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Pharmacology for Nurses

12.3 Intracranial Emergencies and Intracranial Emergency Drugs

Pharmacology for Nurses12.3 Intracranial Emergencies and Intracranial Emergency Drugs

Learning Outcomes

By the end of this section, you should be able to:

  • 12.3.1 Describe the pathophysiology of common intracranial emergencies.
  • 12.3.2 Identify the clinical manifestations related to common intracranial emergencies.
  • 12.3.3 Identify the etiology and diagnostic studies related to common intracranial emergencies.
  • 12.3.4 Identify the characteristics of drugs used to treat common intracranial emergencies.
  • 12.3.5 Explain the indications, action, adverse reactions, and interactions of drugs used to treat common intracranial emergencies.
  • 12.3.6 Describe nursing implications of drugs used to treat common intracranial emergencies.
  • 12.3.7 Explain the client education related to drugs used to treat common intracranial emergencies.

Intracranial Emergency Overview

In adults, the brain has a constant volume, but the amount of cerebrospinal fluid and blood in the skull changes regularly to control pressure in the brain. Cerebrospinal fluid is produced by the brain and absorbed by the veins in the skull. Normal cerebrospinal fluid pressure varies with age but generally should not exceed 250 mm H2O in adults (Sharma et al., 2023). The skull has a relatively fixed volume of approximately 1400–1700 mL (Cook, 2016), consisting of 80 percent brain parenchyma, 10 percent cerebrospinal fluid, and 10 percent blood. Any increase in the volume of components within the skull or an addition of a pathological element, such as a brain tumor, will result in increased pressure within the skull since the skull’s volume is considered constant.

Intracranial emergencies encompass a range of sudden and serious medical conditions that affect the brain, its surrounding structures, or blood vessels within the skull (see Figure 12.3). These conditions can result from a variety of factors including head trauma, bleeding, blockage of blood vessels within the brain, head or sinus infections, brain tumors, or other underlying medical conditions. Successful treatment of intracranial emergencies requires early recognition and prompt medical intervention. Delayed treatment can lead to irreversible brain damage or death. This chapter will specifically delve into intracranial hypertension and increased intracranial pressure, providing an in-depth examination of their causes, symptoms, and treatment options.

A drawing of a head showing the brain inside has a close up that shows the layers of tissue that surrounds the brain. Starting with the outermost layer and working in, there is the skin, aponeurosis, periosteum, and bone. Next is the Meniges, which consists of dura mater, arachnoid mater, and pia mater. Between the arachnoid mater and pia mater is subarachnoid space and cerebrospinal fluid, also known as CSF. Below the pia mater is brain tissue.
Figure 12.3 The layers of tissue surrounding the brain play an important role during intracranial emergencies, especially when there is an elevation in intracranial pressure. (credit: modification of work from Microbiology. attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Intracranial Hypertension and Increased Intracranial Pressure

Intracranial hypertension and increased intracranial pressure are related conditions, but they have distinct differences. Intracranial hypertension refers specifically to an elevated pressure within the skull that may or may not cause symptoms. However, increased intracranial pressure refers to a rise in the pressure within the skull that can cause various symptoms, such as headache, nausea, vomiting, visual changes, and altered mental status. Intracranial hypertension can be a cause of increased intracranial pressure, but it is not the only cause. Other factors that can lead to increased intracranial pressure include brain tumors, bleeding within the brain, infections, or trauma. Significantly, prompt recognition and management of increased intracranial pressure are critical to prevent irreversible brain damage and ensure the best possible outcomes for clients (Munakomi & Das, 2023).

Intracranial pressure is typically measured at the level of the foramen of Monro and is normally between 7 mm Hg and 15 mm Hg in vertically positioned adults. Intracranial hypertension is a clinical condition that is associated with an elevation of the pressures within the cranium. The cranial vault is measured in millimeters of mercury (mm Hg) and is normally less than 20 mm Hg (Pinto et al., 2022). Therapy to lower intracranial pressure should be initiated when increased intracranial pressure is greater than 20 mm Hg to 25 mm Hg (Munakomi & Das, 2023).

Diagnostic Testing

Intracranial hypertension and increased intracranial pressure can be diagnosed with these tests:

  • Neurologic assessment: A physical examination of the client’s neurological function can provide information about the presence of increased pressure or fluid within the skull and brain.
  • Radiologic imaging: CT and MRI are commonly used to evaluate the brain for structural abnormalities that may cause intracranial hypertension or increased intracranial pressure.
  • Intracranial pressure monitoring: Direct measurement of intracranial pressure can be obtained by inserting a catheter into the skull and connecting it to a pressure transducer. This is the “gold standard” for diagnosing and monitoring increased intracranial pressure.
  • Transcranial doppler: This is a noninvasive test that uses ultrasound to measure the velocity of blood flow in the brain’s blood vessels. It can be used to assess cerebral blood flow and help diagnose and monitor increased intracranial pressure.
  • Ophthalmologic examination: Increased intracranial pressure can cause swelling of the optic nerve, which can be detected by an ophthalmologist during an eye examination.

