Med Brux 1994; 15: 53-4.5. Drazen MJ. Asthma. In: Goldman L, and AusielloD [editors]. Cecil Textbook of Medicine, 22nd

edition, Saunders Co. 2004; p.p. 502-8.6. Weinberger SE, and Drazen MJ. Disturbances ofrespiratory function. In: Kasper D, Fauci A,Braunwald E, et al [editors] Harrisons Principles ofInternal Medicine, 16th edition, McGraw Hill, 2005:p.p. 1511-6.7. Haslett C, Chilvers ER, and Corris PA.Obstructive Pulmonary Disease, In: Haslett C,Chilvers ER, and Corris PA [editors]. Davidson’sPrinciples and Practice of Medicine, 19th edition,Churchill Livingstone, 2002: p.p. 513-6.8. Karwat K. The factors inducing status asthmaticusand changes in physical examination on admission.Wiad Lek 2002; 55: 525-34.9. Rubinsztajn R, Nasilowski J, and Chazan R.Asthma induced myocardial infarction in a 39 yearold woman. Pol Merkuriusz lek 2003; 15: 253-5.10. Hansell AL, Walk JA, and Soriano JB. What dochronic obstructive pulmonary disease patients diefrom. Eur Respir J 2003; 22: 809-14.



11. Abramson MJ, Walters J, and Walters EH.Adverse effect of beta-agonists; are they clinicallyrelevant? Am J Respir Med 2003; 2: 287-97.12. Lemaitre RN, Siseovick DS, Psaty BM, et al.Inhaled beta- 2 adrenergic receptor agonist andprimary cardiac arrest. Am J Med 2002; 15: 711-6.13. Hill SH, and Weiss EB. Status asthmaticus. In:Weiss EB, and Stein M [editors]. Bronchial Asthma,evaluation and therapeutics, 3rd edition, Little, Brownand Company, 1993; p.p. 994-6.14. Siegler D. Reversible electrocardiographicchanges in severe acute asthma. Thorax 1977; 32:328.15. Sessler CN, Ayres SM, and Glauser FL. CardiacInteraction, Arrhythmias and Pathology, In: WeissEB, and Stein M [editors]. Bronchial Asthma, 3rd

editon, Little, Brown and Company, 1993; p.p.1045.16. Robotham JL, and Mitzner WA. A model of theeffect of respiration on left ventricular performance.J Appl Physiol 1979; 46: 411.17. Robotham JL, et al. Effects of respiration oncardiac performance. J Appl Physiol 1978; 44: 703.18. Briker JA. Leftward septal displacement duringright ventricular loading in man. Circulation 1980;61: 626.19. Guzman P, et al. Transeptal pressure gradientwith leftward septal displacement during Muellermaneuver in man. Br Heart J 1981; 46: 657.20. Morris J. Dynamic right ventricular dimension:Relation to chamber volume during cardiac cycle, JThorac Cardiovasc Surg. 1986; 91: 879.21. Chappell AG. Painless myocardial infarction inasthma. Br J Dis Chest 1984; 78: 174.22. Jazayeri MR, Reen BM, and Edward JA. Asthmainduced myocardial infarction in patients withnormal coronary arteries. J Med 1983; 14: 351.23. Straub PW, and Buhlmann AA. Hypovolaemia instatus asthmaticus. Lancet 1969; 2: 923.24. Guy W, Hoo S, and Santiago S. Complications.In: Weiss EB, and Stein M [editors] BronchialAsthma, 3rd edition, Little, Brown and Company,1993; p.p 1167-8.


PLEURAL EFFUSION, ADENOSINE DEAMINASE (ADA) AND LACTATEDEHYDROGENASE (LDH) ENZYMES LEVEL, CORRELATED WITH

CYTOLOGICAL EVALUATION.

F.A. Al-Rawi1 FICPath, N.J. Metib1 MBChB, Z. Talib2 PhD.

Abstract:Background: Measurement of pleural fluidadenosine deaminase (ADA) and Lactatedehydrogenase (LDH) enzymes activity has gainedincreasing popularity as a diagnostic test fortuberculous and non-tuberculous pleuritis, especiallyin countries where the prevalence of TB is high. Itcarries a high sensitivity, inexpensive and easy.

Objective: To demonstrate the diagnostic value ofincreased level of ADA and LDH in pleural effusioncorrelated with the cytological, biochemical andbacteriological assessment.

Methods: seventy-five patients presented withpleural effusions were studied (53 males and 22females) their mean age was 43.8 years. In all casesafter the clinical assessment, evaluation of the pleuralfluid was done and this included cytological examwith biochemical tests (adenosine deaminase "ADA"enzyme, lactate dehydrogenase "LDH", protein andglucose level) and bacteriological tests (Gram stain,and Ziehl-Neelsen stain).

