Intracranial Hypertension


Article Author:
Sandeep Sharma
Muhammad Hashmi


Article Editor:
Anil Kumar


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
9/13/2019 1:41:31 PM

Introduction

Intracranial hypertension is a spectrum of neurological disorders where cerebrospinal fluid (CSF) pressure within the skull is elevated. Normal CSF pressure varies by age. In general, CSF pressure above 250 mm H20 in adults and above 200 mm H2O in children signifies increased intracranial pressure (ICP). It may be idiopathic or arise as a result of neurologic insult or injury.[1][2][3][4]

Etiology

The human skull is a relatively fixed volume structure of approximately 1400 to 1700 mL. Physiologically its components consist of 80% brain parenchyma, 10% cerebrospinal fluid, and 10% blood. Since the skull is considered an unchangeable volume, any increase in the volume of components within the skull or an addition of a pathologic element will result in increased pressure within the skull. Pathologic structures that can cause increased ICP may include mass lesions, abscesses, and hematomas. 

The physiologic volume of the brain parenchyma is a relatively constant value in adults: however, it may be adjusted by mass lesions or in the setting of cerebral edema. Cerebral edema can occur with acute hypoxic encephalopathy, large cerebral infarction, and severe traumatic brain injury. CSF and blood volume in the intracranial space will vary on a regular basis as these are the primary regulators of intracranial pressure. CSF volume is primarily regulated via choroid plexus production at a rate of approximately 20 mL per hour physiologically and through its reabsorption at a similar rate by arachnoid granulations which drain into the venous system of the skull.  The control mechanisms for maintaining appropriate CSF pressures may become damaged in neurological injuries such as stroke or trauma. Increased CSF production above the rate at which it can be reabsorbed such as in the presence of a choroid plexus papilloma leads to increased pressure. 

A failure to reabsorb at a sufficient rate to match normal secretion rate is another possibility and is seen with arachnoid granulation adhesions after bacterial meningitis. Ventricular obstruction may also induce decreased reabsorption of CSF causing hydrocephalus. The primary regulator of blood volume is via cerebral blood flow. Diseases which obstruct venous outflows such as a venous sinus thrombosis, jugular vein compression, or structural changes due to neck surgery may cause blood congestion within the skull, thus increasing pressure. Idiopathic intracranial hypertension, also known as pseudotumor cerebri, is a term for increased intracranial pressure due to unknown causes with no known structural change.[2][5][6]

Etiology of intracranial hypertension can be divided into 2 categories:

Primary or Intracranial Causes

  • Trauma ( epidural hematoma, subdural hematoma, intracerebral hemorrhage or contusions)
  • Brain tumors
  • Stroke
  • Nontraumatic intracerebral Hemorrhage ( aneurysm rupture)
  • Idiopathic or benign intracranial hypertension
  • Hydrocephalus
  • Meningitis

Secondary or Extracranial Causes

  • Hypoventilation (hypoxia or hypercarbia)
  • Hypertension
  • Airway obstruction
  • Metabolic (drug induced)
  • Seizures
  • Hyperpyrexia
  • High altitude cerebral edema

Epidemiology

The exact epidemiology of intracranial hypertension depends on its etiology. However, of special note is idiopathic intracranial hypertension where up to 90% of affected individuals are women of childbearing age. Individuals with chronic hypertension or obesity are also at an increased risk for developing intracranial hypertension. A frequency of occurrence has been established to be 1.0 per 100,000 in the general population, 1.6 to 3.5 per 100,000 in women, and 7.9 to 20 per 100,000 in women who are overweight.

