Journal of Postgraduate Medicine
 Open access journal indexed with Index Medicus & ISI's SCI  
Users online: 4670  
Home | Subscribe | Feedback | Login 
About Latest Articles Back-Issues Article Submission Resources Sections Etcetera Contact
 
  NAVIGATE Here 
  Search
 
 :: Next article
 :: Previous article 
 :: Table of Contents
  
 RESOURCE Links
 ::  Similar in PUBMED
 ::  Search Pubmed for
 ::  Search in Google Scholar for
 ::Related articles
 ::  Article in PDF (24 KB)
 ::  Citation Manager
 ::  Access Statistics
 ::  Reader Comments
 ::  Email Alert *
 ::  Add to My List *
* Registration required (free) 


  IN THIS Article
 ::  Abstract
 ::  Introduction
 ::  Material and method
 ::  Results
 ::  Discussion
 ::  References

 Article Access Statistics
    Viewed14835    
    Printed236    
    Emailed11    
    PDF Downloaded198    
    Comments [Add]    
    Cited by others 3    

Recommend this journal


   
ORIGINAL ARTICLE
Year : 1991  |  Volume : 37  |  Issue : 2  |  Page : 69-75

Natural course of hematogenous pyogenic osteomyelitis (a retrospective study of 110 cases).


Department of Orthopaedic Surgery, Seth G. S. Medical College, Parel, Bombay, Maharashtra.

Correspondence Address:
Department of Orthopaedic Surgery, Seth G. S. Medical College, Parel, Bombay, Maharashtra.


  ::  Abstract

Hundred and ten consecutive cases in acute and various stages of chronicity were studied. Incidence regarding age, sex, bone affected and complications was established. The optimum way to manage osteomyelitis in different stages was sought. It was found that in acute stage early decompression of bone leads to resolution of disease. Hip involvement leads to necrosis of capital epiphysis and should be treated on an emergency basis. In the sub-acute stage it is necessary to protect the weakened bone. In chronic stage, we suggest sequestrectomy only after adequate involucrum has formed properly. Antibiotics in acute stage should be instituted as early as possible and should be continued for three weeks after the fever subsides. Antibiotics in sub-acute and chronic stage are given only in cases of reactivation of infection and around the time of surgery. Surgery, when required should be performed without too much soft tissue damage especially the covering periosteum. But repeated surgery should be avoided as they lead to cicatrization of muscles and further sequestration of bone.

How to cite this article:
Kharbanda Y, Dhir R S. Natural course of hematogenous pyogenic osteomyelitis (a retrospective study of 110 cases). J Postgrad Med 1991;37:69-75


How to cite this URL:
Kharbanda Y, Dhir R S. Natural course of hematogenous pyogenic osteomyelitis (a retrospective study of 110 cases). J Postgrad Med [serial online] 1991 [cited 2019 Nov 18];37:69-75. Available from: http://www.jpgmonline.com/text.asp?1991/37/2/69/786




  ::   Introduction Top

Infection of bones and joints are widely prevalent in our country and form a major portion of our orthopaedic practice. Unfortunately despite this fact, what we read about this condition is largely from the western literature. Although over the years mortality and morbidity has changed for the better, there is still great scope to learn about this disease and to update its management to suit our conditions.
Thus, we took up this project to study the natural course of hematogenous pyogenic osteomyelitis in light of the available literature which is largely western and to design and advocate a way to manage the disease and its complications in our prevailing circumstances.

