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Chief Editor:Ahmad Husari

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2 Editorial Ahmad Husari

Original Contribution / Clinical Investigation

3 Effects of female age of marriage on antisperm antibodies formation among infertile couples in Erbil city, Kurdestan region , IRAQ

Zakarea Abdullah Yaseen Al-khayat7 Manifestation of Myiasis in HIV patients Basel Al- Rawashdeh, Hussein Al- Tarawneh, Sail Abuseif12 Association Between Hepatitis C Virus Infection and Chronic Urticaria Fethi Abed Al-GANI 15 Evaluation of Serum 5’- Nucleotidase, Adenosine deaminase, and Alkaline phosphatase in rheumatoid arthritis patients in Erbil city Sardar Nouri AHMAD, Tayfoor Jalil MAHMOUD, Hamid G. HASSAN 19 The effect of Lidocaine with Fentanyl, or Midazolam on cardiovascular responses during Endotracheal intubation in hypertensive patients on Beta-blocker Kawa Dizaye, Allaa M. Yousif, Muhamed Aydin

Medicine and Society 29 Causes Of Poor Compliance in Ophthalmology Mohannad Qasim Albdour

Education and Training

32 Computed tomography (CT) scan requirements for endoscopic surgery of paranasal sinuses: Current practice Qais Aljfout 37 Inguinal Herniorrhaphy Under Local Anesthesia: Outcome And Tolerance Among Patients In Royal Medical Services: A Prospective Study Jihad Odeh, Mazen Alomari, Abdullah Rababaah, Amjad Maslamani, Laith Khasawneh

Case Reports

41 Pigmented villonodular synovitis of the Ankle and foot: A Case Report Zaid Aleyadah, Jamal Alshawabkeh, Jamal Rahyama

43 Bochdalek’s Hernia: A Rare Underlying Cause of Acute Gastric Volvulus in an Adult Patient

Abdullah Rababaah, Samer Ghazawi, Jihad Odeh, Majdi Rababa

50 Pulmonary Embolectomy After CPR For Post CABG Arrest Razi Abu Anzeh, Khaled Nawaiseh

ISSN 1837 9052 March 2011 - Volume 4, Issue 1

nternal edicine

Middle East Journal of Internal Medicine

M I D D L E E A S T J O U R N A L O F I N T ER N A L M ED I CI N E • VO LU M E 2 , I SSU E 32

Welcome to the Middle East Journal of Internal Medicine. In this issue, we present a study that stresses the importance of Women’s Health in our region. Dr Al-khayat et al conducted a prospective study that included more than 150 females attending an infertility clinic in Erbil city in Iraq. The study noted that the age of the females at the time of marriage correlates significantly with the presence of anti-sperm antibodies detected by ELISA testing. We accepted a study that examined the alarming concerns of multi drug resistance and infections in the intensive care units. (ICUs). Another study reviewed the rate of nosocomial infections in ICU and noted that Pseudomonas Aureginosa continues to be the most common gram-negative microorganism with a significant rise in multi drug resistance.

Dr. Sardar et al examined Synovial of patients with Rheumatoid Arthritis and noted an association between serum 5?- Nucleotidase, Adenosine deaminase, and Alkaline phosphatase activities and patients with active RA. Further studies are needed to determine if these findings can be considered as biomarkers of joint inflammation, particularly for RA. This issue also included a surgical report that evaluates the safety of local anesthesia for surgical intervention of all reducible adult inguinal hernia repairs.

The author concludes that local anesthesia is safe, simple, effective, and economical, for patients undergoing inguinal hernia repair without post anesthesia side effects.

The journal included two stimulating case reports. We report a rare case in which Bochdalek’s hernia was found to be the underlying cause of acute gastric volvulus in an adult patient. The second case report describes an open pulmonary embolectomy for the treatment of hemodynamically unstable patient with massive pulmonary embolism.

Finally, a refreshing study addressing the poor compliance in patients with ophthalmologic illnesses, the study notes the importance of educating the patients about their disease and associated complications.

2

From the Editor

Ahmad Husari (Chief Editor)

Editor, Middle-East Journal of Internal MedicineDirector, American University of Beirut Sleep Disorders CenterDirector, American University of Beirut outpatient clinical care servicesAssistant ProfessorDivision of Pulmonary and Critical Care MedicineAmerican University of Beirut Medical CenterBeirut Lebanon

FR O M T H E ED I TO R

MIDDLE EAST JOURNAL OF INTERNAL MEDICINE VOLUME 4, ISSUE 1

M I D D L E E A S T J O U R N A L O F I N T ER N A L M ED I CI N E • VO LU M E 2 , I SSU E 3 3

Effects of female age of marriage on antisperm antibodies formation among infertile couples in Erbil city, Kurdestan region , IRAQ

Introduction Infertility in general is defined as the inability of a couple to conceive after one year of regular unprotected intercourse (1). Approximately 10-15% of couples desiring children suffer from infertility (2). It is realized that in 40% of infertility cases, the pathology is found in the men alone, while in 40% of cases, the pathology is found in women alone. The remaining 10-20% of cases may be caused by contributing factors by both partners (3).

It is commonly accepted that approximately 15 percent of couples will be determined to have unexplained infertility (IU) i.e. a couplethat has failed to establish a pregnancy despite an evaluation that there is no obvious reason for infertility or after correction of the factors identified as probably responsible for the infertility (4). The current rate of unexplained infertility is probably about 50% for couples with a female partner under age 35 and about 80% by age 40 years (5).

The likelihood of a diagnosis of unexplained infertility increased substantially in women over 35 years. The reason for this is that there are more likely to be egg quantity and quality problems as women aged (6). Since we do not have a “standard category”, these couples sometimes get lumped into the “unexplained infertility” category (7). Unfortunately, there is currently no specific test for “egg quality”. (8)

Experimental studies indicate that infertility may have an immune basis and most clinical evidence for spermatozoa antibodies has come from correlative studies (9) . Materials and Methods This study was carried out on infertile couples attending an infertility care and IVF center in Erbil city from November 2007 to November 2008. From the female partners of 157 couples who were diagnosed as unexplained infertility cases, serum samples were studied for the presence of ASA by ELISA method. For all patients a special questionnaire list was already prepared, including age, address, date of marriage, frequency of marriage, type of infertility, duration of infertility, medical and surgical history. All persons involved in the study had given their acceptance to participate in this research .

Zakarea Abdullah Yaseen Al-khayat

Correspondence: Dr. Zakarea Abdullah Yaseen Al-khayat (M.B.Ch.B, MSc, Ph.D in Microbiology & Immunology)College of Medicine, Hawler Medical University, Kurdestan Region, IRAQ.Email: [email protected]

ABSTRACTBack ground and objectives: Infertility is a serious problem for couples. A tendency to delay childbearing for social reasons has resulted in increasing numbers of women seeking infertility treatment at an advanced age.

Objectives of this study were to delineate the effect of female age at marriage on female fecundity by demonstrating the possible effects of female age on the formation of antisperm antibodies.

Methods: A cross-sectional study carried out on 157 females attending an infertility care and IVF center in Erbil city from November 2007 to November 2008. Serum from 157 females were examined by enzyme linked immunosorbent assay (ELISA) for the presence of antisperm antibodies (ASAs).

Results: The mean of marriage age of females was 29.27±0.52 years. The mean duration of marriage was 5.6±0.8 years .The highest number and percentage of infertile females were 45(28.7%), 76(41.4%) in the age groups (27-32),(33-38) consequently. ASAs had been detected by ELISA in 38(48.8%) of the tested samples. From all the positive serum for ASA , 21 samples (13.4%) were in the age group of 33-38 . The relationship between age of marriage of the females and presence of ASAs in serum was significant (p<0.05).

Conclusions: The female marriage age had a relation to the occurrence, severity and prevalence of infertility. There is a significant relationship between female marriage age with formation of ASAs.

Key words: Age, antisperm antibodies, infertility

O R I G I N A L CO N T R I B U T I O N A N D CL I N I C A L I N V E S T I G AT I O N


M I D D L E E A S T J O U R N A L O F I N T ER N A L M ED I CI N E • VO LU M E 2 , I SSU E 3�4


Results The range and mean of ages were(15-38) and (29.27±0.52year) respectively, which was within the normal ranges of capability of conceiving. (Table 1).The highest number of infertile females were in the age of marriage ranges (33-38) and (27-32).

Table 1: Age of marriage distribution among infertile females Table 2 showed that from the total 157 female serum samples, 38 (24.21%) showed positive presence of ASAs while the remainder 119 (75.79%) showed negative results.

Table 2: Incidence of ASAs in female serum Table 3 clarified that the highest incidence of positive ASAs in female serum was 21(13.4%) observed in the age group (33-38) years. This relation showed a significant difference (P<0.05).

Table 3: Relationship between ASA in female serum and female marriage age


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Discussion This study revealed that most infertile females with positive sera for ASA were in the marriage age group of (33-38). Bayer et al, (2007) (10) concluded that, a woman’s fertility generally begins to decline after the age of 24 years and there is acceleration of the decline after the age of 37 years.

Gardi (2005) (11) reported in his study in Erbil, that the most common age range of female infertility is centered around (25-31) years. Rostard et al, (2006)(12) concluded that, fertility problem is quite common in Norway and has increased in younger age groups. Gnoth et al, (2005) (8) found that, in general cumulative probabilities of conception decline with age. Rowe (2006) (13) concluded that, women showed a progressive decline in fecundity as they pass through the reproductive years. The decline in fecundity can be attributed to numerous potential causes, including changes in oocyte quality, the frequency and efficiency of ovulation, sexual function, the health of the uterus and the risk of pregnancy complications.

Alvarez (2006) (14) shows the increase in the number of women over age 35 years who demand medical attention for infertility. This reflects the more advanced age at which marriage is consumated and the pregnancy postponed when women, either by choice or out of necessity enroll in the labor market.

Te velde et al (2007) (15) concluded that the postponement of childbearing determined by social factors and related to the fact that it is often difficult for women to combine an education, a job or a career with having children and taking care of a family, postponing the first pregnancy which was accompanied by an increased risk of unwanted infertility.

In this study ASAs was found in serum of (24.2%) of females and this is in agreement with Kappor et al, (1999) (16) who detected ASA in 25% of 40 infertile female’s serum by ELISA. Koskimies (1979) (17) found that in 11% of women of 150 infertile couples, their sera contained sperm agglutinating activity.

This controversy in the results of this study and others may be due to different samples of infertile couples selected for the study and to different methods used for detection of ASAs. Other causes may be related to the mechanism of antisperm immune response, or different mechanisms of tolerance to sperm antigens (Hass, 1987) (18).

This study indicated that the highest percentage of serum of ASAs presence was in the marriage age group 33-38 years. This result compares with that of Hossain et al, (2007) (19) which indicated that the age related variations in the incidence of ASAs might suggest that the vulnerability of different age groups of patients to immunological imbalances is not the same. A study by Collins et al, (1993) (20) and Heidenreich et al, (1994) (21) found that ASAs, in both sexes, increased with age, and this probably suggests that age may be a contributing factor in induction of ASAs. Studies done by Turek and

Lipshutz, (1994) ( 22) ; Mazumdar and Levine, (1998) (23) delineate that females have special tolerance to sperm and the female genital tract is endowed with immunological component cells which phagocytes sperm, and processes their antigen for immune recognition.

This female tolerance to sperm antigen may be affected by many factors that lead consequently to abolishment of this tolerance and the production of ASAs in female sera in consequence to its presence in the male sera. This may be due to the exposure of this group of female to spermatozoa more frequently at the time of ovulation .

Observations of potential relevance to understanding the etiology of sperm immunity in women include evidence that they are more likely to have detectable sperm antibodies if their male partner also has sperm antibodies in his semen (24).

Another interesting observation was that in about one-third of cases women apparently react only to their partner’s sperm antigens rather than to sperm-specific antigens (25). Conclusion Female age had a relationship to the occurrence, severity and prevalence of infertility. There is a significant relationship between female age with formation of ASAs. References 1- WHO (World Health Organization) (1999). WHO Laboratory manual for the examination of human semen and sperm cervical mucus interaction:4th edition. World health organization: Cambridge University Press.2- Ghina S, Ghazeen and Kutteh WH (2001). Immunological testing and treatment in reproduction: frequency assessment of practice patterns at assisted reproduction clinics in the USA and Australia. Hum Reprod; 16(10): 2130- 5.3- Walsh P, Retic A, Vaughon D and Wein A (1998). Male Infertility: Campbell’s Urology. 7th edition. Philadelphia: Saunders Company. PP. 1311- 13.4- Capri E, Crosiganani PG (2004).Diagnosis and management of the infertile couple: missing information. Hum Reprod; 10(4): 295-307.5- Siristatidis C, Bhattacharva S(2007). Unexplained infertility: dose it really exist? Does it matter? Hum Reprod Aug; 22(8): 2084-7.6- Bayer RS, Alper MM, Penzias AS (2002). The Boston IVF Hand book of infertility. First edition. USA: The Parthenon.7- Hunault CC, Habbema JDF, Eijkemans MJ, Collins JA, Evers JLH and Velde ER (2004). Two new prediction rules for spontaneous pregnancy leading to live birth among subfertile couples, based on the synthesis of three previous models .Hum Reprod; 19: 2019- 26.8- Gnoth C, Godehardi E, Herrmann PF, Friol K, Tigges J and Freundl G (2005). Debate- contiued: Definition and prevalence of subfertility and infertility. Hum Reprod 2(5): 1144- 7.




9- Rose NR, Hamilton RG, Detrick B (2002). Autoimmunity of testis, Ovary,and Spermatozoa. Manual of Clinical Laboratory Immunology. 6th Edition. Washington: American society for microbiology, DCP. 1054- 9.10- Bayer RS, Alper MM, Penzias AS (2007). The Boston IVF Hand book of infertility. Second edition. USA: The Pathenon Publishing groups.11- Gardi AH (2005). Assessment of Psychosocial aspect of infertile women in Erbil- Kurdistan region - Iraq. (M.Sc thesis). Erbil: University of Salahaddin, College of Nursing.12- Rostard B, Schei B, Sundby J (2006). Fertility in Norwegian women: results from a population -based health survey. Scand J Public Health; 34(1): 5-10.13- Rowe T (2006). Fertility and woman’s age. Reprod Med; 51(3): 157-63.14- Alvarez Nieto C (2006). Infertility: the magnitude of this problem. Rev Enferm. May; 29(5): 59-62.15- Te Velde ER, Habbema JD, HildersCG, Merkus JM (2007). The consequence of postponing pregnancy. Ned Tijdschr Geneeskd. July; 151(28): 1593-6.16- Kappor A, Talib VH, Vermask(1999). Immunological assessment of infertility by estimation of antisperm antibodies in infertile couples. Indian J Pathol Microbiol; 42(1): 37-43.17- Koskimies Al (1979). Sperm-agglutinating antibodies in infertile couples. Arch Androl. May; 2(3): 241-5.18- Hass GG (1987).Antibody mediated causes of male infertility .Urol Clin N Amer; (14): 539- 49 .19- Hossain A, Islam N, Aryal S, Madanes A(2007). The prevalence of circulating antisperm antibodies (ASA) in infertile population representing of all etiologies. Middle East Fertility Society; 12(1): 27-30.20- Collins JA, Burrows EA,Yeo J,YoungLai EV(1993). Frequency and predictive value of antisperm antibodies among infertile couples. Hum. Reprod; 8(4): 592-8.21- Heidenreich A, Bonfig R, Wilbert DM and Engelmann UH (1994). Risk factors for antisperm antibodies in infertile men. Amer J Reprod Immunol; 31: 69-76.22- Turek PJ, Lipshutz LI (1994). Immunologic infertility. Uro Clin North Am. Aug; 21(3): 447- 68.23- Mazumdar S, Levine AS (1998). Antisperm antibodies etiology, Pathogenesis, diagnosis and treatment. Fertil Steril. November; 70(5): 799-810.24- Witkin SS, Chaudhry A (1989). Relationship between circulating antisperm antibodies in women and autoantibodies on the ejaculated sperm of their partners. Am J Obstet Gynecol ;161:900-3.25- Witkin SS, Vogel-Roccuzzo R, David SS, Berkeley A, Goldstein M ,Graf M(1988). Heterogeneity of antigenic determinants on human spermatozoa : relevance to antisperm antibody testing in infertile couples . Am J Obstet Gynecol ;159:1228-31.




Manifestation of Myiasis in HIV patients

Basel Al- Rawashdeh (1) Hussein Al- Tarawneh (2) Sail Abuseif (3)

1. Dr Basel Alrawashdeh,M.D. Dermatology Department, Royal medical services 2. Dr Hussein Al tarawneh,M.D. Plastic surgery Department, Royal medical services 3. Dr Sail Abuseif, M.D. Dermatology Department, Royal medical services

Correspondence: Dr Basel Al Rawashdeh P.o.box 340771, Zip code 11134 Amman, Jordan Mobile 0776333312 Email: [email protected]

ABSTRACT

Objective: To determine the clinical manifestation of myiasis in HIV positive patients.

Patients and methods: This is a prospective study done in Sierra Leone, level III Jordanian hospital, over a period of one year from August 2001 to August 2002.

A total number of 204 patients participated in this study. Age group varied from 20 to 53 years. Diagnosis of myiasis was mainly based on clinical grounds. A specially designed form was used for each patient separately, which included age, gender, source of referral, presentation and diagnosis, and blood samples results along with their consent to rule out HIV.

Clinical data and laboratory results were analyzed for further evaluation.

Results: The most common pattern of presentation was the nodular form, n=128 patients, followed by the abscess form, n=57, while the least common pattern was a non specified one in 19 patients.

The most common age group of patients was the 30-40 years age group, followed by age group 20-30 years then age group 40-50 years, while >50 years was the least common age group.

HIV positive tests were found in 82 (39%).

Abscess formation was the commonest manifestation in patients with HIV, n= 62, followed by the nodular type (n=16).

Abscess formation was more in positive HIV males in age group 30-40 years.

Conclusion: Painful nodule is the most common presentation in myiasis patients in Sierra Leone, while the abscess form was the commonest in HIV positive patients.

We recommended HIV tests in every patient with abscess formation in myiasis infestation.

Introduction Sierra Leone is a country in West Africa. It covers a total area of 71,740 km2 (27,699 sq miles) and has a population estimated at 6.5 million. The country has a tropical climate, with a diverse environment ranging from savannah to rainforests.

The Jordanian level III hospital is located in Freetown the capital of Sierra Leone, which offers medical treatment to all United Nations personnel in that area.

The term myiasis was originally proposed by Hope in 1840 and stems from the Greek (myia), meaning a fly (1), as shown in Figure 1.

Figure 1: Dermatobia hominis fly Myiasis is the infestation of body tissue in living vertebrates by the Diptera larvae. Classifications commonly used include cutaneous, enteric, ophthalmic, nasopharyngeal, auricular, oral, and urogenital (2) . The most common type is cutaneous myiasis, as shown in Figure 2 (next page).




Figure 2: Nodular presentation of myiasis

Cutaneous presentations include furuncular, migratory, and wound myiasis, depending on the type of infesting larvae (3). Insects and their larvae occasionally are found in the human body.

The fly deposits its packet of eggs on a mosquito or other blood-feeding insect, which unknowingly transfers the eggs to a warm blooded animal. When the mosquito lands on the skin, the eggs hatch and penetrate the feeding site. The larva develops in the skin for 4 to 14 weeks, reaching a length of about 2 cm, exits, and drops to the ground to pupate. After 14 to 30 days the adult fly emerges and the life cycle resumes (4).It is a common disease in endemic and tropical regions.

Removal of the larvae is the treatment of choice, followed by administration of systemic antibiotics in cases of associated infection (5).

