About all

What causes swelling in the brain. Cerebral Edema: Causes, Types, and Management of Brain Swelling

by alexxlab

What are the main types of cerebral edema. How does the Monroe-Kellie doctrine explain the consequences of brain swelling. What are the common causes and symptoms of cerebral edema. How is cerebral edema diagnosed and treated.

Содержание

Understanding Cerebral Edema: A Comprehensive Overview

Cerebral edema, in its simplest terms, refers to swelling of the brain. This condition, while common, can have serious and potentially life-threatening consequences if left untreated. The complexity of cerebral edema lies in its various types and numerous underlying causes, making it a critical area of study in neurology and emergency medicine.

The Four Types of Cerebral Edema

Cerebral edema is generally categorized into four main types:

  • Vasogenic edema
  • Cellular (cytotoxic) edema
  • Osmotic edema
  • Interstitial edema

Each type has distinct characteristics and underlying mechanisms, which influence treatment approaches and patient outcomes.

The Monroe-Kellie Doctrine: Explaining the Impact of Brain Swelling

To understand the consequences of cerebral edema, it’s crucial to grasp the Monroe-Kellie doctrine. This principle states that the cranial cavity has a fixed volume, containing specific proportions of brain matter (approximately 1400 ml), blood (approximately 150 ml), and cerebrospinal fluid (approximately 150 ml).

How does the Monroe-Kellie doctrine relate to cerebral edema? When brain swelling occurs, the volume of brain tissue increases. Due to the fixed nature of the cranial cavity, this increase must be compensated by a decrease in either blood volume or cerebrospinal fluid. This compensation can lead to decreased brain perfusion and potentially further damage to both edematous and non-edematous brain regions.

Exploring the Causes of Cerebral Edema

Cerebral edema can result from a wide range of underlying conditions, both neurological and non-neurological. Some common causes include:

  • Traumatic brain injury
  • Stroke or vascular ischemia
  • Brain tumors
  • Infections (e.g., meningitis, encephalitis)
  • Metabolic disorders
  • Acute hypertension
  • Hypoxia

Less common causes may include hepatitis, Reye syndrome, carbon monoxide poisoning, lead poisoning, and high-altitude cerebral edema. In rare cases, a condition called pseudotumor cerebri can also lead to brain swelling.

Vasogenic Edema: The Most Common Type

Vasogenic edema is the most frequently encountered form of cerebral edema. What causes this type of brain swelling? It results from a disruption in the blood-brain barrier, allowing ions and proteins to flow more freely into the extravascular space. This influx creates an osmotic gradient, drawing fluid into the brain’s interstitium.

In cases of brain tumors, for example, factors like vascular endothelial growth factor (VEGF), glutamate, and leukotrienes increase the permeability of surrounding blood vessels. The lack of tight endothelial cell junctions in these vessels further contributes to the problem, allowing proteinaceous solute and fluid to enter the brain parenchyma, particularly affecting the white matter.

Cellular Edema: A Rapid Response to Brain Injury

Cellular or cytotoxic edema typically occurs within minutes of a brain insult or injury. This type of edema affects glial cells, neurons, and endothelial cells within the brain. In cytotoxic edema, the cells’ homeostatic mechanisms fail, leading to an uncontrolled influx of sodium into the cells. Anions follow in an attempt to restore neutrality, resulting in intracellular swelling as water follows the ions.

Recognizing the Symptoms of Cerebral Edema

The clinical presentation of cerebral edema can vary widely, ranging from asymptomatic cases to severe autonomic dysregulation, coma, and even death. Symptoms typically become apparent when intracranial pressure (ICP) rises above 20 cm H2O in most patients.

Common symptoms of cerebral edema may include:

  • Headache
  • Nausea and vomiting
  • Altered mental status
  • Visual disturbances
  • Seizures
  • Weakness or paralysis
  • Loss of consciousness

It’s important to note that the specific symptoms can vary depending on the underlying cause, location, and severity of the edema.

Diagnosing Cerebral Edema: A Multi-faceted Approach

Diagnosing cerebral edema often involves a combination of clinical assessment, imaging studies, and sometimes invasive monitoring. How do medical professionals confirm the presence of brain swelling?

  • Neurological examination: Assessing mental status, pupil reactivity, and motor function
  • Imaging studies: CT scans and MRI can visualize brain swelling and potential underlying causes
  • Intracranial pressure monitoring: In severe cases, direct measurement of ICP may be necessary
  • Laboratory tests: To identify potential metabolic or infectious causes

Early and accurate diagnosis is crucial for implementing appropriate treatment and preventing further complications.

