الجمعة، 11 مايو 2012

Tuberculous Sinuses Re-Visited عامر التواتي

Tuberculous Sinuses Re-Visited


S. Theophilus Bushan,* Amer Irhuma,* Einass Elhudeiri,*


Background:
Tuberculous sinuses occur as a result of long standing T.B. Lymphadenitis, untreated and or its complication. Patients may neglect and delay in seeking medical help due to ignorance, poverty and or lack of education, some times non-availability of medical facility or undiagnosed initially by the primary care physicians who see the patient.

Aims of the Study:
This study was mainly initiated to see why the patients with T.B.sinuses were so much delayed in getting the timely medical treatment even when medical facility is a state sponsored programme to all its citizens and resident foreigners.

Methods:
All patients with peripheral sinuses attended our OPD suggestive of tuberculosis and all cases of T.B. Lymphadenitis / Sinuses attending TB Hospital (Dharan) from Jan 2001 to June 2002  one and half years analysed.

Results:
25 patients had registered with Dharan hospital during this one and half years study period both referred and direct visits. There were 15 male, 7 female, 2 female children and one male child.Age ranged between 3 years to 64 years. Cervical nodes were effected in 16 patients Supra clavicular, submandibular nodes 2 each Tuberculus sinuses were resent in 3 patients Lymph node biopsy   was done in 15 patients, and FNAC Smear in 2 patients. AFB (Z-N) stain was done in sinuses.

Diagnosis was established in 20 patients (80%). PPD (Montox) test was done in 19 patients (76%), PPD was significant diagnostically is 17 patients (68%) Chest X-ray (MMR) was done in all the cases yeilded Hilar Lymphadenopathy in 5 patients (20%).
All the patients received W.H.O regime of anti.T.B. treatment. There were only 2 defaulters



Conclusions:
Most patient are compliant of therapy 92% (23 patients) only 2 had defaulted (8%). There is both neglect, ignorance, lack of medical knowledge on part of the patients as well as delay in diagnosis by the primary care doctors initially when seen first (cases illustrated).
This needs to be remedied by C.M.E  special programme on tuberculosis in chest TB hospital regularly to the primary care doctors who usually see these patients first.

Introduction & History:
Scrofula defined as tuberculosis of lymphglands  has afflicted humans for thousands of years. Hippocrates (460-377BC) mentioned scrofulous tumours in his writings and Herodotus (484 ;- 425 BC) described the exclusion of those patients who had leprous lesions from the general populations1
In Europe in the middleages this illness was known as KNG'S EVIL because of apparent cure of many cases following KING'S ROYAL TOUCH!.
Historians have recorded vivid accounts of the crushing mobs gather to see the royal touch.2
Scrofula most frequently afflicted children between 2-15 years. In 1884 in England out of 133,000 children examined, 24% showed obvious scars of scrofula or had enlarged cervical lymph nodes.3

Patients and Methods:
All the patients registered with  TB (Dharan) hospital referred and direct visits, as tuberculosis have a master card showing medical data, investigations and treatment schedule.
All the 25 patients of TB lymphadenitis and TB sinuses were analysed. All patients had undergone complete general physical examination routine blood investigations, chest X-ray (MMR). FNAC smear and lymph node biopsy in selected cases and PPD (Mantoux) test in majority of the patients.
All the patients were on WHO regime of management with monthly follow up and some patients are admitted needing special monitoring.


* Department of  Gen. Surgery 2nd March Hospital, Sebha, Libya.
* Faculty University of Sebha, School of Medicine, Sebha, Libya.

Case I:
K.M. 31 years old Libyan female attended our clinic in Jan.2002 with h/o non healing ulcers in the left axilla and left hand since 6 months. She had seen 3 different doctors and had many courses of antibiotics and regular dressings.
On examination she was sickly looking young female, anemic with multiple sinuses discharging thin watery pus covered with unhealthy granulation tissue   in the axilla she also had 2 small ulcers over the fourth and fifth fingers of the left hand  covered with unhealthy granulation tissue.
She under went all routine investigations including HIV, HbsAg test, chest x-ray all were negative. AFB smear was negative but PPD (montonx) test was highly positive.
She was started on anti TB treatment from 17.1.2002. She has completed 6 months course and on regular monthly follow up All the sinuses have healed. Her appetite has improved and she has gained weight. Her husband is happy and dedicated to his wife who always accompanies her to the clinic every visit.
In this case delay in starting the proper management was due to non-diagnosis by the  doctors who saw her before.

