Ajaz Nabi Koul

Fat embolism syndrome in long bone trauma following vehicular accidents: Experience from a tertiary care hospital in north India

Background: Fat embolism syndrome (FES) is a clinical problem arising mainly due to fractures particularly of long bones and pelvis. Not much literature is available about FES from the Indian subcontinent. Materials and Methods: Thirty-five patients referred/admitted prospectively over a 3-year period for suspected FES to a north Indian tertiary care center and satisfying the clinical criteria proposed by Gurd and Wilson, and Schonfeld were included in the study. Clinical features, risk factors, complications, response to treatment and any sequelae were recorded. Results: The patients (all male) presented with acute onset breathlessness, 36-120 hours following major bone trauma due to vehicular accidents. Associated features included features of cerebral dysfunction (n = 24, 69%), petechial rash (14%), tachycardia (94%) and fever (46%). Hypoxemia was demonstrable in 80% cases, thrombocytopenia in 91%, anemia in 94% and hypoalbuminemia in 59%. Bilateral alveolar infiltrates were seen on chest radiography in 28 patients and there was evidence of bilateral ground glass appearance in 5 patients on CT. Eleven patients required ventilatory assistance whereas others were treated with supportive management. Three patients expired due to associated sepsis and respiratory failure, whereas others recovered with a mean hospital stay of 9 days. No long term sequelae were observed. Conclusion: FES remains a clinical challenge and is a diagnosis of exclusion based only on clinical grounds because of the absence of any specific laboratory test. A high index of suspicion is required for diagnosis and initiating supportive management in patients with traumatic fractures, especially in those having undergone an invasive orthopedic procedure.

High altitude pulmonary edema among "Amarnath Yatris"

Background: Annual pilgrimage (Yatra) to the cave shrine of Shri Amarnath Ji’ is a holy ritual among the Hindu devotees of Lord Shiva. Located in the Himalayan Mountain Range (altitude 13,000 ft) in south Kashmir, the shrine is visited by thousands of devotees and altitude sickness is reportedly common. Materials and Methods: More than 600,000 pilgrims visited the cave shrine in 2011 and 2012 with 239 recorded deaths. Thirty one patients with suspected altitude sickness were referred from medical centers en-route the cave to Sher-i-Kashmir Institute of Medical Sciences, a tertiary-care center in capital Srinagar (5,000 ft). The clinical features and the response to treatment were recorded. Results: Thirty-one patients (all lowlanders, 19 male; age 18-60 years, median 41) had presented with acute onset breathlessness of 1-4 days (median 1.9 d) starting within 12-24 h of a rapid ascent; accompanied by cough (68%), headache (8%), dizziness and nausea (65%). Sixteen patients had associated encephalopathy. Clinical features on admission included tachypnea (n = 31), tachycardia (n = 23), bilateral chest rales (n = 29), cyanosis (n = 22) and grade 2-4 encephalopathy. Hypoxemia was demonstrable in 24 cases and bilateral infiltrates on radiologic imaging in 29. Ten patients had evidence of high-altitude cerebral edema. All patients were managed with oxygen, steroids, nifedipine, sildenafil and other supportive measures including invasive ventilation (n = 3). Three patients died due to multiorgan dysfunction. Conclusions: Altitude sickness is common among Amaranath Yatris from the plains and appropriate educational strategies should be invoked for prevention and prompt treatment.

Tubercular vertebral osteomyelitis.

