Air & Water Borne Diseases
Open Access

Infectious Diseases and Endocrinology 2019: Dengue fever associated cerebral hemorrhages, a rare, poorly understood entity in an era of dengue epidemic: A case series and literature review, Nayomi Shermila Jayasinghe, Bairnsdale Regional Health Service, Australia

Dengue fever is caused by a flavivirus, which is a vector borne RNA virus with four anti-genically distinct serotypes (DEN 1, DEN 2, DEN 3 and DEN 4). Neurological manifestations are rare compared to other complications of the disease. Encephalopathy, encephalitis, aseptic meningitis, intracranial hemorrhages, thrombosis, mono-neuropathies / polyneuropathies, Guillain-Barre syndrome and myelitis have been reported. Neurological manifestation in dengue hemorrhagic fever usually results from multisystem dysfunction secondary to liver failure, cerebral hypoperfusion, electrolyte imbalance, shock, cerebral edema and hemorrhage related to vascular leak. The occurrence of brain hemorrhage in a case with dengue shock can be serious and leads to death. The occurrence of brainstem hemorrhage can be a very serious fatal situation. We report this case series of dengue hemorrhagic fever with multiple intracranial, sub arachnoid hemorrhages and sub-dural hematoma causing brainstem herniation. Case 1: A 25-year-old previously healthy woman was admitted on third day of fever with thrombocytopenia. Critical phase started on 5th day with evidence of pleural effusion and moderate ascites. 31 hours into critical phase, she developed headache, altered level of consciousness, limb rigidity and respiratory depression without definite seizures. Non-contrast CT brain done at tertiary care level revealed diffuse intra cranial hemorrhages and sub arachnoid hemorrhages in right frontal, parietal, occipital lobes and brainstem, cerebral oedema with an acute subdural hematoma in right temporo-parietal region. Her platelet count was 40,000 at this time with signs of vascular leakage. She was intubated and ventilated with supportive care. Later on, she developed features of cranial diabetes insipidus and it responded to intranasal desmopressin therapy. In spite of above measures signs of brainstem herniation developed and she succumbed to the illness on day 8. Dengue was confirmed serologically. Case 2: A 24 year old previously healthy was admitted on 2nd day of fever with constitutional symptoms and no bleeding manifestations. Clinical, hematological and serological parameters confirmed dengue infection. On 5th day of illness, she entered into leaking phase, but did not have evidence of any bleeding Intra Cranial Hemorrhage (ICH) in right parietal lobe deep white matter area associated with perilesional oedema and midline shift. Bleeding into the right lateral ventricle and Small Subdural Hematoma (SDH) were also noted in right parietal lobe area. Her platelet count at the time of development of hemorrhages was 32,000 and International Normalised Ratio was normal. NCCT brain was repeated 24 hours later and showed progression of hemorrhages. It showed progressive worsening of right occipito-temporal ICH, cerebral oedema, midline shift, right SDH and SAH. Patient remained hemodynamically stable and platelet count was on the rising trend. It was 52,000, 77,000 and 83,000 on 3 consecutive occasions. PCV was stable around 43. There were no other bleeding manifestations neurosurgical interventions were not attempted and patient was managed conservatively. Amidst maximum care provided, patient succumbed to illness on the following day. It can be concluded that diffused cerebral hemorrhages with moderate thrombocytopenia and normal coagulation profile are a very rare and fatal complication of dengue fever. Exact pathophysiological mechanism is not well understood. Increased awareness and high degree of clinical suspicion is needed among clinicians for timely diagnosis of this extremely rare complication of dengue fever. We postulate that immunological mechanisms may play a role in pathogenesis. However further comprehensive research and studies are needed to understand the pathophysiological mechanisms leading to this complication.

Elements relying upon the host, the vector, and the viral operator, related to biological and epidemiological conditions, are engaged with dengue scourges. As indicated by the new World Health Organization (WHO) clinical grouping, suggestive diseases can bring about instances of dengue or serious dengue. Optional contamination is viewed as the primary hazard factor for serious illness, in spite of the fact that T cell reaction and individual hereditary qualities are likewise significant. Dengue avoidance stays endless supply of the vector, albeit a few immunization competitors just as new devices for vector disposal are under assessment and will be presented sooner rather than later. Dengue is as of now the most significant mosquito-borne viral illness all inclusive. While still being worked on, hereditarily adjusted (GM) sterile bug strategies are a conceivably encouraging way to deal with control dengue. GM mosquitoes have been created with the objective of delivering posterity that kick the bucket in the early formative stage, and diminishing the mosquito populace beneath the dengue transmission limit. Here, we present a structure and the fundamental segments of a financial investigation to survey GM mosquito advancements. Consolidating information from different dengue-endemic nations, we create a scientific model of expenses and benefits and aligned it with accessible proof. We talk about the primary presumptions, results, and admonitions around theseThe frequency of dengue has expanded considerably over ongoing decades, with about portion of the total populace now in danger of disease. Vector control is as of now the principle procedure to diminish dengue infection transmission; notwithstanding, vector control has not ended the spread of Aedes aegypti, the fundamental dengue vector, and of dengue episodes. Promising new vector control innovations might spare billions of dollars yearly in turned away clinical costs, efficiency misfortunes, and unexpected losses.Dengue antigens, fundamentally prM and E proteins, can be communicated in microscopic organisms, yeast, mosquito cells, or mammalian cells, and afterward cleaned to plan nonreplicating, subunit immunizations. When all is said in done, a shortened E protein is communicated that does not have its carboxy-terminal hydrophobic film stay locale with an end goal to augment the discharge and solvency of the protein. Dengue transmission happens during the time in endemic tropical regions; be that as it may, in many nations there is a particular occasional example, with expanded transmission as a rule related with the blustery season. Flare-ups happen most as often as possible in regions where different serotypes of dengue infection are all the while endemic or consecutively pestilence and diseases with heterologous sorts are visit. In endemic regions dengue happens most much of the time in youngsters matured somewhere in the range of 2 and 15 years. Extreme dengue is generally connected with auxiliary dengue contamination and during essential disease in newborn children under 1 year, destined to dengue-safe moms.

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