Pathophysiology

Anytime there is an elevation in ICP, there is the risk of subsequent injury from direct brainstem compression or from a reduction in cerebral blood flow. Clinically, cerebral blood flow is evaluated via measurement of cerebral perfusion pressure where:

Cerebral perfusion pressure = Mean arterial pressure - Intracranial pressure

Cerebral perfusion pressure in simpler terms is the pressure of blood flowing to the brain and is the driving force for delivery of oxygen necessary for neuronal functioning. Normally, this is a constant value of 50 to 100 mm Hg due to autoregulation. The impact that cerebral perfusion pressure holds is in the concept that blood flow will occur from an area of higher concentration to an area of lower concentration.  When ICP becomes elevated, cerebral perfusion pressures decrease, and the net driving force of blood flow to the brain becomes decreased.  The physiologic autoregulatory response to a decrease in cerebral perfusion pressure is to increase mean arterial pressures systemically and to vasodilate cerebral blood vessels. This results in increased cerebral blood volume that further increases ICP.  Paradoxically, this further reduces cerebral perfusion pressure producing a feedback cycle that results in the total reduction of cerebral flow and perfusion. The result of this feedback loop is cerebral ischemia and brain infarction with neuronal death. In cases where intracranial hypertension is the result of hemorrhage, increased blood pressure will worsen intracranial bleeding, thus worsening intracranial hypertension.

History and Physical

Symptoms of elevated intracranial hypertension are primarily derived from neurological irritation, compression, or displacement and papilledema. Non-specific headaches are recorded in almost all cases and are likely mediated via the pain fibers of the trigeminal nerve in the dura and blood vessels of the brain. Pain is generally diffuse and worse in the mornings with exacerbation by the Valsalva maneuver. Nausea and vomiting are common presentations of elevated ICP. Patients can present with double vision most frequently with horizontal diplopia associated with CN VI palsy from compression. Transient visual abnormalities occur frequently, often described as a gradual dimming of vision in one or both of the eyes. Visual abnormalities worsen with changes in posture. Peripheral visual loss may be reported and most commonly begins in the nasal inferior quadrant with subsequent loss of the central visual field.  Alterations in visual acuity with blurring or distortion may occur.  Variable degrees of loss of color distinction may occur. In more severe or chronic cases, a sudden visual loss can occur due to intraocular hemorrhage. Tinnitus with a pulsing rhythm exacerbated by supine or bending positions and Valsalva maneuver can occur. Radicular pain, numbness, or paresthesias are possible and most commonly associated with localized compression or possible herniation of the brain. Neurological findings are indications of severe disease. The anatomical locations where herniation is most likely to occur include the subfalcine, central transtentorial, uncal transtentorial, cerebellar tonsillar/foramen magnum, and transcalvarial lobes. These types of changes may lead to decreased consciousness or responsiveness. Focal neurological constellations depend on which region of the brain has herniated. Often this results in a stupor state or more severely with coma due to the local effect of mass lesions or pressure on the reticular formations of the midbrain. It may further lead to respiratory compromise.

Physical exam findings can vary widely depending on etiology. A change in mental status or comatose patient should prompt urgent evaluation. A complete neurological assessment is essential whenever intracranial hypertension is suspected. Cranial nerve assessment is particularly important for identifying lesions. Cranial nerve VI palsy is most common. Blunting of the pupillary reflex with fixed dilation of one pupil is also highly associated with herniation syndromes. Spontaneous periorbital bruising may be present as well. A classic triad of bradycardia, respiratory depression, and hypertension is known as Cushing's triad and is highly indicative of intracranial hypertension. Fundoscopic examination looking for retinal hemorrhages or papilledema is essential. Alterations in respiratory drive and effort may occur leading to failure of respiration and oxygenation.

Infants can have widening of cranial sutures and bulging fontanelle.

