Increased Intracranial Pressure


Article Author:
Venessa Pinto
Prasanna Tadi


Article Editor:
Adebayo Adeyinka


Editors In Chief:
Sebastiano Cassaro
Joseph Lee
Tanya Egodage


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
3/26/2019 5:05:14 PM

Introduction

Intracranial hypertension (IH) is a clinical condition that is associated with an elevation of the pressures within the cranium. The pressure in the cranial vault is measured in millimeters of mercury (mm Hg) and is normally less than 20 mm Hg.

The cranium is a rigid structure that contains 3 main components: brain, cerebrospinal fluid, and blood. Any increase in the volume of its contents will increase the pressure within the cranial vault.  The Monroe-Kellie Doctrine states that the contents of the cranium are in a state of the constant volume.[1] That is, the total volumes of the brain tissues, cerebrospinal fluid (CSF), and intracranial blood are fixed. An increase in the volume of one component will result in the decrease of volume in 1 or 2 of the other components. The clinical implication of the change in volume of the component is a decrease in cerebral blood flow or herniation of the brain.

CSF is a clear fluid found in the subarachnoid spaces and ventricles that cushions the brain and spinal cord. It is secreted by the choroid plexus in the lateral ventricles, travels to the third ventricle via the foramen of Monroe. From the third ventricle, CSF reaches the fourth ventricle through the aqueduct of Sylvius. From here, it flows into the subarachnoid space via the foramina of Magendie and Luschka and is eventually reabsorbed into the dural venous sinuses by arachnoid granulation.

Etiology

The causes of increased intracranial pressure (ICP) can be divided based on the intracerebral components causing elevated pressures:

Increase in brain volume

Generalized swelling of the brain or cerebral edema from a variety of causes such as trauma, ischemia, hyperammonemia, uremic encephalopathy, and hyponatremia

Mass effect

  • Hematoma
  • Tumor
  • Abscess
  • Blood clots  

Increase in cerebrospinal fluid

  • Increased production of CSF
  • Choroid plexus tumor

Decreased re-absorption of CSF

  • Obstructive hydrocephalus
  • Meningeal inflammation or granulomas

Increase in blood volume

  • Increased cerebral blood flow during hypercarbia, aneurysms
  • Venous stasis from
  • Venous sinus thromboses,
  • Elevated central venous pressures, e.g., heart failure

Other causes

  • Idiopathic or benign intracranial hypertension
  • Skull deformities such as craniosynostosis
  • Hypervitaminosis A, tetracycline use

Epidemiology

The true incidence of intracranial hypertension is unknown. The Centers for Disease Control and Prevention (CDC) estimates that in 2010, 2.5 million people sustained a traumatic brain injury (TBI). TBI is associated with increased ICP. ICP monitoring is recommended for all patients with severe TBI. Studies of American-based populations have estimated that the incidence of idiopathic intracranial hypertension (IIH) ranges from 0.9 to 1.0 per 100,000 in the general population, increasing in women that are overweight.[2]

Pathophysiology

The harmful effects of intracranial hypertension are primarily due to brain injury caused by cerebral ischemia. Cerebral ischemia is the result of decreased brain perfusion secondary to increased ICP. Cerebral perfusion pressure (CPP) is the pressure gradient between mean arterial pressure (MAP) and intracranial pressure (CPP = MAP - ICP). CPP = MAP - CVP if central venous pressure is higher than intracranial pressure. CPP targets for adults following severe traumatic brain injury is recommended at greater than 60 to 70 mm Hg, and a minimum CPP greater than 40 mm Hg is recommended for infants, with very limited data on normal CPP targets for children in between.

Cerebral autoregulation is the process by which cerebral blood flow varies to maintain adequate cerebral perfusion. When the MAP is elevated, vasoconstriction occurs to limit blood flow and maintain cerebral perfusion. However, if a patient is hypotensive, cerebral vasculature can dilate to increase blood flow and maintain CPP.

History and Physical

Clinical suspicion for intracranial hypertension should be raised if a patient presents with the following signs and symptoms: headaches, vomiting, and altered mental status varying from drowsiness to coma. Visual changes can range from blurred vision, double vision from cranial nerve defects, photophobia to optic disc edema and eventually optic atrophy. Infants in whom the anterior fontanelle is still open may have a bulge overlying the area.