Treatment Strategies for Cerebral Edema

The management of cerebral edema focuses on addressing the underlying cause and mitigating life-threatening complications. Treatment approaches may include:

  1. Hyperventilation: To reduce cerebral blood flow and intracranial pressure
  2. Osmotherapy: Using agents like mannitol or hypertonic saline to draw fluid out of the brain
  3. Diuretics: To reduce overall fluid volume
  4. Corticosteroids: Particularly effective in reducing vasogenic edema associated with tumors
  5. Surgical decompression: In severe cases, to relieve pressure on the brain

The choice of treatment depends on the specific type of edema, its cause, and the patient’s overall condition. A tailored approach is essential for optimal outcomes.

Emerging Therapies and Research Directions

As our understanding of cerebral edema evolves, new treatment strategies are being explored. These include targeted molecular therapies to address specific mechanisms of edema formation, neuroprotective agents, and advanced monitoring techniques to guide treatment decisions.

The Role of the Interprofessional Team in Managing Cerebral Edema

Effective management of cerebral edema requires a coordinated effort from an interprofessional team. This team typically includes:

  • Neurologists and neurosurgeons
  • Critical care specialists
  • Radiologists
  • Nurses specializing in neurocritical care
  • Pharmacists
  • Rehabilitation specialists

How does this team approach improve patient outcomes? By combining expertise from various disciplines, the team can provide comprehensive care, from accurate diagnosis and prompt treatment to long-term management and rehabilitation.

Continuous Monitoring and Adjustment

Managing cerebral edema is often a dynamic process requiring continuous monitoring and adjustment of treatment strategies. The interprofessional team must work closely to assess the patient’s response to interventions and make timely modifications as needed.

Prevention and Long-term Management of Cerebral Edema

While not all cases of cerebral edema can be prevented, certain measures can reduce the risk or severity of brain swelling in some situations. These may include:

  • Proper management of underlying conditions (e.g., hypertension, diabetes)
  • Wearing protective gear during high-risk activities to prevent traumatic brain injury
  • Prompt treatment of infections that could affect the brain
  • Careful monitoring and management of patients at risk for cerebral edema

Long-term management often involves addressing any residual neurological deficits through rehabilitation and ongoing medical care.

Patient Education and Support

Educating patients and their families about cerebral edema, its causes, and potential long-term effects is crucial for optimal recovery and prevention of future episodes. Support groups and resources can provide valuable assistance for those dealing with the aftermath of severe brain swelling.

In conclusion, cerebral edema represents a significant challenge in neurology and critical care medicine. Its complex pathophysiology, diverse causes, and potentially severe consequences necessitate a thorough understanding and a multidisciplinary approach to management. As research continues to unveil new insights into the mechanisms of brain swelling, we can expect more targeted and effective treatments to emerge, improving outcomes for patients affected by this condition.

Cerebral Edema – StatPearls – NCBI Bookshelf

Continuing Education Activity

The most basic definition of cerebral edema is swelling of the brain. It is a relatively common phenomenon with numerous etiologies. Cerebral edema categorizes into either vasogenic, cellular, osmotic, and interstitial causes. It can arise from a variety of causes, including head trauma, vascular ischemia, intracranial lesions, or obstructive hydrocephalus resulting in interstitial edema. The consequences of cerebral edema can be devastating, even fatal, if untreated. This activity reviews the causes, presentation, and diagnosis of cerebral edema and highlights the role of the interprofessional team in its management.

Objectives:

  • Review the causes of cerebral edema.

  • Describe the presentation of cerebral edema.

  • Summarize the treatment options for cerebral edema.

  • Explain modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by cerebral edema.

Access free multiple choice questions on this topic.

Introduction

The most basic definition of cerebral edema is swelling of the brain. It is a relatively common phenomenon with numerous etiologies.  Cerebral edema categorizes into either vasogenic, cellular, osmotic, and interstitial causes. [1]  It can arise from a variety of causes, including head trauma, vascular ischemia,[2] intracranial lesions, or obstructive hydrocephalus resulting in interstitial edema.  The consequences of cerebral edema can be devastating, even fatal, if untreated.  

The explanation of the mechanism of injury arising from cerebral edema comes via the Monroe-Kellie doctrine.  The Monroe-Kellie doctrine states that space of the cranial cavity is fixed in volume and contains fixed proportions of brain matter (approximately1400 ml), blood (approximately 150 ml) and cerebrospinal fluid (approximately 150 ml).  Because of this fixed space, an increase in the volume of one of these components must, therefore, result in the loss of another component in equal amounts. [3]  In cerebral edema, the relative volume of brain tissue increases as the brain tissues swells with edema.  This increased relative brain volume decreases perfusion (blood) to the brain, and the pressure can cause further damage to both the edematous and non-edematous brain. Clinical presentation of cerebral edema is variable, ranging from asymptomatic to severe autonomic dysregulation, coma, and death.  Symptoms appear as the intracranial pressure (ICP) rises above 20 cm h3O in most patients.  Treatment for cerebral edema targets the underlying cause and any life-threatening complications. Treatments include hyperventilation, osmotherapy, diuretics, corticosteroids, and surgical decompression.