The more frequent trips to tropical and subtropical areas led this study to consider this diagnosis for a non follicular furuncular swelling on exposed skin in a patient who had been in an endemic area. Patients and Methods This is a prospective study done in Sierra Leone, level III Jordanian hospital over a period of one year from August 2001 to August 2002.

A total number of 204 patients participated in this study. Age group varied from 20 to 53 years. Diagnosis of myiasis was mainly based on clinical grounds. A specially designed form was used for each patient separately, which included age, gender, source of referral, presentation and diagnosis and blood samples results, along with their consent to rule out HIV.

Clinical data and laboratory results were analyzed for further evaluation. Results The most common pattern of presentation was the nodular form, n=128 patients, followed by the abscess form, n=57, while the least common pattern was a non specified one in 19 patients.

The most common age group of patients was 30-40 years, followed by age group 20-30 years then age group 40-50 years

while >50 years was the least age group. HIV positive tests were found in 82 (39%).

Abscess formation was the commonest manifestation in patients with HIV, n= 62, followed by the nodular type (n=16). Abscess formation was more in positive HIV males with age group 30-40 years. Discussion All patients who visited the dermatology clinic with the diagnosis of myiasis during the study period were included (n=204). Distribution of the patients according to age is shown in Table 1, which shows that the nodular pattern is the commonest presentation n=128, especially in the age group (30-40) years, which forms n=59 patients, followed by the abscess form, n=57 patients. Male patients were more common than female patients; the ratio was 3:1 as shown in Diagram 1. The commonest age group was 30-40 years, n=96 paients, followed by the age group 20-30 years, n=72, while the least age group was > 50 years.

Further simple analysis was done for the positive HIV patients according to their age which showed that the commonest presentation was the abscess form, n=62 patients, followed by the nodular form, n=16, as shown in Table 3, and was more common in males as shown in Table 4. Myiasis is the infestation of humans with the larvae of the Diptera order of fly species. More than a hundred species of Diptera have been reported to cause human myiasis. Some of the most important are as follows: Dermatobia hominis (human botfly) causes furuncular myiasis, Cordylobia anthropophaga also causes furuncular myiasis, Cochliomyia hominivorax (America) and Chrysomyia bezziana (Africa, Australia, Asia) both cause wound myiasis (6).

A few case reports of myiasis have been published in the medical literature, mostly related to D hominis in travelers returning from the tropical areas of South and Central America(7).

So we conducted our study in Sierra Leone which is considered an endemic area for myiasis which also had a high percentage of positive HIV patients therefore, it was clear from the result of this study, that as the immunity was impaired, the body’s reaction towards abscess formation is the result.

Almost all cases originated in the tropical area of Bolivia in the area of Madidi National Park with an estimated attack rate of 1:190 travelers (8) . The diagnosis is simple once the physician becomes familiar with the typical skin lesions and the specific anamnesis of traveling to an endemic region. With an inexperienced physician, the lesions are frequently misdiagnosed and confused with impetigo, insect bites, folliculitis, and other skin disorders, as happened to many of our patients who were seen by several doctors without a prompt diagnosis (9).




Table 1: Distribution of patients’ presentation according to age

Table 2: Distribution of patients according to age

Diagram 1: Distribution of patients according to sex




Table 3: Distribution of HIV +ve patients’ presentation with myiasis according to age

Table 4: Distribution of HIV +ve patients with myiasis according to sex

Figure 3: Ulcerative abscesses Figure 4: Maggots extracted presented in HIV+ve patient


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No reported studies in the literature had been done to assess the clinical presentation of myiasis in positive HIV patients, hence most of them were discussing the clinical types of myiasis or case reports of patients regardless of the immune status, so this study is the first one that looked for the immunodeficient patients’ clinical pattern with myiasis which showed the abscess pattern is the commonest in HIV positive patients. Figures 3 and 4 show one of the positive HIV patients with abscess formation and the maggots that had been extracted.

The treatment can be conservative or surgical putting a sealing ointment and occluding the breathing opening that causes suffocation of the larva, which causes it to migrate from the skin (10). Brewer et al applied bacon to the larval apertures and caused them to migrate sufficiently far out of the skin to be removed with tweezers, Nunzi, Rongioletti, and Rebora (11, 12).

Injected lidocaine underneath the larva produced sufficient pressure to push the larva out of the skin. Olumide (5) described a method to extract the larva using pressure applied by two wooden spatulas. We treated 76 patients with soft paraffin ointment applied to the lesions without success. A reasonable explanation for our conservative treatment failure is having seen the patients at the late stage of the larva. At an early stage, when it is still small and more superficial, it can be removed non surgically with no difficulty. As the larva matures, it grows numerous concentric rows of backward projecting spines that lock the larva in place and causes difficulty in dislodging it from the skin. In such a case we can use dermoscopic or Doppler ultrasound to confirm the diagnosis (13, 14). From our experience, supported by others, (12) the best method of evacuating the larva is by making a small incision through the opening, inserting a small hemostat, and pulling the larva out; the wound usually heals with no complications. Any attempt to probe the wound with non sterile equipment can result in a bacterial infection, cellulitis, and an abscess formation (15, 16).

We discourage self extraction of the larva, although it is a legitimate possibility when there is no medical facility nearby. An attempt to seal the opening can lead to the death of the larva in situ and formation of a foreign body granuloma, secondary infection, or calcification (11).

Awareness of this skin disorder is the key to correct diagnosis. The treatment is simple and should be done appropriately to evacuate the larva completely. References 1. Hope FW. Insects and their larvae occasionally found in the human body. Trans R Soc Entomol London 1840; 2:256.2. Magnerelli L, Andreadis T. Human cases of furuncular, traumatic and nasal myiasis in Connecticut. Am J Trop Med 1981; 30:864-96.3. Cushing E, Patton W. Studies on higher Dipteria of medical and veterinary importance: Cochliomyia Americana sp, screw-worm fly of the New World. Ann Trop Med 1933; 27: 539-51.

4. Tamir J, Haik J, Orenstein A. and Schwartz E. Dermatobia hominis myiasis among travelers returning from South America. J Am Acad Dermatol 2003; 48:630-2.5. Olumide YM. Cutaneous myiasis: a simple and effective technique for extraction of Dermatobia hominis larva. Int J Dermatol 1994; 33:148-9.6. Maier H, Honigsmann H. Furuncular myiasis caused by Dermatobia hominis, the human botfly. J Am Acad Dermatol 2004; 50(2 Suppl):S26-30.7. Jelinek T, Nothfurft HD, Rieder N, and Loscher T. Cutaneous myiasis: review of 13 cases in travelers returning from tropical countries. Int J Dermatol 1995; 34:624-6.8. Schwartz E, Gur H. Dermatobia hominis myiasis among Israeli travelers to South America: an emerging disease in the Amazon basin of Bolivia. J Travel Med 2002; 9:97-9.9. Brewer TF, Wilson ME, Gonzalez E and Felsenstein D. Bacon therapy and furuncular myiasis. JAMA 1993; 270:2087-8.10. White G, Cook G and Zumla A. Ectoparasites: leeches and leech infestation, myiasis, jigger fleas, scabies, louse infestation. Manson’s tropical diseases. 21st ed. Edinburgh:Elsevier Science Limited; 2003. pp. 1727-32.11 Gordon P, Hepburn N, Williams A and Bunney M. Cutaneous myiasis due to Dermatobia hominis: a report of six cases. Br J Dermatol 1995; 132:811-4.12. Nunzi E, Rongioletti F, Rebora A. Removal of Dermatobia hominis larva. Arch Dermatol 1986; 122:140.13. Quintanilla-Cedillo MR, Leon-Urena H, Contreras-Ruiz J and Arenas R. The value of Doppler ultrasound in diagnosis in25 cases of furunculoid myiasis. Int J Dermatol 2005; 44: 34-7.14. Bakos RM, Bakos L. Dermoscopic diagnosis of furuncular myiasis. Arch Dermatol 2007; 143:123-4.15. Safdar N, Young DK and Andes D. Autochthonous furuncular myiasis in the United States: case report and literature review. Clin Infect Dis 2003; 36:e73-80.16. Maier H, Honigsmann H. Furuncular myiasis caused by Dermatobia hominis, the human botfly. J Am Acad Dermatol 2004; 50(2 Suppl):S26-30.






ABSTRACT A total of 55 (fifty five) patients with chronic urticaria were examined for the presence of hepatitis C virus infection by serological techniques and 1500 control population were tested for the presence of antibody to hepatitis C virus. The aim of this study was to determine whether there is an association between HCV(Hepatitis C Virus) Infection and urticaria.

A retrospective study carried out at Prince Rashid Bin Al-Hassan military hospital in the north region of Jordan over a two year period in 1999-200. Fresh blood samples were drawn from all patients. Serum was separated and routine tests including kidney function tests, liver function tests, complete blood count, erythrocyte sedimentation rate, fasting blood sugar, stool analysis, urinalysis and chest x-ray were also done. Serum was separated and stored at -20 c until it was tested for the presence of anti-hepatitis C antibodies and hepatitis B-surface antigen.

A total of fifty-five patients (23 males, 32 females) were in the study and included all patients with chronic urticaria (urticaria 7 weeks duration) who had been followed up in the dermatology clinic at Prince Rashed Bin Al-Hassan military hospital. None had known hepatic disease prior.

The results obtained in this study , of all fifty-five patients with chronic urticaria, showed negative results for anti-hepatitis C virus, whereas 37 of the 1500 control population showed positive results for anti-hepatitis C virus(2.5%).

This study revealed that there was no increased incidence of hepatitis C virus infection among patients with chronic urticaria.

Key words: Hepatitis C, Chronic urticaria, Viral infection

Introduction Hepatitis C virus (HCV) is the primary cause of transfusion-associated hepatitis and may affect intravenous drug users, organ-transplant recipients and hemodialysis patients, as well as medical personnel. Although routine screening of blood products has substantially reduced the risk of post-transfusion hepatitis the medical establishment continues to grapple with this disease because other modes of transmisson have maintained the overall frequency of HCV infection. Approximately 50% of patients with acute hepatitis C infection will develop chronic disease and about 20% of these will progress to cirrhosis and possible hepatocellular carcinoma.Hepatitis C is caused by RNA virus that enters the body parenterally. The commonest clinical manifestation of chronic hepatitis C is fatigue. Jaundice rarely occurs. The laboratory features resemble those of hepatitis B, although serum aminotransferase levels are generally lower and show a wider fluctuation. Serologic tests for the virus include the enzyme-linked immunosorbent assay (ELISA) and radio-immunoblot assay (RIBA). Viral antigen may be identifed by the polymerase chain reaction test(PCR). The diagnosis of chronic hepatitis C infection is made by liver biopsy in association with one or more of the above blood tests (1).

Chronic urticaria is not uncommon and at times, a challenging problem that causes irritation and discomfort for the patient. Different etiological factors have been described and search for other possible causes continues. Basic routine investigations are usually used for assessment of any patient with chronic urticaria. These include complete blood count, blood sugar, kidney function tests, liver function tests, chest X-ray, stool analysis and urinalysis. Recently, Kazuaya Kanazawa et al. (2) have found that there is a significant association between hepatitis C virus infection and chronic urticaria and there is an increased incidence of hepatitis C virus infection among patients with chronic urticaria. Other research(3), as well as the present study, have not concurred with these findings. Hepatitis C virus infection induces

Association Between Hepatitis C Virus Infection and Chronic Urticaria

Fethi Abed Al-GANI

Senior Lab. Officer Rashid Bin Al-Hassan Military Hospital / Laboratory Department JORDAN, IRBID

Correspondence: Fethi ABDÜLGANI, Phone: 0096277416581,0096226475896 Email: [email protected]

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variable skin manifestations, so we decided to investigate the role of hepatitis C virus infection in a group of our patients with chronic urticaria. Method From March 1999 to March 2001, fifty-five patients with chronic urticaria were studied for hepatitis C virus infection. Twenty-three were males (mean age: 33.3 12.7 years) and thirty-two were females (mean age:35.2 14.4 years). None had known hepatic disease prior. The study included all patients with chronic urticaria (urticaria 7 weeks duration) who had been followed up in the dermatology clinic at Prince Rashid Bin Al-Hassan Hospital. The control group included 1500 apparently healthy persons of both sexes who were among blood donors at Rashid Bin Al-Hassan Hospital.

Fresh blood samples were drawn from all patients. Serum was separated, and routine tests including kidney function tests, liver function tests, complete blood count, erythrocyte sedimentation rate, fasting blood sugar, stool analysis, urinalysis, hepatitis B-surface antigen and chest X-ray were also done. Anti hepatitis C virus antibodies were detected by enzyme immunoassay using the commerical kit murex anti-HCV(Version )-Murex VK 47/48.

Results All of the 55 patients tested for anti-hepatitis C virus antibodies showed negative results. Of the healthy 1500 control group, 37 persons were positive for anti-hepatitis C virus antibodies(2.5%). HBs Ag (Hepatitis B-Surface Antigen) was also negative in all of the 55 patients. Other requested routine tests revealed elevated ALT and AST(Transaminases) in three patients, elevated fasting blood sugar in two patients , anemia in two patients, elevated erythrocyte sedimentation rate in two patients and showed Blastocystis hominis by stool analysis in one patient. Apart from these all the requested tests in the other patients were normal. Table 1 shows the relevant clinical data and laboratory findings. Discussion Urticaria caused by underlying leukocytoclastic vasculitis or panniculitis, palpable purpura and livedo reticularis have been reported as the chief cutaneous manifestations of hepatitis C virus infection(4).

Hepatitis C virus infection has also been found to be the most common cause of mixed cryoglobulinemia which can lead to vasculitis in various organs including the skin (5).

* HCV: Hepatitis C- Virus; ** HBs Ag:Hepatitis B Surface Antigen, ***Erythrocyte Sedimentation Rate, + ALT:Alanine Transaminase; ++ AST:Aspargine Transaminase Table 1: Relevant clinical data and laboratory findings

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Urticarial vasculitis without cryoglobulinemia has been reported to be associated with hepatitis C virus infection and response to interferon treatment has been achieved (2).

Vasculitis has been found in patients with urticaria with or without evidence of systtemic disease. Urticaria associated with HCV infection might represent a particular form of chronic urticaria caused by immune complexes elicited by the HCV infection (6) .

HCV circulates complexed with antibodies in chimpanzees experimentally infected with HCV and levels of circulating immune complexes are high in serum of patients with HCV. These lines of evidence would implicate circulating immune complexes in the pathogenesis of urticaria in patients with HCV infection(7).

Other cutaneous manifestations like porphyria cutanea tarda, lichen planus, erythema nodosum, erythema multiforme, polyarteritis nodosa, prurigo and pruritus have been described to be associated with hepatitis C virus infection (2,3,8,9,10). Kazuya Kanazawa et al(2) found that 19 patients(24%) of the total 79 patients with urticaria that were included in their study, were positive for Anti-HCV. In contrast, the percentage of positive Anti-HCV in their control group was 1.1%. They concluded that hepatitis C virus could be a significant cause of urticaria, especially chronic urticaria. Reichel M.et al (8) conclude that the urticaria was associated with seroconversion to HCV positivity. Llanos F.et al (3) did not observe a higher incidence of hepatitis C virus infection in patients with chronic urticaria; only 1.6% of their patients showed positive anti-HCV which was similar to that found in the general population in France(3). Tarawneh A., et al.(10) also did not observe a higher incidence of hepatitis C virus infection among 55 patients with chronic urticaria. Our results concur with the results of Llanos F.et al (3) and with the results of Tarawneh A.et al (10). No increased incidence of hepatitis C virus infection among patients with chronic urticaria was detected but in our study the finding that was observed was the high rate of anti-hepatitis C virus antibody positive cases among our control group (37 out of 1500) which necessitates more epidemiological studies and screening for this serious problem in the north region of Jordan.

The association of urticaria and hepatitis C remains tenuous. HCV could be a significant cause of urticaria. It was found that there was increased incidence of hepatitis C virus infection among patients with chronic urticaria. The increased rate of anti-hepatitis C virus antibody positive cases among our control group necessitates further epidemiological evaluation for hepatitis C virus infection in the north region of Jordan. Routine laboratory tests done for chronic urticaria are helpful.

References 1. Mitchell J.Schwaber,Abraham Zlotogorski.Dermatologic manifestations of hepatitis C infection.International Journal of Dermatology.;36:251-254. 1997.2. Kanazawa K. Yaoita H. Tsuda F.et al. Hepatitis Cviruse infection in patients with urticaria. J Am Acad Dermatol .;35:195-198. 1996.3 .Llanos F.Peyron NR.Meunier L. et al.Hepatitis C virus infection in patients with urticaria. Jam Acad Dermatol 1998;38:38-616. )4. Pawlotsky JM, Dhumeaux D, Bagot M. Hepatitis C virus in dermatology.Arch Dermatol .;131: 1185-1193. 1995.5. Agnello V,Chung RT, Kaplan LM. A role for hepatitis C virus infection in type 2 cryoglobulinemia N Engl J Med .;327:1490-1495. 1992.6.Berg RE,Kantor GR,Bergfeld WF.Urticarial vasculitis.Int J Dermatol .;27:468-72. 1988. 7. Hijikata M, Shimizu YK,Kato H,et al.Equilibrium centrifugation studies of hepatitis C virus: evidence for circulating immune complexes.J Virol 1993;67:1953-8.8. Reichel M,Mauro TM.Urticaria and hepatitis C .Lancet.;336:822-823. 1990. 9.Chuang Tl, Stitle L, Brashear R. Et al. Hepatitis Cvirus and lichen planus: A case -control study of 340 patients. J Am Acad Dermatol .,41.787-789. 1999.10. Tarawneh A.,Halalat M, Rihani G. Hepatitis C virus infection and chronic urticaria.J of the Royal Medical Services.;8(29):70-71. 2001.




Evaluation of Serum 5’- Nucleotidase, Adenosine deaminase, and Alkaline phosphatase in rheumatoid arthritis patients in Erbil city

ABSTRACT

Background and Objectives: The 5’-nucleotidase ( 5’ NT ), adenosine deaminase ( ADA ) and alkaline phosphatase ( ALP ) are three subclasses of the enzyme class hydrolases. They are present in various organs and many cells and they catalyze the hydrolysis of 5’nucleotide to a ribonucleoside, adenosine to inosine and ammonia and hydrolysis of a number of organic phosphate esters to inorganic phosphate and phosphate radical respectively.

The aim of the present study was to measure the serum activities of these enzymes in healthy individuals and rheumatoid arthritis (RA) patients in Erbil city.

Materials and methods: The study was carried out during the period from March 2008 to April 2009 on 162 (47 males and 115 females) apparently healthy volunteer individuals and 124 (43 males and 81 females) newly diagnosed or known (RA) patients. Serum 5’ NT, ADA and ALP activities were estimated by UV/VIS, method of Giusti and Galnti, method of Belfield and Goldberg respectively.

Results: The mean activities of serum 5’ NT, ADA and ALP were significantly higher in RA patients than those of controls (P < 0.01).

Conclusions: Synovial fluid 5’ NT, ADA and ALP activities increase in RA patients leading to an increase in the serum level of these enzymes, so they can be considered as biomarkers of joint inflammation, particularly for RA.

Key words: 5’ NT , ADA , ALP activities, serum RA

Introduction Rheumatoid arthritis (RA) is a chronic systemic inflammatory autoimmune disorder that causes the immune system to attack the joints(1). In its typical form RA is a symmetric, destructive and deforming polyarthritis affecting small synovial joints with associated systemic disturbance. A variety of extra articular and large features and the presence of circulating antiglobulin antibodies are present in RA(2).

Until now, there was no specific laboratory test for diagnosis of RA, only some traditional tests such as erythrocyte sedimentation rate ( ESR ), C-reactive protein ( CRP ), rheumatoid factor ( FR ), and complete blood count with differential are used. However none of these tests are specific for diagnosis of RA(3).

