Pharmacy Pearls: How to Identify a Ruptured Brain Aneurysm and Subarachnoid Hemorrhage

By: Maha Sohail, PharmD Candidate c/o 2024

In the United States, about 6.5 million, or 1 in 50 people, have an unruptured brain aneurysm, with one rupture occurring every 18 minutes.1 Worldwide, there are almost half a million deaths each year from this medical emergency, of which half the victims are younger than 50 years old. Ruptured brain aneurysms are fatal in about 50% of cases, and those who do survive must often struggle with long-term debilitating health obstacles.1 It is important to be able to identify the clinical presentation of a suspected rupture and its result, an aneurysmal subarachnoid hemorrhage, as well as recognize patient treatment and brain health lifestyle management after this occurrence. 

Cerebral Aneurysms

A cerebral aneurysm, also known as a brain or intracranial aneurysm, is characterized by the inflation of an artery in the brain. The causes are unknown; however, some proposed mechanisms are genetic artery abnormalities or structural changes caused by hypertension or smoking.2 There are three different types of cerebral aneurysms, including berry (saccular), fusiform, and mycotic.3 Berry aneurysms are the most common, representing 90% of cerebral aneurysms, where there is a ballooning that inflates from a weakened area of an artery wall, and the balloon is attached to the artery like a berry hanging from a vine.3 Fusiform aneurysms are rare and characterized by an expansion of the artery bulging out from all sides.3 Mycotic aneurysms are bulging aneurysms similar in shape to fusiform, and they are caused by an infection that affects the brain arteries, leading to the weakening of the artery wall.

Aneurysmal Subarachnoid Hemorrhage

An aneurysmal subarachnoid hemorrhage (aSAH) is the result of a ruptured aneurysm, causing extravasation of blood into the subarachnoid space, which irritates the lining of the brain and damages the brain cells.4 Additionally, the area of the brain where the damaged artery was previously supplying oxygen-rich blood with, becomes blood deprived otherwise known as delayed cerebral ischemia (DCI).5 An aSAH is a medical emergency, as it is a life-threatening hemorrhagic stroke.

The subarachnoid space is filled with cerebrospinal fluid (CSF), which protects the brain by acting as a floating cushion. As blood from the aSAH fills up the space, it leads to increased intracranial pressure (ICP), causing the brain to either shift and herniate or be crushed against the skull.5 Blockage of CSF circulation will lead to enlarged ventricles, known as hydrocephalus, resulting in confusion, lethargy, and loss of consciousness.5

Ruptured Cerebral Aneurysm Presentation and Risk Factors

A ruptured aneurysm presents as the extremely sudden onset of a severe, thunderclap headache with maximal intensity. Symptoms include a stiff neck, nausea, vomiting, blurred or double vision, photophobia or sensitivity to light, loss of consciousness, seizures, and an altered mental status ranging from mild lethargy to a profound coma.6 Brain aneurysms are most prevalent in people ages 35 to 60; however, they can occur in children as well. Women are more likely to suffer from a brain aneurysm than men at a ratio of 3:2.6 Other risk factors include having a past medical history of a previously ruptured brain aneurysm, genetics, African-American ethnicity, Hispanic ethnicity, arteriovenous malformation (AVM), and certain connective tissue disorders. Some modifiable risk factors include excessive alcohol consumption, hypertension, smoking, and illicit drug use of sympathomimetics such as cocaine and/or methamphetamine.6

Rupture Treatment and aSAH Management

According to the American Heart Association and American Stroke Association guidelines for rupture treatment and aSAH management, there is emerging data that indicates early aneurysm repair combined with aggressive management of complications such as hydrocephalus and DCI leads to improved functional outcomes.4 It is recommended to use surgical or endovascular methods of treatment for a rupture, such as open surgery craniotomy (in which a surgical clipping is used) or less invasive therapies, including endovascular surgical coilings, stents, liquid agents, or flow diversion devices.7 

Since aSAH is frequently misdiagnosed, patients with an acute onset of a severe headache should be highly suspected. Determining the initial clinical severity of aSAH through the use of simple validated scales such as the Hunt and Hess Scale (Table 1) or the World Federation of Neurosurgical Societies Scale (Table 2) is crucial for appropriate management and prognosis prediction.7