  ::   Material and method Top

A total of 110 consecutive cases of hematogenous pyogenic osteomyelitis which were admitted for treatment in one of the orthopaedic units in King Edward Memorial Hospital, Mumbai since 1980 were studied. Hence the patients being treated in the outpatient department without getting admitted even once could not be included in this study.
Through this study, it was sought to establish an incidence of age, sex, bone involvement and relationship between acute osteomychtis and affection of adjacent joint, loss of movements and function and growth disturbance in pyogenic osteomyelitis. Sequential radiological changes during its natural course were identified. Process of sequestrurn formation, pathological fracture and its repair by involucrum formation during its course were studied and an attempt was made to correlate these changes with various sequential ongoing pathological processes. While doing so, it was attempted to find out the optimum way to manage osteomyelitis in different stages.
In acute stage, fever was controlled by starting antibiotics, antipyretics and local glycerine magnesium sulphate compresses. Decompression of bone was done when localising signs were present. Two or three drill holes were made through a window in the periosteum avoiding elevation. No drilling was done when sub-periosteal abscess was encountered. Antibiotics were changed according to sensitivity reports. During all this time, the limb was splinted and hydration and nutrition of the patient maintained. Any incidence of involvement of adjacent joint was looked for and arthrotomy and lavage was carried out if necessary. Antibiotics were continued for at least 3 weeks after the fever subsided.
During sub-acute stage, we studied serial radiographs over several months to know separation of sequestrum and development of sub-periosteal new bone formation. The limb was protected in a cast to prevent a pathological fracture from displacing and to facilitate adequate involucrum formation (See [Figure - 5]). Drainage of pus was done if an abscess was encountered. No removal of sequestrum was advised during this stage to avoid damage and collapse of the periosteal tube. During the chronic stage, sequestrum was removed through cloaca or small window in the bone. We preferred to crush larger sequestrum into smaller pieces for their removal through small windows rather than sacrificing larger chunk of involucrum. Saucerization was avoided to prevent permanent weakening of the bone (See [Figure - 1]). We carried on with conservative treatment in cases where bone was diffusely involved with multiple small sequestra till they were either resorbed or thrown out through sinus. Meanwhile antibiotics in sub-acute and chronic stages were given only in case of reactivation of infection and or during surgery.
Joint affection due to osteomyelitis in early childhood often caused severe joint damage leading to gross instability but in grown up children such joints developed painful ankylosis and deformity. Shortening of various grades were seen due to epiphyseal damage and displaced pathological fracture. Contractures and periarticular adhesions, subluxation and/or dislocation of joints were some of the other causes for deformity (See [Figure - 2]). Painful joints were treated with either excision arthroplasty or arthodesis. Joint deformities were corrected by soft tissue release and arthrolysis. Osteotomics of infected bones were avoided. Pseudarthrosis as a result of tubular sequestration in subcutaneous bones like tibia, ultia, clavicle was treated by free fibular grafting or by tibialisation of fibula with its myofascial attachments (See [Figure - 4]). Shortening was treated by providing shoe raise. Epiphyseal sepration (See [Figure - 3]) and joint dislocation were treated by reduction and immobilization. Rarely internal fixation by Krishner's wires or intramedullary nail was used to align the displaced pathological fracture or epiphyseal separation till they were stabilized by involucrum formation.