Many diseases that cause tissue damage result in an increased release of intracellular (non plasma specific ) enzymes into plasma. The serum activity of many of these enzymes are routinely determined for diagnostic purposes in disease of heart, liver, skeletal muscle and others. The serum activity of a specific enzyme frequently correlates with the extent of tissue damage(4).

The enzyme 5’- ribonucleotide phosphohydrolase ( 5’ NTP ) or 5 ‘nucleotidase ( 5’ NT ) is a glycoprotein that acts only on nucleoside-5-phosphates such as adenosine - 5’-phosphate ( Adenosine-5’-monophosphate ( AMP = adenylic acid ) releasing inorganic phosphate and a nucleoside adenosine) (5). This enzyme belongs to the hydrolase class of enzymes and its classification number is ( EC 3.1.3.5 ) and catalyzes the following reaction : 5 ‘ AMP + H2O Adenosine + Orthophosphate Adenosine deaminase (ADA) is an enzyme involved in the metabolism of purine through the salvage pathway, and catalyzes the irreversible hydrolytic cleavage of deoxy adenosine to deoxy inosine and ammonia (1). Adenosine deaminase is also a glycoprotein, widely distributed in human tissues and has two iso-enzymes (ADA-1 and ADA-2 ) with different optimal pH (2). During the last decade, different disorders have been investigated and revealed elevation in serum ADA activity in different diseases (3) . This enzyme belongs to the hydrolase class of enzymes and its classification number is ( EC 3.5.4.4 ) and catalyzes the following reaction : Adenosine + H2O Inosine +NH3

Sardar Nouri AHMAD (1) Tayfoor Jalil MAHMOUD (2) Hamid G. HASSAN (3)

(1) Clinical Biochemistry, Lecturer, Dept. of Clinical Biochemistry, College of Medicine, Hawler Medical University, Hawler, Iraq (2) Clinical biochemistry, Assistant professor, Dept. of Clinical Biochemistry, College of Medicine, Hawler Medical University, Hawler, Iraq (3) Clinical biochemistry, Professor, Dept. of Biochemistry, Ibn-Al-Haitham College, Baghdad University, Baghdad, Iraq

Correspondence: Hamid G. Hassan Dept. of Biochemistry / Ibn-Al-Haitham College / Baghdad University / Baghdad / Iraq Email: [email protected]




Alkaline phosphatase (ALP) or orthophosphoric monoester phosphohydrolase -alkaline medium is a group of enzymes that catalyze the hydrolysis of a number of organic phosphate esters, liberating inorganic phosphate and the organic radical at alkaline pH (6). Alkaline phosphatase (class hydrolase) is present in all mammalian tissues, especially at or in the cell membrane (7).

Patients with bone disease accompanied hypophosphatasia prove that the ALP is needed for normal bone mineralization by calcium and phosphate (8).

Normal serum ALP consists of a mixture of iso-enzymes derived primarily from liver, intestine, and bone (9). Serum activity of ALP increases in bone inflammation, osteomalacia, osteoporosis and osteosarcoma (10). This enzyme belongs to the hydrolase class of enzymes and its classification number is (EC 3.1.3.1 ) and catalyzes the following reaction : Organo phosphate + H2O Organic compound + Inorganic phosphate Several investigators reported that there is a relationship between raised serum 5’ NT activity and the incidence of RA and suggested that this enzyme can be used as a biomarker of RA (7, 8) . To our knowledge, no reports have dealt with serum activities of 5 ‘ NT, ADA and ALP in RA around Erbil city so the present study may be of value in this regard. Materials and Methods SubjectsThis study was conducted from March 2008 to April 2009 at the Department of medical biochemistry, College of medicine, Hawler medical university, Erbil, Iraq.

The present investigation was carried out on (286) volunteers, which were divided into two groups:

A- Group 1 (Control group): One hundred and sixty two randomly selected subjects (47 males and 115 females) were served. All are apparently healthy volunteers. B-Group 11 (RA patient group): One hundred and twenty four (43 males and 81 females) RA patients (diagnosed by consultants) participated in the study. Details concerning both groups are shown in Table 1.

SamplesSix to eight ml of peripheral blood samples were drawn early morning (12 hours fasting) from controls and RA patients using disposable syringes. The samples were transferred into

glass tubes, sitting for 30 minutes for clotting and centrifuged at 900xg for (15) minutes. The separated serum was used for measurement of serum 5’ NT, ADA, and ALP activities on the same day of the estimation.

Methods Serum 5’ NT activity was estimated according to a method described by Tietz (6).

This method depends on the releasing of phosphate and adenosine by incubating the serum with the substrate (5 ‘ monophosphate) at optimum condition ( T 37 0 C and pH 7.5 ) for half an hour. Serum proteins are precipitated by tri-chloroacetic acid, and phosphate is converted to phosphomolybdate (Mo V1 ) complex by addition of sodium molybdate. The addition of p-methylaminophenol sulphate (metol compound) reduces (Mo V1) in the complex to yield an intensely blue-colored phosphomolybdate complex (Mo V ). The absorbance of the solution is measured at 700 nm and is proportional to the serum phosphate concentration.

Serum ADA activity was determined for the two groups according to the method of Giusti and Galanti (11). In this method serum ADA is easily assayed by measuring the amount of ammonia formed during the incubation for 60 minutes. Ammonia reacts in the presence of phenol-nitroprusside as a catalyst with sodium hypochlorite at pH 5 producing blue indophenol. The ammonia concentration is directly proportional to the absorbance of the indophenol at 630 nm.

Serum ALP activity was measured for the two groups by an enzymatic colorimetric method of Belfield and Goldberg (12).

Colorimetric determination of serum ALP activity was performed according to the following reaction: . ALP ( pH 10 ) Phenylphosphate Phenol + Orthophosphate The liberated phenol was measured in the presence of 4-aminoantipyrene and potassium ferricyanide. The presence of sodium arsenate in the reagent stops the enzymatic reaction. Results Table 2 provides the mean serum 5 ‘ NT activity in both groups. The results obtained reveal that the mean serum 5 ‘NT activity was (22.87 ± 10.21 IU / L) and the range was (8.9-73.1 IU / L) in RA patients. The activity was seen to exceed significantly (P < 0.01) those obtained in the normal group, (mean = 7.71 ± 4.21 , and range = 1-22.3 IU / L).

Table 1 : Details of number, age, sex and BMI of both groups




Serum 5 ‘ NT activity in RA patients was found to be three times higher than that of normal activity ( 3: 1). The activity shows a 79.5% increment in RA serum than normal activity. However there was no significant difference (P>0.01) between males and females in both groups. Table 3 shows the mean serum ADA activity in both groups. The data obtained indicates that the mean serum ADA activity was (24.83 ± 7.72 IU / L), (Mean ± SD) in RA patients. This value exceeds significantly (P < 0.01) that obtained in the normal group (10.26 ± 2.48 IU / L).

Serum ADA activity in RA patients compared to normal were two and half times higher (2.5: 1), and it was increased by about 64.5 % in RA patients compared with normal activity. However there was no significant difference (P > 0.01) between males and females in both groups.

Table 4 provides the mean serum ALP activity in both groups. The results obtained reveal that the mean serum ALP activity was (134 .19 ± 6.95 IU / L), (Mean ± SD) in RA patients. The activity of ALP enzyme was found to be significantly higher (P<0.01) than that obtained in normal group (90.38 ± 5.9 IU / L), and it was greater (by one and half times) with 59.5% than

Table 2 : Details 5 ‘ NT activity (Mean ± SD) in normal and RA Groups

Table 3: Details ADA activity ( Mean ± SD ) in both groups

Table 4: The Mean±S.D of S. ALP activity in normal and RA groups




that of the normal group.

However there was no significant difference (P > 0.01) between males and females in both groups. Discussion The mean serum activity of 5 ‘NT in RA patients was significantly higher than that of control subjects (P < 0.01). This finding is in agreement with the results obtained by Thompson et al (8).

The serum 5 ‘ NT activity comes mostly from the liver, and could be used as a biomarker of general inflammation, whereas 5 ‘ NT in the synovial fluid is mostly produced locally, and could be used as a biomarker of joint inflammation, particularly for RA (6).

The mean serum activity of ADA in RA patients was significantly higher than that of control subjects (P < 0.01). The similar results were obtained by Sari et al (12) and Komar et al (13).

It is well established that the serum levels of ADA reflect the activity of stimulated T-lymphocytes and its level is raised whenever cell mediated immunity is stimulated. Adenosine activity has been shown to be increased in disease characterized by T-lymphocyte proliferation and activation. Therefore.it has been considered as a non specific marker for T-cell activation (14).

In another study by Surekha et al (15), they estimated serum ADA activity in RA patients and found that the mean serum ADA activity in RA patients was significantly higher (P < 0.001) than that of controls. The authors suggested that this result is due to the immunological and inflammatory reaction that plays a pivotal role in the initiation and perpetuation of RA. Similar results were obtained by Spooner et al (16) and Aida(17).

The mean serum ALP activity of ALP in RA patients was significantly higher (P < 0.01) than that of controls. Similar results were obtained by Aida (17)

Namke et al(18) who conducted a study to evaluate the serum activity of ALP in RA patients and reported an increase in activity and suggested that bone-type ALP derived from the synovial tissue may contribute to the raised activity in RA patients.

The mean BMI (Kg/M2) in RA patients was significantly lower (P<0.01) than that of controls, and this is due to normocromatic anemia which is one of the major symptoms of RA(19). Similar results were obtained by Malgorzata (20).

The ratio of RA patients in females to males is about 2:1, while in most research the ratio is about 3:1, and this is due to a difference in sex hormones (21).

Conclusion As a result of this study, the following conclusions are drawn:

1- The mean serum activities of 5 ‘ NT, ADA and ALP in RA patients were significantly higher than that of controls so measurement of the serum activities of these enzymes may be used as a biomarker in the diagnosis of RA.2- Estimation of the serum activities of 5 ‘ NT, ADA and ALP are easy and reliable methods.3- The most appropriate conditions for optimum activities of 5 ‘ NT, ADA and ALP were at T 37 0 C, pH 7.5, T 370 C, pH 6.5 and T 37 0, pH 10 respectively. References 1-C Kieth Stone and Robert L. Humphries Current emergency: Diagnosis and treatment , 5th ed., Medical application division , 2004 .2-Parveen Komar , and Mkieaide Clinical medicine (2008). 6th ed., London.3-Rindfleisch JA and Muller D. (2005). Diagnosis and management of rheumatoid arthritis. A physician: 72(6):1037-1047. 4-Vasudevan DM , and Sreekumaris Textbook of biochemistry for medical students , 4th ed, . Japee brothers , New Delhi, India , 2005 .5-Varley Harold et al Practical clinical biochemistry , 5th ed. , Vol . 1 , London , 1980 6-Tietz NW Textbook of clinical chemistry , second edition., W.E.Sounders , London , 1986 .7-Joseph SA, and Roger G. Clinical chemistry : Principles and procedures, 4th ed., Little Brown, Boston, Mass., USA, 1980 .8-Thompson PW , Jones DD , and Moss DW The source and significance of raised serum enzymes in RA .J .Med. 1999 ; 76 : 869-779-Kaplan LA, and Pesce AJ. Clinical chemistry : Theory, analysis and cortrelation, 2nd ed, .Pub. C.V. Mosby company , USA , 1989 .10-Liu PP , Leng KS et al. Bone specific ALP in plasma as tumor marker of osteosarcoma Oncolog . 1996 ; 53 : 275-80 11-Giusti J , and Galanti B. Estimation of serum adenosine deaminase Mal.Inf. Paris 1968 ; 20 : 980 12-Sari RA et al. Correlation of serum levels of ADA activity and its iso-enzymes disease activity in RA .Clin. Exp. Rheimatol . 2003 ;21 (1).13-Kumar R et al. Study of ADA activity in various arthritic conditions (1994). Vol,1, No.2;92-4.14-Hovi T et al Role of ADA in lymphocyte proliferation Clin. Exp.Immunol. 1976 ; 23 : 39515-H. Surekha et al. (2006). Lymphocyte ADA activity in rheumatoid arthtritis Clin. Exp.Immunol. 95:12316-Schgal VN;Bhattachary SN; andShahi. (1992). Lymphocyte ADA activity in lyprosy during and after treatment of reaction. Clin. Exp. Dermatol 17:20-23.17-Aida S. Alkaline phosphatase iso-enzyme activity in RA and hepatobiliary enzyme dissociation and relation to disease activities .Ann .Rhem. Disease 1993 ; 52 (7) : 511-16(continued page 36)




The effect of Lidocaine with Fentanyl, or Midazolam on cardiovascular responses during Endotracheal intubation in hypertensive patients on Beta-blocker

ABSTRACT

Background and Objectives: Endotracheal intubation (ETT) is always associated with marked increases in heart rate and systemic blood pressure. These hemodynamic changes are well tolerated in normotensive individuals, but are of greater significance in patients with cardiovascular disorders, and have been recognized as a potential source of a number of complications. This single blind study was done to evaluate and compare the efficacy of Lidocaine alone, Lidocaine with Fentanyl, or Lidocaine with Midazolam in attenuating the hemodynamic responses to endotracheal intubation in hypertensive patients on Beta-blocker.

Methods: Sixty one hypertensive patients were divided into three groups: Group L (receiving Lidocaine alone); included 11 controlled hypertensive patients (5 male, and 6 female).

Group F+L (receiving Fentanyl+Lidocaine); included 32 controlled hypertensive patients (12 male, and 20 female).

Group M+L (receiving Midazolam+Lidocaine); included 18 controlled hypertensive patients (8 male, and 10 female).

Results and Conclusion: Midazolam+Lidocaine combination was more effective in controlling and stabilizing blood pressure (MBP, SBP, and DBP) than Lidocaine alone and Fentanyl+Lidocaine combination after applying endotracheal intubation. Midazolam+Lidocaine combination have better effect in controlling pulse rate than Lidocaine alone, and Fentanyl+Lidocaine combination after applying endotracheal intubation.

Key words: Lidocaine, Midazolam, Fentanyl, endotracheal intubation

Dr. Kawa Dizaye Dr. Allaa M. Yousif, Dr. Muhamed Aydin

Correspondence: Dr. Kawa Dizaye Assist. Prof. of Pharmacology Head of department of Pharmacology College of medicine, Hawler medical University, Iraq Tel: 009647504452392 Email: [email protected]

Introduction Airway maintenance is essential following induction of anesthesia, as nearly all general anesthetics reduce or eliminate both ventilatory drive and the reflexes that maintain airway patency. Therefore, ventilation generally must be assisted or controlled for at least some period during surgery. Endotracheal intubation was introduced by Kuhn in the early 1900s and has been a major reason for a decline in the number of aspiration deaths during general anesthesia (1, 2). Endotracheal intubation not only provides protection for the airway, but it also permits manipulation of ventilation as required (3, 4).

Stimulation of the upper airways is associated with a reflex increase in sympathetic activity and increased catecholamine secretion. Consequently, arrhythmias may occur during laryngoscopy, bronchoscopy, and endotracheal intubation (5). Endotracheal intubation and administration of inhalation agents are common procedures during general anaesthesia (6, 7). However, induction of anesthesia and endotracheal intubation are often a period of hemodynamic instability for hypertensive patients, regardless of the level of preoperative blood pressure control. Many patients with hypertension display an accentuated hypotensive response to induction of anesthesia, followed by an exaggerated hypertensive response to endotracheal intubation (8). Translaryngeal intubation of the trachea stimulates laryngeal and tracheal sensory receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline). This sympathetic stimulation results in tachycardia and elevation in blood pressure (9, 10). In normotensive patients, this rise is approximately 20 to 25 mm Hg; it is much greater in hypertensive patients (10, 11, 12). These hemodynamic changes are well tolerated in normotensive individuals, but are of greater significance in patient with cardiovascular diseases, that have been recognized as a potential source of a number of complications such as; increase in blood




pressure, increase in heart rate, tachyarrhythmia, cerebral haemorrhage, left ventricular failure, and myocardial ischemia (6, 13, 14, 15).

Many drugs and techniques have been used to prevent the hemodynamic responses induced by laryngoscopy and endotracheal intubation (16, 17), such as; Deep inhalational anaesthesia (18), antihypertensive drugs (Angiotensin-converting enzyme inhibitors [ACE-I], Beta-Blockers, Calcium channel blockers, (19, 20, 21), peripheral vasodilators (22), use of large doses of opiates notably fentanyl and alfentanyl (23, 24), alpha-2-agonist (25,26), .i.v administration of Lidocaine (14,27,28), topical Lidocaine spray(29,30) and benzodiazepine (13, 31, 32). All have been used but with some disadvantages related to either cardiovascular or respiratory depression.

The aim and objective of the study is to evaluate and to compare the efficacy of (Lidocaine), (Fentanyl+Lidocaine), or (Midazolam+Lidocaine) in attenuating the hemodynamic responses to laryngoscopy and endotracheal intubation in ASA (American Society Of Anestheiologists) class II patient (hypertensive patient treated with b blocker).

Materials and Methods STUDY DESIGN This study is a prospective, single blind, comparative study. It was carried out in the General operation theater in; Rizgary Teaching Hospital, Erbil Teaching Hospital, Shaqlawa Hospital, Private Hawler Hospital, and Private Resul Hospital, from January, 2008 to April, 2009 after obtaining scientific Committee approval from the college of medicine. A total of (61) hypertensive patients (patients were controlled hypertensive and they were on cardio-selective b blocker {Atenolol}), who belonged to ASA class II category, scheduled for elective surgery were taken into this study.

PATIENTSSixty one (61) patients were divided into three groups:1-Group L (receiving Lidocaine alone); included 11 controlled hypertensive patients (5 male, and 6 female).2-Group F+L (receiving Fentanyl+Lidocaine); included 32 controlled hypertensive patients (12 male, and 20 female).3-Group M+L (receiving Midazolam+Lidocaine); included 18 controlled hypertensive patients (8 male, and 10 female).

METHODS1. The patients were kept fasting from 2200 the night prior to surgery. 2. All the patients received no premedication neither at the night before surgery nor in the morning before surgery. 3. All the patients received their morning dose of beta blocker (Atenolol) before surgery.4. Routine pre-operative check-up was done in all patients and baseline vitals were noted.

5. In the Operation Theater, intravenous line was started.6. Patients were attached to the following monitors: ECG, Noninvasive blood pressure monitor, pulse oximeter. 7. The baseline values (pre-anesthetic reading) for; mean arterial pressure (MAP) {MAP=DBP+1/3(SBP-DBP)}, systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were recorded. 8. Patients were allocated into three main groups. Group L: receiving Lidocaine alone, Group F+L: receiving, Fentanyl+Lidoocaine andGroup M+L receiving Midazolam+Lidocaine before the Endotracheal intubation to prevent post-intubation hemodynamic change.9. Inducing agents: Anesthesia was induced by Thiopental (given in a dose of 3-5 mg/kg) with (Lidocaine, Lidocaine+Fentanyl, or Lidocaine+Midazolam), then Suxamethonium was given in a dose 1-1.5 mg/kg (Suxamethonium given approximately 30-60 second before ETT), and induction was confirmed by loss of eyelash reflexes.10. Lidocaine, given in a dose of 1.5 mg/kg (given 2 minutes prior to intubation) while Fentanyl was given in a dose of 2-5 mcg/kg (given 2-3 minutes prior to intubation) and Midazolam given in a dose of 0.1-0.3 mg/kg (given 1 minute prior to intubation). 11. The hemodynamic variables; mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were recorded after giving inductive anesthetic agents and trial drugs (before performing endotracheal intubation). 12. Then laryngoscopy was performed by professional anesthetist with a standard Macintosh laryngoscope blade and trachea intubated with an appropriate size cuffed endotracheal tube and ventilated with oxygen, and halothane. 13. Then hemodynamic variables; mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were recorded after 2,5 and 5 minutes after performing endotracheal intubation

STATISTICAL ANALYSISAll the results were expressed as mean ± SE. Hemodynamic variables in the present study were analyzed statistically by using ANOVA Test. P values < 0.05 were considered significant.