Case II.
A.M. 27 years chadian female attended our OPD in March 2002 with Repeated episodes of abscess over the chest since 12 months.
She is from Hoon about 600 Km and was taking medical treatment from different clinics from the near by Village.
Fortunately she was known to some hospital staff here who brought her to our clinic for management.
On examination she had partially opened abscess  over the left mammary region which was incised and drained. Pus was sent for AFB stain.
We carried out all routine investigations including a chest x-ray, ESR was 70 mm/1st  hour PPD was highly positive. Chest x-ray showed bilateral hilar adenitis.
She was registered with TB hospital and anti TB treatment was given from 24.3.2002.
Within 1 month her appetite improved, sinuses are getting better. She is well and regularly visiting Dharan hospital for the treatment (see the photo).
Case III.
25 years Nigerian male and an inmate of the jail hale and hearty before imprisonment, developed a swelling over the  Lt  sterno clavicular joint, slowly increasing in size with minimal general symptoms. Since April 2002. He was referred to the 2nd March Hospital by the attending Physician, where he underwent all the routine tests. The abscess was drained in June 2002. Pus sent for AFB smear, (chest x-ray was negative PPD was not available he was on IV antibiotics for 1 week (inj Rocephin 1g daily) and discharged.
The residual abscess did not respond to routine medications and he started developing neck swelling as well. The doctor sent him to Dharan hospital and on clinical grounds he was started  anti T.B. treatment as an in patient with short course of steroids and he dramatically responded. He is undergoing full anti TB treatment.
The above 3 cases were success stories sadly there are unsuccessful stories as well. There were 2 young Libyan male patients with Bilateral cervical lymphadenopathy one a cold abscess and another with sinus were advised FNAC and cytology after routine investigations and a chest x-ray. Both the patients did not return inspite of our firm instructions these two cases show the negligence and ignorance on the part of the patients.

Discussions:
Tuberculosis (TB) remains one of the deadliest diseases in the world mycobacterium tuberculosis kills more people than any other single infectious agent  TB is a social disease with medical implications.
In 1993 world health organisation took a unique step of declaring TB to be a world emergency.
WHO estimates each year 8 million new cases of TB occur and 3 million people die from the disease. About 95% of TB occur on the developing countries.
Between 2000 to 2020 about 19-43% of world populaiton will be infected tuberculosis nearly 1 Billion people will newly be infected, 200 million will be sick and 3.5 million will die from the disease. About 95% of TB occur in the developing countries. Other factors may contribute to increase TB such as HIV/ AIDS poverty, over crowding multidrug  resistance etc..4
Tuberculosis of the lymphnodes is one of the most common form of extrapulmonary tuberculosis.5
In developing countries tuberculosis is the most common cause of cervical lymphadenopathy.6
There is racial difference in the form of presentation of extra pulmonary TB in whites 37%  present with cervical node involvement where as 52% the patients originating from Indian sub. Continent.7
Scrofula has been historically a disease most common in children.8
However numerous recent studies from developed countries peak  age is between 20 to 40 yrs.8,9