Results: From the clinical data and lab tests, patientswere divided into six groups according to theetiology of pleural effusion. Most (32 patients) weretuberculous, malignant effusion13 patients, infection10 cases, heart failure 8 cases, idiopathic effusion 6cases and miscellaneous 6 cases. Significantdifference was found in ADA level in differenteffusions (P

Pleural effusion, ADA & LDH Enzymes level …. Al-Rawi et al


where as ADA2 is found mainly inmonocytes11-13.

ADA in TB pleuritis increases at theexpense of ADA2 because it produces bymonocytes and that the ADA1/ADA totalactivity ratio improves performance in termsof sensitivity, specificity, and accuracy. Butthis procedure is highly elaborate 3-5, 11-13.Studies on this enzyme show wide range ofcut-off values (from 25u/l to 70u/l) 3-5,8,9.

Two possible causes in the variationof cut-off values were suggested. The first isrelated to the method of ADA activityestimation, which is either colorimetric orspectrophotometric method 8. The secondsource of discrepancy is related to thecharacteristics of the population studied ineach case, considering areas with a highincidence of both HIV and TB infection..Further studies show that ADA isindependent of HIV serology 1,2,6,7.

ADA level of more than 33u/lconsidered diagnostic for TB effusion, thesensitivity raised to 100%, the specificity to95%, and the accuracy to 96% 9. Othersreported that ADA above 70u/l is highlysuggestive of tuberculous effusion, whereaslevel below 40u/l rules out this diagnosis 3-7.Cytology is an important test for diagnosingmalignant cells in pleural effusion withoverall accuracy 50-90%, increases bysubmission of a second specimen and orcombined cytology and pleural biopsy 14,15.Acid fast smears are positive in less than20% of tuberculous effusions and culturesare positive in 67%, but culture combinedwith histological examination establish thediagnosis in about 95% of tuberculouspleuritis 6,16. The aim of this study is todemonstrate the diagnostic value ofincreased level of ADA in the tuberculouseffusion with the application of cytological,biochemical and bacteriological tests. .Ideally the workup of a pleural effusionbegins with classification of fluid into eithertransudate or exudates according to Light etal criteria (1972) 17.Patients & Methods

This prospective study was carried outduring the period from December 2003 to

June 2004 in Dept of Pathology andMedical Research Center in College ofMedicine Al-Nahrin University, and Al-Kadhemia Teaching Hospital in Baghdad-Iraq. Seventy-five patients with pleuraleffusion (53 males and 22 females) their ageranged from 6-79 years (mean=43.8 years)were enrolled in this study. Detailed clinicalhistory, physical examination was done.

Pleural fluid specimens wereaspirated and submitted for cytological,bacteriological (direct smears and culture)and biochemical exam. Five smears for eachcase were prepared from the sediment, 3smears were fixed in 95% alcohol for 20minutes and stained with H&E forcytological exam and two air dried smearsone for gram stain and the second for Ziehl-Neelsen stain. The supernatant of pleuralfluid were submitted for biochemical tests(ADA enzyme level measured bycolorimetric method (Galanti and Guistimethod) 17 and the cutoff value used in thisstudy was 33u/l, LDH activity wasmeasured according to Wroblewski andLadue method 18 total protein wasdetermined by Biuret method 18 and Glucosewas measured by enzyme colorimetricmethod 18.

Total and differential cell count ofpleural fluid was done by dilution of 0.4mlof fluid with 0.4ml of glacial acetic acidusing counting chamber for calculation anddifferentiation. The results were analyzed byappropriate computer soft ware program(SPSS 10.0).

ResultsFrom the clinical data, and lab tests,

patients were divided into six groupsaccording to the etiology of pleural effusion.Tuberculous (TB) effusion 32 cases,malignant effusion13 cases, infection 10cases, heart failure 8 cases, idiopathiceffusion (no specific etiology demonstrated)6 cases and miscellaneous (include uremia,connective tissue disorders, and other rarecauses of pleural effusion) 6 cases. All TBeffusions, malignant effusions and infectioncases were exudates. (Table 1).



Table 1: Levels of Different Parameters in Transudates and Exudates.

Effusion type ADA U/Lmean±SD

LDH U/Lmean±SD

Protein gm/Lmean±SD

Glucose mol/Lmean±SD

Transudate (n =20)Exudate (n = 55)

11.9±9.255.4±45.9

174.6±23.9301.5±70.6

21.2±7.543.8±9.6

5.3±1.72.1±1.1

TB effusions (n=32); Form 43% ofthe cases of idiopathic pleural effusion.Twenty three cases were left sidedeffusions, and 9 were right sided. The meanADA value was 76.7u/l, in 30 cases (93.7%)exceeded the cutoff value (33u/l) and only 2cases (6.3%) were below the cutoff value.

