Neurol India Home 

Year : 2010  |  Volume : 58  |  Issue : 4  |  Page : 598--599

Dengue myositis and myocarditis

Shashikala A Sangle, Abhijit Dasgupta, Shripad D Ratnalikar, Rahul V Kulkarni 
 Department of Medicine, Byramjee Jeejeebhoy Medical College, Pune - 411 001, India

Correspondence Address:
Shashikala A Sangle
Department of Medicine, Byramjee Jeejeebhoy Medical College, Pune - 411 001

How to cite this article:
Sangle SA, Dasgupta A, Ratnalikar SD, Kulkarni RV. Dengue myositis and myocarditis.Neurol India 2010;58:598-599

How to cite this URL:
Sangle SA, Dasgupta A, Ratnalikar SD, Kulkarni RV. Dengue myositis and myocarditis. Neurol India [serial online] 2010 [cited 2023 Feb 3 ];58:598-599
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Dengue is a common viral infection in the tropics. Neurological complications of dengue fever are being increasingly recognized in the recent years. Dengue commonly presents with a varying degree of myalgia; however, muscle weakness is distinctly uncommon. A few cases of myositis [1],[2] and even rhabdomyolysis [3],[4] have been reported. Muscle involvement can be histopathological. [5] Myocarditis has also been reported in dengue fever. [6],[7],[8] We report a case of dengue shock syndrome with myositis and myocarditis.

A 16-year-old girl presented with moderate-grade fever with severe malaise and myalgia. Around day 3, she developed a reddish rash over her abdomen that rapidly spread to involve the limbs. She also reported bleeding from her gums while brushing. On admission (day 7 of fever), she was found to be febrile, 38.3ΊC, pulse rate 116/min and blood pressure 90/70 mmHg. She had subconjunctival hemorrhages bilaterally and confluent, reddish macules all over her trunk and limbs. Muscles were tender. Neurological examination did not reveal any deficits. All other systems were clinically normal. Laboratory investigations showed hemoglobin of 14 g%, hematocrit of 43%, platelet count of 80,000/mm 3 and blunting of both costophrenic angles bilaterally on the chest X-ray. Dengue serology: IgM titers were elevated (day 9) with normal IgG titers.

Hemodynamic stability was achieved with intravenous fluid resuscitation. However, she was found to have persistent resting tachycardia. The electrocardiogram showed sinus tachycardia with low-voltage complexes in all leads. A 2D-echocardiogram performed on day 3 of hospitalization showed poor septal motion, left ventricular internal diameter-diastolic [LVID-(D)] = 50 mm, left ventricular internal diameter-systolic [LVID-(S)] = 30 mm. There was a thin pericardial effusion. Creatine phosphokinase-MB (CPK-MB) was 92 IU/L (normal -0-50 IU/L).

On day 3 (day 10 of symptoms onset), she was found to have difficulty in getting up from squatting position. Neurological examination revealed hypotonia and proximal muscles weakness in both upper and lower limbs. Her trunk muscles were also weak. Sensory system was normal with normal deep tendon reflexes and plantar response. Muscles were tender. Weakness progressed over the next few days and the patient developed neck muscle weakness and dysphagia. Her gag reflex was sluggish, necessitating the placement of a nasogastric tube.

Laboratory data: serum SGOT 120 IU/L, serum CPK 310 1U/L and normal serum electrolytes. Urine for myoglobin was negative. Electrodiagnostic evaluation showed normal motor and sensory conduction and electromyogram (EMG) showed small-amplitude polyphasic potentials with a normal interference pattern, suggestive of myopathy. However, there was no abnormal insertional or spontaneous activity. Muscle biopsy was essentially normal. Magnetic resonance imaging (MRI) of the brain was also normal.

The patient was treated symptomatically and physiotherapy was introduced gradually. She made a gradual recovery and was discharged after 1 month of hospitalization. At the time of discharge, her neurological evaluation was essentially normal. At discharge, her laboratory values were: Hb 12.2 g%; hematocrit 37%; platelet count 2.5 lakh/mm 3 ; SGOT 22 IU/L; CPK 135 IU/L. ECG was normal and 2D-echocardiographic findings were LVID-(D) 42 mm and LVID-(S) 20 mm.

Dengue can cause acute pure motor quadriplegia [1],[2] and even rhabdomyolysis. [3],[4] In the series by Kalita et al., [1] CPK was elevated in all the seven patients; one patient had myopathic features on EMG and in one muscle biopsy was suggestive of myositis. Malheiros et al. [5] reported muscle biopsy findings in 15 patients with dengue fever and myalgia without any weakness: mild to moderate perivascular mononuclear infiltrates in 12 patients and lipid accumulation in 11 patients. Muscle biopsy in our case was normal.

Myocarditis has also been reported in dengue fever. [6],[7] Wali et al. [6] reported a patient with dengue hemorrhagic fever/dengue shock syndrome with transient cardiac involvement with poor left ventricular ejection fraction. Cardiac involvement in this patient had worsened the hypotension and shock. Arrhythmias involving sinus node dysfunction have also been reported. [7] Recently, Salgado et al. [8] have demonstrated infection of heart tissues in vivo and striated skeletal cells in vitro. It has been proposed that the derangements of Ca 2+ storage in the infected cells may directly contribute to the presentation of myocarditis.

We conclude that acute, flaccid quadriparesis with tender muscles signifying myositis and myocarditis may be novel complications of dengue fever. One must be vigilant for these complications as they may lead to potentially disastrous consequences like respiratory failure, rhabdomyolysis, aspiration pneumonia and heart failure.


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