Duret Hemorrhages

Etiology

Duret hemorrhages are small areas of bleeding in the brainstem, primarily attributed to descending transtentorial herniation, which occurs due to increased intracranial pressure (ICP) and resultant intracranial compartmental shifts (see Image. Duret Hemorrhage, Computed Tomography Scan). The most common causes include traumatic brain injury, subdural and epidural hematomas, intraparenchymal hemorrhages, acute diffuse cerebral edema, brain neoplasms, hyponatremia, and, in rare cases, administration of thrombolytics.[3][4][5][6][7] While typically associated with increased ICP, there have also been a few reported cases of Duret hemorrhages resulting from intracranial hypotension.[8][9] 

Duret hemorrhages develop when a significant mass effect, as with cerebral edema, hematomas, or tumors, forces brain tissue out of its normal anatomical position, leading to uncal or transtentorial herniation. This downward displacement of the brainstem stretches and tears the penetrating arteries supplying the midbrain and pons, particularly the paramedian branches of the basilar artery. This vascular compromise results in hemorrhagic infarction, typically in the midline, paramedian, and ventral regions of the tegmentum of the upper pons and midbrain. The direct mechanical damage, disruption of blood flow, and sustained increase in ICP further exacerbate brainstem injury. Duret hemorrhages serve as a critical marker of severe brain injury and often indicate a poor prognosis. Their presence signifies impending brainstem failure and is frequently associated with irreversible neurological deterioration.

Epidemiology

The precise epidemiology of Duret hemorrhages is not widely documented, as they are typically postmortem findings in cases of severe brain injury. They occur secondary to conditions that cause significant brain herniation, such as large intracranial hematomas, severe traumatic brain injury, or brain tumors. Since Duret hemorrhages are often a marker of irreversible brainstem injury, the condition is rarely diagnosed in living patients, and its true prevalence remains uncertain.

The incidence of Duret hemorrhages varies significantly between neuropathological and radiological studies. Autopsy-based studies report an incidence of 30% to 60%, whereas radiological studies estimate a much lower occurrence of 5% to 10%.[1] This discrepancy may be explained by the fact that up to 20% of secondary brainstem hemorrhages occur at a microscopic level, making them undetectable on conventional imaging. Additionally, there may be a delay in developing Duret hemorrhages, meaning that initial computed tomography scans may not capture their presence. Risk factors associated with Duret hemorrhages include arterial hypertension and advanced age, which may contribute to increased vascular fragility and susceptibility to hemorrhagic infarction.[1]

Pathophysiology

Most believe the hypothesis underlying Duret hemorrhage is due to the distortion of the arteries' pontine perforating branches against the relatively immobile basilar artery due to caudal displacement of the upper brainstem by descending transtentorial herniation coupled with an anterior-posterior elongation of the brainstem by the side to side compression. However, some authors have also postulated a venous origin of these hemorrhages due to obstruction of venous return resulting from a sudden increase in intracranial pressure, which results in venous thrombosis, infarcts, and hemorrhages.[2][10]

Duret hemorrhages are essentially bleeding in the brainstem (midbrain and pons), typically seen in cases of severe brain trauma or other conditions causing increased intracranial pressure. Here's a brief overview of the pathophysiology:

• Increased ICP
  • Conditions like traumatic brain injury, brain tumors, large intracranial hematomas, or brain edema can cause a significant increase in ICP.
• Brain herniation
  • The increased pressure can force parts of the brain to move from their normal position, a process known as herniation. Specifically, uncal or transtentorial herniation can occur, where part of the temporal lobe is pushed against or through the tentorial notch.
• Impaired blood flow
  • This abnormal movement and pressure can compress or stretch the small, penetrating arteries that supply the brainstem, disrupting blood flow to those areas.
• Ischemic injury and hemorrhage
  • The reduced or blocked blood supply can cause ischemic injury to the brain tissue. This damage makes the blood vessels in that area more susceptible to rupture, leading to hemorrhaging (bleeding).
• Duret hemorrhages
  • These areas of bleeding in the midbrain and pons are associated with the disrupted blood supply and ischemic injury caused by the herniation process.

Notably, Duret hemorrhages are usually a secondary event following significant brain injury or increased intracranial pressure, and they generally indicate severe brain damage with a poor prognosis. They are most often identified post-mortem during an autopsy.

Histopathology

In the eighteenth century, Henri Duret confirmed that trauma resulted in variations in cerebrospinal fluid distribution, which in turn caused changes in pressure in the spaces where the fluid circulates, eg, the cerebral aqueduct. He noted microhemorrhages in the brainstem in the surrounding tissue as “action of a pressure increases in the cerebrospinal fluid due to sudden accumulation, which caused a linear hemorrhage on the medulla’s thickness and around the central canal.”[1] Histopathologically, Duret hemorrhages are characterized by small, linear areas of bleeding in the brainstem, often in the midbrain and pons. They are usually associated with severe brain injury, particularly transtentorial herniation.

Upon microscopic examination, one might observe:

• Acute hemorrhage
  • In the acute phase, red blood cells and hemorrhagic necrosis of the surrounding brain tissue would be evident.
• Chronic lesions
  • If the person survives for a period after the hemorrhage, the lesion may evolve. Over time, the hemorrhage may become organized, with macrophages infiltrating the area to clear the debris. In the later stages, gliosis, a process where glial cells proliferate to form a glial scar, may occur.
• Vascular disruption
  • There may be evidence of disruption to the small, penetrating arteries of the brainstem, which is thought to be the underlying cause of Duret hemorrhages.
• Associated findings
  • Since Duret hemorrhages are usually associated with significant brain herniation, there may also be histopathological findings consistent with this, such as evidence of neuronal injury or necrosis in other areas of the brain, particularly those affected by the herniation.