Pathology:
Mycobacterum tuberculosis infection is spread from the primary focus to regional lymphnodes in almost all cases.10
This often results in greater volume of the diseased tissue in regional lymphnodes than at the original site of infection.11
Infection from the regional lymphnodes may continue to spread via lymphatic system to other nodes or may pass through the nodes and reach the blood stream in small numbers, from here virtually it can spread to any organ in the  body. This form of lymph-hematagenous spread is usually self limited and more than 90% of primary infectious heal with a positive tuberculosis reaction and perhaps a little pulmonary calcification.12
The primary (childhood) versus secondary (adult) tuberculosis is distinctly different relative to lymphnode involvement.13
In untreated tuberculosis of children (primary TB) almost all patients will have enlargement of hilar and or paratracheal lymphnodes apparent on chest radiographs (14-15%) and 5% will develop scrofula within 6 months of tuberculous infection.16
The node involvement occurs shortly after the onset of primary infection is supported by the fact that more than 80% of children with cervical lymph node involvement have radiological evidence of pulmonary tuberculosis.17, 18
In contract, adult tuberculous lymphadentis is accompanied  by abnormal
chest radiographs only in 30% of the cases and represent old healed lesions suggesting nodal disease is from reactivation of previous infection.19, 20, 21
Historically lymphnode tuberculosis was caused by Bovine Mycobacteria but nearly all lymphnode tuberculosis now a days is due to mycobacterium tuberculosis.22
The major pathological events of lymphnode tuberculosis include compression of surrounding tissue,  caseation and breakdown of nodes and fibrosis from healing of the eroded nodes.
Mortality is uncommon but morbidity and chronic illness are the rule.23
Lymphnode enlargement within the mediastinum may also be accompanied by compression of major blood vessels, nerves, occlusion of lymphatic drainage erosion into the chest wall and sternum.24,25
Involvement of the superficial lymph node usually results in enlarging mass lesions if untreated swelling progresses and nodes within a group become matted eventually caseation leading to rupture causing chronic sinuses.26,27

Clinical Picture:
More than 90% of superficial tuberculous lymph nodes are found in the head and neck regions. In the cervical region anterior and posterior cervical group, supra-clavicular and sub mandibular groups are commonly involved and occasionally pre-auricular and submental nodes get involved.28
Most infected nodes heal but the organisms may lie dormant and viable for years or decades and can again multiply and produce active disease.
In severe immuno compromise, tuberculous  lymphadenopathy may be acute and resemble acute pyogenic lymphadentis.29

Symptoms:
It presents as painless swelling of one or more lymphnodes clinical presentation of lymphdenitis include mildly tender slowly progressive swelling of the involved lymphnodes.30
Most patients give a fairly long history and usually seek medical advise because the lumps have become painful.
In Asia the presentation is different , 20% have discharging sinuses, 10% have cold abscess , 10% are adherent to the skin, these patients usually have negative chest X-ray 90% are unilateral and 90% involve one node group commonest being deep jugular chain followed by submandibular and posterior triangle group.31
Generalised lymphdenopathy and hepato splenomegaly, occur in less than 5% of most series. In cases of childhood miliary tuberculosis generalised lymphadenopathy may be found in 10% to 15% of cases.32
In less than 20% of patients there are associated symptoms such as weight loss, raised temperature, anorexia, fatigue, malaise and or pain.33
Other uncommon presenting symptoms of tuberculous lymphadenitis include chronic right sided chest pain caused by intercostal lymph node involvement.34
A neck mass with dysphagia caused by a traction diverticulum of the oesophagus35 and generalised lymph node enlargement suggesting reticulo histocytic tumours.35
On examination peripheral tuberculous nodes are initially firm or rubbery, discrete and non tender. The painless quality usually persists despite caseation  and erosion through the skin. Occasionally in young children the nodes may be  swollen and tender owing to secondary bacterial infection.36
The physical appearance of superficial tuberculous lymphadenitis has been classified into five stages by Jones and Campbell.37

Stage I.   Enlarged, firm, mobile discrete nodes showing non-reactive hyperplasia.
Stage II.  Larger rubbery nodes fixed to surrounding tissues due to periadenitis.
Stage III. Central softening due to abscess formation.
Stage IV.  Collar stud abscess.
Stage V.  Rupture and sinus formation
Majority of cases fall into stage 2 & 3 at the time of presentation.38

Diagnosis:
1. The differential diagnosis of tuberculous lymphadenitis is extensive.
      Consideration must be given to infections, sarcoidosis, non tuberculous mycobacteria, viruses, chlamydia, fungi, toxoplasma and agent of cat scratch ferver.39, 40, 41
2. Neo plastic diseases such as lymphoma, kaposi's sarcoma, Hodgkin's disease and metastatic carcinoma42 .
3. Drug reactions e.g.  hydantion sodium.43
4. Non-lymphoid neck swellings
- partotid gland.
- sub-mandibular gland.
- branchial arch cyst.
- cystic hygroma.
- carotid body tumour.