The choice of diagnostic test depends on the suspected cause of intracranial hypertension and increased intracranial pressure, the severity of the symptoms, and the availability of resources. A combination of these tests may be necessary to make an accurate diagnosis and to develop an appropriate plan of treatment.

Clinical Manifestations

Clinical manifestations of intracranial hypertension and increased intracranial pressure can vary depending on the underlying cause and the individual client factors. A thorough evaluation by a health care provider is necessary to accurately diagnose and manage these conditions.

Clinical manifestations of intracranial hypertension may include:

  • Headache
  • Nausea
  • Blurred vision
  • Dizziness
  • Tinnitus
  • Confusion or altered mental status

Clinical manifestations of increased intracranial pressure may include:

  • Headache
  • Seizures
  • Papilledema
  • Altered mental status, including drowsiness, confusion, or coma
  • Changes in vital signs, such as bradycardia (slow heart rate) or hypertension

In severe cases, increased intracranial pressure can lead to brain herniation, a condition in which a portion of the brain is displaced due to increased intracranial pressure, a life-threatening condition. Symptoms of brain herniation can include changes in breathing pattern, dilation of one or both pupils, loss of consciousness, coma, and death.

Clinical Tip

Nursing Interventions to Lower/Stabilize Increased Intracranial Pressure

Along with administering drugs to decrease elevated intracranial pressure, the nurse must keep the head of the client’s bed at a 30-degree angle, or as directed by the health care provider, and keep the client’s neck in a neutral position to help stabilize and lower intracranial pressure (Faraj et al., 2022).

Drugs Used for Intracranial Emergencies

The health care provider selects drugs to treat intracranial hypertension and increased intracranial pressure based on the underlying cause and severity of the condition. For example, in some cases of cerebral edema, osmotic diuretics or carbonic anhydrase inhibitors (CAIs) may be used to reduce brain swelling and lower intracranial pressure. Non-pharmaceutical treatments—such as radiation or surgery—may also be needed as adjuvant treatment, particularly if there is a mass, tumor, bleeding, or trauma to the brain. The health care provider may also need to monitor the client’s response to treatment and adjust the drug regimen accordingly. Common drugs used to treat issues with intracranial hypertension and increased intracranial pressure include glucocorticoids, hyperosmolar therapy (mannitol and hypertonic saline), barbiturates, sedatives, and antiepileptic drugs (Faraj et al., 2022). This section of the chapter will focus on drugs that are aimed at reducing intracranial pressure and cerebral edema including CAIs and osmotic diuretics.

Carbonic Anhydrase Inhibitors (CAIs)

CAIs are a class of drugs that are commonly used to treat a range of conditions, including intracranial hypertension, altitude sickness, and glaucoma. In managing intracranial emergencies, CAIs work by blocking carbonic anhydrase on the luminal membrane and inside the proximal renal tubule, which results in a reduction in the secretion of bicarbonate ions through the sodium and hydrogen antiporter. This decrease in bicarbonate ion secretion leads to a reduction in cerebrospinal fluid and intracranial pressure, making CAIs an important therapeutic option for managing intracranial hypertension (Aslam & Gupta, 2022).

Adverse effects of CAIs include changes in taste, fatigue, abdominal pain, nausea, diarrhea, blurred vision, tinnitus, paresthesia, rash, and headache. Serious adverse effects include hypokalemia, metabolic acidosis, aplastic anemia, fulminant hepatic necrosis, and nephrolithiasis. CAIs are contraindicated in clients with hepatic disease, in those with certain electrolytes imbalances—such as hypokalemia and hyponatremia—and in those with hypersensitivity to the drug or its components (Aslam & Gupta, 2022).

Safety Alert

Aspirin and Acetazolamide

Caution is advised for client’s receiving concomitant high-dose aspirin and acetazolamide, as anorexia, tachypnea, lethargy, metabolic acidosis, and death have been reported.