  ::   Results Top

Total number of patients studied since 1980 were 110 cases. Mean age group was 12.22 years with minimum age of one month and maximum age of 50 years (47 patients were under 10 years, 41 patients between 10 and 19 years and 22 were above 20 years). Eighty patients were males and 30 females. Sixty-six per cent of patients gave history of predisposing trauma. The organism isolated was staphylococci (40%), streptococci (4%), klebsiella (4%), proteus (6%) mixed organism (30%). In 16% cases, reports were not available.
Possible sources of infection in children were found to be upper respiratory tract infection and pyoderma whereas in adults it was inconclusive.
Totally 125 bones were affected in 110 cases: femur (60), tibia (35), humerus (12), fibula (6), radius (2), ulna (1) clavicle (2) and small bones (7). Two or more than two bones were involved in 15 cases.
We observed that in greater majority of cases, the initial site of involvement was metaphysis of long bone. Femur (upper end - 13, lower end 26, diaphyseal involvement - 21); tibia (upper end-14, lower end-6), diaphyseal involvement - 15. humerus (upper end - 10, lower end - 2)5 fibula (upper end - 4, lower end - 2), radius (lower end - 2), ulna (lower end -1 case).
Thirty-two cases presented in acute stage and 78 cases in chronic stage.
Periosteal reaction as the first definitive radiological sign of osteomyelitis was seen in about 10-14 days (See [Figure:1A]). While studying the radiographs, we observed that avascular bone could usually be distinguished from the surrounding hypervasular osteoporotic living bone by 3rd week after the onset of disease (See [Figure:1a]). This avascular bone gradually separated from the living bone by the osteoclastic process to form a sequestrum. Simultaneously subperiosteal new bone was laid down to develop a strong involucrum in 3-5 months (12% of cases), 6-8 months (22% of cases), 9-12 months (36% of cases), and after 12 months in 10% of cases.
Ten per cent of cases, which were treated early did not show any of the subsequent changes of osteomyelitis. Another 10% of cases showed diffuse diaphyseal involvement having many small sequestra in different stages of their development distributed throughout the bone. Such affection did not get resolved during the follow up for many years (See [Figure - 2] on page 68C).
Avascular bone appeared more dense on radiographs. The new sub- periosteal bone was less towards the metaphyseal ends but abundant around the diaphysis (See [Figure:1b]).
Tubular sequestrum involving a part of diaphysis was present in 48 cases and those involving whole of diaphysis in 8 cases. Pathological fracture during sub-acute stage occurred in natural course after separation of tubular sequestra, however when properly splinted, they remained undisplaced and were stabilized by involucrum formation subsequently. Pathological fracture with displacement occurred in 12 cases. These cases presented late to us and were not immobilised in early stage of ostesmyelitis. Pathological fracture was associated with non-union in 4 cases and shortening due to overlapping and deformity in 11 cases.
There was a natural tendency of a sequestrum to extrude through the existing cloaca (See [Figure:1c]). Larger sequestrum, with time, became thinner and smaller and even disintegrated by osteoclastic activity over several months or years to be extruded in small pieces.
We observed that sinus persisted in the presence of sequestrum. Once the sequestrum was resorbed or was extracted, the sinus healed. However, at times, the sinus, stopped draining even in the presence of sequestrum for a few days, which usually caused exacerbation of infection leading to septicaemia. This lead to reformation of abscess requiring surgical drainage along with institution of antibiotics. In case there was only inflammation, it could be controlled by systemic antibiotics alone. Such recurrences usually initiated fresh sequestration.
Adult osteomyelitis was seen in 20% of total cases. We observed that the sequential changes of osteomyelitis in adults remained same as in children. However unlike children they did not show tubular sequestration. The bone was diffusely involved with formation of multiple small cortical sequestra. The diagphyseal involvement with large sub-periosteal abscess was more common. Joint involvement was rare.
Joint was involved in 18 cases (hip - 10, knee-4), elbow-2, shoulder and ankle-1 each).
Contractures due to cicatrization of muscles resulting into deformity were present in 5 cases of knee and 3 cases of hip. Stiffness due to involvement of joint was present in 9 cases of hip, 4 cases of knee, 2 cases of elbow and 1 case each of shoulder and ankle.
Epiphyseal involvement resulted in deformity in 3 cases and shortening due to arrest in 12 cases.