Etiology

Cerebral edema can result from a variety of derangements.  The major types include vasogenic, cellular, osmotic, and interstitial.

Through these mechanisms, cerebral edema stems from tumor, trauma, hypoxia, infection, metabolic derangements, or acute hypertension.  Causes are widespread and divide into neurological and non-neurological categories.   Other non-neurologic causes include hepatitis, Reye syndrome, carbon monoxide poisoning, lead poisoning, and high altitude cerebral edema. A rare cause of cerebral edema is pseudotumor cerebri.

Epidemiology

Cerebral edema affects all age groups, genders, and ethnic groups.  The actual frequency of cerebral edema may be under-reported secondary to its sometimes non-specific symptoms.

Pathophysiology

Vasogenic cerebral edema, the most common form,  results from the disruption of the blood-brain-barrier.  With the disrupted blood-brain-barrier ions and proteins flow more freely into the extravascular space which causes osmotic draw of fluid into the brain interstitium.  For example, vascular endothelial growth factor (VEGF), glutamate, and leukotrienes produced locally increase the permeability of vessels around tumors.[4]  These factors and a lack of tight endothelial cell junctions in the vessels around the tumors cause this increased permeability, which allows for an influx of proteinaceous solute and fluid into the brain parenchyma, particularly in the white matter. [5]  Peritumor edema, for example, leads to 65% of patients developing cognitive impairment resulting from displacement and damage to white matter tracts.[6]

Cellular or cytotoxic edema often results within minutes of the insult/injury and affects glial, neuronal, and endothelial cells within the brain.  In cytotoxic edema, the cells lack hemostatic mechanisms, and primarily sodium enters the cell freely, with the failure of the export mechanism.  Anions then follow, attempting to return neutrality to the cell, resulting in intracellular edema as the cells swell with increased water following the ions into the intracellular compartment.[7]  Traumatic brain injury and stroke cause this form of edema.

Interstitial cerebral edema results from the outflow of cerebrospinal fluid from the intraventricular space to the interstitial areas of the brain. Patients with hydrocephalus or meningitis are examples of those affected by this etiology.  The increased pressure, against the cerebrospinal fluid (CSF) and brain, drives fluid into the brain parenchyma.   The fluid accumulates in the extracellular space of mostly the white matter causing the cerebral edema.

Osmotic edema generally stems from derangements affecting osmolarity, such as hyponatremia, diabetic ketoacidosis (DKA), or similar metabolic pathologies.  The cells of the brain pull water from the plasma in these instances, resulting in widespread edema. 

Histopathology

The histopathology of cerebral edema may show both the underlying pathology (tumor, infection, anoxic changes) as well as diffuse swelling of either the cell bodies in cytotoxic edema or interstitial spaces.

History and Physical

Cerebral edema can be asymptomatic, merely seen on imaging, or it can cause life-threatening complications. The history can help provide insights as to the etiology of the cerebral edema.  Patients may have a history of trauma, a hypoxic event, cancer, metabolic diseases or other factors which can help identify the possible etiology of the cerebral edema. 

The physical exam findings of cerebral edema can vary widely depending on the location and extent of the cerebral edema.   Localized cerebral edema can cause dysfunction of the edematous brain and include weakness, visual disturbances, seizures, sensory changes, diplopia, and other neurologic disturbances.  For diffuse cerebral edema, the patient may have headaches, nausea, vomiting, lethargy, altered mental status, confusion, coma, seizure or other manifestations.  With diffuse or focal cerebral edema the patient can develop increased intracranial pressure (ICP) which typically presents with headaches, nausea, vomiting, lethargy, cranial neuropathy, altered mental status to coma and death.

Evaluation

It is extremely important to identify severe cerebral edema as early as possible to prevent herniation and death. For example malignant middle cerebral artery stroke presenting with severe cerebral edema. Malignant middle cerebral artery stroke is seen more commonly in the younger population. Usually, these patients are admitted to the ICU setting. Following the Neurological exam closely is very important. Usually, there is an altered mental status and development of fixed and dilated pupil. Patients presenting with findings suggestive of cerebral insult should undergo computed tomography (CT) scan of the brain; this can show the edema, which is visible as areas of low density and loss of gray/white matter differentiation, on an unenhanced image.  There can also be the obliteration of the cisterns and sulcal spaces.  A CT scan can also reveal the cause in some cases.  If flattened gyri or narrowed sulci, or compression of the ventricles, is seen, this suggests increased ICP.  Serial CT scans are used to show the progression or improvement of the edema.

Magnetic resonance imaging (MRI) can show increased T2 and FLAIR signal changes (hyperintensity) within the brain.

If increased ICP is a concern from the cerebral edema, then an ICP monitor or ventriculostomy may be needed to monitor ICP and can provide better outcomes by helping to tailor therapy.[8]

Treatment / Management

Treatment of cerebral edema is two-fold: prevent further injury from the cerebral edema and remediate the original insult causing the cerebral edema if able.

