Duret Hemorrhages

Etiology

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

Duret hemorrhages develop when significant mass effect from cerebral edema, intracranial hematomas, or brain tumors causes brain tissue to shift from its normal anatomical position, resulting in uncal or transtentorial herniation. This downward displacement of the brainstem stretches and tears the penetrating arteries that supply the midbrain and pons, in particular the paramedian branches of the basilar artery. This vascular compromise leads to hemorrhagic infarction of the midline, paramedian, and ventral regions of the tegmentum of the upper pons and midbrain. Direct mechanical damage, disruption of blood flow, and sustained increase in ICP further exacerbate the brainstem injury. Duret hemorrhages represent a critical indication of severe brain injury and often indicate a poor prognosis. Their presence signifies impending brainstem compromise and is often associated with irreversible neurological damage.

Epidemiology

The precise epidemiology of Duret hemorrhages is not widely documented because they are usually found on postmortem examination in cases of severe brain injury. These hemorrhages occur due to conditions that result in brain herniation, such as large intracranial hematomas, severe TBI, or brain tumors.[10] Since Duret hemorrhages are often a marker of irreversible brainstem injury, the condition is rarely diagnosed in patients who survive, and their 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% compared to radiological studies that estimate a much lower occurrence rate of 5% to 10%.[1] This discrepancy may be explained by the fact that up to 20% of secondary brainstem hemorrhages occur at the microscopic level, which makes them undetectable on conventional imaging. Additionally, there may be a delay in developing the Duret hemorrhages, which indicates that the initial computed tomography scans may not demonstrate their presence. Risk factors associated with the development of Duret hemorrhages include arterial hypertension and advanced age, both of which may contribute to increased vascular fragility and a susceptibility to hemorrhagic infarction.[1]

Pathophysiology

Most clinicians believe that the hypothesis underlying Duret hemorrhage is related to the distortion of the pontine perforating arterial branches that extend from the relatively immobile basilar artery due to the caudal displacement of the upper brainstem, due to descending transtentorial herniation, which is coupled with an anterior-posterior elongation of the brainstem from the side-to-side compression. However, some authors have also postulated that there may be a venous origin of these hemorrhages due to obstruction of the venous return that results from a sudden increase in ICP, which results in venous thrombosis, infarction, and hemorrhage.[2][11]

Duret hemorrhages represent bleeding in the midbrain and pons of the brainstem that is usually seen in cases of severe brain trauma or other conditions causing increased ICP. Here is a brief overview of the pathophysiology:

• Increased ICP
  • Conditions such as TBI, brain tumors, large intracranial hematomas, or brain edema can cause a significant increase in ICP.
• Brain herniation
  • The increased ICP can cause parts of the brain to shift from their normal position in a process known as herniation.[12] Specifically, uncal or transtentorial herniation can result where the medial temporal lobe is pushed against the brainstem or through the tentorial notch.
• Impaired blood flow
  • This abnormal ICP and movement of the brainstem can compress or stretch the small, penetrating arteries that supply the brainstem, which prevents blood flow to those areas.
• Ischemic injury and hemorrhage
  • Reduced or absent blood flow to the brainstem can cause ischemic injury to brain tissue. This vascular damage makes the blood vessels in that area more susceptible to rupture, which results in hemorrhage.
• Duret hemorrhages
  • These areas of hemorrhage in the midbrain and pons are associated with the decreased blood flow to the brainstem and the resultant ischemic injury caused by the herniation process.

Duret hemorrhages are usually a secondary event that occurs after a significant brain injury or in the presence of increased ICP, where they indicate severe brain damage with a poor prognosis. They are most often identified postmortem at the time of the autopsy.

Histopathology

In the 18th century, Henri Duret confirmed that trauma resulted in variations in cerebrospinal fluid distribution that caused changes in the ICP in the spaces where the fluid circulates, such as the cerebral aqueduct. Duret noted microhemorrhages in the brainstem and 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 midbrain and pons of the brainstem. They are usually associated with severe brain injury, such as transtentorial herniation.