Ziehl Neelsen stain was positive in twosmears (6.3%). Cytological smears and cellcount revealed moderate-severe chronicinflammatory reaction with paucity ofmesothelial cells. LDH, mean value was314.2u/l. (Table-2).

Table 2: Mean Age of Patients and Levels of Different Parameters in the Pleural Fluid of the studiedgroups

*Undiagnosed conditions inspite of all possible clinical and lab tests. **Non-specific infection.*** Include nephrotic syndrome, celiac disease, liver cirrhosis, hypothyroidism & connectivetissue disorders.

Diagnosis(Cause of pleural

effusion)

AgeYears

ADA U/Lmean±SD

LDH U/Lmean±SD

Proteingm/L

mean±SD

Glucosemmol/L

mean±SD

Cellcount/ccm

Idiopathic*(N=6)

57.2 14.9±10.6 177.2±16.2 24.0±7.7 4.5±2.0 816.7±1075.5

Infection**(N=10) 36.7

21.1±14.32 cases > 33U/L8 cases < 33U/L

279.8±42.4 38.5±4.6 2.6±1.2 3650.0±2848.5

TB(N=32) 32.4

76.7±41.130 cases > 33U/L2 cases < 33U/L

314.2±69.7 43.7±8.6 2.1±.9 3218.8±2232.2Lymphocytesform 98% of

the cells.Heart failure

(N=8) 63.6 24.8±17.8171.9±16.0 27.1±5.8 4.9±1.7 1137.5±1627.2

Malignancy(N=13 60.8

32.4±51.33 cases > 33U/L10 cases < 33U/L

321.1±60.2 50.5±11.3 1.6±.9 2007.7±1651.0

Miscellaneous***(N=6)

39.5 6.7±5.9 165.3±11.8 16.5±7.8 6.0±1.3 366.7±310.9



Malignant effusions (n=13); Form17% of the cases. ADA was below thecutoff value in (77%) 10 cases and only in 3cases (23%) were above the cutoff value(Table 2). Five were right sided, 6 were leftand 2 were bilateral effusions. Cytologicalsmears were positive in 7 cases (53.8%) andnegative in 6 (46.2%). Nine cases weremetastatic adenocarcinoma, 3 weresquamous cell carcinoma, and one small celllung carcinoma. LDH, mean values were321.1u/l. (Table-2). Details of other testsand other effusions are listed in table 2.

DiscussionEvaluation of pleural effusion

usually includes complete clinicalassessment, radiographic studies lab tests ofpleural fluid and pleural biopsy. Howeverfollowing these procedures approximately20% of patients still has undiagnosedconditions 19. Current study shows marginalsignificant correlation between finaldiagnosis and age of the patients, but notwith the side of effusion. Highest level ofADA activity in this study was measured intuberculous effusions.

Cutoff value of ADA was 33u/l gave93.7% sensitivity, 86.1% specificity and89.3% accuracy. These results werecomparable with other studies [20,21]. Therelationship between ADA and finaldiagnosis was significant (P



and non-tuberculous effusions. The LDH,protein and glucose level were useful inseparation of exudative and Transudatepleural effusions.

References1. Valdes L, Alvarez D, and San Joes E. Value ofADA in the diagnosis of TB PE in young patients ina region of high prevalence of TB. Thorax 1995; 50:600-3.2. Lezama SM, Rosales QH, and Mendez BJL .Diagnostic methods of primary TB effusion in aregion of high prevalence of TB, a study in Mexicanpopulation. Rev Invest Chin 1997; 49: 453-6.3. Villegas MV, Labrada LA, and Saravia NG.Evaluation of polymerase chain reaction, ADA, andiF-Y in pleural fluid for the differential diagnosis ofpleural TB. Chest 2000; 118: 1355-64.4. Rodriguez PE, and Castro JD. The use of ADAand ADA isoenzymes in the diagnosis of TBpleuritis. Curr Opin Pulm Med 2000 July; 6(u): 259-66.5. Gakis C. ADA isoenzymes ADA1 & ADA2diagnostic and biologic role. Eur Resp J 1996; 9:632-3.6. Valdes L, Alvarez D, and San Jose E . Tb pleurisy.Arch Inter Med 1998; 158: 2017-21.7. Bernard LTCJ, and Roth MC. Searching for TB inpleural space. Chest 1999; 116: 1.8. Chalhoub M, Cruz AA, and Marcilio C. Value ofdetermining the activity of ADA in the diagnosis ofPE. Rev Aassoc Med Bras 1996; 42: 139-46.9. Banales JL, Pineda PR, and Fitzgerald JM. ADAin the diagnosis of TB PE. Chest 1991; 99: 355-7.10. Garylee YG, Jeffery T, and Rogens RT. ADAlevel in non-TB lymphocytic PE. Chest 2001; 120:356-61.11. Perez RE, Perez WJ, and Sanchez J.ADA1/ADA2 ratio in pleural TB, an excellentdiagnostic parameter in leural fluid. Resp Med 1999;93: 816-21.12. Valdez L, San Jose E, and Alvarez D. ADAisoenzymes analysis in PE. Diagnostic role andrelevance to the origin of increased ADA in TBpleuritis. Euro Resp J 1996; 9: 747-51.13. Valdez L, and San Jose E. Diagnosis of TBpleurisy using the biological paeameters, ADA,lysozymes, and IF-Y. Chest 1993; 103: 458-65.14. Assi Z, James L, Caruso MD, et al. Cytologicallyimproved malignant effusions. Chest 1998; 113:1302-8.15. Andrew A, Renshaw MD, Barbara RD, et al. Therole of cytological evaluation of PE in diagnosis ofmalignant mesothelioma. Chest 1997; 111: 106-9.16. Aoki Y, Katoh O, and Nakanishi Y. Acomparison study of interferon gamma, ADA CA-125 as the diagnostic parameters in TB pleuritis.Resp Med 1994; 88: 139-43.

