During the febrile phase of symptomatic dengue infection, which typically lasts 2 to 7 days, the patient may exhibit warning signs of progression to severe disease characterized by increased capillary permeability and consequent distributive shock (dengue shock syndrome [DSS]), usually accompanied by serious bleeding complications (dengue hemorrhagic fever [DHF]). Among the clinical warning signs are hepatomegaly, alteration of consciousness, mucosal bleeding, and “third space” accumulation of fluid. Concurrent elevation of hematocrit and fall in platelet count at this juncture is an ominous finding that reflects hemoconcentration and a predisposition to bleeding, respectively. A positive tourniquet test, whereby numerous petechiae appear after a sphygmomanometer cuff is inflated on the arm and then released, raises the index of suspicion for incipient DHF. The moment of defervescence marks the onset of the critical phase, which lasts 24 to 48 h and may be characterized by transition to recovery or progression to DHF/DSS. Patients with warning signs are often hospitalized for close observation, supportive care, and IV hydration. Even with early and appropriate intervention, the course taken by a particular patient depends on both host and viral characteristics; higher risk for progression is conferred by female sex, young age, high BMI, and certain dengue strains. The severe trajectory is also more likely in those who have been previously infected with a different serotype in a phenomenon blamed on incomplete immunity that, although not protective, facilitates viral entry and spread, thereby enhancing the inflammatory cascade. Rather than direct viral toxicity, the pathogenesis of DHF/DSS is believed to involve virally mediated cytokine activation leading to endothelial dysfunction and permeability. The resultant clinical entity behaves in a manner reminiscent of septic shock with disseminated intravascular coagulation. Patients may initially compensate and manifest a narrowed pulse pressure without overt hypotension. Further deterioration, however, results in refractory hypotension with multiorgan dysfunction syndrome complicated by GI or other life-threatening hemorrhage in the context of consumptive coagulopathy and severe thrombocytopenia. Inability to protect the airway due to profound encephalopathy frequently mandates endotracheal intubation. The presence of pulmonary edema may reflect overzealous fluid administration in the setting of a porous endothelium, viral myocarditis causing left ventricular systolic dysfunction, or noncardiogenic fluid as part of ARDS.