  ::   Discussion Top

Hematogenous osteomyelitis is an infection of bone and marrow cavity. It is still a major problem in a developing country like India. It is seen in low income group of population due to low resistance because of poor nutrition, illiteracy and poor hygienic surroundings. The most common organism causing this infection has been found to be staphylococcus[7]. This fact is also seen in our study. Other organisms include streptococci, H. influenza, proteus and klebsiella. It occurs most commonly in infants and children although of late, more and more cases of acute osteomyelitis are being seen in the adults also [22],[24]. Our study comprises 20% of adult hematogenous osteomyelitis.
Acute osteomyelitis is a disease which when treated appropriately in the initial stages, can result into early resolution of bone. Some of our cases showed complete resolution when treated within 48 hours of onset. However, due to illiteracy, among poorer patients and lack of transportation, only a few seek early treatment. Hence, various stages of advanced disease can be seen in this population. Acute process of hematogenous osteomyelitis usually starts either in the upper or the lower metaphysis of a long bone. Faster growing epiphyseal ends are liable to get infected more commonly than the slower growing ends[22]. In our series, the lower end of femur, upper end of tibia and humerus were common sites of affection.
In acute bacillaemia and septicaemia along with the localisation of the infection are the major problems and require treatment with antibiotics[4],[5],[12],[13] and decompression[17] of bone abscess. This stage gets over within three weeks. A possibility of joint involvement should be looked for. Sub-acute stage is concerned with active repair of the damage done to the affected bone during acute stage. The process although quite slow, is very effective. In the presence of infection necrosed bone gradually separates from the living bone by osteoclastic activity of the invading granulation tissue. This process considerably weakens the bone. Simultaneously a subperiosteal new bone is also laid down to develop into involucrum. Pathological fracture develops during this stage as a natural course during separation of a tubular sequestrum, or as a result of minor trauma through a weakened segment of bone. By the time, the hematogenous osteomyelitis has reached a chronic stage, the repair process is almost over. The necrosed bone has separated into a sequestrum, and the bone has thickened and regained its strength by formation of involucrum (See [Figure - 1]). Often there are one or more discharging sinuses. The patient is fully active and does not require immobilisation.
The purpose of treatment in acute stage is to control the systemic infection and to prevent spread of intraosscous abscess to limit bony damage. Systemic antibiotic is the mainstay of the treatment and when needed an early decompression of bone abscess must be done. Once the abscess has tracked to subperiosteal space, bone naturally gets decompressed and limits further damage. Decompression of bone is not required if frank sub- periosteal abscess is found on incising the periosteum. While decompressing the bone any inadvertent damage to the periosteurn must be avoided to prevent any further avascularity of the bone. The bone is splinted and weight bearing avoided till bone damage is fully assessed after the acute inflammation has settled down. Immobilisation is extended to 6 weeks if drilling of bone has been done in absence of other bony changes.
Prolonged immobilisation in sub-acute stage is required to protect weak bone till involucrum becomes strong enough to take over the function. Inadequate protection would often cause deformation of bone and hamper adequate involucrum formation. This process takes 6 months (3 months to 15 months) on an average. Antibiotics are used in this stage, only if there is reactivation of the infection denoted by increase in local discomfort and onset of fever. Apart from occasional drainage of abscess, practically no other surgery is required during this stage. Sequestrectomy is not performed till the involucrum is well formed. It may not be possible to prevent a premature extrusion of the sequestrum and subsequent development of pseudarthrosis in superficial bones like tibias, clavicle and ulna (See [Figure - 4]).
In chronic stage, sequestrectomy leads to healing of sinuses. This however, requires utmost precaution.
i) Multiple repeated operations through muscle planes are avoided lest it would cause muscle cicatrization and its adherence to the bone limiting movements.
ii) The involucrum and its periosteal blood supply is not unduly damaged in the process of sequestrectomy lest it would cause more necrosed bone leading to further sequestration. Wide excision of the involucrum to remove large sequestrum or wide saucerization to make deep bony defects shallower[3],[10],[11] should be avoided lest the bone would be weakened permanently requiring prolonged protection to prevent pathological fracture. In natural course small sequestrum gets thrown out through cloacae. In case of larger sequestrum we advocate them to be broken into small pieces rather than unduly damaging the involucrum. We have found that even large bone defects left alone often sequestrectomy healed by fibrosis and wide saucerization was not usually required. We have left alone multiple small sequestra in a diffusely involved bone. In the course of time, most of them would become smaller and break up in pieces by osteoclastic activity of the surrounding granulation tissue and would then get resorbed or discharged through existing sinus. Only relatively larger sequestra may ultimately need removal.
Acute hematogenous osteomyelitis, when it occurs concurrently with adjacent joint sepsis [1], the problems of treatment are further complicated and the risk of chronic disability and disordered growth is increased. Acute septic arthritis usually affects the hip joint[19], rarely knee, ankle and elbow also get involved. Concumence of the two diseases is most common in the proximal femur and adjacent hip joint. Sequestration of the femoral head, subluxation or dislocation of joint are common sequelae (See [Figure - 2]) in early childhood, however painful ankylosis is more common later in life. HBS Kemp and Lloyd-Roberts[16] have published a paper in which they emphasised the danger of avascular necrosis of the capital femoral epiphysis arising as a late complication of osteomylitis of the proximal metaphysis of the femur. A possibility of joint involvement can be prevented by early decompression and drainage of bone abscess through extra capsular route. Damage to an already infected joint can be prevented by early drainage and through lavage.
Pseudarthrosis would require some reconstructive procedures like live bone grafting from a fibula or a rib. Old joint affection, epiphyseal damage and deformities would require salvation by definite planned proceures. A possible role for local instillation or implantation of antibiotics (gentamycin beads), silver ionisation or electromagnetic therapy seems to exist in persistent diffuse grumbling infections of bone like Brodie's abscess and osteomyelitis of Garre. We however, have not used these procedures in our cases.