Evaluation

Complete blood count (CBC) and complete metabolic panel (CMP) are usually checked in all patients with suspected intracranial hypertension to evaluate for infection, anemia, and electrolyte abnormalities. Initial evaluation should include a head CT scan. CT scan findings of cerebral edema such as compressed basal cisterns and midline shift are predictive of elevated ICP. However, the absence of these findings does not rule out intracranial hypertension. A head MRI is more accurate than head CT in evaluating elevated ICP and to looking for potential etiology. Bedside ultrasonography also can be used to measure the diameter of the optic nerve sheath to determine intracranial hypertension. However, this study is limited by operator skill and not frequently used. A lumbar puncture may sometimes be needed for diagnosis. However, it should be delayed until neuroimaging, especially in those with suspicion of impending herniation. When LP is performed, in addition to measuring opening pressures, CSF should also be tested for infection and other potential etiology. Invasive measurement of ICP is definitive for diagnosis and improves the physician’s ability to maintain adequate cerebral perfusion pressure (CPP). There are 4 main anatomical sites used for clinical measurement of intracranial pressure: intraventricular, intraparenchymal, subarachnoid, and epidural. Ventriculostomy catheter is preferred device for ICP monitoring and can be used even for therapeutic CSF drainage to lower ICP. When ventricles cannot be cannulated, intraparenchymal devices using microsensor and fibreoptic transducer may be used. Subdural and epidural monitors are not as accurate as ventriculostomy and parenchymal monitors.[7][8][9][10]

Treatment / Management

Treatment of chronic intracranial hypertension is mainly focused on treating and reversing the etiology.

A sudden increase in ICP is a neurosurgical emergency, requiring close monitoring in an intensive care unit (ICU) setting. For acute intracranial hypertension, a patient should first be stabilized with healthcare professionals aiming for hemodynamic stability, and preventing and treating factors that may aggravate or precipitate intracranial hypertension. These patients should have close monitoring of heart rate, blood pressure, body temperature, ventilation and oxygenation, blood glucose, input and output, and ECG. Patients with suspected intracranial hypertension, especially with severe traumatic brain injury, should also have ICP monitoring.[11][12][13]

It is vital to prevent and treat factors that may aggravate or precipitate intracranial hypertension. These interventions are used to buy time until the underlying etiology is identified and corrected.

  • Keep the head elevated to 30 degrees and neutrally positioned to minimize venous outflow resistance and improve cerebral spinal fluid displacement from the intracranial to the spinal compartment.
  • Hypoxia and hypercapnia can increase ICP. Controlling ICP through optimal respiratory management is crucial. It is essential to control ventilation to maintain a normal PaCO2 and maintain adequate oxygenation without increasing the PEEP.
  • Agitation and pain can increase blood pressure and ICP. Adequate sedation and analgesia is an important adjunctive treatment. Since most sedating medications can have effects on blood pressure, medications with minimal hypotensive effect should be preferred. Hypovolemia can precipitate the hypotensive side effects and should be treated before administering sedative agents. Shorter-acting agents have the advantage of allowing brief interruption of sedation to evaluate neurological status.
  • Fever can increase brain metabolic rate and is a potent vasodilator, which in turn, increase the cerebral blood flow and increased ICP. Fever should be controlled with antipyretics and cooling blankets and infectious causes must be ruled out.
  • Elevated blood pressure is commonly seen in patients with intracranial hypertension especially when due to traumatic brain injury. In patients with untreated intracranial mass lesions, cerebral perfusion is maintained by the higher blood pressure, and systemic hypertension should not be treated. The absence of an intracranial mass lesion presents a more individualized, controversial decision when treating systemic hypertension. When antihypertensive are used, the preferred treatment includes beta-blockers like labetalol and esmolol or calcium channel blockers because they reduced blood pressure without affecting ICP. Agents with short half-lives should be preferred. Avoid vasodilators like sodium nitroprusside, nitroglycerin, and nifedipine.
  • Seizures can contribute and complicate elevated ICP and should be prevented by prophylactic medications, especially in severe traumatic brain injuries.

For patients with sustained intracranial hypertension, additional measures are needed to control the ICP.  

  • Emergent surgical management should be considered when there is sudden intracranial hypertension, or it is refractory to medical management.
  • Nondepolarizing muscle relaxants along with sedatives may be used to treat intracranial hypertension caused by posturing, coughing or agitation. When a neuromuscular blockade is used, EEG should be monitored to rule out convulsive states.
  • Hyperosmolar therapy is used for severe, acute intracranial hypertension.

Mannitol is commonly used as a hyperosmolar agent and is usually given as a bolus of 0.25 to 1 g/kg body weight. Serum osmolality should be kept less than 320 mOsm to avoid side effects of therapy like renal failure, hypokalemia, and hypo-osmolarity.