Upon microscopic examination, those findings may represent:

• Acute hemorrhage
  • In the acute phase, red blood cells and hemorrhagic necrosis of the surrounding brain tissue may be evident.
• Chronic lesions
  • If the person survives after the hemorrhage, the lesion may evolve. Over time, the hemorrhage may become organized, with macrophages infiltrating into the area to clear the dead tissue. 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 that represent the underlying cause of the Duret hemorrhages.
• Associated findings
  • Because Duret hemorrhages are usually associated with significant brain herniation, there may also be histopathological findings such as neuronal injury or necrosis in other areas of the brain that have been affected by the herniation.

These histopathological features will depend on the time of the analysis and the severity of the brain injury. As Duret hemorrhages typically indicate severe brain damage and have a poor prognosis, they are often identified postmortem during an autopsy.[12]

History and Physical

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

In some cases, ipsilateral weakness can present due to the “Kernohan notch” phenomenon, where there is compression of the cerebral peduncle on the contralateral side of the brainstem against the tentorium cerebelli.[13] With downward transtentorial herniation, the patient can demonstrate progression from decorticate to decerebrate posturing with the loss of brainstem reflexes and alteration in the respiratory pattern from Cheyne-Stokes to ataxic breathing. With the upward transtentorial herniation that results following cerebral spinal fluid diversion procedures, there may be an associated Perinaud syndrome.[14][15]

Evaluation

The initial evaluation of the patient requires a computed tomography (CT) scan of the head to discern whether there are supratentorial and infratentorial abnormalities, such as brain tumors with vasogenic edema causing mass effect or epidural, subdural, or intraparenchymal hemorrhage. Central herniation results in complete obliteration of the 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 occasionally be kinked at the tentorial edge, resulting in occipital lobe infarction. Required laboratory investigations include a serum sodium level, arterial blood gases, and a basic metabolic profile. 

Treatment / Management

First and foremost, the airway, breathing, and circulation of the patient should be addressed. An emergent noncontrast CT scan of the head should be obtained, followed by the aggressive treatment of the intracranial hypertension if it is present on the scan. Identification of the underlying cause of the elevated ICP, with the timely management of the cause, represents the therapeutic course of action for the patient. The necessary basic labs include blood count, metabolic panel, and coagulation profile. If the clinician establishes that trauma is the cause of epidural or subdural hemorrhage leading to herniation, then the rapid surgical evacuation of the hematoma should be pursued.[16](A1)

Steps for managing increased intracranial hypertension include:

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

The clinical goal in the intensive care unit is to maintain normotension, normovolemia, normonatremia to hypernatremia, normoglycemia, and normothermia to hypothermia. Such patients are followed with serial neurological examinations and head CT scans in the intensive care unit. 

Differential Diagnosis

The most common differential diagnosis includes primary brainstem hemorrhages, which are petechial in appearance and represent hypertensive bleeds. Radiologically, Duret hemorrhages have a linear configuration that extends in the brainstem from a ventral and dorsal location, but may be of any shape in the clinical setting of supratentorial abnormalities that cause transtentorial herniation. Primary hypertensive hemorrhages are usually larger and occur spontaneously in patients with an antecedent history of uncontrolled hypertension without supratentorial abnormalities. Petechial hemorrhages are multifocal and small in size and are seen around the dorsal midbrain in periaqueductal and tectal locations in cases with diffuse axonal injuries following TBI.[17]

Prognosis

The presence of Duret hemorrhages has invariably been regarded as a poor prognostic sign. However, increasing case report numbers suggest functional recovery may be possible after a Duret hemorrhage.[18] The presence of a Duret hemorrhage alone should in itself not be considered a poor prognostic indicator and should not by itself result in the decision to withdraw care.[19] Depending on the underlying cause of the transtentorial herniation, there have been a few case reports that resulted in a good prognosis in patients with severe hyponatremia, subdural hemorrhage, and TBI.[20][21][22] 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 contains 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 this vital autonomic function.

Motor dysfunction is another major complication of Duret hemorrhage, often presenting as quadriplegia due to corticospinal tract involvement. Cranial nerve deficits may occur with abnormalities in the pupillary response, ocular movement, and ability to swallow. Patients who survive the acute phase of the injury may experience persistent neurological impairment that includes spasticity, dysphagia, and the locked-in syndrome. Additionally, the severe elevation in ICP 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.