21/12/22, 12:49 Charcot Bouchard Aneurysm - StatPearls - NCBI Bookshelf

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Charcot Bouchard Aneurysm

Authors

Kashvi Gupta1; Joe M Das2.

Affiliations
1 University of Michigan
2 Bahrain Specialist Hospital, Juffair, Bahrain

Last Update: July 25, 2022.

Continuing Education Activity

The rupture of Charcot Bouchard aneurysms causes intracerebral bleeds in the deep structures of the brain, especially
in patients predisposed to this condition due to multiple risk factors. Rapid diagnoses and management of patients
with this condition are crucial. This activity reviews the evaluation and management of Charcot-Bouchard aneurysms
and highlights the healthcare team's role in improving care for patients with this condition.

Objectives:

Identify the etiology of Charcot-Bouchard aneurysms and intracerebral hemorrhage.

Review the evaluation of Charcot-Bouchard aneurysms and intracerebral hemorrhage.

Summarize the treatment and management options available for Charcot-Bouchard aneurysms and intracerebral
hemorrhage.

Describe interprofessional team strategies for improving care coordination and outcomes in patients presenting
with Charcot-Bouchard aneurysms and intracerebral hemorrhage.

Access free multiple choice questions on this topic.

Introduction
Charcot-Bouchard aneurysms are minute aneurysms (microaneurysms) in the brain that occur in small penetrating
blood vessels with a diameter that is less than 300 micrometers. The most common vessels involved are the
lenticulostriate branches (LSA) of the middle cerebral artery (MCA). LSAs originate from the MCA just before its
bifurcation, and they can vary between 2 to 12 in number (average 8.1). Most branches arise medially (99.2%), close
to the internal carotid artery. They supply the basal ganglia, and more specifically, the putamen and caudate, followed
by the thalamus, pons, and cerebellum.[1] 

Charcot-Bouchard aneurysms are named after the French physician Jean-Martin Charcot and his student Charles
Joseph Bouchard. In the 19th century, Bouchard discovered these aneurysms during his research under Charcot. Cole
and Yates strengthened Charcot and Bouchard's work by demonstrating that aneurysms truly exist using
microangiographic techniques in the 1960s. However, it has been a topic of lively debate if it is, in fact, the rupture of
these aneurysms that are responsible for the intracerebral bleeds.[2]

Individuals with chronic systemic hypertension are at high risk of developing atrophy of the outer muscular layer.
With the loss of integrity of the vessel wall, microaneurysms develop in LSA, which are at high risk of rupture.
Bleeding of aneurysms into the deep structures of the brain parenchyma is also referred to as intraparenchymal
hemorrhage or, more broadly, as intracerebral hemorrhage. Clinically the deficits that present can point towards the
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location of the bleed. The first line diagnostic modality for these patients is a non-contrast computed tomography (CT)
of the head to visualize the bleed. Depending on the severity and location of the hemorrhage, the treatment options
vary from observation to neurosurgical intervention.[3][4]

Etiology
Chronic systemic hypertension is the most critical risk factor for developing Charcot Bouchard aneurysms that
subsequently rupture and cause hemorrhage. The risk factors broadly classify as follows:

Modifiable Factors 

Hypertension

High-fat diet

High waist to hip ratio

Smoking

Excessive alcohol consumption

Low low-density lipoprotein and triglyceride levels 

Illicit drug use such as cocaine, heroin

Non-Modifiable Factors

Old age

Male sex

Race and ethnicity such as Asians and African Americans who are at higher risk 

Systemic diseases such as chronic kidney disease, cerebral amyloid angiopathy, vascular malformations, and
coagulopathies, whether hereditary, acquired, or due to drugs such as warfarin and antiplatelet medications, also
increase the risk of the development of microaneurysms and intracerebral hemorrhages.[5][6][3]

Epidemiology
Intracerebral hemorrhage contributes to 10 to 20% of all strokes worldwide and about 8 to 15% of all strokes in the
United States. The lifetime risk of stroke in individuals 25 years and older in 2016 was estimated to be 24.7% among
men and 25.1% in women. The overall risk is thus, an estimated 24.9% compared to 22.8% in 1990. The highest risk
is in East Asia and Europe, and the lowest risk is in countries with a low sociodemographic index, such as Sub-
saharan Africa. Similarly, stroke incidence and mortality are highest in Asia, especially in China and East European
countries. Although the rates are declining, the absolute number of incidence cases in 2016 has doubled since 1990,
with the majority of individuals being under the age of 70. The estimated case fatality of intracerebral at one month is
40% and at one year is 54%. Long-term functional independence occurs in only 13 to 49% of the patients.[7][3]

