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| CASE IN POINT: CLINICS IN ORTHOPEDIC SURGERY |
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| Year : 2015 | Volume
: 2
| Issue : 3 | Page : 145-147 |
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Case of tropical myositis sans suppuration
Arun Kumar Harith1, Ajay Malik1, Mukesh Chandra2, Chandra Mohan Singh3
1 Department of Pathology, Delhi Cantt, New Delhi, India
2 Department of Radiodiagnosis, Delhi Cantt, New Delhi, India
3 Department of Orthopedic Surgery Base Hospital, Delhi Cantt, New Delhi, India
| Date of Web Publication | 2-May-2016 |
Correspondence Address:
Arun Kumar Harith
Department of Pathology, Base Hospital, Delhi Cantt, New Delhi - 110 010
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2349-0977.181512
A rarely reported condition, tropical myositis is a microbial condition. Caused most commonly by Staphylococcus aureus, it may also be triggered by Streptococci and Gram-negative bacilli like Klebsiella. A pocket of pus, identifiable on ultrasound or magnetic resonance imaging is the usual hallmark. We present a rare case of the disease in a 32-year-old patient who had tropical myositis without any pus collection. The disease ran an extremely aggressive course and despite not being immunocompromised, the patient succumbed to the condition. Keywords: Tropical myositis, pus, immune status
How to cite this article:
Harith AK, Malik A, Chandra M, Singh CM. Case of tropical myositis sans suppuration. Astrocyte 2015;2:145-7 |
| Introduction | |  |
Tropical myositis (TM) is common, albeit a rarely reported condition in the country. The disease presents with nonspecific findings of fever, malaise and muscle pain and progresses to a state of sepsis. The disease is usually seen in the backdrop of some immunecompromise, be it in the form of human immunodeficiency virus (HIV) infection, as a complication of diabetes or rarely in cases of leukemia. The incidence of this disease has been reported to be around 4% in African population.[1] The corresponding figures in Indian population is lacking, probably due to under-reporting. The most common etiological agent for this disease is Staphylococcus aureus. Other organisms implicated in this disease include Streptococcus and Gram-negative bacilli like Klebsiella.[2] It is not uncommon to misdiagnose these cases for other common tropical diseases like viral infection, septic arthritis, osteomyelitis, dengue, etc. However in most of the cases reported so far, after the initial nonspecific findings at clinical presentation, a focus of pus is found using imaging techniques like ultrasonography/magnetic resonance imaging (MRI), and drainage of the same with appropriate therapy results in the cure of the patient. We present a rare case of the disease in which there was no pus collection, and despite best management, the patient succumbed to the disease.
A 32-year-old patient with no comorbitities presented to the hospital with history of pain in the left hip joint of 20 days duration. There was no history of trauma or taking of any injections. He progressively became febrile, and routine investigations showed a raised total leukocyte count (22,000/µl) which consisted predominantly of neutrophils. The neutrophils showed a shift to the left and toxic granules. He was not seroreactive for HIV and there was no evidence of diabetes. He was managed with broad spectrum antibiotics but without any significant improvement. He was suspected to be suffering from septic arthritis and referred to the orthopedic surgeon for further management. T1-weighted images and STIR MRI images [Figure 1] and [Figure 2] showed diffuse hyperintensity with swelling of the gluteus maximus, medius, minimus, iliacus, piriformis, and inferior fibers of the psoas muscle on the left side suggestive of edema. Marrow edema was seen involving the left iliac bone [Figure 3] and left side of the sacrum. Diffuse perineural hyperintensity was also seen along the neural elements of sacral nerve roots on the left side. The patient progressively developed perianal paresthesia associated with loss of ankle jerk and inability to dorsiflex the great toe of the left foot. On suspicion of an illiopsoas abscess, extraperitoneal exploration was done to drain out any pus and relieve the muscle tension. However, no pus was located peroperatively. Subsequently, the individual developed radicular pain with inability to move both the lower limbs. The pain was severe enough to warrant epidural bupivacaine. The patient had raised creatinine kinase (1750 IU/L) levels along with raised levels of aspartate amino transferase (AST) (220 IU/L) while the alanine amino transferase (ALT) was within normal limits (30 IU/L). Repeated cultures of the blood, urine, and an intraoperative muscle biopsy done on a fully automated Vitec System did not reveal any microorganisms. The patient showed a progressively downhill course as he developed coagulopathy, acute renal failure, and respiratory failure. Subsequently, he had a cardiorespiratory arrest and died. The diagnosis of TM was made mainly due to the characteristic MRI features, biochemical evidence of myositis (in the form of raised Creatine Kinase [CK] and AST>ALT) and the persistence of leukocytosis (22,000–27,000/µl) comprising of 80–88% of neutrophils with features of sepsis. | Figure 2: Coronal T2-FatSat image showing marrow edema in the left iliac bone with muscle edema involving iliacus and gluteal muscles.