Remediation of the original and ongoing insult can include correcting metabolic derangements, controlling hypertension, removing intracranial lesion(s) or shunting hydrocephalus depending on the etiology of the cerebral edema.

The edema should be controlled to prevent further injury, and complications such as increased ICP should be mitigated.  Glucocorticoids have shown potential benefit in cerebral edema secondary to vasogenic edema but have limited utility in other forms of edema and should be avoided altogether in the face of trauma.[9] Avoidance of hypotonic fluids is a strong recommendation in instances of cerebral edema as they can worsen cerebral edema and cause elevations in ICP.  If the cerebral edema is causing elevated ICP, various methods are available to help control ICP including positioning, hyperosmolar therapy, antipyretics, sedatives,[10][11] paralytics, modulation of PcO2,[12][13] and surgical intervention.[14] 

 In the management of malignant middle cerebral artery stroke presenting with severe cerebral edema, osmotic agents can be used to create an osmotic gradient across blood thereby drawing fluid intravascularly and decreasing cerebral edema. Mannitol is the primary agent used at doses of 0.25 to 1 g/kg body weight and is thought to exert its greatest benefit by decreasing blood viscosity and to a lesser extent by decreasing blood volume. Side effects of mannitol use are eventual osmotic diuresis and dehydration as well as renal injury if serum osmolality exceeds 320 mOsm. Three percent hypertonic saline is also commonly used to decrease cerebral edema and can be administered as a 5 ml/kg bolus or a continuous infusion, monitoring serum sodium levels closely. It is considered relatively safe while serum sodium is < than 160mEq/dl or serum osmolality is less than 340 mOsm. A decompressive craniectomy is a neurosurgical procedure wherein a part of the skull is removed, and dura lifted, allowing the brain to sell without causing compression. It is usually considered as a last resort when all other ICP lowering measures have failed. When considered it is a good idea to do this procedure sooner rather than later. [15]

 Hypertonic saline has also been used to treat cerebral edema and is preferred over the diuretics.

Other supportive treatments include

1.Extraventricular drainage of the CSF

2.Avoiding straining and coughing

3. Inducing paralysis in patients who are intubated

4.Keeping the neck straight and elevated to allow for the brain to drain with ease

5.Inducing coma with barbiturates

6.Minimizing the use of PEEP

7. Inducing hypothermia to suppress cerebral metabolism. This is often done for several days but extended hypothermia makes the patient susceptible to systemic infections and hypotension.

Differential Diagnosis

The differential diagnosis for cerebral edema includes shaken baby syndrome, encephalitis, toxin poisoning, stroke, metabolic derangements, seizures, and tumors.

Prognosis

The prognosis for cerebral edema is highly variable and depends on the amount of brain involved, the severity, and the etiology of the edema.  If the patient is comatose upon discovery, the prognosis may be poor.  If the edema is widespread and severe enough to cause significantly elevated intracranial pressure, and treatment is not initiated, the patient may die or develop persistent and irreversible brain injury.   An example is seen in prolonged cardiac arrest causing diffuse anoxic brain injury.  The basis for prognosis in milder forms is usually the diagnosis and underlying cause (i.e., tumor, stroke, traumatic brain injury, infection, etc.) and early recognition and treatment.  Cerebral edema as a consequence of reversible diagnoses, such as diabetic ketoacidosis or uncontrolled hypertension or mild head trauma can be reasonably good.

Complications

Complications of cerebral edema range from mild cognitive impairment to death.  Untreated, severe cerebral edema is fatal due to brain and brainstem compression and herniation.  The presence of significant cerebral edema can cause diffuse brain injury, precipitate seizures in some cases, or create large areas of ischemic brain tissue.  Cerebral edema, particularly when widespread, can increase ICP, and this is the most life-threatening sequelae of this condition due to the potential for herniation and brainstem injury.  Permanent brain injury can occur in more severe cases.   Many of the complications are related to the underlying cause(s) of the edema.

Deterrence and Patient Education

Not all cases can are preventable.  Due to the causes, identifying a single preventive measure is challenging. However, in general, patients should focus on keeping their blood pressure under control through lifestyle modification and adherence to recommended medical treatment, maintain optimal control of diabetes to prevent diabetic ketoacidosis. They should also get regular preventive care from their primary care providers, and avoid high-risk behaviors concerning potential injuries, such as not wearing seat belts, or engaging in sports in which there is a high concussive risk, especially if the patient has a history of concussions or head trauma.