Hypertonic saline can also create an osmotic shift from the interstitial space of brain parenchyma into the intravascular compartment in the presence of an intact blood-brain barrier. Hypertonic saline has an advantage over mannitol for hypovolemic and hypotensive patients. Adverse effects of hypertonic saline administration include hematological and electrolyte abnormalities. Hyponatremia should be excluded before administering hypertonic saline to reduce the risk of central pontine myelinolysis.

  • Hyperventilation can be used for rapid reduction in ICP if there are clinical signs of herniation or with severe intracranial hypertension. Hyperventilation decreases PaCO2 which causes vasoconstriction of cerebral arteries, resulting in reduced cerebral blood flow and reduced intracranial pressure.
  • Barbiturate coma should be considered for patients with refractory intracranial hypertension.
  • Routine induction of hypothermia is not indicated; however, moderate hypothermia may be an effective adjunctive treatment for increased ICP refractory to other medical management.
  • Steroids are commonly used for primary and metastatic brain tumors to decrease vasogenic cerebral edema. For other neurosurgical disorders like traumatic brain injury or spontaneous intracerebral hemorrhage, steroids have not been shown to have a benefit, and sometimes may even be detrimental.

Surgical Interventions

  • Resection of intracranial mass lesions producing elevated ICP should be done as soon as possible.
  • CSF drainage lowers ICP immediately by reducing intracranial volume. This modality can be an important adjunct treatment for lowering ICP. However, it has limited utility when the brain is diffusely swollen and the ventricles are collapsed.
  • Decompressive craniectomy is used to treat severe uncontrolled intracranial hypertension. It involves surgical removal of part of the calvaria to create a window in the skull, allowing for herniation of swollen brain through the bone window to relieve pressure.

Differential Diagnosis

  • Acute nerve injury
  • Benign intracranial hypertension (Pseudotumor cerebri)
  • Cerebrovascular ischemia/hemorrhage
  • Hydrocephalus
  • Intracranial epidural abscess
  • Intracranial hemorrhage
  • Leptomeningeal carcinoma
  • Low-grade astrocytoma
  • Lyme disease
  • Meningioma
  • Meningitis
  • Migraine headache
  • Papilledema
  • Subarachnoid hemorrhage
  • Venous sinus thrombosis

Prognosis

Prognosis is highly variable depending on etiology and varies from benign to lethal. Children usually can tolerate higher intracranial pressure (ICP) for a longer period.

Enhancing Healthcare Team Outcomes

The management of intracranial hypertension is with a multidisciplinary team consisting of a neurologist, neurosurgeon, intensivist, ICU nurses, internist, and a pulmonologist. Treatment of chronic intracranial hypertension is mainly focused on treating and reversing the etiology. These patients need ICU admission and continuosu monitoring. In addition, the patients  should have close monitoring of heart rate, blood pressure, body temperature, ventilation and oxygenation, blood glucose, input and output, and ECG. Patients with suspected intracranial hypertension, especially with severe traumatic brain injury, should also have ICP monitoring. In patients in whom the intracranial pressure is short lived and treated the prognosis is good but in those patients with delay in treatment or a malignant cause, the prognosis is abysmal. even those who survive develop permanent neurolgocial deficits.[14][15](Level V)

 


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Intracranial Hypertension - Questions

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A 16-years-old male presents with sudden onset of severe headache, low-grade fever, and diplopia. A few days ago he underwent surgical drainage for a furuncle on his midface. On examination, there is a sick looking young male with periorbital edema, chemosis, lateral gaze palsy, and ptosis on the right side. On fundoscopy, there is bilateral disc edema. Lumbar puncture reveals elevated cerebrospinal fluid (CSF) opening pressure. What is the most appropriate initial management option?