Results Change in mean blood pressure (MBP): MBP in (Lidocaine) group in the pre-anesthetic period was 109.6±2.58 (basal value), after giving Lidocaine and anesthetic inducing agents MBP was decreased non-significantly to 99.5±3.23. Meanwhile at 2.5 minute after ETT, MBP was increased non-significantly to 107.8±5.48, but it did not reach the basal value. At 5 minutes after ETT, MBP was decreased significantly to 92±4.74, compared to basal value (Table 1) and (Figure 1).

M I D D L E E A S T J O U R N A L O F I N T ER N A L M ED I CI N E • VO LU M E 2 , I SSU E 3 2�


MIDDLE EAST JOURNAL OF INTERNAL MEDICINE VOLUME4, ISSUE 1

MBP in the (Lidocaine+Fentanyl) group in the pre-anesthetic period was 109.28±1.28 (basal value), after giving (Lidocaine+Fentanyl) and anesthetic inducing agents, MBP was decreased significantly to 95.37±2.88. Meanwhile at 2.5 minutes after ETT, MBP was increased non-significantly to 105.56±3.05, but it did not reach the basal value. At 5 minutes after ETT, MBP was decreased significantly to 90.12±2.57, compared to the basal value.(Table 1) and (Figure 1).

MBP in the (Lidocaine+Midazolam) group in the pre-anesthetic period was 107.3±1.78 (basal value), after giving (Lidocaine+Midazolam) and anesthetic inducing agents, MBP was decreased non-significantly to 101.4±2.93. Meanwhile at 2.5 minutes after ETT, MBP was decreased non-significantly to 100.7±2.59. At 5 minutes after ETT, MBP was decreased significantly to 98±2.62, compared to the basal value (Table 1) and (Figure 1 - next page).

Change in pulse rate (PR)Pulse rate in the (Lidocaine) group in the pre-anesthetic period was 82.9±4.22 (basal value), after giving Lidocaine and anesthetic inducing agents, PR was increased non-significantly to 85.9±4.94, subsequently at 2.5 minutes after ETT, PR was increased non-significantly to 87.1±5.39, it reached a value higher than the basal value. At 5 minutes after ETT, PR was decreased non-significantly to 79.3±4.83, compared to the basal value (Figure 2).

Pulse rate in the (Lidocaine+Fentanyl) group in the pre-anesthetic period was 81.4±2.69 (basal value), after giving (Lidocaine+Fentanyl) and anesthetic inducing agents, PR was decreased non-significantly to 79.6±2.62, subsequently at 2.5 minutes after ETT, PR was increased non-significantly to 83.8±2.72, it reached a value higher than the basal value. At 5 minutes after ETT, PR was decreased non-significantly to 76.6±2.34,, compared to the basal value (Figure 2).

Pulse rate in the (Lidocaine+Midazolam) group in the pre-anesthetic period was 85.6±2.52 (basal value), after giving (Lidocaine+Midazolam) and anesthetic inducing agents, PR was increased non-significantly to 89±3.41, subsequently at 2.5 minutes after ETT, PR was decreased non-significantly to 87.8±3.68. At 5 minutes after ETT, PR was decreased non-significantly to 82.2±3.5, compared to the basal value (Figure 2).

Comparison Haemodynamic variables among the three groups:The percentage (%) of change in Mean (MBP, SBP, DBP and PR) in each group at each measuring point compared with its previous value, respectively are shown in figures 3, 4, 5, & 6: (next pages). Discussion Endotracheal intubation is stressful noxious powerful stimuli. It stimulates laryngeal and tracheal sensory receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline), and this increase in the sympathetic amines may cause serious complications especially in patients with cardiovascular diseases (9, 10). Reflex response to endotracheal intubation is mainly due to sympathetic stimulation causing increases in blood pressure, increases in heart rate and tachyarhythmia.

In healthy patients, these responses are significantly high but are generally well tolerated whereas in patients with cardiovascular diseases, many complication may occur such as; increase in blood pressure, increase in heart rate, tachyarrhythmia, cerebral haemorrhage, left ventricular failure, and myocardial ischemia (13, 14) . Haemodynamic variables in Lidocaine Group:MBP, SBP, and DBP in the Lidocaine group were non-significantly decreased after giving Thiopental, Lidocaine, and muscle relaxant (Suxamethonium). This reduction in MBP, SBP, and DBP at this period might be due to that, Lidocaine has both myocardial depression property and vasodilatation effects (33, 2), besides that, Thiopental has circulatory depressant effects (8). At 2.5 minutes after ETT, MBP, SBP, and DBP were non-significantly increased,. The reasons behind elevation of the MBP, SBP, and DBP at this point might be due to that, ETT of the trachea stimulating laryngeal and tracheal sensory receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline). This sympathetic stimulation results in tachycardia and elevation in blood pressure (9, 10), and in addition, Lidocaine at 1.5 mg/kg IV bolus dose (the dose used in this study) has minimal depressive effect on the cardiovascular system, and cannot completely attenuate hemodynamic response to ETT (13), and subsequently at 5 minutes after ETT MBP, SBP, and DBP were significantly

(Note: a, b, and c are sign of Significance).Table 1: Mean blood pressure (mm of Hg) in the pre-anesthetic period, in Pre-ETT period after giving Trial drug and anesthetic inducing agents (after induction), and at 2.5, 5 minutes after endotracheal intubation (Post-ETT) in (L), (L+F), and (L+M) group




Figure 1: Blood pressure change with time in (L), (L+F), (L+M) group

decreased, because the action of Lidocaine remains up to 20 minutes (34). Beside that the released sympathetic amines decreased at this point, either by; simple diffusion away from the receptor site, diffusing out of the cleft (with eventual metabolism in the plasma or liver), and reuptake into the nerve terminal (1, 35). From this study it was found that the MBP, SBP, and DBP in the Lidocaine group were un-stable, and weakly controlled throughout the measurement period. From this result it was clear that, Lidocaine was slightly effective in controlling MBP, SBP, and DBP following endotracheal intubation. This result was in agreement with studies done by Chraemmer et al (1986) (36), Miller and Warren (1990) (28) ,Pathak et al (1990) (37), Allen et al (1991) (23), Helfman et al (1991) (38), Singh et al (1995) (39), Kindler et al (1996) (40), Vandenberg et al (1997) (41), Pokharel (2004) (14) , Woon et al (2006) (10) , and Malde & Sarode (2007) (42), while disagree with studies done by Abou Madi et al (1977) (27), Tam et al (1985) (43) , and Wang et al (2003) (44).

PR was non-significantly increased after giving Thiopental, Lidocaine, and muscle relaxant. This elevation in PR at this period might be due to the fact that Lidocaine produces vascular smooth muscle relaxation, which causes vasodilatation. This vasodilatation leads to a fall in blood pressure, and a fall in the blood pressure causes reflex increase in the heart rate to compensate the fall in blood pressure (1, 8). After this at 2.5 minutes after ETT PR was non-significantly increased. This elevation in PR at this point might be due to the fact that ETT of the trachea stimulates laryngeal and tracheal sensory receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline). This sympathetic stimulation results in tachycardia and arise in blood pressure (9, 10), and also because Lidocaine in a 1.5 mg/kg IV bolus dose (the dose that used in this study) has minimal depressive effect on the cardiovascular system (13), and then PR at 5 minutes after ETT was non-significantly decreased, because released sympathetic amines were decreased either by; simple diffusion away from the receptor site, diffusing out of the cleft (with eventual metabolism in the plasma or liver), and reuptake into the nerve terminal (1, 35).




Figure 2: Pulse Rate (beat/minute) in pre-anesthetic period, in Pre-ETT period after giving Lidocaine and anesthetic inducing agents (after induction), and at 2.5, 5 minutes after endotracheal intubation (Post-ETT) in (L), (L+F), and (L+M) group

From the present study it was clear that, Lidocaine was slightly more effective in controlling PR following endotracheal intubation. This was in agreement with studies done by Helfman et al (1991) (38), Bruder et al (1992) (45) ,Feng et al (1996) (46) , Woon et al (2006) (10), Malde & Sarode (2007) (42).

Haemodynamic variables in (Lidocaine+Fentanyl) Group:MBP, SBP, and DBP in Lidocaine+Fentanyl group were significantly decreased after giving Thiopental, Lidocaine+Fentanyl, and muscle relaxant. This reduction in MBP, SBP, and DBP at this period might be due to the fact that, Lidocaine has both myocardial depression and vasodilatation action which leads to a fall in the blood pressure (2, 33) in addition to the fact that IV administration of Fentanyl is associated with a vagus-mediated bradycardia (47, 48, 8). Also Fentanyl produces peripheral vasodilatation by depressing vasomotor centers in the medulla and leads to a decrease in blood pressure, besides the above responses, Thiopental has circulatory depressant effects (8),. Meanwhile at 2.5 minutes after ETT, MBP, SBP, and DBP were non-significantly increased, the reasons for this elevation of MBP, SBP, and DBP at this point might be due to the fact that ETT

of the trachea stimulates laryngeal and tracheal sensory receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline). This sympathetic stimulation results in tachycardia and arise in blood pressure (9, 10), and Lidocaine in a 1.5 mg/kg IV bolus dose (the dose used in this study) has minimal depressive effect on the cardiovascular system, and can not completely attenuate hemodynamic response to ETT (13) Additionally direct depressant effects of Fentanyl on the myocardium are minimal (1), therefore Lidocaine+Fentanyl cannot completely attenuate hemodynamic response to ETT. Subsequently at 5 minutes after ETT MBP, SBP, and DBP were significantly decreased, because Fentanyl redistributes away from the central nervous system after 13 minutes (49), also because the released sympathetic amines were decreased either by simple diffusion away from the receptor site, diffusing out of the cleft (with eventual metabolism in the plasma or liver), and reuptake into the nerve terminal (1, 35). From these results it was shown that; MBP, SBP, and DBP in the Lidocaine+Fentanyl group were unstable, and weakly controlled throughout the measurement period. From this study it was clear that Lidocaine+Fentanyl were slightly more effective in controlling MBP, SBP, and DBP following




Figure 3: Percentage of change in mean blood pressure throughout measurement period in each group

endotracheal intubation. This was in agreement with studies done by Helfman et al (1991) (38), Abdel-Razek, and Attar (1995) (50), Salihoglu et al (2002) (51), while it disagrees with studies done by Young et al (1992) (52), Mi,Wei-Dong (1997) (53), Kim et al (2006) (54).

PR in the Lidocaine+Fentanyl group was non-significantly decreased after giving Thiopental, Lidocaine+Fentanyl, and muscle relaxant. This reduction in the PR at this period might be due to the fact that, Fentanyl produces bradycardia by a specific stimulant effect on the central nuclei of the vagus nerves (17, 55). Then PR was non-significantly increased at 2.5 minutes after ETT. The reasons for this elevation in PR at this point might be due to the fact that ETT of the trachea stimulates laryngeal and tracheal sensory receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline). This sympathetic stimulation results in tachycardia and arise in blood pressure (9, 10), in addition to the fact that direct depressant effects of Fentanyl on the myocardium are minimal (1), and also because Lidocaine in a 1.5 mg/kg IV bolus dose (the dose that used in this study) have minimal depressive effect on the cardiovascular system (13). Therefore Lidocaine+fentanyl can not totally prevent tachycardia produced by increased adrenaline and noradrenaline concentaration produced by ETT, and subsequently PR was non-significantly decreased at 5 minutes after ETT, because the released sympathetic

amines were decreased either by; simple diffusion away from the receptor site, diffusing out of the cleft (with eventual metabolism in the plasma or liver), and reuptake into the nerve terminal (1, 35).

From these results it was found that the Lidocaine+Fentanyl were slightly more effective in controlling PR following endotracheal intubation. This was in agreement with studies done by Helfman et al (1991) (38), Feng et al (1996) (46), Salihoglu et al (2002) (51), and in disagreement with studies done by Kay et al (1985) (56), and Malde & Sarode (2007) (42).

Haemodynamic variables in (Lidocaine + Midazolam) Group:MBP, SBP, and DBP in the Lidocaine+Midazolam group were non-significantly decreased after giving Thiopental, Lidocaine+Midazolam, and muscle relaxant. This reduction in MBP, SBP, and DBP at this period might be due to the fact that, Lidocaine has both myocardial depression and vasodilatation action s which lead to a fall in blood pressure (33, 2), Additionally Midazolam produces decreases in systemic vascular resistance and reduction in blood pressure when large doses are administered. Besides the above responses, Thiopental has circulatory depressant effects (8). Then at 2.5 minutes after ETT MBP was non-significantly decreased, SBP was significantly decreased and DBP was




Figure 4: Percentage of change in systolic blood pressure throughout measurement period in each group

very slightly (negligibly) non-significantly increased (increased from previous value by 0.8 %). The reason for this reduction of MBP, SBP, and DBP at this point, instead of high elevation as in the (Lidocaine) and (Lidocaine+fentanyl) groups, is that Midazolam has the ability to abolish the adverse haemodymanic response and to modify the increase in plasma catecholamine concentrations associated with laryngoscopy and tracheal intubation (57). Meanwhile at 5 minutes after ETT MBP, and SBP were significantly decreased, and DBP was non-significantly decreased. This reduction at this point might be due to the fact that, Midazolam produces; decreases in systemic vascular resistance and reduction in blood pressure when large doses are administered.

From these results it was shown that; MBP, SBP, and DBP in the Lidocaine+Midazolam group were stable, and controlled. From this study it was clear that Lidocaine+Midazolam were highly effective in controlling MBP, SBP, and DBP following endotracheal intubation. This was in agreement with studies done by; Kawar et al (1985) (32), Chraemmer-Jorgensen et al (1992) (57), Chytra et al (1997) (58), while in disagreement with studies done by Celleno and Capogna (1993) (59), and Koju (2004) (13).

Pulse rate in the Lidocaine+Midazolam group was non-significantly increased after giving Thiopental, Lidocaine+Mdazolam, and muscle relaxant. This elevation in PR at this period might be due to the fact that Lidocaine produces vascular smooth muscle relaxation, which causes vasodilatation. This vasodilatation leads to a fall in blood pressure, and a fall in the blood pressure causes reflex increase in pulse rate to compensate the fall in blood pressure (1, 8), Additionally Midazolam decreases vagal tone (i.e. drug-induced vagolysis) (8), after that at 2.5 minutes. After ETT PR was non-significantly decreased (but at the same time it was higher than basal value), The reason for this reduction in PR at this point (if we compared it with the previous value) might be due to the fact that Midazolam produces transient drug-induced vagolysis and transient depression of the baroreceptor mediated heart rate response following IV administration (13) and the reason for its elevation (if we compared it with basal value) at this point might be due to the fact that; ETT of the trachea stimulates laryngeal and tracheal receptors, resulting in marked increase in the elaboration of sympathetic amines (adrenaline and noradrenaline). This sympathetic stimulation results in tachycardia and arise in blood pressure (9, 10), and subsequently PR was non-significantly decreased at 5 minutes after ETT, because released sympathetic amines were

M I D D L E E A S T J O U R N A L O F I N T ER N A L M ED I CI N E • VO LU M E 2 , I SSU E 32�



Figure 5: Percentage of change in diastolic blood pressure throughout measurement period in each group

decreased either by simple diffusion away from the receptor site, diffusing out of the cleft (with eventual metabolism in the plasma or liver), and reuptake into the nerve terminal (1, 35).

From this result it was shown that the Lidocaine+Midazolam was slightly effective in controlling PR following endotracheal intubation. This was in agreement with studies done by Forster et al (1980) (60), Kawar et al (1985) (32), Celleno, and Capogna (1993) (59), and Koju (2004) (13), while in disagreement with studies done by Berggren, and Eriksson (1981) (61). Conclusion Midazolam+Lidocaine combination was more effective in controlling and stabilizing blood pressure (MBP, SBP, and DBP) than Lidocaine alone and a Fentanyl+Lidocaine combination after applying endotracheal intubation. And Additionally Midazolam+Lidocaine combination has better effect in controlling pulse rate than Lidocaine alone, and Fentanyl+Lidocaine combination after applying endotracheal intubation.

References 1. Goodman, L. S. & Gilman, A. G. (2006): The Pharmacological Basis of Therapeutics. 11’th Edition. Chapter 6, 13, 14, 16, 21. McGraw-Hill company. ISBN: 0-07-142280-3.

2. Longnecker, D. E., Brown, D. L., Newman, M. F., Zapol, W. M.(2008): ANESTHESIOLOGY. Chapter 40, 41, 42, 44, 49, 51, 55. McGraw-Hill Companies, New York. 3. Filipi, C. J., Fitzgibbons, R. J., Salerno, G. M. (1992): Laparoscopic herniorrhaphy. Surg Clin North Am.;75:1109. 4. Langeron, O., Birenbaum, A., Amour, J. (2009): Airway management in trauma. Minerva Anestesiol; May; 75(5):307-11. 5. Calvey, T. N., Williams, N. E. (2008): Principles and Practice of Pharmacology for Anaesthetists. Fifth Edition. Chapter 4, and 15. Blackwell Publishing. ISBN: 978-1-405-15727-8. 6. Prys-Roberts, C., Greene, L. T., Meloche, R., Foex, P. (1971): Studies of anaesthesia in relation to hypertension. II. Hemodynamic consequences of induction and endotracheal intubation. Br J Anaesth., 43: 531-47. 7. Ugur, B., Yuksel, H., Odabasi, A. R., Ogurlu, M., Onbasili, A., Aydin, O. (2006): Effects of Intravenous Lidocaine on QTd and HRV Changes Due to Tracheal Intubation During Sevoflurane Induction. Int Heart J. July , Vol 47 , No 4.



Figure 6: Percentage of change in Pulse Rate throughout measurement period in each group

8. Morgan, G. E., Mikhail, M. S., Murray, M. J. (2006): Clinical Anesthesiology. Fourth Edition. Chapter 8, 20. The McGraw-Hill Companies. ISBN 0-07-110515-8. 9. Shribman, A. J., Smith, G., Achola, K. J. (1987): Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. Br J Anaesth.,59:295-9. 10. Woon, Y. K., Yoon, S. L., Moon, S. C., Jae, H., Young, C. P.; Hye, L. (2006): Lidocaine does not prevent bispectral index increases in response to endotracheal intubation. Anesth Analg., 102:156-159. 11. Asad, N., Ali, K., Iqbal, M. (2006): Effect of nalbuphine and midazolam on haemodynamic response to intubation. Canadian Journal of Anesthesia. 53:26192. 12. Yao, F. F., Fontes, M. L., Malhorta, V. (2008): Yao & Artusio’s Anesthesiology: Problem-Oriented Patient Management. sixth edition. Section 2. Chapter 12., Lippincott Williams & Wilkins Publisher. ISBN: 0781736412. 13. Koju, R. B. (2004): Haemodynamic response to Laryngoscopy and Tracheal Intubation after induction of Anesthesia with Midazolam or Propofol. PHD thesis. Department of Anesthesiology. Bir Hospital, Kathmandu. 14. Pokharel, M. (2004): Comparative study of intravenous Magnesium Sulphate and Lignocaine in attenuation of Hemodynamic responses to Laryngoscopy and Tracheal intubation. Ph.D Thesis. Tribhuvan University. 15. Lee et al, 2007. Lee, S. H., Han, J. I., Kim, C. H. (2007): Target-controlled Infusion of Remifentanil during Propofol Induction in Hypertensive Patients: Effects of Three Different Remifentanil Concentrations on Hemodynamic Changes. Korean J Anesthesiol Vol. 53, No. 6, December.