Pathophysiology
LSAs branch off at right angles from the MCA, rendering the blood flow through the LSA disturbed and non-laminar.
The friction between the blood flow and lateral walls of the blood vessels gives rise to a shear force. Furthermore, the
changes in blood pressure, velocity, and diameter that occur at the branching of arterioles to capillaries increase the
shear force in LSAs. Over time the increase in blood pressure and wall stress upregulates atherogenic factors and
smooth muscle cell proliferation, causing abnormality in the cell junctions and formation of microaneurysms. Rupture

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of the microaneurysms leads to bleeding and hematoma formation in the deep structures of the brain - commonly in
the basal ganglia. 

Following this sequence of events is the disruption of the surrounding parenchymal structure, mass effect on
surrounding structures, disruption in neurotransmitter release, and membrane depolarisations. Through different
mechanisms, several inflammatory pathways become activated. Some of these mechanisms include: 

Release of inflammatory substances from the blood into the perihematomal region  

Mechanical destruction of surrounding neural and glial tissue

Breakdown of hemoglobin that causes neuronal insult

Activation of the clotting cascade and increase in thrombin levels that further increases pro-inflammatory
processes

Most of the hematoma enlargement occurs within the first 3 hours of onset, but it can continue to expand post 12
hours of onset. The perihematomal edema peaks at five days from onset. With increased intracranial pressure, cerebral
perfusion decreases, and patients are at risk of global cerebral hypoxia.[8][4]

Histopathology
Like in any other blood vessel, the wall is comprised, from the inside out, of the tunica intima, media, and adventitia.
The intima layer is sensitive to endothelial nitric oxide synthase, which produces potent vasodilation in response to
acetylcholine, substance P, and bradykinin. The nerve fibers, the majority of which are sympathetic, are distributed in
the tunica media and adventitia layers.[1] 

Chronic hypertension causes hypertrophy of the smooth muscle layer in response to the consistently higher pressures
within the vessel lumen. Hypoxia to the outer smooth muscle layers leads to their degeneration and fibrinoid necrosis.
Following this is sclerosis of the media layer and over time of the entire vessel wall.

A similar sequence of events occurs in cerebral amyloid angiopathy, where there is a deposit of beta-amyloid in the
vessel wall that leads to hypoxia and fibrinoid necrosis.

Finally, the collagen fiber network is then replaced with hyalin. These hyalinized areas are points of low resistance
and are thus susceptible to aneurysmal dilatation and rupture with sudden increases in blood pressure. The size of the
hematoma correlates with the size of the ruptured aneurysm. The LSAs are especially vulnerable since the deep
structures in the brain surrounding these arterioles and capillaries do not allow them to withstand high-pressure
variations.[9]

History and Physical

History

The history should begin with asking the patient about the time of symptom onset and progression of symptoms.
Intracerebral hemorrhage could present during physical activity, emotional stress, or even at rest in individuals with
risk factors. General symptoms that the patient (or accompanying bystanders) complain of at presentation include[10]

Headache due to meningeal irritation

Vomiting (usually projectile in nature) and nausea due to increased intracranial pressure appears in 50% of
patients. 

A decreased level of consciousness ranging from confusion to coma depending on the size of the hematoma;
usually, only very large bleeds cause coma due to a mass effect causing compression of the brain stem. 
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Seizures within the first 24 hours that occur in about 10% of patients

Also, screening for risk factors such as systemic hypertension and medications such as anticoagulant
drugs/antiplatelet drugs is crucial. Important comorbid states to look for in these patients include liver disease and
malignancies, as they are associated with coagulopathies. In patients with cerebral amyloid angiopathy, cognitive
dysfunction might be additionally present.[4]

Physical

Accurate measurement of vital signs, a baseline GCS score, and a complete physical exam with a structured
neurological exam is required. With the worsening of cerebral edema and increased hematoma size, neurological
symptoms progress within minutes to hours. The specific neurological deficits seen reflect the location of
hemorrhage, such as:

Putamen involvement presents with hemiparesis with depression of consciousness.