17. Tarn AC, and Lapworch R. Biochemical analysisof pleural fluid. Ann Clin Biochem 2001; 38: 311-22.18. Heffner JE, Brown LK, and Celia A. Dianosticvalue of tests that discriminate between exudativeand transudative PE. Chest 1997; 111: 970-8.19. Ferr JS, Xaveir GM, and Ranoon MO. Evaluationof idiopathic pleural effusion. Chest 1996; 109:1508-13.20. Baganha MF, Pego A, and Lima MA. Serum andpleural ADA. Chest 1990; 97: 605-10.21. Talib Z. Kanan MJ, and Husam A. Biochemicaland ytological studies of pleural and peritonealfluids. PhD thesis submitted to College of Medicine-AlNahrin University, 2001.22. Cobben MA, Belle AF, and Pennings HJ.Diagnostic value of LDH in pleural fluid. Euro J ClinChin Bioch 1997; 35: 523-8.23. Romero S, Candela A, and Maryin C. Evaluationof different criteria for separation of pleuraltransudate from exudates. Chest 1993; 104: 399-04.24. Candeira SR, Harnandez L, Susana RB, et al.Biochemical markers to discriminate betweentransudate and exudates PE. Chest 2002; 122: 1524-9.


BLEEDING AND THROMBOSIS IN PATIENTS WITH CHRONICMYELOGENOUS LEUKEMIA

Saad Sh Mansour1 FRCPath, Raad J Musa1 FICMS,Wakas F Al-Sammerai2 MSc.

AbstractBackgroud: There is considerable variation in theincidence of bleeding and thrombotic complicationsnoted among patients with myeloproliferativedisorders (cMPDs).

Objective: To explore the rate of thrombotic andhemorrhagic complications in cMPD and to identifyparameters that might be associated with thesecomplications.

Methods: Fourty five patients with various entitiesof cMPDs were enrolled in this study, which wasconducted from January, 2003 to July, 2004 andinvolves three medical centers in Baghdad.Additionally, 25 apparently healthy individuals wereincluded as control group. The patients and healthysubjects were submitted for the followinginvestigations; (plasma fibrinogen concentration,factor VIII:C, factor VII:Ag, plasma factor X:Agand plasma D-Dimers.

Results: The total rate of haemostatic complicationsamong cMPD patients was 20 %. Thesecomplications was significantly associated withincreasing patients' ages (P=0.005) and inverselycorrelated with the disease duration (r =-315,P

Bleeding and thrombosis in patients with CML …. Mansour et al


age (± SD) 41.4 years (range between 24and 66 years) were enrolled in this series asa control group. The patients and healthysubjects were submitted for the followinginvestigations; (plasma fibrinogenconcentration by clotting method of Clauss)5, plasma factor VIII: C (FVIII:C) level byactivated partial thromboplastin time (aPTT)based assay6, plasma factor VII:Ag(FVII:Ag)7 and plasma factor X:Ag(FX:Ag)8 levels by enzyme linkedimmunosorbent assay (ELISA), and plasmaD-Dimers determonation by latexagglutination test 9.

Statistical analysis:Statistical analyses were done using SPSSversion 7.5computer software (StatisticalPackage for Social Sciences). The statisticalsignificance of the difference in mean ofage, fibrinogen c

iraqi journal of medical sciences jms - volume 5 (2) 2007/… · volume 5 (2) 2007 issn 1681-6579...

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