Medical and social history and chest x-ray is very important particularly in children. More than 80% of children have a history of exposure to active tuberculosis and chest x-ray shows active tuberculosis and this is uncommon in adults.
Diagnostic sensitivity  by lymph node aspirate and AFB smear is 70% In ymphnode excision, examination of the cut surface and smear for AFB yields about 80% positivity.
Lymphnode biopsy and routine histological examination and finally Culture of the tissue are confirmatory.

Newer methods:
Fluro-chrome staining advanced laboratories use auramine-rhodomine stain for the lymphnode aspirate and mycobacteria fluresee with bright orange colour under low power microscopy.45

Tuberculin skin test:
Mantoux test is preferred and  a standard skin test for detecting T.B. is Performed by using 5TU (purified protein derivative) usually 0.1 ml is injected intra dermally and the induration is measured at 48-72 hours Mantoux test is positive in more than 90% of cases in tuberculous lymphadenitis.46

Culture Technique:
Lowenstein-Jensen culture medium is most commonly used for myo-bacteria, but the growth takes upto 6-8 weeks.
Now-a-days modern laboratories simultaneously culture specimen in broth based medium that takes only 2-3 weeks for mycobacterial growth.Mycobacteria grown in liquid medium are usually spaciated and sub cultured in the presence of different anti mycobacterial agents to assess drug sensitivity.

Firefly Luciferase:
This ingenious assay uses the fluorescent capabilities of fireflies genetically implanted in mycobacteria tuberculosis. The procedure offers the possibility of testing mycobaterial drug   sensitivity in hours.47

Treatment:
Management of tuberculous lymphadenitis involves appropriate use of antituberculous drugs and judicious use of surgical excision in minority of cases.
Chemotherapy is nearly always curative in cases of superficial lymphadenitis before caseation and sinus formation.48
Surgery should be limited to those patients who fail to show improvement Even after an adequate course of chemotherapy or who have discomfort from enlarged tense & fluctuant nodes.49
Surgery of choice is always complete excision of the involved nodes and surrounding tissue with a healthy margin. Surgical excision does not affect the outcome of the disease process.50

Catogory 3 of WHO guidelines

Sputum smear-negative, PTB with limited parenchymal involvement, extrapulmonary T.B. ( a new, less severe forms like lymph, plearal effusion, bone (exduding spine) peripheral joint, adrenal gland.
Initial phase                   Continuous phase
2 HR2 …………………………….. 6 HE
2 HR2 …………………………….. 4 HR
2 HR2…………………………….. 4 H3  R3
2 H3 R3 23* …….………………….. 4 H3 R3*

* Applied in the revised national tuberculosis programme in India Initial phase includes 2 months of H -isonazid
R-rifampicin and Z pyrizinamide and Continuos phase of 6 months with H. isonazed, E. ethambutol or 4 months of H. isoniazid, R, Rifampicin, or 4 months H.isoninzed, R. Rifampicin ( x 3 times per week ).



Dosage of 1st line ant tubercular agents

Anti TB drugs
Mode of action
Recommended dose mg / Kg /day
Reduce dose is
Renal failure
Liver failure
Isoniazid (H)
Bactericidal
5 (4-6)
No
Only in severe liver impairment
Rifampicin  (R)
Bactericidal
10 (8-12)
Yes
No
Pyrizinamole (Z)
Bactericidal
25 (20-30)
Yes
No
Streptomycin (S)
Bactericidal
15 (12-18)
Yes
No
Ethambutol (E)
Bacteriostatic
15 (12-20 )
Yes
No
Thiactazone (T)
Bacteriostatic
2-5
yes
-


Results:
There were total of 243 patients registered in the study period of 1½  years including pulmonary, extrapulmonary and suspected cases.