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| Discussion | | |
TM is a generic name given to a condition presenting with myositis and gradually progressing to sepsis if not treated. The groups of muscle commonly affected in the descending order of frequency include quadriceps, glutei, pectoralis major, serratus anterior, biceps, iliopsoas, gastrocnemius, abdominal, and spinal muscles.[3] The name tropical is not very appropriate for this condition as cases are now being reported even in temperate regions too.[4] The hallmark of this condition is a rapidly progressively disease starting with nonspecific findings and progressing to a state of suppuration in the muscles followed by septicemia. Classically, the disease has been grouped in three stages.[2] The first stage, called the invasive stage in which there are mild local and systemic symptoms. There is no evidence of pus. Usually, no history of trauma/injections are elicited from the patient. Because of the innocuous nature of this phase, it is invariably missed. In the second stage called the suppurative stage, the patient has more severe pain and features of systemic toxicity. Radiological imaging of the involved area invariably shows features of pus collection. Drainage of the pus from the affected area confirms the diagnosis, as well as gives clue of the causative agent. The late stage is Stage III in which there is evidence of septicemia and if it is not treated properly, progress to death. Drainage of pus and institution of appropriate treatment usually results in the complete cure of the condition. However, in the modern era, where there is excessive use of broad spectrum antibiotics, the culture positivity in cases of TM is very low. Blood culture is usually negative in more than 90% of the cases and culture of the pus obtained on aspiration may be sterile in nearly 30% of the cases.[5]
The present case is unique in many ways. Even in the presence of septicemia, there was no evidence of pus formation anywhere in the involved muscle. Surgical exploration of the involved muscles too did not reveal any pus collection. Cultures-blood, urine, and swabs taken peroperatively over the involved muscles too did not yield any organism. There was evidence of myonecrosis in the form of a raised CK and AST. Traditionally, these markers are usually not raised in TM.[6] Our case had evidence of neural involvement in the form of radicular pain and paraparesis. Features of neural involvement are very rare in TM.[7]
In our case, the diagnosis of TM was made late, mainly due to the lack evidence of pus collection or culture. It is a rare presentation in which the patient has progressed from Stage I to Stage III without a Stage II where pus formation is present. While most of the cases of TM survive, our case even though on broad spectrum antibiotics did not have a good outcome. This case is interesting in the fact that our patient was not immunocompromised and yet progressed to a fatal end despite being managed in a Tertiary Care Center.
The aim of the case report was to highlight the point that TM is a rapidly progressive condition and needs to be treated aggressively. While it has been traditionally been considered that it occurs in the backdrop of immunocompromised state, this is not always true. We also want to highlight the fact that cases can rapidly progress from Stage I to Stage III without any intermediate State II of the disease.
Acknowledgment
We acknowledge the help provided by Dr. Rajat Sharma for providing and reporting the MRI films of the case.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Pike MC, Taylor E, Taylor JF. The epidemiology of tropical myositis in the Mengo Districts of Uganda. Trans R Soc Trop Med Hyg 1978;72:46-53.  |
| 2. | Jain S, Varma S, Chauhan SS. Tropical pyomyositis (myositis tropicans): Current perspective. Postgrad Med J 2004;80:267–70. |
| 3. | Ashken MH, Cotton RE. Tropical skeletal muscle abscesses (pyomyositis tropicans). Br J Surg 1963;50:846-52. |
| 4. | Weinberg J, Friedman S, Sood S, Crider RJ. Tropical myositis (pyomyositis) in children in temperate climates: A report of 3 cases on Long Island, New York, and a review of the literature. Am J Orthop (Belle Mead NJ) 2007;36:E71-5. |
| 5. | Shepherd JJ. Tropical myositis: Is it an entity and what is its cause? Lancet 1983;2:1240-2. |
| 6. | Bickels J, Ben-Sira L, Kessler A, Wientroub S. Primary pyomyositis. J Bone Joint Surg Am 2002;84-A: 2277-86. |
| 7. | Brik R, Braun J, Bialik V, Zuckerman N, Berant M. Non-tropical pyomyositis in children – With report of severe neurological complications. Acta Paediatr Scand 1989;78:331-4. |
[Figure 1], [Figure 2], [Figure 3]
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