Rebound intracranial hypertension (RIH) is an overlooked phenomenon in intensive care medicine. This is characterized by a secondary rise in intracranial pressure (ICP) after an initial period of ICP control (Fig. 1). Some of the common causes include withdrawal of osmotherapy, cerebrospinal fluid drainage limitation, or decompressive craniectomy effect, hence resulting in clinical deterioration.

Rebound intracranial hypertension is a secondary rise in ICP following a period of successful medical or surgical control of intracranial hypertension¹⁾. It typically emerges during recovery or while tapering therapies such as osmotic agents, cerebrospinal fluid (CSF) drainage, or after decompressive surgery^1,2). This is in contrast to primary intracranial hypertension, which results directly from the underlying acute insult, such as trauma, hemorrhage, or ischemia. It remains iatrogenic in nature and is unable to maintain a stable intracranial environment once the effect is reduced^3,4).

According to illustrations in Fig. 1, the pathophysiological cascade leading to rebound intracranial hypertension initiates with the primary brain insult, beginning with edema formation through mechanisms of brain swelling, impaired lymphatic drainage, altered CSF circulation, and venous outflow obstruction. These processes together raise intracranial pressure (ICP), initiating transient stabilization through compensatory responses including CSF displacement, venous blood volume reduction, autoregulatory vasoconstriction, and cellular osmotic buffering. However, as depicted in the “Rebound Mechanisms” phase of Fig. 1, exhaustion of these compensatory processes leads to a secondary rise of ICP. This is characterized by impaired autoregulation, worsening edema, venous congestion, and loss of intracranial compliance. The mechanistic progression explains why RIH manifests after initial ICP control and highlights its potential to produce cerebral ischemia, brainstem compression, herniation syndromes, and Cushing’s triad, as shown in the downstream impact section of Fig. 1.

The exact incidence is unknown, but rebound intracranial hypertension is increasingly recognized in critical care settings, most probably in patients undergoing aggressive ICP management^1,2). Its detection is often difficult because clinical deterioration may be attributed to the primary disease rather than to rebound physiology. If not recognized at the correct time, it can lead to secondary brain injury, herniation, and poor neurological outcomes, emphasizing the importance of careful monitoring, gradual weaning of therapies, and individualized management strategies^3-5).

Hyperosmolar agents such as mannitol and hypertonic saline are the most important aspects in the management of elevated ICP as they lead to an osmotic gradient that facilitates the movement of water from the brain parenchyma to the intravascular compartment^6-8).

When these agents are withdrawn too rapidly—particularly after prolonged administration—the osmotic gradient can reverse, causing a reaccumulation of water within the brain tissue. This effect is most pronounced in regions with a disrupted blood-brain barrier, resulting in RIH^9-11).

This rebound physiology is in line with the mechanisms depicted in Fig. 1, particularly the component labelled “BBB Disruption – Fluid Leak,” where withdrawal of hyperosmolar therapy unmasks increased blood–brain barrier permeability, allowing a renewed influx of water into the parenchyma. Continuing the process, the figure's “Cellular Osmotic Adjustment” pathway illustrates how astrocytes gradually accumulate osmolytes during prolonged osmotherapy; once therapy is discontinued suddenly, the retained intracellular osmolytes pull the water back into the brain, producing a rebound rise in ICP. Both of the above components together, these Fig. 1 elements emphasize that the pathophysiology of rebound intracranial hypertension is not just a passive reversal of osmotic gradients but a structured, mechanistically predictable failure of osmotic and vascular compensatory systems.

Patients with renal dysfunction, systemic inflammation, or pre-existing blood-brain barrier injury are especially susceptible due to altered osmotic homeostasis^4,5).

External ventricular drains are commonly used to control ICP by diverting cerebrospinal fluid. Cerebrospinal accumulation and rebound rise in ICP are a result of sudden discontinuation or premature clamping, without gradual tapering of intracranial pressure^1-3).

This is common in clinical conditions of subarachnoid hemorrhage, obstructive hydrocephalus, or impaired CSF reabsorption, where normal CSF dynamics are compromised¹²⁾.

In case of failure of EVD weaning trial, it often results in a gradual rise of ICP with neurological deterioration¹³⁾.

Recent consensus-based guidelines advocate for stepwise reduction of hyperosmolar therapy and controlled EVD weaning or trial of clamping the external ventricular device with optimal output. Multimodal monitoring of ICP and brain tissue oxygenation to minimize rebound events and optimize neurological outcomes should also be taken into account¹⁴⁾.

Decompressive craniectomy and other modes of surgical decompression effectively lower ICP by allowing expansion of swollen or congested brain tissue and restoring intracranial compliance. However, compensatory alterations in cerebral hemodynamics, venous drainage, and cerebrospinal fluid flow after decompression—if not adequately regulated—can paradoxically trigger a secondary rise in ICP^4,5).

As edema subsides, evolving changes in compartmental compliance and intracranial elastance may lead to delayed shifts in ICP, producing a rebound pattern of intracranial hypertension. These events are frequently associated during the recovery phase with disrupted autoregulation, impaired cerebrospinal fluid absorption, or increased venous outflow resistance^9,10).

After cranioplasty, rebound cranial hypertension has been reported, due to sudden restoration of the rigid cranial vault, which causes a change in the CSF hydrodynamics and venous return, decreasing the intracranial compliance^11-13). Along with this, postoperative monitoring of ICP and gradual adjustment of pressure targets in cerebral perfusion are recommended to reduce secondary intracranial pressure surges¹⁴⁾.

Recent evidence and consensus statements emphasize the importance of stepwise management, ensuring hemodynamic stability and multimodal monitoring—including ICP and brain oxygenation—during decompressive surgery and the cranioplasty phase to prevent rebound phenomena^12,14).

The development of RIH presents significant diagnostic and therapeutic challenges, consistently associated with a variety of adverse clinical outcomes. Early recognition and prompt actions are important, as unrecognized or not treated adequately, this leads to a rise in ICP, posing neurological decompensation and poor outcomes^12,15).

Rebound intracranial hypertension remains a clinically significant complication in neurocritical care. The importance of gradual weaning of ICP-lowering therapies, vigilant monitoring, and individualized management protocols should be taken into account. Multimodal monitoring and stepwise ICP control strategies should be brought into existence in the standard practice of management to reduce secondary injury and optimize neurological recovery.