Conclusions:
1) Hematogenous osteornylitis continues to be a major orthopaedic problem in developing countries.
2) The natural course of hematogenous osteomyelitis can be divided into acute, sub-acute and chronic stages. Acute stage is concerned with acute onset of the disease with symptoms and signs of septicaemia and localisation of the infection in the bone. During sub-acute stage, the avascular bone gets sequestrated, in process pathological fracture develops and new subperiosteal bone is laid down to form involucrum. In chronic stage, the residual effects of these changes may persist for a long period with remission and exacerbation of infection.
3) Joint involvement, epiphyseal damage and deformity are common outcome of this disease and should be looked for while treating these patients.
4) Antibiotic and decompression of bone abscess form basis of treatment in acute stage while protection of weak bone in a splint or a cast is essential to prevent its deformation and to facilitate involucrum formation. In chronic stage treatment is required to remove the sequestrum and to salvage residual effects of osteomyelitis and to prevent exacerbation of infection.
5) Repeated exacerbation of infection and their incision and drainage would cause muscle cicatrization and joint stiffness. Excessive damage of involucrum would weaken the bone and is liable to spontaneous fracture. Premature removal of sequestrum would cause failure of involucrum formation leading to gap non-union.
6) A possible role for local instillation or implantation of gentamycin beads, silver ionisation or electromagnetic therapy seems to exist in persistent diffuse grumbling infections of bone.
Acknowledgments
We are very grateful to the Dean, Seth GS Medical College and King Edward Memorial Hospital for his kind permission to allow us to use the hospital data for this article.

