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Increased intracranial pressure


Description


Increased intracranial pressure (ICP) is a potentially life-threatening situation that results from an increase in any or all of the three components within the skull: brain tissue, blood, and cerebrospinal fluid (CSF).


Pathophysiology


Common causes of increased ICP include a mass lesion (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation). These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, increase the formation and spread of cerebral edema. This edema distorts brain tissue, further increasing the ICP, and leads to even more tissue hypoxia and acidosis.


Regardless of the cause, cerebral edema results in an increase in tissue volume that has the potential to increase ICP. The extent and severity of the original insult are factors that determine the degree of cerebral edema. Figure 9 illustrates the progression of increased ICP.



There are three types of cerebral edema, including vasogenic, cytotoxic, and interstitial. More than one type may occur in the same patient.



■ Vasogenic cerebral edema, the most common type of edema, occurs mainly in the white matter and is characterized by leakage of macromolecules from the capillaries into the surrounding extracellular space. This edema may produce a continuum of symptoms ranging from headache to disturbances in consciousness, including coma and focal neurologic deficits.


■ Cytotoxic cerebral edema results from disruption of the integrity of the cell membranes. This type of edema develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia and syndrome of inappropriate antidiuretic hormone (SIADH) secretion.


■ Interstitial cerebral edema is usually a result of hydrocephalus. It can be due to excess CSF production, obstruction of flow, or an inability to reabsorb the CSF.


Clinical manifestations


Manifestations of increased ICP can take many forms, depending on the cause, location, and rate of increase of ICP.



■ Change in level of consciousness (LOC). LOC is a sensitive and reliable indicator of the patient’s neurologic status. Changes in LOC may be dramatic, as in coma, or subtle, such as a change in orientation or a decrease in the level of attention.


■ Changes in vital signs. Manifestations such as Cushing’s triad (systolic hypertension with widening pulse pressure, bradycardia with a full and bounding pulse, and irregular respirations) may be present but often do not appear until ICP has been increased for some time or markedly increased (e.g., head trauma). The effect of increased ICP on the hypothalamus can cause a change in body temperature.


■ Ocular signs. Compression of the oculomotor nerve (CN III) results in dilation of the pupil on the same side (ipsilateral) as the mass lesion, sluggish or no response to light, an inability to move the eye upward, and ptosis of the eyelid. A fixed, unilaterally dilated pupil is a neurologic emergency that indicates brain herniation. Other cranial nerves may also be affected, with signs of blurred vision, diplopia, and changes in extraocular eye movements. Papilledema, a nonspecific sign associated with persistent increases in ICP, is also seen.


■ Decrease in motor function. As ICP continues to rise, the patient manifests changes in motor ability. A contralateral (opposite side of the mass lesion) hemiparesis or hemiplegia may develop. If a painful stimulus is used to elicit a motor response, the patient may localize to the stimulus or withdraw from it. Decorticate (flexor) and decerebrate (extensor) posturing may also be elicited by noxious stimuli (see Fig. 57-5, Lewis et al, Medical-Surgical Nursing, ed 9, p. 1360).


■ Headache. Although the brain itself is insensitive to pain, compression of other intracranial structures, such as the walls of arteries and veins and the cranial nerves, can produce headache. The headache is often continuous but is worse in the morning. Straining or movement may accentuate the pain.


■ Vomiting. Vomiting, usually not preceded by nausea, is often a nonspecific sign of increased ICP.


The major complications of uncontrolled increased ICP are inadequate cerebral perfusion and cerebral herniation.


Diagnostic studies



Collaborative care


The goals of management of increased ICP are to identify and treat the underlying cause of increased ICP and to support brain function. The earlier the condition is recognized and treated, the better the patient outcome. A careful history is an important diagnostic aid that can direct the search for the underlying cause.


Ensuring adequate oxygenation to support brain function is important. Arterial blood gas (ABG) analysis guides the oxygen therapy. To meet the goal of maintaining the partial pressure of oxygen in arterial blood (PaO2) at 100 mm Hg or greater and to keep PaCO2 in normal range at 35 to 45 mm Hg, an endotracheal tube or tracheostomy and mechanical ventilation may be necessary.



Drug therapy


Drug therapy plays an important part in the management of increased ICP.