16. Kovac, A. L. (1996): Controlling the hemodynamic response to laryngoscopy and endotracheal intubation. J Clin Anesth.;8:63-79. 17. Yushi, U. A., Maiko, S., Hideyuki, H., Kazuhiko, W. (2002): Fentanyl attenuates the hemodynamic response to endotracheal intubation more than the response to laryngoscopy. Anesth Analg.;95:233-7. 18. Boralessa, H., Senior, D. F., Whitwan, J. G. (1983): Cardiovascular response to intubation. Anaesthesia. 38:623-627. 19. Sear, J. W, Jewkes, C., Tellez, J. C., Foex, P. (1994): Does the choice of antihypertensive therapy influence hemodynamic responses to induction, laryngoscopy and intubation?. BJA.; 73:303-308. 20. Mikawa, K., Nishina, K., Maekawa, N., Obara, H. (1996): Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation. Br J Anaesth. Aug; 77(2):296-7. 21. Figueredo, E., Garcia-Fuentes, E. M. (2001): Assessment of the efficacy of esmolol on the haemodynamic changes induced by laryngoscopy and tracheal intubation: A meta-analysis. Acta. Anaesthesiol. Scand., Sep; 45(8): 1011-22. 22. Godet, G., Fusciardi, J., Bernard, J.M., Bertrand M., Kieffer E., Viars. P (1986): Role of fentanyl and nitroglycerine in prevention of myocardial ischemia associated with laryngoscopy and tracheal intubation in patients undergoing operations of short duration. Anesthesia and analgesia.65(6):617-24.



23. Allen, R. W., James, M. F., uys, P. C. (1991): Attenuation of the pressure response to tracheal intubation in hypertensive proteinuric pregnant patients by Lignocaine, Alfentanyl and Magnesium Sulphate. BJA., Vol. 66, No. 2: 216-223. 24. Miller, D. R., O’Brien, H. (1993): Effect of alfentanyl on the hemodynamic and catecholamine response to tracheal intubation. Anesth Analg 76:1040-1046. 25. Yokota, S., Komatsu, T., Yano, K. (1998): Effect of oral clonidine premedication on hemodynamic responses during sedated nasal fiber optic intubation. Nagoya J. Med Sci. May,Vol 61. 26. Zalunardo, M. P. (2000): Preoperative clonidine attenuates stress response during emergence from anesthesia. J. Clin. Anesth. 12. (5):343-9. 27. Abou Madi, M. N., Keszler, H., Yacoub, J. M. (1977): Cardiovascular reactions to laryngoscopy and tracheal intubation following small and large i.v doses of lidocaine. Can anaesth Soc J, Jan; 24(1):12-19. 28. Miller, C. D., Warren, S. J. (1990): I.V. Lignocaine fails to attenuate the cardiovascular response to laryngoscopy and tracheal intubation. B.J.Anaesthesia:Vol.65:216-219. 29. Mostafa, S. M., Murthy, B. V., Barrett, P. J., Hugh, M. C. (1999): Comparison of the effects of topical lignocaine spray applied before or after induction of anaesthesia on the pressure response to direct laryngoscopy and intubation. European Journal of Anaesthesiology, 16:1:7-10. 30. Takita, K., Morimoto, Y., Kemmotsu, O. (2001): Tracheal lidocaine attenuates the cardiovascular response to endotracheal intubation . Can J Anaesth. Sep;48(8):732-6. 31. Lebowitz, P. W., Cote, M. E., Daniels, A. L., Ramsey, F. M., Martyn, J. A., Teplick R. S., Davison J. K. (1982): Comparative cardiovascular effects of midazolam and thiopental in healthy patients. Anesth Analg. Sep; 61(9):771-5. 32. Kawar, P., Carson, I. W. , Clarke, R. S., Dundee, J. W., Lyons, S. M. (1985) Haemodynamic changes during induction of anaesthesia with midazolam and diazepam (Valium) in patients undergoing coronary artery bypass surgery. Anaesthesia. Aug;40(8):767-71. 33. Rang, H. P., Dale, M. M., Ritter, J. M., Flower, R., (2007): pharmacology. 6th edition. Chapter, 36, 37, 44. Churchill Livingstone company. ISBN: 0443069115. 34. McEvoy, G. K., Miller, J., Snow, E. K., Welsh, O. H. (2004): AHFS Drug Information. Amer Soc Health-Syst Publisher. ISBN:1-58528-033-x. 35. Katzung, B. G. (2007): Basic and clinical pharmacology. 10 edition. Chapter 6, 26, 31. McGraw-Hill lange. ISBN 10: 0-07-145154-6. 36. Chraemmer Jorgensen, B., Hoilund-Carlsen, P. F., Marving, J. (1986): Lack of effect of i.v lidocaine on hemodynamic responses to rapid sequence induction of general anaesthesia : a double-blind controlled clinical trial.. Anaesthesia and Analgesia; 65:1037-1041. 37. Pathak, D., Slater, R. M., Ping, S. S., From, R. P. (1990): Effects of alfentanil and lidocaine on the hemodynamic responses to laryngoscopy and tracheal intubation. J Clin Anesth. 2(2):81-5. 38. Helfman, S. M., Gold, M. I., DeLisser, E. A., Herrington, C. A. (1991): Which drug prevents tachycardia and hypertension associated with tracheal intubation: lidocaine, fentanyl, or esmolol? Anesth Analg; 72(4):482-6. 39. Singh, H., Vichitvejpaisal, P., Gaines, G. Y., White, P.

F. (1995): Comparative effects of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation. Clin Anesth; 7(1):5-8. 40. Kindler, C. H., Schumacher, P. G., Schneider, M. C., Urwyler, A. (1996): Effects of intravenous lidocaine and/or esmolol on hemodynamic responses to laryngoscopy and intubation: a double-blind, controlled clinical trial. Clin Anesth;8(6):491-6. 41. Vandenberg, A. A., Savva, D., Honjol, N. M. (1997): Attenuation of the hemodynamic responses to noxious stimuli in patients undergoing cataract surgery.A comparison of Magnesium Sulphate, Esmolol, Lignocaine ,Nitroglycerine and placebo given I.V with induction of anaesthesia. Eur J Anaesthesiol. Mar;14(2):134-47. 42. Malde, A. D., Sarode, V. (2007): Attenuation of the hemodynamic response to endotracheal intubation: Fentanyl Versus Lignocaine. The Internet Journal of Anesthesiology. Volume 12 Number 1. 43. Tam, S., Chung, F., Cambell, J. M. (1985): Attenuation of circulatory response to endotracheal intubation using i.v lidocaine :a determination of the optimal time of Injection. Canadian Journal of Anaesthesia: 32:565. 44. Wang, Y. M., Chung, K. C., Lu, H. F., Huang, Y. W., Lin, K. C., Yang, L. C., Lin, C. R. (2003): Lidocaine: the optimal timing of intravenous administration in attenuation of increase of intraocular pressure during tracheal intubation. Acta Anaesthesiol Sin; 41(2):71-5. 45. Bruder, N., Ortega, D., Granthil, C. (1992): Consequences and prevention methods of hemodynamic changes during laryngoscopy and intratracheal intubation Ann Fr Anesth Reanim.; 11(1): 57-71. 46. Feng, C. K., Chan, K. H., Liu, K. N., Or, C. H., Lee, T. Y. (1996): A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin.; 34(2):61-7. 47. Vickers, M. D., Morgan, M., Spencer, P. S. J., Read, M. S. (1999): Drug In Anaesthetic and intensive care practice. 8’th edition. Oxford. Butterworth-Heinemann publisher. ISBN: 0750637277. pp.109,180. 48. Koda-Kimble, M. A., Young, L. Y., Kradjan, W. A., Guglielmo, B. J., Alldredge, B. K., Corelli, R. L. (2005): Applied Therapeutics; The Clinical Use of Drugs. Eighth edition. Chapter 9, 10, 76. Lippincott Williams & Wilkins Publisher. ISBN: 0-7817-4845-3. 49. Nissen, D. (2002): Mosby’s Drug Consult. Mosby company ISBN 0-323-01766-5. (page III-1119,1898-1900). 50. Abdel razek, A., Attar, A.M. (1995); nifedipine versus fentanyl to prevent pressor response to tracheal intubation: Middle East J. Anesth feb; vol 13. (1):88-99. 51. Salihoglu, Z., Demiroluk, S., Demirkiran, K. Y. (2002): Comparison of effects of remifentanil, alfentanil and fentanyl on cardiovascular responses to tracheal intubation in morbidly obese patients. Eur J Anaesthesiol.; 19(2):125-8. 52. Young, S. L., Sook, Y. L., Kwang, W. P., Jong, R. K.,Youn, W. L. (1992): The Effects of Fentanyl Preloading on the Hemodynamic Responses to Endotracheal Intubation. Korean J Anestheisol. Jun; 025(03): 477-484. 53. Mi, Wei-Dong (1997): haemodynamic and electroencephalograph response to intubation during induction with ptopofol/fentanyl. Can. J. Anesth, 45/19-22. (Continued page 36)




M ED I CI N E A N D S O CI E T Y

Causes Of Poor Compliance in Ophthalmology

ABSTRACT

Objective: To evaluate the causes of poor compliance in patients using their eye drops long term, depending on the nature of their disease.

Patients and methods: During the period between October 2007 and October 2008, 132 patients using eye drops long term for various reasons, were asked in the ophthalmology clinic in Royal Medical Services about their compliance of using these eye drops during their regular follow up. Questions included inquiry about the number of eye drops used and dose, if the patient misses their medication, and about the cause of poor compliance. The diseases which needed long term eye drop treatment included glaucoma, vernal catarrh, chronic uveitis, and dry eyes. Non compliance was defined if the patient didn’t use medications properly in the last three months.

Results: Poor compliance was seen in 27 patients (20.5%). The most common cause for non-compliance was forgetting to use eye drops; it was seen in 10 patients (37.0%). Other causes of poor compliance include costly medications when not available, multiple eye drops usage, poor understanding of the disease, and side effects of the medication. Patients with vernal catarrh were the most compliant, followed by chronic uveitis patients, glaucoma patients, and patients with dry eye who were the least compliant.

Conclusion: It is important to educate patients about their disease and its complications since the most common cause for poor compliance is forgetfulness. Also it is important to try to give the patients other substitutes if a costly medication is unavailable.

Key Words: compliance, glaucoma, chronic eye diseases

Mohannad Qasim Albdour

Mohannad Qasim Albdour, M.D, JBO Glaucoma Specialist Department of Ophthalmology, King Hussein Medical Center, Amman, Jordan

Correspondence: Dr. Mohannad Albdour Amman-Jordan PO.Box 412 Mobile: 0016304871148 Email: [email protected]

Introduction Compliance can be defined as the extent to which a patient’s behaviour coincides with medical advice(1). Poor compliance may produce adverse effects on the quality of medical care and may waste resources. Firstly, it interferes with therapeutic efforts by reducing the benefits of the preventive or curative services offered. Secondly, non-compliance may cause unnecessary diagnostic and treatment procedures, thus generating further costs. Thirdly, poor compliance with treatment for infectious disease can increase the probability of the development of drug resistant strains and the possibility of infecting others. Finally, low compliance during a clinical trial may lead to overestimation of therapeutic dosage, causing drug toxicity for compliant patients in actual practice(2). On the other hand, non-compliance can sometimes reduce the cost and adverse effects of treatment, particularly if treatment is inappropriate. In this study we tried to elaborate the causes of poor compliance in patients who need the long term use of eye drops. Patients and Methods During the period between October 2007 and October 2008, 132 patients using eye drops long term for various reasons were asked in the ophthalmology clinic in Royal Medical Services about their compliance of using these eye drops during their regular follow. Questions included inquiry about the number of eye drops used and its dose, and if the patient misses their medications sometimes, and about the causes of poor compliance. The diseases which needed long term eye drops treatment included glaucoma, vernal catarrh, chronic uveitis, and dry eyes. Non compliance was defined if the patient didn’t use their medications properly in the last three months. As it is well known that compliance is difficult to be measured, we depended on verbal information from patients to measure it.



Table 1: Causes of poor compliance

Table 2: Distribution of patients according to their disease and compliance

Table 3: Number of patients with specific disease according to cause of poor compliance




Results Poor compliance was seen in 27 patients (20.5%). The most common cause for non-compliance was forgetting to use eye drops; it was seen in 10 patients (37.0%). Other causes of poor compliance include costly medications when not available, multiple eye drop usage, poor understanding of the disease, and side effects of the medication. They were seen in 29.6%, 22.2%, 7.4%, and 3.7% of the patients respectively (Table 1). Patients with glaucoma were the least compliant, followed by dry eyes, chronic uveitis, and vernal catarrh patients who were the most compliant (Table 2). 21 patients with glaucoma were non-compliant and this was attributed to costly medications in 8 patients, multiple eye drops usage in 6 patients, forgetfulness in 5, and poor understanding of the disease in 2 patients. 2 patients with dry eyes said that they forgot to take the medication. Forgetfulness was also attributed to poor compliance in 2 patients with vernal catarrh and in 1 patient with chronic uveitis. The cause of non-compliance for 1 patient with vernal catarrh was burning sensation after installing the eye drops (Table 3). Discussion Compliance to medications for diseases that are considered as risk factors for ocular complications is an important issue in decreasing the risk for developing these complications. Many studies attempted to measure the extent towards which compliance occurs(3-5). Different methods have been used for estimating compliance such as self reported compliance, pill counts, and measurement of drug concentrations in serum or urine(2,6). In our study compliance was estimated by self reporting from patients. Many factors are responsible for poor compliance; among these are patient forgetfulness, the cost of the drugs, multiple drug regimens and the side effects of the drugs. To improve compliance it is important to explain to the patient how to take their medications properly and regularly and to explain the sequelae and dangers of poor compliance. Methods for improving compliance included simple medication regimens(7), and providing written and verbal information(8,9). All our patients were given clear verbal and written instructions on how to use their medications.

In our study the least compliant patients were those with glaucoma. Poor compliance in glaucoma patients was mostly attributed to two factors. Firstly, some drugs when not available are costly, and secondly, patients may need to use three or four eye drops and this decreases compliance. We instructed our patients about the serious blinding complication of uncontrolled high intraocular pressure. Non compliant patients with dry eyes thought that artificial tears were not necessarily to be used all the time so were easily forgotten. Again, patients were instructed about the complications of dry eyes especially in hot and humid climates. Patients with vernal catarrh and chronic uveitis were more compliant, possibly due to availability of the medication and from the relatively shorter nature of the illness.

Poor compliance has an effect on morbidity, with many patients receiving suboptimal treatment. The financial cost of non-compliance also needs to be considered. Many strategies have been suggested to improve compliance. These include

simplifying medication regimens(7), providing written and verbal information(8,9), and more appropriate packaging of drugs(10). Self medication in hospital has also been suggested as a way of improving compliance on discharge(11-13). A scheme of self medication allows patients to give themselves their drugs in hospital, after education. The last principle can be extended and applied in patients using eye drops.

Conclusion It is important to educate patients about their disease and its complications since the most common cause for poor compliance is forgetfulness. Also it is important to try to give the patients other substitutes if a costly medication is unavailable. References 1. Haynes RB. Compliance in health care. Baltimore: Johns Hopkins University Press, 1979.2. Melnikow J, Kiefe C. Patient compliance and medical research: issues in methodology. J Gen Intern Med 1994;9:96-105.3. Ley P. Communicating with the patient. London: Croom Helm, 1988.4. Sacket DL, Snow JC. The magnitude of compliance and non-compliance. In:Haynes RB. Compliance in healthcare. Baltimore: Johns Hopkins University Press, 1979.5. Parkin DM, Henney CR, Quirk J, Crooks J. Deviation from prescribing drug treatment after discharge from hospital. BMJ 1976;ii 686-688.6. Urquhart J. Role of patient compliance in clinical pharmacokinetics. A review of recent research. Clin Pharmacokinet 1994;27:202-215.7. Asplund J, Danielson M, Ohman P. Patient compliance in hypertension-the importance of the number of tablets. Br J Clin Pharmacol 1984;17:547-552.8. Raynor DK, Booth TG, Blenkinsopp A. Effects of computer generated reminder charts on patients’ compliance with drug regimens. BMJ 1993;306:1158-1161.9. Sandler DA, Mitchell JRA, Fellows A, Garner ST. Is an in information booklet for patients leaving hospital helpful and useful? BMJ 1989;298:870-874.10. Rudd P. Medication packaging: simple solutions to non-adherence problems? Clin Pharmacol Ther 1979;25:257-65.11. Baxendale C, Gourlay M, Gibson IIJM. A self-medication retraining programme. BMJ 1978;ii:1278-9. 12. Bird C. Taking their own medicines. Nursing Times 1988;84:28-32.13. Webb C, Addison C, Holman AH, Saklaki B, Wagner A. Self-medication for elderly patients. Nursing Times 1990;86:46-9.




ABSTRACT Objective: To evaluate the current practice in requesting and performing paranasal sinuses computed tomography scan for patients scheduled for endoscopic sinus surgery and to describe the current hospitals’ practice in performing these scans.

Methods: Three forms were specially designed to collect data from our study groups which included: ENT surgeons, and radiologist and radiology sections in three hospitals. Data collection was done on May 2010 during an international meeting organised in Amman. The first form was designed for ENT surgeons and aimed at knowing whether they perform endoscopic sinus surgery or not, and to know if they have specific requirements on requesting sinuses CT scan. The second was designed for radiologists and aimed at knowing their current practice and specifications in performing paranasal sinuses CT scan. The last one was designed to evaluate the current practice of performing paranasal sinuses CT scan at three different hospitals; King Hussein Medical Centre, Prince Zaid Hospital and Prince Rashid Hospital.

Results: A total of 24 ENT surgeons participated in this study. 20 surgeons (83.3%) perform endoscopic sinus surgery and (83.3%) requested specification for the sinuses CT scan. About 88% usually gave antibiotic treatment before requesting the CT scan unless there was a suspicion of malignancy, and the most requested specification was coronal plane in 42%. Of the total 24 radiologists who responded to our study 71% prefer the prone position, 71% prefer the coronal plane and 71% preferred the direct coronal rather than the reconstructed images. In all three hospitals axial plane with reconstructed coronal images is the present practice with slice thickness between 2-3 mm and a total number of image scans ranging from 40 to 50 images.

Conclusion: Differences between ENT surgeons, radiologist and hospitals’ practice and other hospitals guidelines found in literature is present, so we are in need of a guideline protocol agreed upon by both groups in order to have the best required data with the least exposure for radiation dose.

Key words: computed tomography, sinuses, coronal

Introduction Computed tomography (CT) scan is currently the most important radiological investigation of paranasal sinuses.

