Post-stroke fever is a frequent complication following an acute cerebral event, affecting 40% to 60% of hospitalized patients. This elevated temperature represents a serious complication that requires immediate intervention. High body temperature in the acute phase of stroke is consistently associated with worse neurological outcomes, increased disability, and higher rates of mortality. The presence of fever acts as a marker for a compromised clinical state and signals the need for a rapid search for its underlying cause.
The Link Between High Temperature and Secondary Brain Injury
Elevated body temperature, regardless of its origin, directly worsens the damage to already vulnerable brain tissue, a process known as secondary brain injury. The core mechanism involves a significant increase in the cerebral metabolic rate (CMR), demanding more oxygen and glucose. This increased demand is detrimental because the area surrounding the stroke, called the ischemic penumbra, is already struggling with a severely limited blood supply.
The temperature rise exacerbates a process called excitotoxicity, primarily by promoting the release of excitatory neurotransmitters like glutamate. High levels of glutamate overstimulate neurons, leading to an uncontrolled calcium influx that is toxic to the cell and triggers neuronal death. Even small changes, such as a 1°C increase in brain temperature, can affect the extent of this secondary injury.
Furthermore, fever intensifies the inflammatory response within the brain, making the blood-brain barrier (BBB) more permeable. This breakdown allows harmful substances and immune cells from the bloodstream to enter the brain parenchyma, contributing to cerebral edema and further neuronal damage. Prompt control of the temperature is considered a neuroprotective strategy to limit the expansion of the initial injury.
Identifying the Sources of Post-Stroke Fever
Fever after a stroke can originate from two main categories: infectious causes, which are the most common, and non-infectious causes related to the brain injury itself. Infectious fevers account for a large portion of cases, with stroke patients being particularly susceptible due to complications like swallowing difficulties and immobility.
The most frequent infectious complications are pneumonia and urinary tract infections (UTIs). Impaired swallowing, or dysphagia, is a major risk factor for aspiration pneumonia, as it allows oral secretions and food particles to enter the lungs. UTIs are also common, especially in patients who require indwelling urinary catheters, which introduce a pathway for bacteria.
Non-infectious, or endogenous, fever can result directly from the stroke, sometimes called central fever. This type of fever is often seen early, typically within the first 24 hours, and is caused by the stroke lesion affecting the hypothalamus, the brain’s thermoregulatory center. Non-infectious fever can also be a consequence of massive tissue necrosis or the presence of blood in the brain following a hemorrhagic stroke. Differentiating between infectious and non-infectious fever is important because the former requires antibiotics, while the latter is primarily managed with temperature control.
Clinical Assessment and Diagnostic Steps
A temperature above 37.5°C (99.5°F) in a stroke patient triggers an aggressive diagnostic workup to pinpoint the source. Continuous or frequent temperature monitoring is the first step, often occurring every four hours, or more frequently if a temperature-reducing intervention is started. This monitoring helps to track the fever pattern and assess the effectiveness of treatment.
Diagnostic tools focus on identifying the most likely infectious sources. Blood tests, including a complete blood count (CBC) and inflammatory markers, help determine if a systemic infection is present. A chest X-ray is routinely performed to look for signs of pneumonia, which may not present with a typical cough in a stroke patient.
A urine analysis and culture are necessary to diagnose a urinary tract infection, especially if a catheter is in place. In cases where the fever source remains unclear, blood cultures may be taken to check for bloodstream infections. The rapid completion of this assessment is essential because the choice between administering antibiotics for an infection or focusing solely on physical cooling for a central fever depends on these results.
Medical and Supportive Management Strategies
Management of post-stroke fever involves a dual strategy: symptomatic treatment to lower the temperature and definitive treatment aimed at the underlying cause. Symptomatic treatment typically begins with antipyretic medications like acetaminophen (paracetamol), often administered at a dose of 650-1000 mg every four to six hours. However, oral antipyretics alone are sometimes only marginally effective at achieving normothermia, which is the goal of maintaining a normal body temperature.
If medications are insufficient, physical cooling methods are employed, which may include external cooling blankets or devices. These non-pharmacologic approaches can be more effective at reducing temperature but must be used carefully to avoid inducing shivering, which paradoxically increases the body’s metabolic rate and heat production.
Definitive treatment is guided by the diagnostic findings, most commonly involving the prompt initiation of appropriate antibiotics if an infection is suspected or confirmed. For example, if a UTI is diagnosed, the antibiotic choice is tailored to the likely bacterial source. Supportive measures are equally important, particularly aggressive pulmonary hygiene (positioning and suctioning) to prevent aspiration and subsequent pneumonia. Hydration management also helps to maintain overall physiological stability, supporting the patient’s recovery from the acute stroke event.