These histopathological features will depend on the analysis timing relative to the injury and the severity of the underlying brain injury. As Duret hemorrhages typically indicate severe brain damage and have a poor prognosis, they are often identified postmortem during an autopsy.[11]

History and Physical

In most cases, there is a prior history of head trauma, brain tumor, or a space-occupying lesion. Often, there is an altered sensorium ranging from confusion to a comatose state due to underlying transtentorial herniation and consequent perturbation of the reticular activating system. There is often anisocoria due to the involvement of the ipsilateral third cranial nerve with contralateral weakness.

In some cases, ipsilateral weakness can present due to the “Kernohan notch” phenomenon, an indentation of the cerebral peduncle on the contralateral side against the tentorium cerebelli.[12] With the progression of downward transtentorial herniation, the patient can demonstrate progression from decorticate and decerebrate posturing with loss of brainstem reflexes and changes in the respiratory pattern from Cheyne-Stokes to ataxic breathing. With the upward transtentorial herniation, especially following cerebral spinal fluid diversion procedures, there may be accompanying Perinaud syndrome.[13][14]

Evaluation

The initial evaluation requires a computed tomography scan head to discern supratentorial and infratentorial abnormalities such as tumors with vasogenic edema causing mass effect, epidural, subdural, or intraparenchymal hemorrhage. Central herniation results in complete obliteration of perimesencephalic and perimedullary cisterns with or without small hemorrhages in the midline, paramedian, and ventral regions in the tegmentum of the upper pons and midbrain (see Image. Computed Tomography Scan of a Duret Hemorrhage). The posterior cerebral artery may sometimes be kinked at the tentorial edge, resulting in occipital infarction. Necessary laboratory investigations include serum sodium, arterial blood gases, and a basic metabolic profile. 

Treatment / Management

First and foremost, the patient's airway, breathing, and circulation should be managed. An emergent noncontrast computed tomography (CT) scan of the head followed by aggressive management of intracranial hypertension. Identification of the underlying cause with timely intervention of the cause is the key to subsequent management. Basic labs include blood count, metabolic panel, and coagulation profile. If the clinician establishes trauma as the cause of epidural or subdural hemorrhage leading to herniation, then a rapid evacuation of the hematoma should be pursued. 

Steps for managing increased intracranial hypertension include:

• Raising the head of the bed 30 to 60 degrees.
• Hyperventilation may be needed to keep PaCo₂ (partial pressure of carbon dioxide) at 30 to 35 mm Hg.
• Osmotherapy, including hypertonic saline and mannitol therapy, can help manage the condition.
• ICP monitoring and keeping ICP <20 mm Hg is helpful.
• In cases of brain tumors and associated vasogenic edema, dexamethasone might help reduce the mass effect. 
• Surgical interventions (eg, decompression of mass/hematoma) may also be warranted.

In the intensive care unit, the goal is to maintain normotension, normovolemia, normonatremia to hypernatremia, normoglycemia, and normothermia to hypothermia. Such patients are followed through serial neurological examinations and head CTs in the intensive care unit. 

Differential Diagnosis

The most common differential diagnosis includes primary brainstem hemorrhages, which are petechial and hypertensive bleeds. Radiologically, Duret hemorrhages typically have a linear configuration, extending from ventral and dorsal, but may be of any shape in the clinical setting of supratentorial abnormalities leading to transtentorial herniation. Primary hypertensive hemorrhages are usually larger and occur spontaneously in patients with an antecedent history of uncontrolled hypertension without any supratentorial abnormality. Petechial hemorrhages are multifocal and small, which are seen around the dorsal midbrain (periaqueductal and tectum) in cases of diffuse axonal injuries following traumatic brain injury.[15]

Prognosis

The presence of Duret hemorrhages has invariably been regarded as a poor prognostic sign. However, an increasing number of case reports suggest possible functional recovery after a Duret hemorrhage. The presence of a Duret hemorrhage alone should in itself not be considered a poor prognostic marker and should not in itself trigger a decision to withdraw care.[16] Depending on the underlying cause of the transtentorial herniation, there are few case reports with good prognosis in patients with severe hyponatremia, subdural, and TBI.[17][18][19] The direct correlation between recovery and the rapid reversibility of the underlying cause remains uncertain.

Complications

Duret hemorrhages are typically associated with severe brain injury and carry a poor prognosis due to their location in the brainstem, which houses critical autonomic and motor functions. The most significant complications arise from direct damage to the midbrain and pons, leading to devastating neurological deficits. Patients may develop loss of consciousness, coma, and ultimately, brain death due to disruption of the reticular activating system. Respiratory failure is common, as the brainstem regulates vital autonomic functions.

Motor dysfunction is another major complication, often presenting as quadriplegia due to corticospinal tract involvement. Cranial nerve deficits may also occur, leading to abnormalities in pupillary response, ocular movement, and swallowing. Patients who survive the acute phase may experience persistent neurological impairment, including spasticity, dysphagia, and locked-in syndrome. Additionally, the severe elevation in intracranial pressure associated with Duret hemorrhages increases the risk of secondary ischemia and further brain injury. Due to the often fatal nature of these hemorrhages, survivors typically require prolonged intensive care, mechanical ventilation, and rehabilitative support.