Thalamic hemorrhages produce hemianesthesia more prominently than hemiparesis, along with an upward
gaze.

Pontine hemorrhages present with pinpoint pupils, quadriparesis, dysconjugate ocular mobility disorder, and
coma.

Lobar hemorrhages present with hemiparesis, hemisensory deficits, and speech impairment.

Cerebellar hemorrhages present with vertigo, ataxia, and paralysis of conjugate gaze on one side.

Evaluation
Laboratory Evaluation

A complete blood count to check for infection and anemia. Coagulopathy (PT, INR, aPTT) and lipid profile are
essential in all patients, along with daily electrolytes, creatinine, and liver function tests. As patients may
develop hyperglycemia as a complication of intracerebral hemorrhage, it is essential to establish the baseline
blood glucose and HbA1c levels and monitor them closely. Blood culture and sensitivity are necessary for
patients with suspected systematic infections.

Cardiac-specific troponins are associated with worse outcomes in these patients. 

A urine toxicology screen must be ordered as drugs such as cocaine are risk factors for intracerebral
hemorrhage.

Lumbar puncture, only to rule out infection in patients with clinical suspicion or patients with subarachnoid
hemorrhage and look for hemolysis where the diagnosis is unclear.

Radiographic Evaluation

Non-contrast CT head is the first line for diagnosing intracerebral hemorrhage. The findings on the non-contrast
CT can be staged based on the timing from the onset of initial symptoms. In the hyperacute state, the hematoma
shows as smooth and hyperdense. Over 48 hours, the hematoma begins to show some fluid collection alongside
the hyperintensity. Blood-fluid volumes have high specificity for coagulopathies. Next, over 72 hours, a mass
effect with midline shift and a hypodensity due to edema surrounding the hematoma becomes visible. Finally, 3
to 20 days later, the hypodense region shrinks and has uneven borders with a ring-like appearance. A repeat CT
scan is required with signs of neurological deterioration to diagnose complications. The spot sign is visible in a
contrast-enhanced CT in patients with hematoma expansion.

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Magnetic Resonance Imaging (MRI) MRI of the brain with gradient-echo can be used to more accurately detect
microhemorrhages that appear as hyperintense areas surround by hypointense boundaries. However, to
distinguish an acute bleed from a chronic bleed, a non-contrast CT head is performed. 

Cerebral angiography is useful to diagnose secondary causes of intracerebral hemorrhages, such as

microaneurysms and arteriovenous malformations.[11]

Electroencephalography

Electroencephalography is indicated for patients with unexplained neurological deterioration or suspected

seizures. 

Electrocardiogram

To assess cardiac events and arrhythmias. 

Treatment / Management
Management of intracerebral hemorrhage begins with securing the airway, breathing, blood pressure control, and
maintaining circulation using pressors. Patients with a Glasgow Coma Scale less than 8 often require intubation and
ventilation. An anticoagulation reversal would follow this if the patient were on any pertinent medications. The risk of
rapid deterioration in patients with intracerebral hemorrhage is maximum in the first 24 hours and requires intensive
care unit monitoring. 

The blood pressure should be lowered cautiously in these patients. For patients with initial systolic blood pressure
between 150 and 220 mm Hg, without contraindications to acute lowering of blood pressure, the target systolic blood
pressure should be between 140 mm Hg and lower. For patients with systolic blood pressure over 220 mm Hg, the
blood pressure goal should be between 140 to 160 mm Hg. However, lowering blood pressure must be balanced with
maintaining adequate cerebral perfusion pressure, and blood pressure should be monitored closely (every 5 minutes)
in these patients. Appropriate antihypertensives include nicardipine, clevidipine, labetalol, esmolol, enalaprilat,
fenoldopam, and phentolamine. 

After stabilization of the patient, a neurosurgical consult is necessary to evaluate for intracranial hypertension. Short-
term intravenous mannitol boluses, hypertonic saline, or hyperventilation could be considered in acutely worsening
cerebral edema to maintain cerebral perfusion greater than 70 mm Hg. Surgical procedures such as decompressive
craniectomy for intracerebral hemorrhages merit consideration for two purposes, firstly to decrease the mass effect of
the hematoma, thereby improving cerebral perfusion, and second, to halt the inflammatory processes caused by the
breakdown of blood. In patients with lobar hematomas of 10 to 100 mL located within 1 cm from the brain surface
and without intraventricular hematomas or coma, early surgical intervention has a favorable outcome at six months. 