Year 2001            year 2002 (6 minths)
Pulmonary            - 65        -  49
Extrapulmonary   - 34         - 22

Suspect                 - 39         - 34

                              138         105

Peripheral lymphadenitis with sinuses were 25 patients (10.28%) there is high number 73 patients (30.04%) forming the suspects group whose diagnosis not confirmed but clinically strongly suspected. Biopsy or FNAC cytology was not done or patients came from far distances and could not come again for full investigations. But in cases of tuberculous lymph nodes diagnosis was established in 20 patients (80%).
We used all available modalities such as FNAC for AFB smear, lymphnode biopsy and montoux test. There were only 2 defaulters and they could not be traced as we do not have a social worker who can go to their houses.

Conclusions:
There is definite delay of patients with TB lymphadenitis and sinuses seeking medical help partly due to ignorance, neglect, lack of education of the patients and also we have noticed that the primary care physicians who could not make the proper diagnosis for timely referral to the TB hospital. We propose that there should be C.M.E. programme about tuberculosis every 6 month to the primary care physician in the TB (Dharan) hospital so that the attending doctors are updated about tuberculosis as per W.H.O guidelines.

Acknowledgement:
We wish to thank Dr.  Mohammed AA. Abusaifi MPH director Dharan hospital, Zahid Al Hamid DTCD and their staff for co-operation and fruitful discussion in data collection and suggestions in the over all management.





 


CLINICAL PHOTOGRAPHS



 



                                    




 













                     A.M. 27 years Female                                                Nigerian male 25 years

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3. Lomax L: hereditary or acquired disease ; early nineteenth century     debates on the cause of infantile scofula and tuberculosis J Hist med    1977 ; 32:356-374.
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11.Pratt PC: pathology of tuberculosis semin Roentgenol, 1979;14:196-203.
12&13. Stead, WW: pathogenesis of the sporadic case of tuberculosis New Engl J Med, 197=67; 277:1008-1012.
14. Kendig EL: tuberculosis in Kendig EL, Chernick V (Eds) disorders of respiratory tract in children Philadelphia, WB Saunders 1977, P 787.
15. Sewell EM, Tuberculosis in Krugman S, KatzSL (Eds) infectious diseases in children St Louis CV Morby 1981 p. 427.
16. Lincoln EM, Sewell EM (Eds) tuberculosis in children New York Mc Graw Hill 1963.
17. Schuit KE, Powel DA: Mycobacterial lymphadenitis in children Am J Dis child 1978: 132; 675-677.
18.  Remngton RM : tuberculous cervical lymphadenitis letter can med Assoc. J. 1979; 121:1572.
19. New Combe  JF: Tuberculous cervical lymphadenopathy post grad  Med J 1971; 47: 713-717.
20. Tomblin JL, Toberts FJ : Tuberculous cervical lymphadenitis can  Med Assoc J 1979; 121:324-330.
21. Cantrell RW Hansen JH Reid D: Diangosis and management of tuberculous cervical adeniits Arch otolaryngol 1975; 101:53-57.
22. Tuberculosis Ed. David Schloss berg. Springer vorlag   - 3rd ed. 1994 p. 145
23. Dhand S, Fisher M, Fewell JW: Intrathoracic tuberculosis lymphadenopathy in adult JAMA 1979; 241: 505-507.
24. Rana SR, Saena SB, Gumb, SAV, tuberculous mediastinal lymph adenitis with chest wall mass. Paediatra radiol 1985; 15: 127-128.
25. Appling D, Miller RH: mycobacterial cervical lymphadenopathy: 1981 update Laryngoscope 1981; 91:1259-1266.
26&27. Ord RF, Matx GJ: tuberculous cervical lymphadenitis Arch  otolaryngeal 1974; 99: 327-329.
28&29.  T.B management companion hand book (IMS 74 booket (July- Sep2001) by K. Fenkatraman  Bio gard pvt Ltd pp 12, 13.
30. Essential surgical practice ed by A. Cuscheri, GR. Giles  A.R.  Moosa Butter worth Heinmann. 3rd Ed. 1995 pp 579.
31. Schuit KE: Miliary tuberculosis in children, clinical and laboratory manifestations in 19 patients Am J. dis child 1979;133:583-585.
32. Kendig EL: Tuberculosis in Kendig El, chernick V (Eds) Disorders of the respiratory tract in children Philadelphia, WB Saunders, 977, p. 787.
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Typhoid Perforation of the Appendix: a Rare Clinical Entity عامر التواتي