The article entitled “ Vertebral osteomyelitis: Retrospective review of 11 years of experience ” [1], is an excellent retrospective study that emphasizes the staphylococcal etiology as a causative agent in the majority of vertebral osteomyelitis (VO) cases. In our part of the world we see cases of VO that have a differing etiology from that of developed countries. In our clinical practice we have seen Mycobacterium tuberculosis as a cause of VO more frequently than reported in the literature. During the past 5 y we have admitted and treated 12 cases of VO caused by Mycobacterium tuberculosis. In these cases, the disease process was localized to the thoracic and lumbosacral spine. The patients presented with fever and limitations of ambulation. Scanning and work-up indicated VO compounded by paraspinal abscess formation. The patients were given an extended course of anti-tubercular drug therapy (ATT) along with steroids; the duration of ATT was individualized, with all patients receiving 18 to 20 months of therapy. The sequelae of this disease remained even after a full course of ATT and compliance with the directly observed therapy short-course (DOTS) regime along with regular physiotherapy. In endemic areas of the world, especially India, any patient with fever coupled with limitation of movement should be investigated for a suspected infected spine disease. In such patients, apart from suspecting staphylococcal sepsis or septic VO, tuberculosis (TB) must also be considered. The typical features of spinal TB have been identifi ed in Egyptian mummies dating back to almost 4000 BC [2]. TB is following human history like a shadow. The reservoirs of this chronic debilitating disease remain in the under-developed and developing world, but immune suppression in various forms has made TB a threat to the developed world too. Proper introspection and early institution of ATT ameliorates the burden of TB to a great extent. Spinal TB (Pott disease) most often affects the lumbar and lower thoracic region; upper thoracic and cervical disease is less common but is potentially more disabling [3,4]. Tuberculous abscess, a complication of spinal TB, is frequently bilateral. The goal of achieving a lesser burden of TB is hampered by delays in diagnosis together with a lack of drug compliance. Insuffi ciencies in the identifi cation of the attainment of complete cure among TB patients and their care-givers affect the achievable targets in the management of TB. Areas affected by TB such as the vertebrae add to the challenges of treating the VO secondary to TB effectively. The value of the conventional Mantoux test is high in spinal TB, with sensitivity ranging from 92% to 94% [5]. Radiologically, magnetic resonance imaging (MRI) remains the gold standard in establishing the anatomy of the spine and surrounding structures with precision. It provides a reasonable description of the vertebrae, disc, disc spaces, neuro-anatomy, and surrounding structures, especially the localization of abscesses and neural disruption [6 – 8]. Although aspiration from the infected vertebrae, disc, or paraspinal collection helps in establishing the etiology of VO, computed tomography (CT)-guided aspiration of VO is diffi cult in practice. In those cases of VO that are complicated with a paraspinal collection, ultrasound-guided or CT-guided aspiration helps in documenting the tuberculous etiology. These patients often require a neurosurgical intervention to relieve the acute neural or myelitic compression. In such cases, establishing the tissue diagnosis is less taxing. Sc an d J In fe ct D is D ow nl oa de d fr om in fo rm ah ea lth ca re .c om b y Im pe ri al C ol le ge L on do n on 0 4/ 06 /1 5

Moxifloxacin-associated neutropenia.

Moxifl oxacin is a fl uoroquinolone that is used for the treatment of acute bacterial sinusitis, acute exacerbation of chronic bronchitis, community-acquired pneumonia, intra-abdominal infections, and skin and soft tissue infections [1]. It is a broad-spectrum antibiotic that has activity against Gram-positive and Gram-negative bacteria. It has a unique place in the management of drug-resistant tuberculosis. It acts by inhibiting topoisomerase II and topoisomerase IV. The commonly encountered side effects are nausea, diarrhoea, vomiting, skin rashes, interstitial nephritis, liver injury, and hepatic failure. The quinolones group is notorious for causing thinning of tendons and their rupture. Serum sickness and anaphylaxis is known to occur in susceptible groups. In some vulnerable groups it can cause QT prolongation, fatal arrhythmias, and sudden cardiac death [2]. We wish to relate a few observations on the communication by Berk et al. regarding moxifl oxacinassociated neutropenia, published in a recent issue of your esteemed journal. The quinolones are known to have an idiosyncratic reaction towards bone marrow. In clinical practice we have observed, more often than not, that quinolones, in particular ciprofl oxacin and moxifl oxacin, cause a depression of cell series in the marrow [3,4]. We have used ciprofl oxacin for typhoid fever over a period of 12 y in our clinical practice, and leukopenia, especially neutropenia, is sometimes observed. To add to this dilemma, many typhoid fever patients have varying degrees of bone marrow suppression due to the disease. It is our observation that the institution of quinolones worsens cell suppression. In these patients, thrombocytopenia is also observed due to the disease, which many times is compounded by quinolone administration, mandating a change of quinolones to cephalosporins. Another situation where we use moxifl oxacin is multidrug-resistant tuberculosis (MDRTB). Two of our patients with nodal MDRTB required moxifl oxacin treatment. They developed neutropenia, which was rectifi ed on cessation of the drug. A large subset of patients with communityacquired pneumonia is placed on third-generation cephalosporins and quinolones, especially fl uoroquinolones, for atypical cover. We have observed moxifl oxacinand levofl oxacin-induced cell suppression in the form of mild leukopenia, neutropenia, and thrombocytopenia. This clinical effect of these drugs is rectifi ed on cessation of the offending agent. The leukopenia and thrombocytopenia associated with ciprofl oxacin, levofl oxacin, and moxifl oxacin is short-lived. There was no morphologic or pathologic signifi cance attached to it in our patients. Recovery was complete and in all cases without any sequelae [5 – 7]. We believe that quinolone-associated mild to moderate haematological disturbances are more prevalent than reported and are frequently reversible, without sequelae.

Heparin-induced thrombocytopenia in a patient with colon cancer

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