Lastly, the management of concomitant intraventricular hemorrhage and obstructive hydrocephalus with
ventriculostomy and external ventricular drainage is warranted in patients with enlarging ventricles on CT scan and
neurological deterioration. If the patient is experiencing seizures or has cortically located lobar hemorrhages, seizure
prophylaxis with anti-seizure medications such as phenytoin can be administered. 

Other important therapeutic interventions include:

Elevating the head of the bed to 30 degrees

Avoiding hyperthermia

Treating hypoglycemia with 50% dextrose and hyperglycemia (serum glucose over 200 mg/dl) with insulin

Continuous cardiac monitoring 

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Bladder catheterization if urinary incontinence or retention has occurred, as well as to monitor urine output

Maintaining the patient nil per oral and maintaining adequate tube feeds with a nasogastric tube. 

Prevention of deep vein thrombosis  

Prevention of bedsores 

Mild sedation as needed for comfort

In summary, the key to management is stabilizing the patient, cautious lowering of blood pressure, and
maintaining adequate cerebral perfusion while actively managing complications as they arise.[4][12][13]

Differential Diagnosis
It is critical to differentiate intracerebral hemorrhage from lacunar hemorrhages. Intracerebral hemorrhages occur due
to microaneurysm formation in the LSAs versus lacunar hemorrhages that occur secondary to ischemia and
reperfusion injuries. Although they both have systemic hypertension as an important predisposing risk factor, patients
with lacunar hemorrhage are more likely to have type 2 diabetes mellitus and a higher body mass index.[14]

Pertinent Studies and Ongoing Trials

The following are relevant studies for the management of intracerebral hemorrhage and its complications:

The FAST trial was critical in establishing the efficacy of recombinant factor VIIa in controlling the expansion
of the hematoma in intracerebral hemorrhage and the associated survival and functional benefits.[15]

However, the SPOTLIGHT and STOP-IT trials did not show radiographic or clinical improvement in patients
with spot sign positive, representing hematoma expansion in patients with intracerebral hemorrhage treated at a
median 3-hour from symptom onset.[16]

The STITCH, I, and STITCH II trial evaluated the benefit of early surgical intervention versus medical
management in patients with intracerebral hemorrhage. The study concluded that early surgical intervention has
a clinically relevant survival advantage in patients with intracerebral hemorrhage with no ventricular
hemorrhage. It does not increase the rate of death or disability at six months in these patients.[17]

The ATTACH II trial evaluated the efficacy of rapidly lowering the systolic blood pressure in patients with
acute hypertensive intracerebral hemorrhage. The study found that intensive lowering of the systolic blood
pressure to 110 to 139 mm Hg did not lower mortality compared to standard lowering of systolic blood pressure
to 140 to 179 mm Hg.[18]

The INTERACT II trial aimed to analyze if the rapid lowering of blood pressure would improve outcomes in
patients with acute intracerebral hemorrhage. The target systolic blood pressure in the study arm with intensive
lowering was below 140 mm Hg, and this compared to the standard reduction of systolic blood pressure to over
180 mm Hg. The trial concluded that intensive lowering blood pressure does not significantly reduce mortality
or severe disability in patients with intracerebral hemorrhage.[19]

Prognosis
Determining prognosis in patients with intracerebral hemorrhage is critical. Underestimating the prognosis would lead
to unnecessary procedures and prolonged hospitalization, while overestimation would lead to a limitation of care.
Three important independent prognostic indicators of early neurologic deterioration and mortality are hematoma
expansion with perihematomal edema, intraventricular hemorrhage, and hyperglycemia.

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Complications
Complications of intracerebral hemorrhage secondary to rupture of Charcot-Bouchard aneurysms are as follows,

Hematoma E xpansion

Hematoma expansion also referred to as a rebleed, is an independent predictor of early neurological deterioration and
mortality. Maximal hematoma expansion occurs in the first 3 hours and can occur up to 24 hours from symptom
onset. The "spot sign" or contrast extravasation into the hematoma is seen on the CT angiogram and is an indication of
the expansion of the hematoma. The spot sign has been described as a heterogeneous marker due to its different
shapes and sizes, depending on the timing of imaging relative to the onset of symptoms. Management of hematoma
expansion includes administering hemostatic therapy with recombinant factor VIIa, cautious lowering of blood
pressure, and craniotomy with surgical evacuation.