Typhoid Perforation of the Appendix: a Rare Clinical Entity

Theophilus Bhushan,* Amer  T. Irhuma,**  Mahmood Hussein***

Abstract: Bleeding and perforation of the intestine are the most major complications of typhoid fever. Perforation usually occurs in the 2nd or 3rd week of the illness. Common sites of perforations are ileum, jejunum and caecum in order of frequency but perforation can occur in any part of the gut at any time during the illness.1
Key words:-  Typhoid fever, perforated appendix, laparotomy.


Introduction:

Intestinal perforation mainly occurs in ileum, jejunum, or caecum but can occur in any part of the gut. We report two cases of typhoid perforation of the appendix: one in a child and another in an adult. A 7-year old boy was presented with febrile convulsions and peritonitis. His widal test was positive both pre-operative as well as post-operative period.  Appendical perforation due to typhoid fever is a rare clinical presentation; hence it is being reported.

Case report: first Case.
A 7-year old Libyan boy was initially admitted to the pediatric ward on 23/3/2002 with h/o high fever and convulsions lasting for periods of 5 minutes and 30 minutes prior to admission.
Seven days of fever preceding admission he was treated with anti pyretics at home.  The boy had constipation for 4 days and lower abdominal pain with dysuria for one day prior to admission. He was immediately treated with IV diazepam, cold sponging and rectal paracetamol suppository. There was no past medical history of any major illness or epilepsy; immunization was complete.
O/E the child was ill, febrile (38.5 c) and dehydrated but conscious and oriented.
Vital signs were BP 90/60 P 120/mm RR 20/mm. Blood sample was obtained for investigations.  (see table 1).
On the 2nd day of admission, the child was more alert, but still ill, febrile and mildly dehydrated. His abdominal examination showed guarding, tenderness and rigidity more in the lower abdomen.
The child had vomited twice and complained of lower abdominal pain and dysuria .
Surgical consultation was sought and the patient was transferred to the surgical ward.
A surgical team reviewed the history and examination and confirmed the diagnosis of peritonitis and further investigations were carried out as to the cause of peritonitis. He was kept on N.P.O. I.V. fluids started with other supportive treatment.
The patient started having a foul smell due to a large quantity of loose stool about 6 times in the surgical ward. The stool was sent for routine examination and culture.
On PR examination there was no boggy mass only mild rectal wall tenderness.
Chest X-ray and abdominal X-ray was non-contributory; all blood examination was repeated. Widal test was done. Ultra sonography was performed by a senior radiologist, which was reported as highly suggestive of acute appendicts. The patient was well dehydrated, fever was controlled, triple antibiotics regimen (ampicillin, gentamycin & flagyl in appropriate dosage) was started. The patient was taken up for surgery on 25th March 2002. Under G.A. with E.T.T. After routine aseptic cleaning and drapping, right lower oblique incision was made. Findings were: there was congestion with a few areas of hyperemiea over the ileum and caecum.
Appendix was acutely inflamed, thick and edematous having tiny perforation at the tip, surrounded by a small amount of peri appendical fluid. There was no free pus or collection in the pelvis.
Classical appendectomy was performed and warm saline lavage done. Abdomen was closed with a tube drain. Post-operative period was uneventful except for a gradually subsiding fever and loose stools. Sutures removed on the 7th day and the patient was discharged on the 8th  day. He was put on augmentin and multivitamin syrup as pre-operative and post-operative widal test was positive.


* Lecturer in Surgery, 2nd March Hospital (University Teaching Hospital) Sebha, Libya.
** Con. Surgeon &   HOD Surgery, 2nd March Hospital (University Teaching Hospital) Sebha, Libya.
*** Consultant radiologist, 2nd March Hospital (University Teaching Hospital) Sebha, Libya.