■ IV mannitol (Osmitrol) (25%) is an osmotic diuretic that decreases ICP in two ways: plasma expansion and osmotic effect. The immediate plasma-expanding effect reduces the hematocrit and blood viscosity, thereby increasing cerebral blood flow and cerebral oxygenation. The osmotic effect causes fluid to move from the tissue into the blood vessels, resulting in a decrease in total brain fluid content.


■ Hypertonic saline is another drug treatment used to manage increased ICP. It produces massive movement of water out of edematous swollen brain cells and into the blood vessels.


■ Corticosteroids (e.g., dexamethasone [Decadron]) are used to treat vasogenic edema surrounding tumors and abscesses, but are not recommended for head-injured patients. Corticosteroids stabilize the cell membrane and inhibit the synthesis of prostaglandins. These drugs also improve cerebral blood flow and restore autoregulation.


■ Metabolic demands such as fever (above 38° C), agitation/shivering, pain, and seizures can also increase ICP. The health care team should plan to reduce these metabolic demands in order to lower the ICP in the at-risk patient.


■ High-dose barbiturates (e.g., pentobarbital [Nembutal] and thiopental [Pentothal]) are used in patients with an increased ICP refractory to other treatments. These drugs lower cerebral metabolism, which causes a decrease in ICP.


Nutritional therapy


The patient with increased ICP is in a hypermetabolic and hypercatabolic state that increases the need for glucose to provide the necessary fuel for metabolism of the injured brain. If the patient cannot maintain an adequate oral intake, other means of meeting the nutritional requirements, such as enteral or parenteral nutrition, should be started. Current fluid therapy is directed at keeping patients normovolemic.


Nursing management


Goals


The overall goals are that the patient with increased ICP will have ICP within normal limits, maintain a patent airway, demonstrate normal fluid and electrolyte balance, and have no complications secondary to immobility and decreased LOC.


Nursing diagnoses



Nursing interventions


Respiratory function.

Maintenance of a patent airway is critical in patients with increased ICP and is a primary nursing responsibility. As the LOC decreases, the patient is at increased risk of airway obstruction.



■ Be alert to altered breathing patterns. Snoring sounds indicate obstruction and require immediate intervention. An oral airway facilitates breathing and provides an easier suctioning route in the comatose patient.


■ In general, any patient with a Glasgow Coma Scale score of 8 or less (see Glasgow Coma scale, p. 766) or an altered LOC who is unable to maintain a patent airway or effective ventilation needs intubation and mechanical ventilation.


■ Prevent hypoxia and hypercapnia. Proper positioning of the head is important.


■ Elevation of the head of the bed by 30 degrees enhances respiratory exchange and aids in decreasing cerebral edema.


■ Suctioning and coughing can cause transient increases in ICP and decreases in PaO2. Suctioning should be kept to a minimum.


■ Try to prevent abdominal distention, as it can interfere with respiratory function. Insertion of a nasogastric tube to aspirate the stomach contents can prevent distention, vomiting, and possible aspiration. In patients with facial and skull fractures, a nasogastric tube is contraindicated, and oral insertion of a gastric tube is preferred.


■ ABGs should be measured and evaluated regularly. The appropriate ventilatory support can be ordered on the basis of the PaO2 and PaCO2 values.


Fluid and electrolyte balance.

Fluid and electrolyte disturbances can have an adverse effect on ICP. Closely monitor IV fluids. Intake and output, with insensible losses and daily weights taken into account, are important parameters in the assessment of fluid balance.



Monitoring intracranial pressure.

ICP monitoring is used in combination with other physiologic parameters to guide the care of the patient and assess the patient’s response to routine care. Valsalva maneuver, coughing, sneezing, hypoxemia, and arousal from sleep are factors that can increase ICP. Methods of monitoring ICP are discussed in detail in Chapter 57, Lewis et al, Medical-Surgical Nursing, ed 9. Also see Intracranial Pressure Monitoring, p. 770.


Body position.

Maintain the patient with increased ICP in the head-up position. Take care to prevent extreme neck flexion, which can cause venous obstruction and contribute to elevated ICP. Adjust the body position to decrease the ICP maximally and to improve cerebral perfusion pressure (CPP).



Protection from injury.

The patient with increased ICP and a decreased LOC needs protection from self-injury. Confusion, agitation, and the possibility of seizures increase the risk of injury. Use restraints judiciously in the agitated patient. The patient can benefit from a quiet, nonstimulating environment. Touch and talk to the patient, even one who is in a coma.