Perihematomal Edema

Perihematomal edema develops secondary to vasogenic and cytotoxic effects due to the hematoma formation and
exerts a mass effect on surrounding structures. It is maximal at two weeks from the onset of symptoms. The
management goal is to minimize any increase in the intracranial pressure by elevating the head to 20 to 30 degrees,
analgesics for pain, infection control, sedatives, osmotic diuretics such as mannitol, and hyperventilation. 

Seizures

Seizures can be either a presenting symptom or complication of intracerebral hemorrhage. Treatment includes

antiepileptic drugs based on the patient's medication regimen and contraindications. 

Intraventricular Hemorrhage (IVH) With Hydrocephalus

IVH is also an independent predictor of early neurological deterioration and mortality due to IVH-induced
inflammation and damage to periventricular structures, the brain stem, and leading to hydrocephalus with subsequent
herniation. Relieving the IVH with external ventricular drainage is a life-saving procedure. For stable clots,
intraventricular fibrinolytic (low-dose alteplase) can be administered. Lumbar drainage is less invasive, with a lower
complication rate for communicating hydrocephalus. 

Other complications include:

Venous thromboembolism presenting as deep vein thrombosis or pulmonary embolisms 

Hyperglycemia due to stress

Hyperpyrexia due to brain damage or infections

Hypertension due to activation of the neuroendocrine systems[15][16][20]

Deterrence and Patient Education

It is critical to set age-appropriate blood pressure goals for patients and motivate them to comply with their
medications. Counseling regarding modifiable risk factors such as smoking, excessive alcohol consumption, and high-
fat diets must be pursued as appropriate. 

Since the initial symptoms of a stroke are non-specific, patients (and caregivers) might delay getting medical
attention, limiting their treatment options. Ischemia greater than 4 to 6 hours can produce permanent damage to the
neurovascular tissue. Yet, a study found only half the patients present within the first 24 hours of the onset of stroke.
[21] It is essential to educate them (and reiterate for patients with uncontrolled hypertension and multiple risk factors)
on the presenting symptoms of headache with nausea and vomiting to encourage them to come to the hospital sooner.
[22]
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Enhancing Healthcare Team Outcomes

It is imperative to have a multi-specialty interprofessional team approach to care for patients with Charcot-Bouchard
aneurysms and intracerebral hemorrhage.

Optimizing management for hypertension and other risk factors by the primary care team is the first step, along with
adequate patient education about the signs and symptoms of a stroke to encourage early presentation to the emergency
department. 

Next, the clinician must establish a baseline severity score in the emergency department for patients with spontaneous
intracerebral hemorrhage followed by rapid neuroimaging with CT or MRI to distinguish between an ischemic and
hemorrhagic stroke. 

Initial management of patients with intracerebral hemorrhage must be in intensive care set up or stroke unit with
neuroscience expertise amongst physicians and nursing staff. 

Hemostasis Management

Factor deficiency or thrombocytopenic patients should receive factors and platelets respectively. 

Pneumatic compression for lower extremities to prevent deep vein thrombosis (DVT) from day 1 of
hospitalization

Patients on vitamin K antagonists should have them held and have the INR normalized with intravenous
vitamin K and replacement of vitamin K dependent factors. 

Patients presenting with systolic blood pressure between 150 to 200 mm Hg and without contraindications to acutely
lower blood pressure should have systolic blood pressure lowered to 140 mm Hg. 

Monitoring of glucose to avoid hyper- or hypoglycemia, treatment of seizures, and assessment of dysphagia to prevent
aspiration pneumonia should be performed in all patients.

All medications, including IV fluids, should have pharmacist feedback in the context of the patient's entire medication
record, ruling out interactions, verifying dosing and administration, and consulting with the team in the event there are
any issues in the regimen. Nursing needs to be aware of proper administration and the adverse events associated with
the drugs given to alert the clinicians of any concerns. These interprofessional interactions can help drive improved
patient outcomes. [Level 5]

Lastly, patients requiring surgical interventions due to neurological deterioration should receive a referral to
neurosurgery as early as possible to improve results. 

Patients with intracerebral hemorrhage must have access to interprofessional rehabilitation as an inpatient and have
continued rehabilitation services available in the community and at home to promote recovery.[12] [Level 1]

Review Questions

Access free multiple choice questions on this topic.

Comment on this article.

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