Table  1: investigations of first case


1
Urine examination
Pus cells 10-12. RBC 6-8, Bacteria ++
Epeth cells ++ sugar – Neg. proteins  -+
2
Stool examination
Cyct, larva ova –neg. puscell, RBC 0-1/HPF


         23rd
     25th
    30th
3
CBE
11.800
7.4x103 M/L
9.3x103 M/L

Hb
     -
10.5 g%
12g%

PLT
     -
144x103
618x103

Poly
     -
73.4%
62%
4
Stool Cls
No growth
5
Widal test
S. typhi H. 1:160
S. paratyphi’B’ 1:80

0n 24th & 30th
6
Chest X-ray
No gas under diaphragm
7
Abdomen X-ray
Few gaseous distention of Colon
8
Sr. chemistry
BS 74 mg%  BU 19mg%, Na 138, K 2.8 Cal 168
9
Bl group
A +
10
US- abdomen
Appendix distended Non-compressible with small periappendical collection. Highly suggestive of Acute appendicitis

Table 2: Investigation of second case

23/5
25/5
26/5
29/5
Hb
16.28%
168%
15.79%
15
TLC
14.200/-
4.400/-
7.400/-
9.900/-
BU
24
30
32
--
Creat
--
--
--
--
Na
133
134
138
--
K
3.7
3.5
3.8
--
Ca
0.99
0.98
1.06
--
Plt
121x103
--
--
104x103
BS
176
87
--
--


Widal 25.5.02 pre-op.
  STO - +
  STH - +
  SPTH.A +
  SPTH. B +
Widal  29.5.02
       STO 1:320
       STH 1:320

CXR no gas under diaphragm
Abdominal x-ray  – few gaseous distended large bowel no air fluid level
USG – 1st appendicular mass 6.5 x 5.5 well defined hydrogenous no free fluid in the abdomen or pelvis.
USG – 2nd appendix thick walled 5.2 x3.4 with calcification. No localized collection, no free fluid. Bowel engorged thick walled no perforation.

2nd Case:
A.S. 27 years Libyan male from Marzuk was admitted on 23.5.02 with acute pain abdomen of 4 days duration associated with vomiting and fever for one day.
He was admitted in Marzuk hospital for one day and transferred here for further management.
On examination the patient is tall, well built, febrile, ill looking and dehydrated.
His vital signs were Bp 130/80 p. 120/min RR 18/min and T-39˚c. Respiratory and cardiovascular systems were unremarkable. Abdominal examination revealed, mild distension, tenderness over RIF with guarding and rigidity.
There was palpable mass in RIF about 4.5 cmx 5 cm. There were no signs of generalized peritonitis.
Clinical diagnosis of Appendicular mass was made and conservative line of treatment adopted. He was kept n.p.o, fluids started, antibiotics Rocephin 1gx2, flagyl 500mgx3 iv given with other supportive measures.
Blood was obtained for detailed investigations including widal which was positive (see the table). The patient was on conservative line of management but did not improve.
His pyrexia, tachycardia and abdominal tenderness and toxic state made us to decide for laparotomy. Laparotomy was performed on 25.5.02 under G.A. with E.T.T. and the abdomen was opened through ® lower paramedian incision.
The findings were inflamed, supprative, gangrenous appendix with perforation at the tip surrounded by localized collection of pus.
The caecum, ileum were thick, edematous, adherent with fibrinous plaques.
Careful lysis of adhesions, through warm saline lavage performed appendectomy done by gentle handling of the bowel.
Tube drain put and the abdomen was closed in layers.
Postoperative period was less stormy as fever, tachycardia abdominal pain gradually settling down.
Catheter, NGT were removed subsequently in 3-4 days time after resumption of good bowel movements.
Post-operative widal test was positive. STO 1:320 and STH 1:320. He was put on CIPROX 500mgx2 and B complex tablets with advise on regular follow up 2 wkly.
He was discharged on 29.5.02 in good general condition.