  ::   References Top

1. Alderson M, Speers D, Emslie K, Nade S. Acute hematogenous osteomyelitis and septic arthritis-a single disease. An hypothesis based upon the presence of transphyscal blood vessels. J Bone & Joint Surg 1996; 68B; 268-274.  Back to cited text no. 1    
2.Anderson LD. Infections. In: "Campbell's Operative Orthopaedics." Vol. 1 Sixth Edn. CV Mosby Company; 1980, pp 1034-1058.  Back to cited text no. 2    
3.Bickel WH, Bateman JG, Johnson WE. Treatment of chronic hematogenous osteomyelitis by means of saucerization and bone grafting. Surg Gynecol & Obstet 1953; 96:265-274.  Back to cited text no. 3    
4.Blockey, N. J. and Watson J. T.: Acute osteomyelitis in children. J Bone & Joint Surg 1970; 52B:77-87.  Back to cited text no. 4    
5.Blockey NJ, McAllister TA. Antibiotics in acute osteomyelitis in children. J Bone & Joint Surg 1972; 54B: 299-309.  Back to cited text no. 5    
6.Blockey NJ. Osteomyelitis. Children's Orthopaedics -Practical Problems." Butterworth & Co Ltd; 1976, pp, 15-58.  Back to cited text no. 6    
7.Boland AL (Jr). Acute hematogenous osteomyelitis. Orthop Clin North Amer 1972; 3:225.  Back to cited text no. 7    
8.Duthie RB, Bentley G. In: "Mercer's Orthopaedic Surgery". Eighth edn. London: Edward Arnold Ltd; 1983, pp 472-485.  Back to cited text no. 8    
9.Emslie KR, Nade S. Acute hematogenous staphylococcal osteomyelitis: A description of the natural history in an avian model. Amer J Pathology 1983; 110:333-345.  Back to cited text no. 9    
10.Ger R, Adar U. The management of chronic cavities in the region of the hip joint. J Bone & Joint Surg 1973; 55-A:758-760.  Back to cited text no. 10    
11.Ger R, Efron G. New operative approach in the treatment of chronic osteomyelitis of the tibial diaphysis. A preliminary report. Clin Orthop 1970; 70:165-169.  Back to cited text no. 11    
12.Gillespie WJ, Mayo KM. The management of acute hematogenous ostesmyelitis in the antibiotic era. A study of the outcome. J Bone & Joint Surg 1981; 63B:126-131.  Back to cited text no. 12    
13.Green JH. Cloxacillin in treatment of acute osteomelitis. Brit Med J 1967; 2:414-416.  Back to cited text no. 13    
14.Kelly PJ. Osteomyelitis in the adult. Orthop Clin North Amer 1975; 6:983-989.  Back to cited text no. 14    
15.Kelly PJ. Chronic osteomyelitis in adults. Recent advances in orthopaedic number four edited by B McKibbin. Edinburgh: Churchill Livinstone; 1983, pp 119-129.  Back to cited text no. 15    
16.Kemp HBS, Lloyd-Roberts GC. Avascular necrosis of the capital epiphysis following osteomyelitis of the proximal femoral metaphysis. J Bone & Joint Surg 1974; 56B:688-697.  Back to cited text no. 16    
17.Mollan RAB, Piggot + J. Acute osteomyelitis in children. J Bone & Joint Surg 1977; 59B:27.  Back to cited text no. 17    
18.Morrey BF, Peterson HA. Hematogenous pyogenic osteomyelitis in children. Orthop Clin North Amer 1975; 6:935-951.  Back to cited text no. 18    
19.Nade SML. Acute haematogenous osteomyelitis in infancy and childhood. J Bone & Joint Surg 1983; 65B:109-119.  Back to cited text no. 19    
20.O'Brien T, McManus R, MacAuley PH, Ennis JT. Acute hemotogenous osteomyelitis. J Bone & Joint Surg 1982; 64-B:450-453.  Back to cited text no. 20    
21.Sharrard WJW. Infections of bones and joints. In: “Paediatric Orthopaedics and Fractures.” Vol. 2, Second Edition. Oxford: Blackwell Scientific Publications; 1979; 1309-1395.  Back to cited text no. 21    
22.Truet J. The three types of acute hematogenous osteomyelitis: a clinical and vascular study. J Bone & Joint Surg 1959; 41B:671-680.  Back to cited text no. 22    
23.Turek SL In: "Othopaedics. Principles and their Application", Vol. 1, Fourth Edition. Philadelphia: JB Lippincott Company, 1984, pp 258-266.  Back to cited text no. 23    
24.Zadek L. Acute osteomyelitis of the long bones of adults. Arch Surg 1938; 37:531-545.   Back to cited text no. 24    

Top
Print this article  Email this article
Previous article Next article
Online since 12th February '04
© 2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
Published by Wolters Kluwer - Medknow