The advent of less invasive techniques of endoscopic sinus surgery have provided an important role for coronal computed tomography of the paranasal sinuses both as a diagnostic tool and for preoperative planning(1). Over the last 20 years a search for the best protocol in performing these scans, with least radiation dose to the lens of the eye, was extensive. Many protocols were published and different reports came with best possible guidelines to reduce the amount of radiation and to obtain the maximum information. In Jordan, there is no agreed upon protocol and the scan protocol is usually individualised according to the preference of the radiologist and/or ENT surgeon. So we have conducted this study to evaluate the current practice in requesting and performing paranasal sinuses computed tomography scan and to describe the current hospital practice in performing these scans. Methods Specially designed forms were used to collect data from the study groups which include: ENT surgeons, radiologists and radiology sections in three different hospitals. The first two groups represent different populations of doctors working in both private and public health sectors in our country, to get a wider representation of what is usually going on, and data collection was done during an ENT workshop organised as part of an international meeting and a radiology symposium organised on May 2010. The first form was designed for ENT surgeons and our aim was to know whether they perform endoscopic sinus surgery or not since the paranasal sinuses CT scan is a mandatory preoperative investigation and it provides the surgeon with the anatomic details they need. The medical record abstract forms aimed to collect the following data: whether the surgeon asked for special specifications for the CT scan or not, what are these specifications, if they

Computed tomography (CT) scan requirements for endoscopic surgery of paranasal sinuses: Current practice

Qais Aljfout

Dr Qais Aljfout, MD MRCSI DOHNS Department of Otolaryngology Royal medical services, Jordan

Correspondence: Dr Qais Aljfout PO Box 1643 Tareq Amman, Jordan Email: [email protected]


ED U C AT I O N A N D T R A I N I N G


if they give treatment before requesting the CT scan, what is the duration of treatment and when they perform the CT scan. The second form was designed for the radiologists and aimed to know their specification for the paranasal sinuses CT scans in regard to: the patient’s position, plane, slice thickness, table increment and the number of scan images, and at the end they were questioned as to whether they prefer the direct coronal or the reconstructed coronal images. The last form was designed to evaluate the current practice of performing paranasal sinuses CT scan at three different hospitals: King Hussein Medical Centre (KHMC), Prince Zaid Hospital (PZH) and Prince Rashid Hospital (PRH), and here we have collected data regarding the following: the patient’s position, plane, slice thickness, radiation dose (Kv and milliamperes-second {mAs}) and the number of scan images. Results Forty eight doctors participated in this study. 24 were ENT surgeons who responded to the first form and we found that: 20 surgeons (83.3%) perform endoscopic sinus surgery, 20 (83.3%) ask for specification while writing the request form, coronal plane is the most requested specification 10 (42%) while 6 (25%) ask for axial and coronal planes and 4 (16.7%) ask for specification regarding slice thickness (ask for thin slice thickness). Results are shown in Table 1. Of the twenty four radiologists involved in this study, 17 (71%) ask for prone position, 17 (71%) specify coronal plane, 2-3mm is the preferred slice thickness by 18 (75%) of the radiologists. Tere was a wide range in the number of scan images with the largest group 8 (33%) asking for 40-50 images, and the direct coronal is preferred over reconstructed coronal in 17 (71%) of them. (Table 2 next page). Regarding current practice in our three hospitals: the supine position, axial and reconstructed coronal plane and slice thickness 2-3mm are shared by the three hospitals. The radiation dose is highest at prince

Rashid hospital with 440 mAs since it has the oldest CT scan machine as shown in Table 3. Discussion Currently, the best radiological investigation for the evaluation of paranasal sinuses is CT scan since it displays both bone and soft tissue efficiently. The optimal CT technique for imaging the sinonasal complex is still a matter of debate (2). In our analysis we have noticed few differences between ENT surgeons and radiologists, between ENT surgeons in the same group and between radiologists themselves. Although there are similarities in the current practice in our three hospitals which might represent an unwritten protocol, they have major differences with other published protocols such as John Hopkins hospital (1, 2). Royal National Throat Nose Ear hospital (RNTNE) (3) and Charing Cross Hospital (4). Table 4 represents the current protocols for these hospitals. Some consider that direct coronals are a pre-requisite to virtually all protocols even with the advent of the fast spiral scanners which have considerably improved the quality of reconstructed images on both the axial and the sagittal (3). However, it is not uncommon for departments to continue using the same protocol utilized for early scanners (5). The coronal plane is the plane closest to the view of the endoscopist. It is also the imaging plane that displays the ostiomeatal unit (1). One of the major disadvantages of direct coronal scan is that it requires prone positioning for a prolonged period (6), and when patients are unable to assume the prone position, the reconstructed coronal can be used (1). In children the sinuses CT scan demonstrates an excellent diagnostic accuracy (7) and others have suggested that CT scan may help identifying patients with allergic fungal sinusitis (8) and invasive fungal sinusitis (9). The radiation dose to the lens of the eye and the thyroid gland in the paranasal sinuses CT scan is of concern.


Table 1: ENT Surgeons’ Response in the specially designed record form



Table 2: Radiologist Response



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Table 3: Our three hospital’s current practice

Table 4: Published protocols

Table 5: Radiation dose to the lens at different mAs

Table 6: Suggested protocol

Studies showed that this radiation dose is significantly lower in the axial than the coronal plane (10). Table 5 shows mean radiation dose to the lens of the eye at different mAs settings (11). Recent studies proved that sinuses CT scans can be performed in patients prior to endoscopic surgery at greatly reduced mAs without loss of diagnostic quality of the images (5, 11). This should be done paying attention to the capability of the CT scanners. Table 6 shows a suggested protocol to be adopted by our group of hospitals. In this protocol we have added axial scans as we think they gave us the third dimension that we need to know prior to surgery. In addition, axial scans optimally demonstrate the relationship between the posterior ethmoids and sphenoid to the optic nerve and the carotid artery (3).

Conclusion Although we have seen differences intra and inter our study groups, we recommend a meeting between ENT surgeons and radiologists in order to form a protocol agreed upon by both groups, taking into consideration the information ENT surgeons require, and the lowest radiation dose that can give this information and the minimum number of scan images required, in order to reduce the expenses.


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Reference1. Zinreich SJ, kennedy DW, Rosenbaum AE, Gayler BW, Kumar AJ, Stammberger H. Paranasal Sinuses: CT Imaging Requirements for Endoscopic Surgery. Radiology. 1987; 163:769-775.2. Melhem ER, Oliverio PJ, Benson ML, Leopold DA, Zinreich SJ. Optimal CT evaluation for Functional Endoscopic sinus Surgery. Am J Neuroradiol. 1996 January; 17:181-188.3. Lund VJ, Savy L, Lloyd G. Imaging for endoscopic sinus surgery in adults. The Journal of Laryngology & Otology. 2000 May; Vol.114,pp. 395-397.4. Rowe-Jones J, Mackay I, Colquhoun I. Charing Cross CT protocol for endoscopic sinus surgery. The Journal of Laryngology & Otology. 1995 Nov; Vol. 109, pp. 1057-1060.5. Kearney SE, Jones P, Meakin K, Garvey CJ. CT scanning for paranasal sinuses - the effect of reducing mAs. The British Journal of Radiology. 1997 Oct; 1071-1074.6. Witte RJ, Heurter JV, Orton DF, Hahn FJ. Limited Axial CT of the Paranasal Sinuses n Screening for Sinusitis. AJR.1996; 167: 1313-1315.7. Bhattacharyya N, Jones DT, Hill M, Shapiro NL. The Diagnostic Accuracy of Computed Tomography in Pediatric Chronic Rhinosinusitis. Arch Otolaryngol Head Neck Surg. 2004;130:1029-1032.8. Mukherji SK, Figueroa RE, Ginsberg LE, Zeifer BA, Marple BF, Alley JG, et al. Allergic Fungal sinusitis: CT Findings. Radiology 1998;207:417-422.9. DelGaudio JM, Swain Jr RE, Kingdom TT, Muller S, Hudgins PA. Computed tomographic Findings in Patients with Invasive Fungal Sinusitis. Arch Otolaryngol Head Neck Surg. 2003;129:236-240.10. Zammit-Maempel I, Chadwick CL, Willis SP. Radiation dose to the lens of eye and thyroid gland in paranasal sinus multislice CT. The British Journal of Radiology,. 2003 June; 418-420.11. Sohaib SA, Peppercorn PD, Horrocks JA, Keene MH, Kenyon GS, Reznek RH. The effect of reducing mAs on image quality and patient dose in sinus CT. The British Journal of Radiology. 2001 Feb; 157-161.

(References continued from Evaluation of Serum 5’- Nucleotidase, Adenosine deaminase, and Alkaline phosphatase in rheumatoid arthritis patients in Erbil city , page 18)18-Namke Y et al. Alkaline phosphatase in RA : Possible contribution of bone type ALP to the raised activities of ALP in RA patients. Clin Dermatol . 2002 ; 21 (3) : 198-202. 19-Drazen; Gill; Griggs etal. (2006). Cecil text book of medicine 23rd edition, Losculzo. 20-Malgorzata Magliano (2008). Obesity and arthritis. Menopouse international 14 (4). 149-154. 21-Aderioli; Carpenter, and Griggs.(2005).Cecil essential of medicine,5th edition.Losculzo.

(References continued from The effect of Lidocaine with Fentanyl, or Midazolam on cardiovascular responses during Endotracheal intubation in hypertensive patients on Beta-blocker page 28) 54. Kim, H. T., Kim, C. K., Lee, J. H., Kwon, Y. E., Lee, J. W., Kim, D. C. (2006): Effects of Fentanyl and Remifentanil on Hemodynamic Responses to Endotracheal Intubation during the Induction of Anesthesia with Propofol. Korean J Anesthesiol. Nov;51(5):552-557. 55. Anila, D. M., Vineet, S. (2007): Attenuation of the hemodynamic response to endotracheal intubation: Fentanyl versus Lignocaine. The Internet Journal of Anesthesiology. Volume 12 Number 1.56. Kay, B., Healy, T. E., Bolder, P. M. (1985): Blocking the circulatory responses to tracheal intubation. A comparison of fentanyl and nalbuphine. Anaesthesia.; 40(10):960-3. (s)57. Chraemmer-Jorgensen, B., Hertel, S., Strom, J., Hoilund-Carlsen, P.F., Bjerre-Jepsen, K.(1992): Catecholamine response to laryngoscopy and intubation. The influence of three different drug combinations commonly used for induction of anaesthesia. Anaesthesia. Sp;47(9):750-6.58. Chytra, I., Kasal, E., Pradl, R., Bosman, R., Machart, S. (1997): Study on the Haemodynamic response to tracheal intubation after induction of anesthesia using propofol or Midazolam. Br. J Anesth ;200.59. Celleno, D. Capogna, G. (1993): induction drug for cesarean section? A comparison of thiopentone sodium, propofol and midazolam. J Clin Anesth. Jul-Aug; 5(4): 284-8.60. Forster, A., Gardaz, J. P., Suter, P. M., Gemperle, M. (1980): midazolam as an induction agent for anaesthesia: a study in volunteers. Br J Anaesth. Sep; 52(9):907-11.61. Berggren, L., Eriksson, I. (1981): Midazolam for induction of anaesthesia in outpatients: a comparison with thiopentone. Acta Anaesthesial Scand. Dec;25(6):492-6.



Inguinal Herniorrhaphy Under Local Anesthesia: Outcome And Tolerance Among Patients In Royal Medical Services: A Prospective Study

ABSTRACT

Background: Hernia repairs comprise one of the most common procedures performed in our patients. The aim of this study was to evaluate outcome and tolerance of elective inguinal hernia repair under local anesthesia among Jordanian patients.

Methods: A prospective study was made of 72 (70 male and 2 female) patients who underwent inguinal hernia repair under local anesthesia, between June 2008 and June 2010 at the surgical department of our hospital. The patients’ ages ranged from 18 to 84 years (mean age 60 years). Concomitant diseases were present in 16 (22.2%) patients.

Results: Seventy two patients were involved in this study. Sixty of the patients (83.3%) denied any discomfort during the operation. Five patients (7%) experienced mild discomfort which was tolerable, but no actual pain. Four patients (5.5%) had slight pain which settled with further sedation and local anesthetic infiltration, allowing uneventful completion of the procedure. Four percent (3/72) of patients required conversion to general anesthesia due to patient anxiety. The mean volume of local anesthetic solution used was 50 ml (range, 30-90 ml). Overall morbidity rate was 12.5%. The mean duration of post-operative analgesia was 8.8 hours (2 to 24 hours). During the follow-up period none of our patients developed recurrence.

Conclusions: The preferred choice of anesthesia for all reducible adult inguinal hernia repairs is local. It is safe, simple, effective, and economical, without post anesthesia side effects. Furthermore, local anesthesia administered before the incision produces longer postoperative analgesia. In elderly patients with comorbidities local anesthesia might be the best in order to avoid the increased risks of general anesthesia.

Jihad Odeh Mazen Alomari Abdullah Rababaah Amjad Maslamani Laith Khasawneh

Department of Surgery, Prince Ali Hospital, Royal Medical Services, Amman, Jordan

Introduction For several years groin hernia repair has been one of the most commonly performed surgical operations worldwide. Several studies have reported advantages of Local anesthesia over other techniques with regard to safety, reduced postoperative pain, and shorter hospital stay (1, 2, 3). This procedure was found to be acceptable widely to patients, whether they were admitted and stayed in hospital throughout the postoperative period or ambulatory patients who just stayed for one day. The main exceptions to this practice were multi-recurrent hernias, very large scrotal hernias and extremely anxious patients (4). Local anesthesia-based techniques fulfill all the requirements for the ideal ambulatory anesthesia (5). Furthermore, the feasibility of routinely using local infiltration anesthesia for inguinal hernia repair has been convincingly demonstrated (6, 7, 8, 9, 10). However, local anesthesia is used in only 6% to 18% of cases (11, 12). The major advantages of local anesthesia have been reported to be a reduction in hospital costs, a reduction of long waiting lists and a reduction in postoperative complications including recurrences (13, 14). A long duration of postoperative analgesia made it more comfortable for the patients (15). In spite of the many advantages of local anesthesia, inguinal herniorrhaphy is still mostly performed under general or spinal anesthesia. The aim of this study was to assess the results and outcome of using local anesthesia for elective inguinal hernia repair in our community.

Materials and Methods The success of local anesthesia requires good rationalization to the patients. All patients undergoing elective inguinal herniorrhaphy at Prince Ali hospital between June 2008 and June 2010 were informed during their original outpatient visit about this prospective study and inguinal herniorrhaphy under local anesthesia procedure; its advantages and disadvantages. Excluded were patients requiring operation for obstruction, strangulation, or recurrence, age less than 18 years, recurrent hernia, femoral hernia, pregnancy, bleeding abnormalities and anticoagulant treatment. Seventy two patients participated; seventy were males and two females with mean age of 60 years (18 to 84). Admissions were either on the afternoon before or on the morning of the operation.


3� MIDDLE EAST JOURNAL OF FAMILY MEDICINE • VOLUME � , ISSUE �MIDDLE EAST JOURNAL OF INTERNAL MEDICINE VOLUME 4, ISSUE 1

Operative details were as follows: After six hours of fasting, all patients were placed in the supine position on the operating table. All patients should have an intravenous line, and Ringer lactate infusion was started immediately before the operation. Anesthesia personnel were readily available if need for general anesthesia arose. After aseptic draping of the surgical site, the ilio-inguinal block and local infiltration of anesthesia were carried out by the surgeon using a 50:50 mixture of 1% lidocaine and 0.5% bupivacaine. Such a mixture has the following advantages: Lidocaine provides rapid onset, and bupivacaine results in a longer duration of local anesthesia. . Approximately 5 mL of the mixture is infiltrated along the line of the incision. This step blocks the subdermic nerve endings and decreases the discomfort of the intradermic infiltration, which is the most uncomfortable stage of local anesthesia. At this point, without extracting the needle completely, the intradermic infiltration and making of the skin wheal is performed by very slow injection of approximately 3 mL of the mixture along the line of the incision then ten milliliters of the mixture is injected deep into the subcutaneous adipose tissue by vertical insertions of the needle 2 cm apart. Approximately 8 to 10 mL of the anesthetic mixture is injected immediately underneath the aponeurosis of the external oblique. Further, 5ml was injected just above the pubic tubercle in a fan shape extending upward and laterally from the pubic tubercle to peritoneum forming the base of the indirect sac. Skin incision was placed 1 cm above and parallel to the inguinal ligament extending from the pubic tubercle to about 1 cm lateral to the deep ring. Dissection was deepened into the subcutaneous fat, the external oblique aponeurosis was identified and exposed along the length of incision. The inguinal canal was opened, the spermatic cord with its cremasteric covering elevated with a tape. Next, cremasteric fascia was incised along the full length of the cord. The indirect hernia sac was dissected free with sharp dissection up to the neck marked by collar of extraperitoneal fat and transfixed at the neck using 1/0 vicryl and excised. The direct sac was tacked sown by a continuous, placating absorbable suture using 1/0 vicryl. All patients underwent Lichtenstein operation. Having checked for haemostasis and protected the ilio-inguinal nerve, the cord was replaced. External oblique aponeurosis was closed with continuous 1/0 prolene. Skin closure was done by subcuticular 3/0 vicryl suture. Intraoperatively, patients were repeatedly asked about any pain and discomfort that they might have experienced and noted for any facial expression of pain.

Patients were encouraged to ambulate immediately after surgery. The duration of post-operative analgesia up to the time of need for the first dose of post-operative analgesia was noted. Patients were seen usually two weeks after surgery and then followed up at monthly intervals. The mean follow-up was 13 months (5 to 30 months).

Results A total of 72 patients underwent inguinal hernia repair during the study period. Three of them had bilateral hernia. The mean age was 60 years (range, 18-84 years). The majority of the patients were free of any medical illnesses. Patients with medical illnesses (mostly cardiopulmonary diseases) which would have made administration of general anesthesia an unnecessary risk accounted for 22% of all patients.

Lichtenstein mesh repair was the surgical technique used. Intraoperatively 50 (66.6%) of the 75 hernias were indirect, 20 (26.6%) were direct and 5 (6.6%) were pantaloons, having both direct and indirect sacs. The mean duration of the entire procedure was 35.7 minutes (29 to 60 minutes).

Sixty of the patients (83.3%) denied any discomfort during the operation. Five patients (7%) experienced mild discomfort which was tolerable, but no actual pain. Four patients (5.5%) had slight pain which settled with further sedation and local anesthetic infiltration, allowing uneventful completion of the procedure. Three patients (4.2%) required conversion to GA due to patient anxiety. The mean volume of local anesthetic solution used was 50 ml (range, 30-90 ml).

Overall morbidity rate was 12.5% (n=9): hematoma 2.8% (n=2), seroma 4.1% (n= 3), scrotal swelling 2.8% (n=2), superficial surgical site infection 2.8% (n=2). Of the two patients who developed superficial wound infection following surgery; one of them required admission for administration of intravenous antibiotics. No patient required removal of the mesh for infection. The mean duration of post-operative analgesia was 8.8 hours (2 to 24 hours). Follow-up was completed by clinical examination encouraged by telephone contact. During the follow-up period mentioned none of our patients developed recurrence. Discussion Inguinal herniorrhaphy is one of the most frequent operations and can be successfully performed using general, regional, or local anesthesia. Epidemiological data from databases have found that general anesthesia is used in 60%-70% of cases, central neuraxis blockade in 10%-20%, and local infiltration anesthesia in only 5%- 15% of cases(12,16). Even though local anesthesia with sedation (so-called monitored anesthesia care) is a more cost-effective anesthetic technique for inguinal hernia repair (6), general and spinal anesthesia remain the most popular anesthetic techniques at university based teaching programs. Interestingly, specialized hernia centers use local infiltration anesthesia in more than 95% of these cases (7, 8, 9, 10).

The advantages of using local anesthesia in hernia repair are usually cited in relation to its performance as an outpatient procedure, and there is good opportunity to practice outpatient surgery in a developing country because the necessary postoperative supervision is now available.

Limited resources make accurate assessment of priorities the watchword of the medical attendant and any method which preserves resources without jeopardizing clinical care will be welcomed. Advantages in addition to those already outlined became manifest during the study. The nursing staff has indicated that these patients seem to require less attention after the operation: their requirements for analgesia are less; normal motility returns sooner; excretory functions are unimpaired; and they complain less.