Enhancing Healthcare Team Outcomes

The clinical presentation of cerebral edema can easily be mistaken for other issues, such as intoxication, stroke, infection, or post-ictal state.  It requires a high index of suspicion, particularly in milder cases.   In more severe cases, close neurological monitoring and consultation with neurology and neurosurgery are important.  Communication regarding indications/risks/contraindications for ICP monitoring or craniotomy needs to be ongoing, particularly with respect to goals of care.  Nursing care must pay close attention to changes in neurologic status, any change in vitals such as an increasingly erratic heart rate, development of bradycardia, accurate and equal intake and output when having diuresis, and maintenance of proper blood pressure with immediate reporting to the team leader of any significant changes.  Patients at bed rest need DVT and pressure sore prophylaxis. As the patient recovers, physical therapy, occupational therapy, and speech-language pathology can help the patient maximize function after the brain injury and to evaluate patient safety both before and after discharge. 

Patient education regarding avoidance of future complications should come from all team members, with social work involvement to ensure home safety after discharge, and the patient’s primary care provider should be updated, to the appropriate follow-up.   In cases of vasogenic edema due to brain tumor, both oncology, radiation oncology and neurosurgery should be consulted to co-manage the evaluation and management of the neoplasm, determine the best treatment for the tumor (resection/radiation/palliation) based on the tumor type/stage, and follow up with the patient after discharge.  And, finally, the patient and the patient’s family and care providers should be educated about what to watch for that may suggest the need for re-evaluation because of recurrence, or complications from any of the interventions.[15]

Review Questions

  • Access free multiple choice questions on this topic.

  • Comment on this article.

References

1.

Lawrence SE, Cummings EA, Gaboury I, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005 May;146(5):688-92. [PubMed: 15870676]

2.

Yang Y, Rosenberg GA. Blood-brain barrier breakdown in acute and chronic cerebrovascular disease. Stroke. 2011 Nov;42(11):3323-8. [PMC free article: PMC3584169] [PubMed: 21940972]

3.

Jha SK. Cerebral Edema and its Management. Med J Armed Forces India. 2003 Oct;59(4):326-31. [PMC free article: PMC4923559] [PubMed: 27407555]

4.

Senger DR, Van de Water L, Brown LF, Nagy JA, Yeo KT, Yeo TK, Berse B, Jackman RW, Dvorak AM, Dvorak HF. Vascular permeability factor (VPF, VEGF) in tumor biology. Cancer Metastasis Rev. 1993 Sep;12(3-4):303-24. [PubMed: 8281615]

5.

Sorby-Adams AJ, Marcoionni AM, Dempsey ER, Woenig JA, Turner RJ. The Role of Neurogenic Inflammation in Blood-Brain Barrier Disruption and Development of Cerebral Oedema Following Acute Central Nervous System (CNS) Injury. Int J Mol Sci. 2017 Aug 17;18(8) [PMC free article: PMC5578176] [PubMed: 28817088]

6.

Eichler AF, Chung E, Kodack DP, Loeffler JS, Fukumura D, Jain RK. The biology of brain metastases-translation to new therapies. Nat Rev Clin Oncol. 2011 Jun;8(6):344-56. [PMC free article: PMC3259742] [PubMed: 21487419]

7.

Liang D, Bhatta S, Gerzanich V, Simard JM. Cytotoxic edema: mechanisms of pathological cell swelling. Neurosurg Focus. 2007 May 15;22(5):E2. [PMC free article: PMC2740913] [PubMed: 17613233]

8.

Lane PL, Skoretz TG, Doig G, Girotti MJ. Intracranial pressure monitoring and outcomes after traumatic brain injury. Can J Surg. 2000 Dec;43(6):442-8. [PMC free article: PMC3695200] [PubMed: 11129833]

9.

Strandgaard S, Paulson OB. Cerebral blood flow and its pathophysiology in hypertension. Am J Hypertens. 1989 Jun;2(6 Pt 1):486-92. [PubMed: 2757806]

10.

Lassen NA, Christensen MS. Physiology of cerebral blood flow. Br J Anaesth. 1976 Aug;48(8):719-34. [PubMed: 7284]

11.

Ward JD, Becker DP, Miller JD, Choi SC, Marmarou A, Wood C, Newlon PG, Keenan R. Failure of prophylactic barbiturate coma in the treatment of severe head injury. J Neurosurg. 1985 Mar;62(3):383-8. [PubMed: 3882899]

12.

Hoff JT. Cerebral protection. J Neurosurg. 1986 Nov;65(5):579-91. [PubMed: 3534160]

13.

Muizelaar JP, Marmarou A, Ward JD, Kontos HA, Choi SC, Becker DP, Gruemer H, Young HF. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991 Nov;75(5):731-9. [PubMed: 1919695]

14.

Burkert W, Paver HD. [Decompressive trepanation in therapy refractory brain edema]. Zentralbl Neurochir. 1988;49(4):318-23. [PubMed: 3075392]

15.

Pinto VL, Tadi P, Adeyinka A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 1, 2022. Increased Intracranial Pressure. [PubMed: 29489250]

Disclosure: Sara Nehring declares no relevant financial relationships with ineligible companies.

Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.

Disclosure: Steven Tenny declares no relevant financial relationships with ineligible companies.

