12.3: Intracranial Emergencies and Intracranial Emergency Drugs
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 H 2 O 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.
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.
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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. |
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Indications
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
Aminoglycosides Cyclosporine Digoxin Other diuretics Food Interactions No significant interactions |
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Adverse Effects
Acute kidney injury Dehydration Headache Lethargy Confusion Metabolic acidosis Congestive heart failure Pulmonary edema Dry mouth Malaise Urticaria |
Contraindications
Hypersensitivity Anuria Severe hypovolemia Preexisting pulmonary edema Active intracranial bleeding except during craniotomy Caution: Monitor closely in clients who have congestive heart failure because this drug may cause volume overload from fluid shift |
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.