Cushing triad is a clinical syndrome consisting of hypertension, bradycardia and irregular respiration and is a sign of impending brain herniation. This occurs when the ICP is too high the elevation of blood pressure is a reflex mechanism to maintain CPP. High blood pressure causes reflex bradycardia and brain stem compromise affecting respiration. Ultimately the contents of the cranium are displaced downwards due to the high ICP, causing a phenomenon known as herniation which can be potentially fatal.

Evaluation

The evaluation of increased ICP should include a detailed history taking, physical examination, and ancillary studies.

It is extremely important to identify increased ICP as early as possible to prevent herniation and death. For example malignant middle cerebral artery stroke presenting with increased ICP. 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 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. [3]

A funduscopic exam can reveal papilledema which is a tell-tale sign of raised ICP as the cerebrospinal fluid is in continuity with the fluid around the optic nerve.

Imaging- a computed tomography (CT) of the head or magnetic resonance imaging (MRI) can reveal signs of raised ICP such as enlarged ventricles, herniation, or mass effect from causes such as tumors, abscesses, and hematomas, among others.

Measurement of Opening Pressure with a Lumbar Puncture

In this procedure, a needle is introduced in the subarachnoid space. This can be connected to a manometer to give the pressure of the CSF prior to drainage. A measurement greater than 20 mm Hg is suggestive of raised ICP. Brain imaging should precede an LP because LP can cause a sudden and rapid decrease in ICP and the sudden change in volume can lead to herniation.

ICP Monitoring

Several devices can be used for ICP monitoring.

The procedure involves placement of a fiber optic catheter into the brain parenchyma to measure the pressure transmitted to the brain tissue.

External Ventricular Drain (EVD)

A drain placed directly into the lateral ventricles can be connected to a manometer to give a reading for the pressure in the ventricles.

Treatment / Management

Assessment and management of airway, specifically breathing and circulation should always be the priority.[4]

Management principles should be targeted toward:

  • Maintenance of cerebral perfusion pressure by raising MAP 
  • Treatment of the underlying cause.
  • Lowering of ICP. [5]

Measures to lower ICP include:[6]

  • Elevate of the head of the bed to greater than 30 degrees.
  • Keep the neck midline to facilitate venous drainage from the head.
  • Hypercarbia lowers serum pH and can increase cerebral blood flow contributing to rising ICP, hence hyperventilation to lower pCO2 to around 30 mm Hg can be transiently used.
  • Osmotic agents can be used to create an osmotic gradient across blood thereby drawing fluid intravascularly and decreasing cerebral edema. Mannitol was 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.[7]
  • 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.[8]
  • Drugs of the carbonic anhydrase inhibitor class, such as acetazolamide, can be used to decrease the production of CSF and is used to treat idiopathic intracranial hypertension.
  • Lumbar punctures, besides being diagnostic, can be used to drain CSF thus reducing the ICP. The limitation to this is raised ICP secondary to mass effect with a possible risk of herniation if the CSF pressure drops too low.
  • Similar to a lumbar puncture, an EVD can also be used to not only monitor ICP but also to drain CSF.
  • Optic nerve fenestrations can be performed for patients with chronic idiopathic hypertension at risk of blindness. Neurosurgical shunts such as ventriculoperitoneal or lumbar-peritoneal shunts can divert CSF to another part of the body from where it can be reabsorbed.[9]
  • 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.[10] It is usually considered as a last resort when all other ICP lowering measures have failed.

Prognosis

Prognosis depends on the underlying etiology and severity of presentation. Benign intracranial hypertension does not increase the risk of death rate by itself; rather, the death rate is increased by morbid obesity which is a common association with benign intracranial hypertension. Visual loss is a significant morbidity in IIH.

Pearls and Other Issues

A patient who presents with a headache, vomiting, and blurred vision should be evaluated for neurologic deficits and receive head imaging to rule out causes of intracranial hypertension.

All patients with severe TBI (Glasgow coma scale of 3 to 8 on initial presentation) should follow the latest guidelines on the management of severe TBI that includes monitoring of ICP, maintenance of CPP greater than 60 to 70 mm Hg for adults and treatment of ICP greater than 22  mm Hg.

Enhancing Healthcare Team Outcomes

The clinical presentation of increased intracranial pressure 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 increasingly erratic heart rate, development of bradycardia, accurate and equal intake and output when having diuresis, and maintenance of proper blood pressure.  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 ensure 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.


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Increased Intracranial Pressure - Questions

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Which is not a sign of elevated intracranial pressure?