Cerebral Edema (Brain Swelling): Symptoms, Causes, & Treatment

Written by Beth Roybal

  • What Is Brain Swelling?
  • What Causes Brain Swelling?
  • What Are the Symptoms of Brain Swelling?
  • How Is Brain Swelling Diagnosed?
  • What Is the Treatment for Brain Swelling?
  • What Are the Long-Term Effects of Brain Swelling?
  • How Can I Protect my Head?
  • More

If you bump your knee, it’s likely to swell. But what if you injure your brain?

Swelling — also called edema — is the body’s response to many types of injury. It can result from overuse or infection. Usually, swelling happens quickly and is simple to treat with some combination of rest, ice, elevation, medication, or removal of excess fluid.

Your brain can also swell as a result of injury, illness, or other reasons. Brain swelling, though, can quickly cause serious problems — including death. It’s also usually more difficult to treat. As your body’s master control system, the brain is critical to overall function. Yet, the thick, bony skull that snugly protects this vital organ provides little room for the brain to swell.

 

Brain swelling goes by many names:

  • Brain edema
  • Elevated intracranial pressure
  • Cerebral edema

Swelling can occur in specific locations or throughout the brain. It depends on the cause. Wherever it occurs, brain swelling increases pressure inside the skull. That’s known as intracranial pressure, or ICP. This pressure can prevent blood from flowing to your brain, which deprives it of the oxygen it needs to function. Swelling can also block other fluids from leaving your brain, making the swelling even worse. Damage or death of brain cells may result.

Injury, other health problems, infections, tumors, and even high altitudes — any of these problems can cause brain swelling to occur. The following list explains different ways the brain can swell:

  • Traumatic brain injury (TBI): A TBI is also called a head injury, brain injury, or acquired brain injury. In TBI, a sudden event damages the brain. Both the physical contact itself and the quick acceleration and deceleration of the head can cause the injury. The most common causes of TBI include falls, vehicle crashes, being hit with or crashing into an object, and assaults. The initial injury can cause brain tissue to swell. In addition, broken pieces of bone can rupture blood vessels in any part of the head. The body’s response to the injury may also increase swelling. Too much swelling may prevent fluids from leaving the brain.
  • Ischemic strokes: Ischemic stroke is the most common type of stroke and is caused by a blood clot or blockage in or near the brain. The brain is unable to receive the blood — and oxygen — it needs to function. As a result, brain cells start to die and swelling occurs.
  • Hemorrhagic strokes: Hemorrhage refers to blood leaking from a blood vessel in the brain (intracerebral). Hemorrhagic strokes are the most common type of stroke. They occur when blood vessels anywhere in the brain rupture. As blood leaks and the body responds, pressure builds inside the brain. High blood pressure is thought to be the most frequent cause of this kind of stroke. Hemorrhages in the brain can also be due to certain medications and unknown malformations present from birth.
  • Infections: Illness caused by an infectious organism such as a virus or bacterium can lead to brain swelling. Examples of these illnesses include:
    • Meningitis: This is an infection in which the covering of the brain becomes inflamed. It can be caused by bacteria, viruses, other organisms, and some medications.
    • Encephalitis: This is an infection in which the brain itself becomes inflamed. It is most often caused by a group of viruses and is sometimes spread through insect bites. 
    • Toxoplasmosis: This infection is caused by a parasite. Toxoplasmosis most often affects fetuses, young infants, and people with damaged immune systems.
    • Subdural abscess: Subdural abscess (empyema) refers to an area of the brain becoming abscessed or filled with pus, usually after another illness such as meningitis or a sinus infection. The infection can spread quickly, causing swelling and blocking other fluid from leaving the brain.
  • Tumors: Growths in the brain can cause swelling in several ways. As a tumor develops, it can press against other areas of the brain. Tumors in some parts of the brain may block cerebrospinal fluid from flowing out of the brain. New blood vessels growing in and near the tumor can leak and also lead to swelling.
  • High altitudes: Although researchers don’t know the exact causes, brain swelling is more likely to occur at altitudes above 4,900 feet. This type of brain edema is usually associated with severe acute mountain sickness (AMS) or high-altitude cerebral edema (HACE).

Symptoms of brain swelling vary, depending on the severity and the cause. Usually they begin suddenly. You may notice any of these symptoms:

  • Headache
  • Neck pain or stiffness
  • Nausea or vomiting
  • Dizziness
  • Irregular breathing
  • Vision loss or changes
  • Memory loss
  • Inability to walk
  • Difficulty speaking
  • Stupor
  • Seizures
  • Loss of consciousness

The steps used by your doctor to diagnose brain swelling depend on the symptoms and the suspected cause. Common exams and tests used in the diagnosis include:

  • Head and neck exam
  • Neurologic exam
  • CT scan of the head to identify the extent and location of the swelling
  • MRI of the head to identify the extent and location of the swelling
  • Blood tests to check for causes of the swelling
  • Lumbar puncture

Minor cases of brain swelling due to causes such as moderate altitude sickness or a slight concussion often resolve within a few days. In most cases, however, more treatment is needed quickly.

