ACUTE AND INTERMEDIATE PHASE NURSING IN TBI: NEUROLOGICAL AND OTHER ROUTINE NURSING INTERVENTIONS: INCREASED ICP (INTRACRANIAL HYPERTENSION)

  1. Management - Click on TBI Medicine Intensive Care Unit for additional information on medical interventions
    • Follow unit protocol for CSF draining - ICP at either 20 mm Hg or 15 mm Hg for a specific time duration, e.g. 5 minutes - and monitor the color of the drainage, for severe head injured patients with a ventriculostomy

    • Collaborate on the maintenance of physiological parameters:
      • PaO2 at 90-100 mm Hg
      • PaCO2 at 27-30 mm Hg
      • SaO2 at 92-100
      • MAP at 90-100 mm Hg to support CPP > 70 mm Hg
      • Systolic at 140-160 mm Hg
      • CPP at > 70 mm Hg
      • ICP at <20 m Hg
      • CO at 4-6 L/min
      • CI at > 3.0 L/min
      • CVP at 8-10 mm Hg
      • PWCP at 14-16
      • Serum Osm. At <320
      • Hct at <320
      • Normal glucose and electrolytes
      • Hgb at >10 g
      • Normothermia
      • Urine-specific gravity
      • Adequate urinary output
      • Controlled intake and output balance for euvolemia
      • Arterial blood gases

  2. Signs and Symptoms depend on the cause, location of the lesion, and the degree of intracranial compensation and include:
    • Deterioration in the level of consciousness
      • Early signs are confusion, restlessness, lethargy, and disorientation first to time, then to place, and then to person
      • Later signs are stupor and coma

    • Pupillary dysfunction relative to size, shape, and reaction to light:
      • Early signs are a gradual dilation, a slightly ovoid shape, and a sluggish response to light ipsilateral to the lesion
      • Later signs are dilation of the ipsilateral pupil and a non-reactivity to light
      • Final stage signs are bilateral dilation and fixation

    • Motor weakness and sensory deficits
      • Early signs are monoparesis, hemiparesis, and decreased visual acuity, such as blurred vision, diplopia, and field cuts
      • Later signs are hemiplegia, decortication, or decerebration (either unilateral or bilateral) and triple flexion away from the source of stimuli

    • Cranial nerve palsies

    • Headache - Early signs are slight or vague headache which is the worst upon arising in the morning

    • Possible seizures, possible vomiting (including projective vomiting), and possible papilledema

    • Changes in vital signs
      • Blood pressure:
        • Relatively stable in early stages
        • Increased blood pressure and a widening pulse in later stages which signal cerebral dysfunction that may be irreversible
          • Cushing's response (a compensatory response that attempts to provide adequate CPP in the presence of rising ICP) presents as a rising systolic pressure, a widening pulse pressure, and bradycardia and is a late presentation of brain stem dysfunction
          • Cushing's triad (a very late presentation of brain stem dysfunction) presents as hypertension, usually with a widening pulse pressure, bradycardia, and abnormal respiratory patterns
      • Pulse:
        • Relatively stable in early stages
        • Drop in pulse with continued rise of ICP
        • Irregular, rapid, and thready in the decompensatory stage
      • Respirations - acute neurogenic pulmonary edema, adult respiratory distress syndrome, and disseminated intravascular coagulopathy can result from an acute increase in ICP
      • Temperature
        • Within normal ranges during compensatory stage
        • High temperatures can occur during decompensatory stage

    • Impaired brain stem reflexes, such as corneal and gag reflexes

  3. Causes
    • Conditions that increase brain volume, such as space-occupying lesions and cerebral edema

    • Conditions which increase cerebral vasodilation, such as:
      • hypoxemia, or decreased O2 in the blood, which increases cerebral vasodilation when it is < 50 mm Hg; hypoxemia can be due to insufficient oxygen therapy and insufficient ventilation after suctioning
      • vasodilating drugs, including some anesthetics, antihypertensives, and histamines

    • Conditions that increase blood volume, such as:
      • hypercapnia, or excessive levels of CO2 in the blood (>= 45 mm Hg), which increases CBF, which in turn increases CBV and ICP. Can be due to underventilation of the patient during sleep, pulmonary disease, drug sedation, shallow respirations, pressure on brain stem, and improperly calibrated respirators
      • obstruction of venous outflow
      • hyperemia

    • Conditions that increase CSF by:
      • increasing CSF production abnormally
      • decreasing CSF absorption (communicating hydrocephalus, subarachnoid hemorrhage)
      • obstructing the flow of CSF (communicating hydrocephalus)

    • Conditions that increase blood pressure and CVP and decrease venous drainage from the brain, such as:
      • respiratory procedures, including PEEP, asynchronous use of Ambu bags, and intubation
      • some body positions, pressure on neck, isometric muscle contractions, Valsalva's maneuver, and increased tone
      • emotional upset and noxious stimuli which increase blood pressure and CBF
      • coughing, pain, and fecal impaction

    • Conditions which increase cerebral metabolism, such as seizures, hyperthermia and clustering of activities

Based on information in Hickey JV. The Clinical Practice of Neurological and Neurosurgical Nursing, 4th ed., Philadelphia: Lippincott, 1997 and in Chin PA, et al. Rehabilitation Nursing Practice, N.Y.: McGraw-Hill, 1998, except for information where other papers are cited.