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A 65-year-old male patient is brought by his caretaker with the chief complaints of headache, nausea, vomiting, blurring of vision, abdominal pain, and drowsiness. He has been having headaches since the winter started, but the frequency and intensity have gotten worse. He lives in his house alone since his wife passed away last year. On examination, his blood pressure is 110/70 mmHg, pulse 91/min regular, respiratory rate 22/min, and his Glasgow coma scale (GCS) is 11/15. Fundoscopy reveals bilateral disc edema. Having spent some time in the emergency department his GCS declines further and oxygen saturation starts to drop. He is immediately intubated and put on mechanical ventilation. Which of the following should be the target for mechanical ventilation in this case?



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A 16-years-old male presents with sudden onset of severe headache, low-grade fever, and altered behavior. A few days ago, he underwent surgical exploration for complicated middle ear infection. On examination, there is a sick looking young male with periorbital edema, chemosis, lateral gaze palsy, and ptosis on the right side. Pupillary responses are sluggish. Lumbar puncture reveals elevated cerebrospinal fluid (CSF) opening pressure. Which of the following has the highest yield in making a diagnosis in such cases?



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A 16-year-old male patient is brought to the emergency department as he got injured in a road traffic accident. He sustained head and chest trauma. On examination, he has open wounds and bruises all over. His blood pressure 170/110 mmHg, pulse 104/min regular, oxygen saturation 96% on room air, and his GCS is 9/15. His head computed tomography (CT) scan reveals compressed basal cisterns and midline shift. If raised intracranial pressure (ICP) is suspected in this case, which of the following should appear first?



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A 65-year-old male patient is brought to the emergency department with complaints of sudden onset of headache and inability to speak for three hours. On his way to the hospital, he has vomited twice. His previous record reveals that he is suffering from diabetes and hypertension. He has a metallic valve in place because he got mitral valve replacement done 6 years ago and since then he is on anticoagulants. Recently he consulted his family physician for a fungal infection over his skin for which he received a course of antifungals. On examination, blood pressure 180/110 mmHg, pulse 92/min regular, maintaining oxygen saturation on room air, and respiratory rate of 21/min. Nuchal rigidity is positive. Fundoscopy reveals bilateral papilledema. What needs to be administered to counteract the underlying pathology?



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Which imaging study is best to diagnose idiopathic intracranial hypertension (IIH)?



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A 36-years-old female presents with a three months history of headaches which get worse on coughing and postural changes. Sometimes, headache leads to nausea and vomiting. For a few days, she has been hearing a rhythmic sound in both ears that worsens on bending forward. On examination, blood pressure 110/70 mmHg, pulse 89/min regular, and respiratory rate of 18 breaths/min. Fundoscopy reveals bilateral disc edema. Currently, she is only on over-the-counter analgesics and oral contraceptives. Which of the following is the best initial investigation in this case?



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A 32-year-old female comes to the clinic with episodic disturbances of vision and frequent headaches. She also reports incidents of light-headedness and double vision on several occasions. She has a body mass index (BMI) of 35. She has a history of acne on her face for which she has been getting treatment. On fundoscopy, there is bilateral papilledema. On computed tomography (CT) scan, there is no apparent lesion, and she has a raised opening pressure on lumbar puncture. Which of the following risk factors has led to the symptoms of this patient?



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A 35-year-old female presents with the complaint of a 1-week history of generalized, moderate-intensity headaches with bilateral blurring of vision. Her past medical history is not significant, and she is not taking any medications. The exam shows a body mass index of 32, blood pressure 145/95 mmHg, heart rate 88 beats/min, and respiratory rate 16/min. Visual acuity is 20/80 OD and 20/60 OS. On lateral gaze, the right eye will not fully abduct. Visual field testing shows bilaterally enlarged blind spots. Papilledema is present bilaterally. What is the most probable diagnosis?



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A 65-year-old male comes to the emergency department with the complaint of sudden onset of weakness in his right arm and leg. He noticed these symptoms one hour ago. Currently, he is unable to walk, and he has slurred speech. On examination, his blood pressure is 100/60 mmHg and pulse 98/min regular. The neurologist is consulted, and he recommends an imaging study that shows compressed basal cisterns and midline shift. Which of the following is the initial emergent treatment of his condition?



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Intracranial Hypertension - References

References

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