Discussion:
Typhoid fever is endemic in most tropical countries and is caused by ingestion of salmonella organisms. Most severe symptoms are produced by S. Typhi about 200 cases occur per year England and Wales.2
Organisms may survive in gall bladder and urinary tract having invaded through small intestinal mucosa after multiplication in bile rich area in the 2nd part of duodenum.3
Organisms may be take-up by any part of the body but usually enter payers patch mostly in ileum and jejunum. Here ulceration develops and possible hemorrhage and perforation takes place, which occurs, in the 3rd week of the disease.4
Although typhoid fever affects many organ system but the most serious complications occur in .GI. tract. G.I. hemorrhage and intestinal perforation are serious complications of typhoid fever and responsible for most of the fatalities.5
G.I.  Hemorrhage is reported form 0.8% - 5%
Perforation is reported around 5% (0-39%).6



Incubation
Clinical
bacteremia
complication
Mortality
S. Typhi
10 days

Typhoid fever
>90%
Intestinal perforation & hemorrhage
2-32%
S. Typhi
A-B-C
10-14 days
Paratyphoid
fever
>90%
Intestinal complications less common
<2%

……… (7)


Perforation of the gut commonly occurs in the 2nd or 3rd week of typhoid fever and can occur at any time of the illness. In the hospital it may be observed in a child is aten associated with sudden deterioration Hypotension, tachycardia and abdominal rigidity as it was seen in our patient. He was admitted with febrile convulsions. Proceeding 7 days of fever and the next day he was found to have peritonitis.
Some times the perforation is less dramatic resulting in paralytic ileus.8 When perforation occurs, a fit patient will show all the signs of peritonitis as in our patient, but the seriously ill patient may show very little signs of abdominal tenderness guarding and rigidity.
Some times confusion occurs due to the rupture of inf. Epigastric artery in typhoid fever and there is similar tenderness in R.I.F.9
Management of perforation has been controversial in the absence of controlled prospective study most authors currently advocate operative rather than non-operative treatment. Operative treatment is preferred because typhoid fever produces fulminate peritionits unlike other perforations. Patients are usually critically ill, septicemic, often dehydrated and have electrolyte imbalances.10
At laparaotomy, usually a single perforation is found in the antimesentric border of ileum in 80%, and two perforations in 15%, about 50% of the perforations are located within 40 cm of ileum. 2% of perforations are seen in caecum.11
At laparotomy, bowel is very friable and should be handled very gently. Whether perforation is over sewn or resection done depends on the findings at laparotomy.12,13


Mortality:
Intestinal perforation is the leading cause of death in collective series in the developing countries mortality is around 43%. Time interval between the perforation and surgery is critical for better prognosis. And best results are obtained if operated with in 24 hours.14

Conclusion:
Typhoid perforation of the appendix is a rare complication. In our case both pre-op. as well as post op. Widal test was positive in the adult patient, Paratyphoid B, S. typhi H was positive and S.T.O was significantly absent. We are of the opinion it could be paratyphoid perforation which is about 2% in Occurrences. Child is doing well in subsequent follow-ups. Adult male patients went to his home-town and not returned.
We feel in all the unusual type of acute appendicitis with high fever of more than 3-4 days widal test should be done for proper management.

Acknowledgement:
We appreciate the active participation of Dr. Einas, Dr. Awad, SHO surgery and Dr. Ferdous intern pediatrics in patient care.


References:

1. Forefar & Arneils. T.B. of pediatrics. Ed by AGM. Campbell, Neil Mcintosh, churchill & livingstone, 5th ed. 1998. pp1325
2. Public health laboratory science Br. Med. J. 1983;287;1205
3. Cook GC. in: Misiewicz JJ, Pounder RE, Venables CW (eds), Diseases of the gut and pancreas. Blackwell scientific oxford 1987, p. 35.
4. Bitar R, Tarpley J. Rev infect Dis. 1985; 7:257.
5,6,7,10. Oxford T.B. Surgery. ed. By Ronald Malt, Peter Moris, Oxford university press, Vol. II, 1994. pp. 2479-2480.
9. New Airds companion to surgical studies ed by Kevin G. Burnand and Anthony E Young Churchill Livingstone. 2nd ed, 1998 pp 788.
11,14. Oxford T.B. Surgery, Ed by: Ronald Malt, Peter Moris Oxford university press , Vol II, 1994. pp. 2480.2482.
12. Bitar R, Tarpley J. Rev infect Dis, 1985; 7:257
13. Butlar T. et.al. Rev Infect Dis, 1985, 7:244.



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