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A 68-year-old has been hit in the head and his Glasgow coma score is 12. His pupils are equal and reactive and his hemodynamics are stable. One hour later his blood pressure is 190/100 mmHg and right pupil is larger than the left. His GCS drops to 8. Which of the following is not important to the immediate management of this patient?



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Which of the following is not used to decrease intracranial pressure in a patient with a closed head injury?



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In a patient with elevated intracranial pressure, what level of brief hyperventilation is considered safe to acutely reduce the pressure?



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Following a motor vehicle accident, a 35-year-old male is agitated and has multiple cerebral contusions on CT of the head. Hemodynamic measurements show a heart rate of 85 beats/min and a mean arterial pressure (MAP) of 84 mmHg. An intracranial pressure monitor reveals a pressure of 28 mmHg. What is the most appropriate management regimen over the next few days?



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Which of the following is an early feature in a patient with increasing intracranial pressure and impending uncal herniation?



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Which type of respiration may be seen with increased intracranial pressure (ICP)?



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Which may be an appropriate treatment for a patient with increased intracranial pressure (ICP)?



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A patient in the neurointensive care unit has a steady increase of intracranial pressure from 15 to 44 mmHg. What changes would be seen on a physical exam of this patient?



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Which of the following drugs is not used to control elevated intracranial pressure?



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A nurse is taking care of a patient who is being treated for elevated ICP following a head injury. An ICP monitor has been inserted into the brain. Which of the following statements about hyperventilation is incorrect?



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Which osmotic diuretic is most commonly given to reduce elevated intracranial pressure?



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What does the new appearance of pupillary dilatation after neurosurgery indicate?



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A 6-year-old child develops double vision and projectile vomiting. What is the most likely cause of his condition?



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A 6-year-old child has respiratory arrest from septic shock. She is intubated and placed on a ventilator. The next day her blood pressure is 140/105 mm Hg and her heart rate is 40 bpm. What is the next best step in management?



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Which of the following factors cause Lundberg A waves?



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An acute rise in intracranial pressure in a 13-year-old patient causes multiple symptoms. Which of the following would be the last symptom or sign to manifest?



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Which of the following is not appropriate treatment to lower intracranial pressure?



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Which of the following is the most appropriate management of a patient with raised intracranial pressure without any other structural abnormalities?



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Which of the following physical exam findings is an early sign of increased intracranial pressure secondary to a hematoma or mass?



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Which of the following factors affecting the brain cause Lundberg A waves?



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Which of the following intracranial pressure waveforms is indicative of intracranial hypertension?



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What is the definition of "intracranial hypertension"?



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Which is not consistent with increasing intracranial pressure?



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A post-operative patient on the neurosurgical floor is found by the nurse to be moaning incomprehensibly to pain, with minimal withdrawal and no eye-opening. Which of the following measures is not appropriate management?



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A patient presents to the emergency department after a motor vehicle accident. Which of the following signs on the initial exam would not be consistent with intracranial hypertension?



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An obese woman walks into the urgent care center complaining of headache and vomiting for 2 days. Several differential diagnoses are being considered including a migraine and the flu. Which of the following symptoms might be more suggestive of intracranial hypertension?



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A 62-year-old man is in the intensive care unit for altered mental status after a fall. He has an intracranial pressure (ICP) monitor in place that is reading 25 mmHg. Which of the following would not be an appropriate target for his management?



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A nurse is providing care to a client with an epidural hematoma as a result of blunt head trauma. What are important aspects of care necessary to reduce intracranial pressure? Select all that apply.



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A healthcare provider is rounding on a patient newly admitted for observation after a head injury sustained from a fall. After review of the medication reconciliation form and admission history, the provider discovers the patient was on an anticoagulant at home for atrial fibrillation. A CT scan done on arrival yielded negative findings. The patient had ten staples placed to close a scalp laceration. What assessment findings would alert the provider to the fact that the patient may be suffering from elevated intracranial pressure? Select all that apply.



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Increased Intracranial Pressure - References

References

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Role of hypertonic saline and mannitol in the management of raised intracranial pressure in children: A randomized comparative study., Upadhyay P,Tripathi VN,Singh RP,Sachan D,, Journal of pediatric neurosciences, 2010 Jan     [PubMed]
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Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Surgery-General. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Surgery-General, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Surgery-General, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Surgery-General. When it is time for the Surgery-General board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Surgery-General.