Subarachnoid hemorrhage: Clinical sciences

Subarachnoid hemorrhage refers to an intracranial bleed that occurs between the pia and arachnoid layers of the meninges, which are protective layers that cover the brain. If not promptly recognized and treated, blood pooling in the subarachnoid space can lead to a fatal increase in intracranial pressure. Now, based on the underlying cause, subarachnoid hemorrhage can occur as a result of traumatic head injuries, but it could also occur spontaneously, which is also known as non-traumatic subarachnoid hemorrhage.

Now, if your patient presents with a chief concern suggesting subarachnoid hemorrhage, first, perform an ABCDE assessment to determine if they are unstable or stable.

If unstable, stabilize the airway, breathing, and circulation. At this point, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and don’t forget to put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, you might need to manage high intracranial pressure, or ICP for short.

Now, here’s a clinical pearl to keep in mind! In severe cases, subarachnoid hemorrhage can increase ICP, which triggers a physiological response known as the Cushing triad, which consists of bradycardia, hypertension, and irregular breathing. Moreover, important physical exam findings associated with dangerously high ICP and potential brain herniation include dilated pupils that are unresponsive to light!

If you notice any of these signs, place an ICP monitor and start appropriate medical management, which includes elevating the head of the bed, hyperventilation, sedation, and hyperosmolar therapy.

If high ICP is partly due to ventriculomegaly, your patient will require CSF diversion, such as placing an external ventricular drain. Finally, If high ICP persists despite medical management and CSF diversion, you should proceed to emergent decompressive craniectomy.

Let’s go back and look at stable patients. In this case, first, obtain a focused history and physical exam. When taking a patient’s history, it is important to determine the characteristics of headaches and ask about any head trauma. This will help you determine whether the etiology is traumatic or non-traumatic.

First, let’s focus on traumatic subarachnoid hemorrhage. In this case, your patient will usually report a nonspecific headache and recent head trauma. Next, the physical exam will reveal neck stiffness due to blood irritating the meninges, also known as nuchal rigidity. Additionally, your patient might present with altered mental status and focal neurologic deficits. With these findings, you should suspect traumatic subarachnoid hemorrhage, so immediately order a non-contrast head CT. If the CT reveals blood in the subarachnoid space in cortical convexities, meaning on the surface of the brain, with or without blood in other brain compartments such as the epidural, subdural, or intraparenchymal space, you should diagnose traumatic subarachnoid hemorrhage.

Once you diagnose the condition, avoid hypertension to prevent rebleeding and correct any coagulopathy. Finally, don’t forget to consult your surgery team, more specifically, neurosurgery, for possible ICP monitoring and CSF diversion.

Now, let’s go back and take a look at non-traumatic subarachnoid hemorrhage. These patients will typically endorse the worst headache of their life, which is often called a “thunderclap” headache because the pain is maximum at onset. In some cases, a few days or a few weeks before the patient’s presentation, they could also report a sudden, persistent, intense headache called a “warning” or sentinel headache. This type of headache occurs due to aneurysmal wall stretching or minor aneurysmal leak and is often a sign of impending aneurysmal rupture! Next, these individuals will deny a history of recent head trauma, but they might report cardiovascular risk factors, such as hypertension and tobacco use, as well as a family history of cerebral aneurysms. Other important risk factors include a history of autosomal dominant polycystic kidney disease, Ehlers-Danlos type IV, and fibromuscular dysplasia.

Next, the physical exam will reveal nuchal rigidity, possibly in combination with an altered mental status and focal neurologic deficits. Some patients might also present with ptosis and mydriasis, as well as the “down and out” deviation of the pupil.
This clinical presentation is specific for cranial nerve III palsy due to a posterior communicating artery aneurysm because the posterior communicating artery runs next to the cranial nerve III.

Finally, the fundoscopic exam will often reveal papilledema, which indicates increased intracranial pressure, and sometimes, you might notice a boat-shaped hemorrhage called a subhyaloid hemorrhage .

With these findings from the focused history and physical, suspect non-traumatic subarachnoid hemorrhage and promptly order a non-contrast head CT.
If there are no acute findings of hemorrhage, but your suspicion of subarachnoid hemorrhage is strong, perform a lumbar puncture and send a CSF sample for analysis. This is because the CT loses significant sensitivity for picking up subarachnoid hemorrhage after 6 hours of the event. If the CSF analysis shows elevated red blood cell count and xanthochromia, which is a yellow CSF discoloration from bilirubin due to hemoglobin breakdown, you can diagnose subarachnoid hemorrhage.