The most common CAI prescribed for intracranial hypertension is acetazolamide (Farzam & Abdullah, 2022). Table 12.15 is a drug prototype table for CAIs featuring acetazolamide. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Drug Class

Mechanism of Action
Blocks carbonic anhydrase on the luminal membrane and inside the proximal renal tubule, decreasing bicarbonate ion secretion and thereby reducing cerebrospinal fluid and increased intracranial pressure
Drug Dosage
Recommended dose is 500 mg 2 times daily (1 capsule in the morning and 1 capsule in the evening); may increase by 250 mg up to 4000 mg/day.
To treat idiopathic intracranial hypertension
Also used in the treatment of glaucoma, heart failure, altitude sickness, and epilepsy

Therapeutic Effects
Reduces edema
Drug Interactions

Food Interactions
No significant interactions
Adverse Effects
Aplastic anemia
Fulminant hepatic necrosis
Metabolic acidosis
Alterations in taste
Hepatic disease

Monitor closely in clients with hepatic and renal insufficiency and in those with certain electrolyte imbalances such as hyponatremia and hypokalemia
Table 12.15 Drug Prototype Table: Acetazolamide (source:

Osmotic Diuretics

Osmotic diuretics are a class of drugs that primarily function by inhibiting the reabsorption of water in the proximal convoluted tubule, the descending loop of Henle, and the collecting duct, all of which are regions of the kidney that are highly permeable to water. In addition to this mechanism, osmotic diuretics also extract water from the intracellular compartments, thereby increasing extracellular fluid volume, which results in a reduction in edema. Adverse effects include dehydration, heart failure due to the shift of free water, hyponatremia, hypokalemia, and hypocalcemia. Osmotic diuretics are contraindicated in clients with anuria due to renal disease, pulmonary edema, severe dehydration, progressive heart failure, and in those with hypersensitivity to the drug or any of its compounds (Tenny et al., 2022). More information on this topic is included in Diuretic Drugs.

Mannitol administration preparation should include inspecting the injection for particulate matter, discoloration, or crystallization before and periodically during administration. Discard the mannitol solution if particulates, crystallization, or discoloration are present.

Mannitol is the most prescribed osmotic diuretic indicated for decreasing cerebral edema. Table 12.16 is a drug prototype table for osmotic diuretics featuring mannitol. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Drug Class
Osmotic diuretic

Mechanism of Action
Causes osmosis from intracellular fluid (ICF) to extracellular fluid (ECF) by drawing water out of the brain parenchyma and into the intravascular space
Drug Dosage
The total dosage, concentration, and rate of administration depend on the age, weight, and condition of the client being treated, including fluid requirement, electrolyte balance, serum osmolality, urinary output, and concomitant therapy.
Monitor serum osmolarity.
Reduction of intracranial pressure:
Usually a maximum reduction in intracranial pressure in adults can be achieved with a dose of 0.25 g/kg/dose infused intravenously over 30 minutes, which may be repeated every 6–8 hours
Reduction of intraocular pressure:
The recommended dosage is 1.5–2 g/kg of a 20% solution (7.5–10 mL/kg) as a single dose infused intravenously over a period of at least 30 minutes.
When used preoperatively, administer 1–1 ½ hours before surgery to achieve maximal reduction of intraocular pressure before the procedure.
To treat increased intracranial pressure and cerebral edema
To treat increased intraocular pressure

Therapeutic Effects
Reduces intracranial pressure and cerebral edema
Decreases intraocular pressure
Drug Interactions
Other diuretics

Food Interactions
No significant interactions
Adverse Effects
Acute kidney injury
Metabolic acidosis
Congestive heart failure
Pulmonary edema
Dry mouth
Severe hypovolemia
Preexisting pulmonary edema
Active intracranial bleeding except during craniotomy

Monitor closely in clients who have congestive heart failure because this drug may cause volume overload from fluid shift
Table 12.16 Drug Prototype Table: Mannitol (source:

Nursing Implications

The nurse should do the following for clients who are receiving mannitol or other intracranial emergency drugs:

  • Before administering, assess the client’s medical history, current drug list, and allergies.
  • Administer the drug as prescribed by the health care provider.
  • Observe and report symptoms of cerebral edema and intracranial hypertension to the health care provider. These symptoms include headache, confusion, dizziness, convulsions, unconsciousness, bradycardia, or failure of the pupils to react to light.
  • Monitor laboratory tests to detect for possible complications of these drugs such as metabolic acidosis and electrolyte imbalances as hypo/hypernatremia and hypo/hyperkalemia.
  • Monitor intake and output as well as urinary output in response to diuresis.
  • Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Client Teaching Guidelines

If alert and oriented, the client receiving an emergency drug should:

  • Be aware of signs of decreased intracranial pressure and cerebral edema, such as decreased confusion, improved coordination, decreased blood pressure, and increased urine output.
  • Report symptoms of fluid retention including swelling in legs and feet, weight gain, and shortness of breath to their health care provider as these may represent an adverse reaction to the drug.

The client taking an intracranial emergency drug should not:

  • Stop taking the drug unless directed by their health care provider, as this drug class may cause fluid shifts within the body resulting in shortness of breath, peripheral edema, and bradycardia.

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