The goal is to assure that the brain receives enough blood and oxygen to remain healthy while the swelling is relieved and any underlying causes are treated. This may require a combination of medical and surgical treatments. Prompt treatment usually results in quicker and more complete recovery. Without it, some damage may remain.

Supportive care for brain edema may include any combination of the following:

  • Hyperbaric oxygen therapy: Providing oxygen through a respirator or in a chamber helps make sure that the blood has enough oxygen in it. 
  • IV fluids: Giving fluids and medicine through an IV can keep blood pressure from dropping too low. This helps to make sure that the body — including the brain — is receiving enough blood. However, some fluids can make swelling worse. Doctors attempt to use the right amounts of the right fluids in someone with brain swelling.
  • Lowering body temperature (hypothermia): Lowering the temperature of the body and brain helps relieve swelling and allows the brain to heal. Hypothermia as a treatment for brain swelling is not widely used, however.
  • Medication: In some cases of brain edema, your doctor may start a drug to help relieve the swelling. Medication may also be given for other reasons, such as to slow your body’s response to the swelling or to dissolve any clots. The drugs your doctor gives you depend on the cause and symptoms of brain swelling.
  • Ventriculostomy: In this procedure, a surgeon cuts a small hole in the skull and inserts a plastic drain tube. Cerebrospinal fluid is drained from inside the brain, helping to relieve the pressure.
  • Surgery: Surgery may have one or more of these goals:
    • Removing part of the skull to relieve intracranial pressure; this procedure is called decompressive craniectomy.
    • Removing or repairing the source of the swelling, such as repairing a damaged artery or vein or removing a growth

 

It’s common to have lingering effects from brain swelling. The problems you notice depend on the severity as well as the location of the injury. Symptoms may be noticed with any of the following:

  • Sleeping
  • Thinking and attention skills
  • Headaches
  • Depression
  • Communication skills
  • Movement
  • Urinary incontinence 

Your health care team is available to help you deal with these challenges. While some problems may continue to diminish over time, others may require ongoing treatment.

To protect the brain, keep these tips in mind as you go about your daily activities:

  • Use a helmet when biking, skating, playing contact sports, or performing other activities in which you might fall and hit your head.
  • Wear seat belts properly when driving or riding in vehicles.
  • Make sure you are doing all you can to control high blood pressure and heart disease.
  • Avoid smoking.
  • When traveling to high elevations, take your time — allow your body to adjust to the altitude.

Top Picks

Cerebral edema – causes, symptoms, signs, consequences, diagnosis, treatment, prognosis

Signs of cerebral edema occur in a life-threatening emergency. In this condition, fluid is rapidly accumulating in the brain tissues, especially the glial (supporting) and intercellular space. The volume of the brain increases, and since the skull cannot expand, pressure increases sharply in its cavity, and intracranial hypertension develops.

Features of cerebral edema

Cerebral edema is an incomplete term, since two processes occur simultaneously: edema and swelling of the medulla. With edema, the cells move apart and are squeezed by the accumulating fluid, which disrupts the transport of oxygen and intracellular metabolic processes. Swelling increases the volume of the cells themselves. Edema and swelling do not occur in isolation (separately), these processes are interconnected and always occur simultaneously. Medical assistance must be provided immediately, otherwise it is impossible to save the patient.

It should be noted that other organs of the human body also swell during illness. However, in other organs it is not so dangerous. Even swelling of the bone marrow can lead to paralysis or loss of vision, which eventually disappear. The brain is the main control organ of the body, and any damage to it is life-threatening.

The contents of the cranium consists of three types of tissues, their percentage is as follows:

  • brain substance or parenchyma – up to 85%;
  • cerebrospinal fluid or cerebrospinal fluid – up to 9%;
  • blood – up to 6%.

In this case, the amount of the entire fluid (extra- and intracellular, blood, cerebrospinal fluid) is about 1200 ml. This fluid is in dynamic equilibrium, constantly produced and absorbed up to 600 ml daily. All brain tissues are incompressible, therefore, they are quickly damaged when intracranial pressure or ICP increases (the norm is from 7 to 15 millimeters of water column). A slight increase in ICP can be compensated by an increase in absorption, but this has its limits. An increase in ICP leads to compression of the veins, and absorption stops.

The condition is not a disease, but a complication of other diseases or injuries.

Causes of cerebral edema

The brain swells in many conditions:

  • trauma;
  • abscess;
  • tumor;
  • meningitis;
  • encephalitis;
  • oxygen starvation;
  • stroke;
  • infections;
  • intoxication;
  • widespread body burns;
  • malignant hypertension.