This study shows that hernia repair under local anesthesia was acceptable to the majority of patients presenting with inguinal



hernia. The procedure was tolerated well. Only 7% had mild discomfort. The method of assessing intra-operative pain was adapted from Ofili et al (17), where 58% of the patients felt no discomfort and 27% experienced mild discomfort. Baskerville and Jarrett (18) also reported that 93% of their patients denied any pain. Other studies (15,19) have also reported that most of the patients who underwent herniorrhaphy under local anesthesia, including those who had previous hernia repairs under general or spinal anesthesia, favored this procedure and volunteered that they would have it performed in the same way again if required.

The technique used for local infiltration anesthesia has been extensively described in the surgical literature (8) and can be performed by the surgeon and/or the anesthesiologist.

A potential advantage of local infiltration anesthesia is that it can be performed using so-called unmonitored anesthesia (10), although most centers prefer to use sedation as a part of a monitored anesthesia care technique to increase acceptance by patients and surgeons (6,7,8,9). Postoperative recovery is definitely faster with local anesthesia compared with general and regional anesthetic techniques. In addition, it can obviate the need for admitting these patients to the post anesthesia care unit which can facilitate an earlier discharge home after surgery (6,10,20). Postoperative pain is ideally treated with a multimodal approach involving both opioid and nonopioid analgesics (21). Local anesthetics are highly effective in alleviating postoperative pain when administered using both a peripheral nerve block technique (e.g., ilioinguinal-hypogastric nerve block) (22) and local wound infiltration at the fascial level (23). However, the duration of local analgesia after a single injection typically lasts nine hours (24).

In our series, the most common complication was bruising of the skin around the wound (13.6%); this resolved spontaneously and uneventfully within 3 to 5 days, as previously described by other authors (19,25) The 3% of scrotal hematomas occurred in the distal portion of large hernial sacs left behind. Our complication rate was comparable to the 0.75% (42) to 28.9% (15) reported in previous studies on herniorrhaphy under local anesthesia, where wound bruising was reported but not considered a complication. 22% of our patients had medical illnesses which would have made the administration of a general anesthetic more difficult. Young (15) found that the complications in patients with medical illnesses and those over 65 years of age were less under local anesthesia compared to either general or spinal anesthesia.

There were no recurrences in this series; the short follow up was inadequate to assess whether inguinal hernias repaired under local anesthesia were more prone to recur than those done under general anesthesia. It is known that if hernias were to recur, half of them would have recurred by the end of five years and three quarters s by the end of ten years of follow-up (7). The reported recurrence rates for repair under local anesthesia were 0.6% to 4.2% in primary hernias (26) and 0.8% to 4% in recurrent hernias (4, 25). Berliner et al (13) showed that inguinal hernia repair under local anesthesia

resulted in a lower recurrence rate than repair under general anesthesia. This is probably because under local anesthesia, there is less likelihood of a repair being performed under tension. Furthermore, the cough stress test enables the integrity of the repair to be assessed intra-operatively and if defective, further steps can be taken to correct any deficiencies.

The choice of anesthesia depends on several factors, including patient and surgeon preferences, feasibility of the technique in a given patient, intra- and postoperative pain control, early recovery and monitoring requirements, postoperative morbidity, and perioperative costs. Given the recent studies confirming the benefits of local anesthetic-based techniques over both general and spinal anesthesia (6, 10), it is surprising that these techniques are so rarely used outside dedicated hernia centers. Despite the fact that it is safe, simple, and cost-effective, there is a lack of acceptance of local infiltration anesthesia within the surgical community. Conclusion In conclusion, there is a surprising discrepancy between the documented benefits of local anesthesia in reducing postoperative pain and anesthetic-related morbidity (as well as perioperative costs) in patients undergoing inguinal herniorrhaphy and the frequency with which this technique is used for this operation.

It is hoped that this paper has demonstrated how successfully such patients can be managed using local anesthesia. Its outcome and advantages have been described in detail in the hope that it may eventually become the anesthetic of choice in our hospitals. References 1. Nordin P, Zetterstrom H, Carlsson P, et al. Cost-effectiveness analysis of local, regional and general anaesthesia for inguinal hernia repair using data from a randomized clinical trial. Br J Surg 2007;94:500 -5. 2. Kehlet H, Aasvang E. Groin hernia repair: anesthesia. World J Surg 2005;29:1058-61. 3. Nordin P, Zetterstrom H, Gunnarsson U, et al. Local, regional, or general anaesthesia in groin hernia repair: multicenter randomized trial. Lancet 2003;362:853- 8. 4. Glassow F. Inguinal hernia repair using local anaesthesia. Ann R Coll Surg Engl 1984: 66:382-387 5. White PF. Ambulatory anesthesia advances into the new millennium. Anesth Analg 2000;90:1234-5. 6. Song D, Greilich NB, White PF, et al. Recovery profiles and costs of anesthesia for outpatient unilateral inguinal herniorrhaphy. Anesth Analg 2000;91:876-81. 7. Glassow F. Short-stay surgery (Shouldice technique) for repair of inguinal hernia. Ann R Coll Surg Engl 1976;58:133-9. 8. Amid PK, Schulman AG, Lichtenstein IL. Local anesthesia for inguinal hernia repair: step-by-step procedure. Ann Surg 1994; 220:735-7. 9. Kark AE, Kurzer MN, Belsham PA. 3175 primary inguinal hernia repairs: advantages of ambulatory open mesh repair using local anesthesia. J Am Coll Surg 1998;186:447-55.


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10. Callesen T, Bech K, Kehlet H. One-thousand consecutive inguinal hernia repairs under unmonitored local anesthesia. Anesth Analg 2001;93:1373-6. 11. Bay-Nielsen M, Kehlet H, Strand L, et al. Quality assessment of 26,304 herniorrhaphies in Denmark: a prospective nationwide study. Lancet 2001;358:1124-8. 12. Hair A, Duffy K, McLean J, et al. Groin hernia repair in Scotland. Br J Surg 2000;87:1722- 6 13. Berliner S, Burson L, Katz P and Wise L. An anterior transversalis fascia repair for adult inguinal hernias. Am J Surg 1978; 135:633-636. 14. Lichtenstein IL and Shore JM. Exploding the myths of hernia repair. Am J Surg 1978; 44:465-471. 15. Young DV. Comparison of local, spinal and general anaesthesia for inguinal herniorrhaphy. Am J Surg 1987; 153:560-563. 16. Nilsson E, Kald A, Anderberg B, et al. Hernia surgery in a defined population: a prospective three year audit. Eur J Surg 1997;163:823-9. 17. Ofili OP, Osime U and Morgan AA. Local anaesthetic for inguinal hernia repair a system of objective assessment of patients’ tolerance. JR Coll Edin 1988; 33:71-74. 18. Baskerville PA and Jarret PEM. Day case inguinal hernia repair under local anaesthetic. Ann R Coll Surg Engl 1983; 65:224-225. 19. Abdu RA. Ambulatory herniorrhaphy under local anaesthesia in a community hospital. Am J Surg 1983: 145:353-356. 20. Li S, Coloma M, White PF, et al. Comparison of the costs and recovery profiles of three anesthetic techniques for ambulatory anorectal surgery. Anesthesiology 2000;93:1225-30. 21. Callesen T, Kehlet H. Postherniorrhaphy pain. Anesthesiology 1997;87:1219-30. 22. Ding Y, White PF. Post-herniorrhaphy pain in outpatients after pre-incision ilioinguinal-hypogastric nerve block during monitored anesthesia care. Can J Anaesth 1995;42:12-5. 23. Yndgaard S, Holst P, Bjerre-Jepsen K, et al. Subcutaneously versus subfascially administered lidocaine in pain treatment after inguinal herniotomy. Anesth Analg 1994;79:324-7. 24. Møiniche S, Mikkelsen S, Wtterslev J, Dahl JB. A qualitative systematic review of incisional local anaesthesia for postoperative pain relief after abdominal operations. Br J Anaesth 1998; 81:377-83. 25. Flanagan L and Barcona JU. Repair of the groin hernia. Outpatient approach with local anaesthesia. Surg Clin N Am 1984; 64:257-267. 26. Britton BJ and Morris PJ. Localanaesthetic hernia repair. An analysis of recurrence. Surg Clin N Am 1984; 64:245-255.

(References continued from Pigmented villonodular synovitis of the Ankle and foot: A Case Report page 42) 6 Pigmented villonodular synovitis (PVNSAdded by Gregory Mallo, last edited by Matt Steensma on Oct 07, 2008 (view change) Tumor template based on A Clinical Guide to Primary Bone Tumors. Levesque et al7 Pigmented villonodular synovitis of the knee : A case report S Singh, V ChowdhuryDepartment of Radiodiagnosis, Maulana Azad Medical College and Associated Lok Nayak Hospital, Jawaharlal Nehru Marg, New Delhi- 110 002, India8 The use of surgery and yttrium 90 in the management of extensive and diffuse pigmented villonodular synovitis of large joints. S. Shabat1,2,, Y. Kollender1, O. Merimsky3, J. Isakov4, G. Flusser5, M. Nyska2 and I. Meller11 The National Unit of Orthopaedic Oncolog9 Pigmented Villonodular Synovitis. Dr. Bhavuk Garg, Dr. Rajesh Malhotra, Dr Surya Bhan10 Pigmented Villonodular Synovitis dr tylor hospital for special surgery new york,j am acad orthopaedic surg. 2006,14:376.38511 Pigmented Villonodular Synovitis of hip mimicking soft -tissue sarcoma :a case report MKS Lee PFM CHOONG, PJ SMITH, GJ Powell. St Vincents Hospital, Fitzroy,Melbourne,Australia12 Pigmented Villonodular Synovitis wheeless textbook of orthopaedics13 Pigmented Villonodular Synovitis of the ankle :a report of two cases. Amol saxena ,D.P.M., department of sports medicine ,palo alto medical fouyndation.913 emerson street palo alto,ca . 94301 415/853-2943 fax 415/853-600414 Pigmented Villonodular Synovitis Auther:Johnny uv monu,MD,associate professor of radiology and orthopaedics,university of Rochester school of medicine, updated. Jun 21,2007 medscape CME15 Pigmented villonodular synovitis (PVNS) Added by Gregory Mallo, last edited by Matt Steensma on Oct 07, 2008 (view change) Tumor template based on A Clinical Guide to Primary Bone Tumors. Levesque et al.


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Pigmented villonodular synovitis of the Ankle and foot: A Case Report

Introduction Pigmented villonodular synovitis (PVNS) is a locally aggressive disease process of uncertain etiology affecting the linings of joints, tendon sheathes, and bursae. Originally described in 1941 by Jaffe et al., this phenomenon affects 1.8 patients per million population, and presents most commonly in the knee and hip joints followed by the ankle and shoulder. Whereas the onset of this process is insidious in nature, if left untreated, it can become expansive involving adjacent osseous tissue. Although diagnosis in the past relied on combined clinical, radiographic, gross, and histological analyses, magnetic resonance imaging (MRI) has provided a useful means of diagnosis based on the relatively unique appearance of this lesion on T1- and T2-weighted images. Granowitz and Mankin divided PVNS into two forms: localised (nodular) and diffuse. Both forms can occur in the foot and ankle. A nodular variant, the giant cell tumour of tendon sheath (GCT), occurs in the flexor or extensor tendon sheaths of digits. Although now considered a benign tumour, PVNS was considered to be a low-grade synovial malignancy. The spectrum of clinical presentations ranges from a painless nodule or swelling to a diffusely painful, stiff joint. Most cases are monarticular and do not metastasise although they may be locally destructive.

As the natural history of PVNS is one of potential aggression, it is accepted that surgical excision is the only curative treatment, and total synovectomy is required for the diffuse form where recurrence is common. Marginal or intra-lesional excision by curettage may not eliminate the disorder. The nature of the anatomy in the foot and ankle makes complete excision difficult to achieve.

Radiotherapy (RT) has been used in the management of recurrent disease with moderate radiation doses. Where complete synovectomy cannot be achieved, local recurrences have been treated with RT. Blanco et al. combined partial arthroscopic synovectomy with external-beam RT at a dose of 26 Gy for cases of PVNS in the knee where posterior joint access was difficult and only partial excision could be achieved. A recurrence rate of 14% within 1 year of surgery was reported. We present the results of a similar combined approach to PVNS of the foot and ankle. Case Report This 67-year-old male presented with complaints of pain, swelling, and instability of his left ankle that had progressed in both intensity and frequency over the last year, which was out of proportion to mild degree of pain and discomfort. The patient’s past medical history is significantly free from any medical illness, there is no history of any trauma for a left foot and ankle subsequently, the patient developed instability of this ankle. The patient described the pain as insidious, but more intense with weight-bearing and activity. He denied any

Zaid Aleyadah Jamal Alshawabkeh Jamal Rahyama

Royal medical services, Jordan

recent trauma and stated that with immobilization the pain resolved, but that the swelling had become persistent. The patient subsequently underwent an MRI scan after routine X-rays of his ankle appeared normal. T-1 weighted images performed in the sagittal and axial planes demonstrated a diffuse hypodense infiltrative lesion involving the soft tissue structures about both sides of the ankle. The osseous anatomy appeared relatively spared from this pathologic process despite its intra-articular involvement. This decreased signal intensity appeared most predominant on the lateral aspect of the ankle; however, medial involvement was also noted at this level and more distally involving the hindfoot lobulated focal mass representing pvns tissue was seen along the anterior aspect of ankle and subtalor joint, in addition to bone marrow oedema. Bone isotope scan was done which showed evidence of increased flow blood pool around the ankle and foot. Biopsy from the tissue was taken which revealed benign synovial lesion with papillary projection made up of foamy cells admixed with a few hemosiderin laden macrophages and multinucleated giant cells embedded in dense fibrous tissue. Focal areas of osteochondrometaplasia are seen. There is no evidence of malignancy, and final diagnoses features are in keeping with villonodular synovitis with osteochondrometaplasia. The patient then underwent open synovectomy and resection of this mass through medial and lateral approach. Upon dissection through the subcutaneous layer, an infiltrative mass of brownish-yellow tissue was noted in both peroneal tendons. This process appeared to infiltrate extensively both proximally and distally. There was also destruction of the peroneal brevis tendon. Additionally, the mass appeared to involve both the ankle and subtalar joints and extended distally into the hindfoot, to the area of the sinus tarsi. This process infiltrated and destroyed the capsular attachments at the tibiotalar joint. Lateral excision was performed until no further dystrophic tissue was visualized. Medial exploration was then performed. Involvement was found in both the posterior tibial and the flexor digitorum longus tendons. Medial synovectomy with mass excision was additionally performed to a grossly clear margin. Osseous involvement of the tibia or talus was noticed either medially or laterally. Pathology specimens of tendon with their associated sheathes and synovium were sent for analysis. At gross examination, multiple fragments of yellow, red and tan, dense, mottled tissue was received .The cut surfaces displayed areas of soft,

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rusty-red, friable, granular material admixed with white, dense tissue.

Microscopic analysis revealed synovial tissue with several areas displaying a focal villous architecture. The predominant cellular constituents were large mononuclear cells with abundant, eosinophilic cytoplasm, and ovoid nuclei consistent with epithelioid histiocytes. Interspersed amongst these histiocytes were multiple multinucleated giant cells and scattered small lymphocytes. Coarse, granular hemosiderin pigment was present both intra- and extra-cellularly. Varying amounts of collagen bands were also identified dividing the sheets of epithelioid histiocytes. Focally, sheets of foamy histiocytes, were also readily identified. These features were consistent with those described for pigmented villonodular synovitis.

Post-operatively, this patient continues to have mild discomfort and swelling, and associated mild instability in the anteroposterior plane to an anterior drawer test.

The patient is presently bearing full weight in conventional shoes and may require a stabilization procedure in the future for his instability. Discussion PVNS is an aggressive disease, and there is a substantial incidence of re-growth.

When found in the foot and ankle, the large number of joints in this region and the lack of integrity of the superficial muscle layers assist in allowing spread to adjacent articular spaces. Complete excision is therefore difficult to achieve. Radiation oncologists have been reluctant to employ radiation in the treatment of benign disease for several reasons: (1) the small but not negligible risk of late appearance of radiation-induced malignant tumours; (2) the need to reduce the radiation dose if an independent neoplasm was to arise in the same region of the body; and (3) non-malignant tissue changes that might appear subsequently and complicate healing of surgical wounds.

However, the clinical seriousness of many benign processes has liberalised the use of radiation and clinical data indicate that moderate radiation doses can be effective.

The Princess Margaret Hospital reported on their experience with 14 patients with advanced recurrent disease .The dose was 30-50 Gy. There was a complete response in 13 of the 14 patients. These data suggest that a moderate radiation dose is an attractive option in recurrent disease. An alternative has been the injection of radioactive yttrium 90 locally. Blanco et al. combined anterior arthroscopic synovectomy and post-operative RT with a total dose of 2,600 cGy for primary diffuse PVNS of the knee. At an average follow-up of 33 months, 86% of cases did not show signs of recurrence, and there were no apparent harmful effects from RT.

Research is continuing into the anti-inflammatory properties of radiation and the optimal treatment regimes and some of the mechanisms are becoming clear. For example, low radiation doses may have an anti-inflammatory effect through modulation of the NO pathway in macrophages. Since the pathogenesis of PVNS is unclear, it is not possible to infer that radiation affects the disease through the same pathways, but it seems likely that chronic inflammation has some role, and this may be why RT can improve symptoms and prevent recurrence.

Estimates of risk after low radiation doses to joints are also difficult to define. Many studies have addressed the incidence of second malignancy after treatment for childhood cancers and common adult tumours. These studies, whilst instructive for specific populations, should not necessarily be used to estimate risk for patients without malignant disease. This is highlighted by the fact that some of these tumours occur with increasing frequency at non-irradiated sites and are therefore due to factors unrelated to treatment, possibly genetic pre-disposition. After treatment for benign disease such as Grave’s ophthalmopathy in young patients, an absolute lifetime risk of radiation-induced cancer has been estimated at 0.3%. After treatment for joint disease at the knee or ankle in an adult, the only organ for which there is a quantifiable risk ofsecond malignancy is skin, and the estimated absolute lifetime risk is 22×10 -8 per Gy.

For the typical field size used in this study, this gives a risk estimate of three per 100,000. This small risk may be justified in patients with significant disability who may otherwise require radical surgery in order to achieve complete excision.

Although this study is too small to fully evaluate the benefit of radiation in these patients we have demonstrated that low-dose RT can be an effective adjuvant to surgery. References 1 Giant-cell tumour of the tendon sheath in the foot and ankle C. L. M. H. Gibbons, H. A. Khwaja, A. S. Cole, P. H. Cooke, N. A. Athanasou. From the Nuffield Orthopaedic Centre, Oxford, England 2 Case Report Pigmented Villonodular Synovitis, A Disease in Evolution HENDA BOUALI, ERIC J. DEPPERT, LAWRENCE J. LEVENTHAL, BRIAN REEVES, and THOMAS POPEThe Journal of Rheumatology 2004; 31:8 3 Blanco CE, Leon HO, Guthrie TB (2001) Combined partial arthroscopic synovectomy and radiation therapy for diffuse pigmented villonodular synovitis of the knee. Arthroscopy 17:527-531 [PubMed]. 4 Diffuse pigmented villonodular synovitis of the foot and ankle treated with surgery and radiotherapy. Reviewed by M. Lee, 1,3 S. Mahroof,1 J. Pringle,1 S. C. Short,2 T. W.R. Briggs,1 and S. R. Cannon1 Int Orthop. 2005. December; 29(6): 403-405. Published online 2005 August 30. doi: 10.1007/s00264-005-0004-8. 5 Pigmented Villonodular Synovitis in Children:A Report of Six Cases and Reviewof the Literature. Philip Neubauer, MD,A Kristy Weber, MDA, Nancy Hadley Miller, MDA, Edward F. McCarthy, MDA. The Iowa Orthopaedic Journal(continued page 40)

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Bochdalek’s Hernia: A Rare Underlying Cause of Acute Gastric Volvulus in an Adult Patient

ABSTRACT

Background: Gastric volvulus is a rare condition that can lead to significant morbidity and mortality if diagnosed and treated late after strangulation has occurred. Common causes include abnormal laxity of gastric ligaments, hiatal hernia (paraesophageal), and post-gastroesophageal surgery. Bochdalek’s hernia is a type of congenital diaphragmatic hernia that is usually asymptomatic and if present usually does so in childhood.

