Pathophysiology of 3 types of hemorrhage

The classic presenting symptom of SAH is acute onset "thunderclap" headache that may be accompanied by loss of consciousness, vomiting, neck stiffness, or seizure. Thunderclap headaches reach maximum intensity within seconds. The headache is typically occipital or unilateral. A significant proportion of patients will also have a warning (sentinel) headache. Of note, not all patients with SAH present with this classic symptom and a gradual onset headache does not preclude the diagnosis of SAH. The Hunt and Hess Grading System is one method used to describe patients with SAH.

Recent exertion, hypertension, excessive alcohol consumption, sympathomimetic use, and cigarette smoking are risk factors as well for both SAH and intracerebral bleeds. However, the strongest risk factor for SAH is family history, which carries a 3 - 5 fold risk.

Subdural hematomas are extra axial blood collections between the dura and the arachnoid mater. While epidural hematomas are usually ipsilateral to the trauma, subdural bleeds are typically on the contre-coup side. Subdural hematomas form when bridging veins are sheared during acceleration-deceleration of the head.

As the bleeding is venous and low-pressure in nature, the hematoma can grow fairly slowly and the presentation can be delayed by days to weeks. This is particularly true in patients with brain atrophy, whose bridging vessels are more susceptible to shear and who can more readily accommodate the additional intracranial blood volume.

Subdural hematomas have a wide clinical spectrum. Acute SDH is more common in younger patients with a history of trauma. Rapid accumulation of extra-axial blood, the absence of pre-existing atrophy, and the presence of other traumatic brain injuries correspond to a worse neurologic status at presentation. As the younger brain is less atrophic, even small volumes of extra-axial blood can increase ICP and result in severe deficits.

In the pediatric population, presence of acute or chronic SDH should raise suspicion of for child abuse, although SDH can also occur as a result of birth trauma. The physician should search for other signs of 'Shaken Baby Syndrome', including retinal hemorrhages and long bone fractures. Infants with increased ICP might present with a bulging fontanel, enlarged head circumference, emesis, failure to thrive, and seizure.

Chronic SDH is a grand imitator. It occurs more often in elderly and alcoholic patients as they are most prone to atrophy and/or coagulopathy. The most common presentation is altered mental state. Hemiparesis, headache, and falls are other common features. As the symptoms can be subtle, the differential diagnosis broadly encompasses any potential cause of weakness or confusion in the elderly. This highlights the need to perform a CT scan in any elderly patient with a change in mentation that is not convincingly explained by other pathologies.

Computed tomography (CT) is the mainstay of diagnosis, and the CT appearance varies depending on the age of the lesion. In the acute phase (days 0-3), the lesion appears hyperdense relative to the parenchyma. The clot is fresh and jelly-like. Subacutely, between 3 and 14 days, the lesion is isodense or hypodense as a result of fibrinolysis occurring within the clot. An injection of contrast may be helpful in illuminating isodense lesions. Chronic subdural hematomas, older than 2 weeks, are usually hypodense. Unlike epidural hematomas, SDH's can extend past the suture lines. Acute bleeds are typically concave in shape.

As an SDH grows, mass effect becomes evident; midline shift, sulci effacement, obliteration of the basal cisterns, and ventricular compression might be seen. Bilateral hematomas are fairly common, leading to medial compression of both ventricles, making them slit like. This is called "squeezed ventricle" or "rabbit's ears" sign. Small isodense hematomas at the vertex, the base of the skull, and in the posterior fossa can be particularly difficult to visualize. In these cases, MRI can be of assistance in making the diagnosis.

Epidural hematomas are accumulations of blood between the skull and the dura, and typically occur after significant blunt head trauma. Fractures of the temporal bone can disrupt the middle meningeal artery, leading to high-pressure bleeding within the cranial vault. Herniation can occur within hours if the hematoma is not evacuated, so early recognition is key.

Classically, patients with epidural hematomas have a brief loss of consciousness after their injury, followed by a lucid period. Then, they lose consciousness again and deteriorate into herniation and death. You might hear this described as the 'talk and die' phenomenon. In reality, most EDH patients either do not lose consciousness, or do not regain it.