More often than others, cerebral edema occurs during and after a stroke, as well as trauma. Regardless of the cause, the mechanism of edema and swelling is the same. There are local and diffuse edema. Local, or local, develops around a small injury: a tumor, an abscess, a heart attack (blockage by a blood clot), a bruise site. Diffuse develops in systemic diseases (intoxication, malignant hypertension, body burns) and covers the entire brain.

Cerebral edema in adult or elderly patients develops in severe diseases of the internal organs:

  • heart failure;
  • anaphylactic shock;
  • diabetes mellitus;
  • liver and kidney failure;
  • infections – toxoplasmosis, influenza;
  • poisoning with external poisons;
  • status epilepticus.

There is swelling of the brain after surgery to remove tumors and hematomas, in chronic alcoholics due to increased vascular permeability, in lovers of high-mountain sports, after violating the rules of gradual acclimatization to a reduced oxygen content in the mountain air.

Cerebral edema in children occurs with birth trauma, protracted labor, tight entanglement of the umbilical cord, with severe toxicosis during pregnancy. Unclosed fontanel sutures can to some extent compensate for swelling, but are dangerous for damage to the medulla.

Edema of the spinal cord of the spine is a mandatory (universal) reaction of tissues to any injury. All pathological conditions (trauma, surgery, rupture of the hernial protrusion, demyelinating diseases) are accompanied by swelling. The most dangerous period is the first 3-5 days. Mortality and consequences largely depend on the level of the lesion, the most dangerous in the cervical region.

Symptoms of cerebral edema

The clinical picture consists of three syndromes:

  • cerebral;
  • focal and stem;
  • dislocations (displacements) of brain structures.

Cerebral syndrome reflects an increase in ICP. The patient is lethargic or stunned, may complain of severe arching headache, persistent hiccups, nausea and vomiting, photophobia. There are oculomotor disorders, especially double vision, increased blood pressure, and the frequency of respiration and pulse slows down. Muscle tone increases, the head cannot be bent to the sternum. Eye movements are painful, as are the exit points of the cranial nerves on the face.

Focal symptoms appear when the process spreads to the cortex and subcortex, stem symptoms – to the brain stem. Edema of the hemispheres is manifested by narrowing or loss of consciousness, generalized convulsions. Damage to the subcortex and deep structures is manifested by psychomotor agitation, excessive movements (hyperkinesis), grasping reflexes. The pose of the “pointing dog” is characteristic – on its side with an unbent head with legs and arms bent at the knees and pressed to the body. Compression of the trunk is manifested by periodic non-rhythmic breathing, miosis (sharp constriction of the pupils), a drop in blood pressure, and cardiac arrhythmia.

How long they live with cerebral edema depends on whether it is possible to stop the growth of the process, this period is calculated in days or even hours.

Displacement of brain structures is manifested by signs of separation of the cortex and subcortical structures: fever above 40 ° C, lack of consciousness with “floating” eyeballs and divergent strabismus. This is an irreversible state.

In children, the condition is manifested by constant screaming and crying, bulging of a large fontanel, generalized convulsions. Without medical attention, breathing stops quickly.

Diagnosis of cerebral edema

This is an emergency condition, which the doctor has a few minutes to recognize. Diagnosis is based on clinical signs; if the hospital is well equipped, a CT scan is possible.

Lumbar puncture is contraindicated because of the risk of wedging the brainstem into the foramen magnum.

The patient is immediately transferred to the intensive care unit, urgent blood tests are performed, especially the acid-base balance is monitored.

Treatment of cerebral edema

It is carried out individually in accordance with the developing situation, counteracting all emerging violations. First of all, dehydration treatment is performed to remove excess fluid. Various types of diuretics and decongestants are injected intravenously – mannitol, loop diuretics. Substances with neuroprotective properties are used: magnesium sulfate, glucose solution. This helps to prevent the negative consequences of cerebral edema and save the patient’s life.

Give pure oxygen to breathe or transfer the patient to mechanical ventilation, use local head cooling. Metabolic processes are improved with the help of cortexin, citicoline and antioxidants. Cell membranes are stabilized with glucocorticoid hormones.

After stabilization of the state, reduction of hyperthermia, with stable blood pressure, pulse and respiration, they treat the underlying disease: trauma, tumor, hematoma, infarction.

The prognosis for cerebral edema depends on many factors: age, underlying and concomitant diseases, genetic stability, speed of medical care. The outcome can be either a complete recovery or the formation of focal neurological symptoms or a psychoorganic syndrome with a gross decrease in intelligence.

To prevent such a formidable complication, it is necessary to consult a doctor in case of any, even seemingly minor, health disorder. Particularly noteworthy are persistent, growing headache, double vision, unsteadiness. When these signs appear, you should immediately contact a neurologist.

Author of the article:

Markelov Gleb Vladimirovich

neurologist, online consultations

work experience 4 years

reviews Leave a review

Clinic

m. Sukharevskaya

Reviews

Services

  • Title
  • Appointment, consultation of a neurologist primary 2300