Acute Demyelinating Polyneuropathy in a Child with Dengue Shock Syndrome
- PDF / 149,305 Bytes
- 2 Pages / 595.276 x 790.866 pts Page_size
- 24 Downloads / 202 Views
SCIENTIFIC LETTER
Acute Demyelinating Polyneuropathy in a Child with Dengue Shock Syndrome Surjeet Kumar 1 & Vijay Kumar 1 & Renu Suthar 2 & Karthi Nallasamy 1 & Suresh Kumar Angurana 1 Received: 11 May 2020 / Accepted: 8 June 2020 # Dr. K C Chaudhuri Foundation 2020
To the Editor: An 8-y-old boy presented with fever for 5 d, respiratory distress for 3 d, and swelling in lower limbs for 2 d. Examination revealed afebrile child with generalized edema, cold hypotensive shock, tachypnea, bilateral crepitations, SpO2 90% (off oxygen), and hepatomegaly. Treatment included administration of oxygen and a normal saline bolus (20 ml/kg). Investigations revealed hemoglobin 12.4 g/dl, TLC 10400/cumm, platelet count 18000/cumm, transaminitis, positive NS1 antigen and IgM Dengue serology, bilateral diffuse infiltrates on chest radiograph, and normal renal functions. Worsening in respiratory and hemodynamic status warranted vasoactive drugs, conventional mechanical ventilation, and high frequency oscillatory ventilation. Due to gradual improvement in clinical status, vasoactive drugs were stopped on day 5 and switch was made to conventional ventilation. After weaning of sedation, analgesia, and neuromuscular blockers, generalized hypotonia, absent deep tendon reflexes, and respiratory weakness was noted. Cerebrospinal fluid analysis revealed albumino-cytological dissociation. Nerve conduction studies showed grossly delayed latencies, reduced nerve conduction velocities, and prolonged F wave latencies in bilateral common peroneal and posterior tibia nerves, suggestive of demyelinating polyneuropathy for which he received intravenous immunoglobulins (2 g/kg over 2 d) and continued on mechanical ventilation. He was gradually weaned from mechanical ventilation and extubated on day 11 of hospital stay. At discharge, he
was able to walk with support and attained pre-morbid status at 3-mo follow-up. The neurological manifestations of dengue fever are uncommon, ranging from 0.5–20% of cases [1]. Acute demyelinating polyneuropathy associated with Dengue fever is uncommon and reported mainly among adult patients [1–3] and there are limited reports in the Pediatric literature [3–5]. The possible etiology could be the molecular mimicry induced by dengue virus and pro-inflammatory cytokines (tumor necrosis factor, interleukins, and complements) causing immune attack on myelin and axons [1]. Garg et al. reviewed 29 cases of Landry-Guillain-Barré syndrome (LGBS) associated with dengue fever with mean age of 37.7 y (range 1½ y to 79 y) [3]. There were 15 children with age ≤ 16 y. The LGBS occurred within 2 wk (mean 11.4 d and range: 2–30 d) of dengue infection. These patients were afebrile at the time of appearance of neurological manifestations and majority had low platelet count, suggesting that LGBS was a manifestation of the active dengue infection. The common variants noted were demyelinating type; CSF showed albumino-cytological dissociation, half were treated with IVIG, and mean time to start of ambulation was 23.7 (range 7–60) days.
Data Loading...