Objective: To report a rare case in which Bochdalek’s hernia was found to be the underlying cause of acute gastric volvulus in adult patient.

Case report: An adult female patient presented with epigastric pain, frequent vomiting and fever of two day duration. Chest X-ray showed distended gastric fundus above the left hemidiaphragm. Chest and abdomen CT scan confirmed the presence of diaphragmatic hernia containing part of stomach, spleen and bowel. Barium meal study confirmed the presence of gastric obstruction. Patient was diagnosed as a case of diaphragmatic hernia complicated by acute gastric volvulus. At laparatomy a Bochdalek’s hernia was found to be the underlying anatomical defect. Repair of the hernia was done after reduction of abdominal viscera and detortion of the stomach with gastropexy.

Conclusion: Bochdalek’s hernia, although rarely symptomatic and usually presents in childhood if any, can be the cause of significant morbidities in adulthood including acute gastric volvulus.

Keywords: Bochdalek’s hernia, congenital diaphragmatic hernia, acute gastric volvulus, strangulation, adulthood

Introduction Gastric volvulus is a rare clinical entity defined as an abnormal rotation of the stomach of more than 180°, creating a closed loop obstruction that can result in incarceration and strangulation. Most common causes are abnormal laxity of gastric ligaments, hiatal hernia (paraesophageal), and post-gastroesophageal surgery{1}.

Symptomatic Bochdalek’s hernia in adulthood is even rarer {6,7}. Here we present a case in which a Bochdalek’s hernia was found to be the underlying cause of acute gastric volvulus in an adult patient.

Abdullah Rababaah MD Samer Ghazawi MD Jihad Odeh MD Majdi Rababa RN

Correspondence: Dr. Abdullah Rababaah, general surgeon, department of surgery, Royal medical services, Jordan. Tel: 00962777513973 Email: [email protected]

Case Report A 16 year old female patient was admitted to the surgical ward with severe epigastric pain associated with frequent vomiting and fever of two day duration. There were no respiratory symptoms. On examination the patient had tachycardia (104 bpm) and low grade fever (38 c). Abdominal exam was unremarkable except for moderate epigastric tenderness. All lab results were within normal limits except for an elevated WBC count (14,000/mm3). Chest X-ray showed distended gastric fundus above the left hemidiaphragm (Figure 1 - next page). Chest and abdomen CT scan confirmed this in addition to the presence of part of the spleen and bowel along with it. Barium meal study confirmed the presence of gastric obstruction (fig 2). Diagnosis of diaphragmatic hernia complicated with acute gastric volvulus was concluded based on these findings. Adequate resuscitation was done and the decision was made for emergent laparotomy. At laparotomy the stomach, upper two thirds of the spleen, and distal one third of transverse colon were found to be displaced above the left hemidiaphragm through a 3-4 cm defect in the posterolateral aspect of the left hemidiaphragm “Foramen of Bochdalek”. Also there was organoaxial volvulus of the stomach with early ischemic changes. Reduction of all herniated viscerae with detortion of the stomach and gastropexy was done followed by closure of diaphragmatic defect in two layers. Six months has passed since then and the patient is doing well with no symptoms of recurrence. Discussion Bochdalek’s hernia is the commonest type of congenital diaphragmatic hernia {2}. It affects approximately 1 in 2200 to 12,500 live births {3}. Most of them are asymptomatic so that from all patients with a congenital Bochdalek’s hernia only 5% will be diagnosed in childhood or adulthood {4}. It is rare in adults and accounts for about 0.17% to 6% of all diaphragmatic hernias {5}. Symptomatic Bochdalek’s hernia in adulthood is very rare {6,7}. Adult Bochdalek’s hernia can present in two ways. They can give rise to vague, mainly gastrointestinal {2,8,9} (abdominal pain, nausea and vomiting, constipation) or respiratory {4,9} (chest pain, dyspnea, wheezing) symptoms, followed by severe attacks and episodes of incarceration with serious consequences. Characteristically, these symptoms

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can be intermittent, as herniated viscera can spontaneously reduce causing symptom regression. In such cases, radiological investigations demonstrate reduction of the hernia with symptom resolution {7}. Others will present with serious complications associated with strangulation of herniated viscera, especially when the diagnosis has been missed or treatment delayed {10}. There have been reports of Bochdalek’s hernia presenting with “sudden death” from intrathoracic complications {11}. Gastric volvulus is one of the rare but recognized complications of Bochdalek’s hernia and the mortality in these has been high (32%) because of visceral strangulation {12}. Diagnosis can be reached with CXR during an attack especially when hollow viscera herniates though large defects {2}. CT can detect small asymptomatic Bochdalek’s hernias {13} and a definitive diagnosis can be achieved with barium or gastrographin meal and enema {9}. Signs of incarceration or strangulation are absolute indications for emergency surgery {7}. A laparotomy incision represents the best approach because it allows better access to the abdominal viscera after reduction. This can be helpful when resection of an infarcted viscus is necessary or indeed, in cases of gastric volvulus where a gastropexy will be needed. In the age of minimally invasive surgery, laparoscopic repair {14} and video assisted thoracoscopic techniques {15} have been described for elective repair of Bochdalek’s hernia.

In this patient the diagnosis of acute gastric volvulus complicating some type of diaphragmatic hernia - proved to be a Bochdalek’s hernia operatively - was so obvious that the surgery was done after only a little enough time for resuscitation. Conclusion Although rare and usually asymptomatic, Bochdalek’s hernia can be the underlying anatomical defect leading to acute gastric volvulus. To minimize morbidity and mortality surgery should be done as soon as the patient is resuscitated.

References {1} Miller DL, Pasquale MD, Seneca RP. Gastric volvulus in the pediatric population. Arch Surg. Sep 1991;126(9):1146-9. {2} Ahrend TR, Thompson BW. Hernia of the foramen of Bochdalek in the adult. Am J Surgery 1971; 122:612-615 {3} Shin MS, Mulligan SA, Baxley WA, Ho KJ. Bochdalek hernia of diaphragm in the adult. Diagnosis by computed tomography.Chest 1987;92:1098-1101 {4} Osebold WR, Soper RT. Congenital posterolateral diaphragmatic hernia past infancy. Am J Surg 1976 131:748-754. {5} Mark E, Jeffrey SS, Saini SS, Peter RM. Prevalence of incidential Bochdalek’s hernia in a large adult population. AJR 2001;177:363-66

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Figure 2

{6} Losanoff JE, Sauter ER. Congenital posterolateral diaphragmatic hernia in an adult. Hernia 2004; 8:83-85 {7}Nouheim KS. Adult presentation of unusual diaphragmatic hernias. Chest Surg Clin N Amer 1998; 8:359-369 {8} Hines GL, Romero C. Congenital diaphragmatic hernia in the adult. Int Surg 1983; 68:349-351 {9} Perhoniemi V, Helminen J, Luosto R. Posterolateral diaphragmatic hernia in adults.Acute symptoms, diagnosis and treatment. Scand J Thorac Cardiovasc Surg1992; 26:225-227 {10} Niwa T, Nakamura A, Kato T, Kutsuna T, Tonegawa K, Kawai A, Itoh M. An adult case of Bochdale hernia complicated with hemothorax. Respiration 2003; 70(6):644-646 {11} Salacin S, Alper B, Cekin N, Gulmen MK. Bochdalek hernia in adulthood: a review and an autopsy case report. J Forensic Sci 1994; 39:1112-1116 {12} Fingerhut A, Baillet P, Oberlin PH, Ronat R. More on congenital diaphragmatic hernia in the adult (letter). Int Surg 1984; 69:182-183 {13} Wilkins AC, Govodes GF, Hibbeln JF. Imaging findings in adult Bochdalek hernias. Clin Imaging 1994; 18:224-229{14} Swain JM, Klaus A, Achem SR, Hinder RA. Congenital diaphragmatic hernia in adults. Semin Laparosc Surg 2001; 8:246-255

{15}Silen ML, Canvasser DA, Kurkchubasche AG, Andrus CH, Naunheim KS. Video-assisted thoracic surgical repair of a foramen of Bochdalek hernia. Ann Thorac Surg 1995; 60:448-450


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ABSTRACT Background: To prove the importance of clinical diagnosis for pulmonary emboli and to show the important role of embolectomy as a choice of treatment methods

We present the case of an 81-year-old man who had an acute massive pulmonary embolism after CABG surgery. The patient had undergone ACB to major OM and diagonal +LIMA to LAD. 12 hours postoperatively, he required emergent intubation when he suddenly became cyanotic, severely hypotensive, and tachypneic, with an oxygen saturation of 60%. An acute massive pulmonary embolism was suspected, and an emergency transesophageal echocardiogram confirmed the diagnosis. On the basis of the patient’s clinical condition and the echocardiographic findings, we performed an emergent pulmonary embolectomy, with the patient on cardiopulmonary bypass. We evacuated multiple large clots from both pulmonary arteries. The patient recovered and was discharged from the hospital 45 days postoperatively.

This case supports the use of open pulmonary embolectomy for the treatment of hemodynamically unstable patients on the basis of clinical diagnosis.

Key words: Embolectomy, emergencies, pulmonary embolism, Cardiopulmonary resuscitation.

Introduction Pulmonary embolism is one of the life threatening complications of open heart surgery. Pulmonary embolectomy was the mainstay of therapy for pulmonary emboli in 1960s and 1970s.presently, however, with the advent of effective nonsurgical therapy, pulmonary embolectomy is largely reserved for anatomically extensive central emboli with hemodynamic compromise or right ventricular strain, or for cases in which medical therapy has failed or is contraindicated. Massive pulmonary embolism is defined as obstruction of the pulmonary arterial tree that exceeds 50% of the cross-sectional area, causing acute and severe cardiopulmonary failure from right ventricular overload. Depending on the series reviewed, up to 50% of patients with pulmonary embolism experience a massive pulmonary embolism. Studies show that approximately 70% of patients who die of a pulmonary embolus die within the 1st hour after onset of symptoms, thus advocating rapid evaluation and intervention.(2) Definitive diagnosis is made on the basis of imaging studies (ventilation-perfusion scanning,

contrast pulmonary angiography, computed tomographic [CT] angiography, and echocardiography). Anticoagulation and thrombolysis are the basic methods of treatment of pulmonary embolism. Inotropic support for hemodynamic optimization completes the axis of medical therapy. Surgical embolectomy has also been described in extreme cases. Massive pulmonary embolism with cardiopulmonary collapse at times precludes time-consuming imaging studies and requires urgent pulmonary embolectomy on the basis of clinical criteria and a high index of suspicion for pulmonary embolism.(1) Urgent pulmonary embolectomy in the surgical treatment of pulmonary embolism has received mixed reviews in terms of efficacy and associated morbidity and mortality. Opinions range from no need for pulmonary embolectomy in massive pulmonary embolism to pulmonary embolectomy for massive pulmonary embolism in patients without hemodynamic disturbances.(3)

We report a case of a massive pulmonary embolism that required an urgent pulmonary embolectomy on the basis of clinical impression and emergent transesophageal echocardiography (TEE). This report highlights the early use of open pulmonary embolectomy in the surgical treatment of acute massive pulmonary embolism.

Case Report An 81-year-old man underwent CABG surgery. He became acutely cyanotic and went into acute respiratory distress 12 hours postoperatively. He was also hypotensive (systolic blood pressure as low as 50 mmHg) and cyanotic (SaO2 of 60% and PaO2 of 48.8 mmHg) and had to be intubated and started on high-dose inotropic support. At this time, given the acuity of the hemodynamic instability and the risk factors for deep venous thrombosis, an acute massive pulmonary embolism was suspected. The patient became hemodynamically stable for a short period of time after intubation and required high-dose inotropic support; however, he became more hemodynamically labile despite additional inotropic agents, with a blood pressure of 63/39 mmHg and a central venous pressure of 28 mmHg on epinephrine, dobutamine, and vasopressin support. The patient did not require cardiac massage throughout the resuscitative efforts.

Pulmonary Embolectomy After CPR For Post CABG Arrest

Razi Abu Anzeh Khaled Nawaiseh

Razi Abu Anzeh, MD. Khaled Nawaiseh, MD. Department of Cardiac Surgery at Queen Alia Heart Institute,JORDAN

Correspondence: Dr Khaled Nawaiseh. Email: [email protected]

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M I D D L E E A S T J O U R N A L O F I N T ER N A L M ED I CI N E • VO LU M E 2 , I SSU E 3 ��MIDDLE EAST JOURNAL OF INTERNAL MEDICINE VOLUME 4, ISSUE 1

A TEE revealed a severely dilated right ventricle with decreased systolic function. The proximal pulmonary artery was also visualized and appeared dilated with a large floating thrombus within its lumen.

The patient was taken to the operating room, and an emergent sternotomy with aortic and bicaval cannulation was performed. Full normothermic cardiopulmonary bypass on a beating heart was instituted. A longitudinal pulmonary arteriotomy was made, and a #7 Fogarty catheter was passed multiple times down the left and right pulmonary arteries. A large amount of clot was removed from the lumen of the left and right pulmonary arteries. Intraoperative TEE confirmed no residual pulmonary emboli, and the arteriotomy site was closed with 4-0 Prolene sutures. The patient was very slowly weaned off cardiopulmonary bypass over approximately 2 hours. The sternum could not be closed during this operation due to a distended right ventricle, and the patient required closure of the sternotomy along with inferior vena caval filter placement, 2 days later. Postoperatively, the patient did well and slowly recovered. He was discharged from the hospital on the 45th postoperative day, taking an oral anticoagulant. He was seen 8 months later and had no recurrent pulmonary embolism nor congestive heart failure.

Discussion First described in the 1800s, pulmonary embolism can be classified as acute or chronic, as submassive (25%-50% obstruction) or massive (>50% obstruction), and as central or peripheral.(4) Acute pulmonary embolism leads to an abrupt rise in pulmonary vascular resistance. Right ventricular contractile function is compromised, and right ventricular failure ensues. This vicious cycle of cardiogenic shock is augmented by concomitant hypoxia, which inevitably leads to cardiovascular collapse.(5) The interval from the onset of symptoms to death is relatively short. In patients with massive pulmonary embolism, 50% die within 30 minutes, 70% die within 1 hour, and more than 85% die within 6 hours of the onset of symptoms.(6) Therefore, the window for obtaining a definitive diagnosis is small. In an optimal setting, the diagnosis of pulmonary embolism can be made on the basis of the history and physical examination along with selective tests, such as electrocardiography (ECG) to rule out myocardial infarction, chest radiography to rule out pneumothorax, and an arterial blood gas analysis to bolster the diagnosis.(2) Electrocardiographic signs of pulmonary embolism are seen in approximately 75% of cases; however, ECG changes, along with radiographic findings consistent with pulmonary embolism, are often not present.(7) Pulmonary angiography and spiral CT pulmonary angiography, the diagnostic gold standards for pulmonary embolism, are precluded by hemodynamic instability in many patients. A delay in treatment in order to complete a lengthy and invasive diagnostic procedure is not justified. Transesophageal echocardiography is a method that is beneficial and is gaining acceptance in demonstrating, non-invasively, right ventricular dilatation and the presence of emboli within the pulmonary arteries.(4) When the diagnosis of massive pulmonary embolism is made, medical or surgical treatment must be initiated immediately. If the patient is

in extremis, the decision to perform embolectomy may be made primarily on clinical impression. Treatment options for massive pulmonary embolism vary, depending on the clinical picture of the patient. Although anticoagulation and thrombolysis are the standard for treatment of acute massive pulmonary embolism, these treatments are limited to patients who are hemodynamically stable and do not have contraindications. Furthermore, data suggests that patients treated with thrombolysis have a higher death rate, increased risk of major hemorrhage, and increased rates of recurrence of pulmonary embolism, compared with patients treated by means of pulmonary embolectomy.(8) The International Cooperative Pulmonary Embolism Registry found a surprisingly high intracranial hemorrhage rate of 3% among patients with pulmonary embolism who were treated with thrombolytic therapy.(9) Regardless, the risk of fatal hemorrhagic complications of thrombolysis restricts the use of these agents in the immediate postoperative course, as was in the case of our patient. Although interventional catheter-based catheter fragmentation and suction embolectomy are also available for pulmonary embolectomy in some institutions, open surgical embolectomy is indicated in patients who have contraindications to thrombolytic therapy, persistence of thrombi in the right heart or pulmonary arteries after pulmonary embolism, or severe hemodynamic compromise with cardiovascular collapse. Early surgical treatment must also be considered in patients whose course deteriorates in spite of aggressive medical therapy.(10) Depending on the series, the overall mortality rate after pulmonary embolectomy varies from 16% to 46%, with a mean mortality rate of 26%. The high mortality rate, for the most part, is due to the fact that most patients who undergo surgical embolectomy are hemodynamically compromised and arrive at the operating room in cardiac arrest with cardiopulmonary resuscitation (CPR) in progress, or else they have had CPR performed beforehand. Data suggest that preoperative hemodynamic status is the most important prognostic indicator of postoperative outcome after surgical pulmonary embolectomy, and cardiac arrest and CPR are independent factors predictive of postoperative death.(4,10) These findings suggest that earlier surgical intervention may result in improved survival. The present report describes a case in which severe hemodynamic compromise mandated a surgical embolectomy. References 1. Brevetti GR, O’Brien B, Coomer CL, Hall TS, Brevetti LS, Jablons DM. Emergent surgery for massive pulmonary embolism on the basis of clinical diagnosis. Tex Heart Inst J 2003;30:149-51. [PMC free article] [PubMed] 2. Hsieh PC, Wang SS, Ko WJ, Han YY, Chu SH. Successful resuscitation of acute massive pulmonary embolism with extracorporeal membrane oxygenation and open embolectomy. Ann Thorac Surg 2001;72:266-7. [PubMed] 3. Aklog L, Williams CS, Byrne JG, Goldhaber SZ. Acute pulmonary embolectomy: a contemporary approach. Circulation 2002;105:1416-9. [PubMed] 4. Ullmann M, Hemmer W, Hannekum A. The urgent pulmonary embolectomy: mechanical resuscitation in the operating theatre determines the outcome. Thorac Cardiovasc Surg 1999;47:5-8. [PubMed]

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5. Ohteki H, Norita H, Sakai M, Narita Y. Emergency pulmonary embolectomy with percutaneous cardiopulmonary bypass. Ann Thorac Surg 1997;63:1584-6. [PubMed] 6. Stulz P, Schlapfer R, Feer R, Habicht J, Gradel E. Decision making in the surgical treatment of massive pulmonary embolism. Eur J Cardiothorac Surg 1994;8:188-93. [PubMed] 7. Tayama E, Ouchida M, Teshima H, Takaseya T, Hiratsuka R, Akasu K, et al. Treatment of acute massive/submassive pulmonary embolism. Circ J 2002;66:479-83. [PubMed] 8. Gulba D, Schmid C, Borst HG, Lichtlen P, Dietz R, Luft FC. Medical compared with surgical treatment for massive pulmonary embolism. Lancet 1994;343:576-7. [PubMed] 9. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet 1999; 353:1386-9. [PubMed] 10. Meyer G, Tamisier D, Sors H, Stern M, Vouhe P, Makowski S, et al. Pulmonary embolectomy: a 20-year experience at one center. Ann Thorac Surg 1991;51:232-6. [PubMed].

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