Narrowing of the arteries, or vasospasm, after an aSAH is common and occurs 7 to 10 days after an aneurysm rupture and spontaneously resolves after 21 days.  DCI associated with arterial vasospasm is a major cause of death and disability in aSAH patients. 7 The management of aSAH-induced vasospasm and DCI entails nimodipine, a second-generation dihydropyridine calcium channel blocker, 60 mg by mouth every 4 hours for 21 days, with a recent comprehensive meta-analysis study confirming improved neurological outcomes. Nimodipine should be administered to all patients with aSAH, and maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI.7

Seizures associated with aSAH remain a controversy as management on prophylaxis or treatment has been poorly supported by randomized, controlled trials. Around 8 to 15% of patients experience seizure-like episodes; however, there is still uncertainty regarding whether these episodes are epileptic in origin.4 The guidelines recommend that the use of prophylactic anticonvulsants may be considered in the immediate posthemorrhagic period, such as levetiracetam 1000 mg by mouth every 12 hours; however, the routine long-term use of anticonvulsants is not recommended. They may be considered only if patients have known risk factors for delayed seizure disorder, such as prior seizure, intracerebral hematoma, intractable hypertension, infarction, or a middle cerebral artery aneurysm.7

Hypernatremia and hyponatremia are both acutely observed after aSAH, and hyponatremia is chronologically linked with the onset of clinical vasospasm. It can develop via multiple different mechanisms after aSAH, with one being cerebral salt wasting syndrome, which results from an oversecretion of natriuretic peptides.7 This leads to excessive excretion of sodium in the urine, or natriuresis, and ultimately induces hyponatremia as well as volume depletion. Guidelines suggest that the use of fludrocortisone acetate and hypertonic saline solution is reasonable for preventing and correcting hyponatremia.7

Pain management for the head, neck, and other areas is typically treated initially with acetaminophen. However, oftentimes, pain relief is not achieved by the use of acetaminophen alone, warranting the use of opiates such as morphine or codeine.9 Patients with acute aSAH are also given stool softeners and kept at bedrest to ease hemodynamic fluctuations and lower risks of rebleeds.10

Lifestyle Management and Patient Education

Effective lifestyle management plays a crucial role in promoting recovery and reducing the risks of experiencing another aneurysm. These include keeping a healthy body and a healthy mind. Some non-pharmacological therapies for stress reduction include engaging in yoga, meditation, ear plugs or noise-canceling headphones, and aromatherapy such as lavender scents for soothing.11 There is evidence for the use of aromatherapy demonstrating effectiveness in lowering heart rate and blood pressure after massage sessions associated with essential oils of lavender and geranium.11

Adopting the MIND Diet, otherwise known as the Mediterranean-DASH Intervention for Neurodegenerative Delay Diet, targets brain health due to the preservation of cognitive functions via protection against cardiovascular diseases. The diet includes plant-based foods while limiting the intake of animal and high saturated fat foods.11 The MIND Diet guidelines suggest servings of whole grains, green leafy vegetables, nuts, beans, berries, poultry, fish, and olive oil instead of other oils or fats.12 Unhealthy foods include red meat, cheese, butter/margarine, pastries, and sweets.12 

Patient education entails counseling on the symptoms of a stroke. The acronym BE-FAST will allow patients to have awareness of the warning signs and get help quickly. BE-FAST stands for balance, eyes, face, arm, speech, and time. These indicate loss of balance, blurred vision, facial droop, arm or leg weakness, speech difficulty, and time to call an ambulance, respectively. 13


In conclusion, cerebral aneurysms, aSAH, and their complications are a significant public health concern that demands continued research, awareness, improved care pathways, and patient advocacy. The pharmacist’s role includes identification of its clinical presentation and recognition of pharmacological treatment and lifestyle management. With early detection, proper management, and an emphasis on a commitment to a healthy lifestyle, we can work towards reducing the impact of this life-threatening medical emergency and improving the quality of life for those affected. 


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