Introduction

Brainstem hemorrhages classify as primary or secondary. Primary hemorrhages result from direct trauma, hypertension, coagulopathy,  whereas secondary hemorrhages may result from descending transtentorial herniation from diverse etiologies.[1] The latter is known as Duret hemorrhages (DH) named after a French neurologist Henri Duret, who first described the distribution of arterial supply in the brainstem and then in the cerebral cortex. He studied brain trauma and localized the origin of disturbances in autonomic function to the brainstem. These disturbances showed links to microhemorrhages affecting the medulla and pons, as a consequence of DH.[2]

Etiology

Duret hemorrhage is attributable to descending transtentorial herniation from any cause. Herniation syndromes occur secondary to elevations in intracranial pressure leading to intracranial compartmental shifts.  Duret hemorrhage is reported most frequently with increases in intracranial pressure from diverse etiologies, including subdural, epidural, intraparenchymal hemorrhages, trauma, brain neoplasms, acute diffuse cerebral edema, hyponatremia and rarely following administration of thrombolytics.[3][4][5][6][7][8][9][10] There are a  few reported cases of Duret hemorrhage resulting from intracranial hypotension.[11][12] Duret hemorrhages usually occur in the midline, paramedian, and ventral regions in the tegmentum of the upper pons and midbrain. 

Epidemiology

The incidence of Duret hemorrhages is reported more in neuropathological studies (30 to 60%) compared to 5 to 10% in radiological studies.[1] This discrepancy could be because 20% of these secondary brainstem hemorrhages occur at the microscopic level. Secondly, there is possibly a delay in the development of Duret hemorrhage following the initial CT scans. Some of the risk factors associated with the development of Duret hemorrhage are arterial hypertension and advanced age.[1]

Pathophysiology

Most believe the hypothesis underlying Duret hemorrhage is due to the distortion of the 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][13]

Histopathology

In the eighteenth century, Henri Duret confirmed that trauma resulted in variations in the distribution of cerebrospinal fluid, which in turn caused changes in pressure in the spaces where the fluid circulates e.g., 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]

History and Physical

In most cases, there is a prior history of head trauma, brain tumor, or a space-occupying lesion. Often, there is altered sensorium ranging from confusion to comatose state due to underlying transtentorial herniation and consequent perturbation of the reticular activating system. There is 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, which is an indentation of the cerebral peduncle on the contralateral side against the tentorium cerebelli.[14] With the progression of downward transtentorial herniation, the patient can demonstrate decorticate and decerebrate posturing with loss of brainstem reflexes and changes in the respiratory pattern from Cheyne stoke to ataxic breathing. With the upward transtentorial herniation, especially following CSF diversion procedures, there may be accompanying Perinaud syndrome.[15][16]

Evaluation

The initial evaluation requires a CT 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 peri-mesencephalic and peri-medullary cisterns with or without small hemorrhages in the midline, paramedian and ventral regions in the tegmentum of the upper pons and midbrain. In some cases, the posterior cerebral artery may 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 management of airway, breathing, and circulation followed. An emergent non-contrast CT head followed by aggressive management of intracranial hypertension. Identification of the underlying cause with timely intervention is the key to subsequent management. Basic labs, including CBC, CMP, 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:

1. Raising the head of bed 30 to 60 degrees.
2. Hyperventilation to keep PaCo2 30 to 35 mmHg
3. Osmotherapy including hypertonic saline and mannitol therapy
4. Intracranial pressure monitoring and to keep ICP < 20 mmHg
5. In cases of brain tumors and associated vasogenic edema, dexamethasone might help reduce the mass effect. 
6. Surgical interventions (decompression of mass, hematoma, etc.)

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 CT head in the intensive care unit. 

Differential Diagnosis

The most common differentials include primary brainstem hemorrhages, which are petechial and hypertensive bleeds. Radiologically, Duret hemorrhage typically has 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 dorsal midbrain (periaqueductal and tectum) in cases of diffuse axonal injuries following traumatic brain injury.[17]

Prognosis

The presence of Duret hemorrhage has been invariably regarded as a poor prognostic sign. However, an increasing number of case reports are suggesting possible functional recovery after Duret hemorrhage. Depending on the underlying cause of the transtentorial herniation, there are few case reports with good prognosis in patients with severe hyponatremia, subdural, TBI.[3][4][5][6][7][13][17] It remains unclear if a recovery in such cases is directly related to the rapid reversibility of the underlying cause. 

Enhancing Healthcare Team Outcomes

It can be challenging to distinguish Duret hemorrhage from primary brainstem hemorrhages. Traditionally, the presence of Duret hemorrhage was associated with grave prognosis, often leading to the withdrawal of care. With increasingly reported cases in the literature, early identification and aggressive interventions can result in good neurological outcomes. The presence of Duret hemorrhage alone should not be considered as a poor prognostic marker and should not trigger a decision to withdraw care.