Psychologic considerations.

Anxiety over the diagnosis and prognosis for the patient with neurologic problems can be distressing to the patient, caregiver, family, and nursing staff. Short, simple explanations are appropriate and allow the patient and family to acquire the amount of information they desire. There is a need for support, information, and education of both patients and families.


Assess the family members’ desire and need to assist in providing care for the patient and allow for their participation as appropriate.



Inflammatory bowel disease


Description


Inflammatory bowel disease (IBD) is a chronic inflammation of the GI tract. It is characterized by periods of remission interspersed with periods of exacerbation. The cause is unknown, and there is no cure. IBD is classified as either Crohn’s disease or ulcerative colitis based on clinical manifestations (Table 53). Ulcerative colitis is usually limited to the colon. Crohn’s disease can involve any segment of the GI tract from the mouth to the anus.



Table 53


Comparison of Ulcerative Colitis and Crohn’s Disease







































































































Characteristic Ulcerative Colitis Crohn’s Disease
Clinical
Usual age at onset Teens to mid-30s* Teens to mid-30s*
Diarrhea Common Common
Abdominal cramping pain Common Common
Fever (intermittent) During acute attacks Common
Weight loss Rare Common, may be severe
Rectal bleeding Common Infrequent
Tenesmus Common Rare
Malabsorption and nutritional deficiencies Minimal incidence Common
Pathologic
Location Usually starts in rectum and spreads in a continuous pattern up the colon Occurs anywhere along GI tract in characteristic skip lesions; most frequent site is terminal ileum
Distribution Continuous areas of inflammation Healthy tissue interspersed with areas of inflammation (skip lesions)
Depth of involvement Mucosa and submucosa Entire thickness of bowel wall (transmural)
Granulomas (noted on biopsy) Occasional Common
Cobblestoning of mucosa Rare Common
Pseudopolyps Common Rare
Small bowel involvement Minimal Common
Complications
Fistulas Rare Common
Strictures Occasional Common
Anal abscesses Rare Common
Perforation Common (because of toxic megacolon) Common (because inflammation involves entire bowel wall)
Toxic megacolon Relatively more common Rare
Carcinoma Increased incidence of colorectal cancer after 10 yr of disease Increased incidence of small intestinal cancerIncreased incidence of colorectal cancer but not as much as with ulcerative colitis
Recurrence after surgery Cure with colectomy Common at site of anastomosis


Image


*Second peak in incidence after age 60.


Both ulcerative colitis and Crohn’s disease commonly occur during the teenage years and early adulthood, and both have a second peak in the sixth decade. IBD is more prevalent in industrialized countries and in the Ashkenazi Jewish population. Many people with IBD have a family member with the disorder.


Pathophysiology


IBD is an autoimmune disease involving an immune reaction to a person’s own intestinal tract. Some agent or a combination of agents triggers an overactive, inappropriate, sustained immune response. The resulting inflammation causes widespread tissue destruction.


Evidence suggests that IBD is caused by a combination of factors, including environmental factors, genetic predisposition, and alterations in the function of the immune system. The pattern of inflammation differs between Crohn’s disease and ulcerative colitis.


Crohn’s disease


The inflammation in Crohn’s disease involves all layers of the bowel wall and can occur anywhere in the GI tract from the mouth to the anus. It most commonly occurs in the terminal ileum and colon. Segments of normal bowel can occur between diseased portions, the so-called skip lesions.



Ulcerative colitis


Ulcerative colitis usually starts in the rectum and moves in a continual fashion toward the cecum. Although mild inflammation sometimes occurs in the terminal ileum, ulcerative colitis is a disease of the colon and rectum.



Clinical manifestations


Symptoms are often the same (diarrhea, bloody stools, weight loss, abdominal pain, fever, and fatigue) in both conditions. Bloody stools are more common with ulcerative colitis, and weight loss is more common in Crohn’s disease because inflammation of the small intestine impairs nutrient absorption. Both forms of IBD are chronic disorders with mild to severe acute exacerbations that occur at unpredictable intervals over many years.


Crohn’s disease


Diarrhea and colicky abdominal pain are common symptoms of Crohn’s disease.


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Oct 26, 2016 | Posted by in NURSING | Comments Off on I

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