NURSING MANAGEMENT
OF PATIENT WITH
INCREASED ICP
INTRACRANIAL PRESSURE
• IT IS THE PRESSURE EXERTED BY THE CONTENTS INSIDE
THE CRANIAL VAULT-THE BRAIN TISSUE, CSF AND BLOOD
VOLUME
• A PRESSURE READING GREATER THAN 20 mm Hg is
defined as increased ICP
PATHOPHYSIOLOGY AND ETIOLOGY
• COMPONENTS –VOLUME RATIO-BRAIN TISSUE (80%),
CSF (10%) AND BLOOD VOLUME (10%)
• MONROE KELLIE DOCTRINE-
• Intracranial vault is a closed structure with a
fixed intracranial volume. The ratio between
pressure and volume remains constant. Any
increase in the volume of one component must be
accompanied by a reciprocal decrease in one of
the other components. When this volume
pressure relationship becomes unbalanced, ICP
rises.
MONROE KELLIE DOCTRINE-
PATHOPHYSIOLOGY AND ETIOLOGY
• BRAIN COMPENSATE BY
• i) displacing or shunting of CSF from the
intracranial compartment to lumbar sub
arachnoid space
• Normal CSF production-500 ml produced and
absorbed in 24 hrs.
• 125-150 ml circulates throughout ventricular
system and SAS in fol ratio-25 ml in ventricles 90
ml in lumbar subarachnoid space and 35 ml
surrounding subarachnoid space.
PATHOPHYSIOLOGY AND ETIOLOGY
• BRAIN COMPENSATE BY
• ii)increased CSF absorption.
• iii) decreased cerebral blood volume by displacement
of cerebral venous blood in to venous sinuses.
• iv)INCRESED ICP OCCUR-VOLUME OF INTRACRANIAL
MASS EXCEEDS VOLUME COMPENSATED.
• COMPENSATORY MECHANISMS EXHAUSTED-slight
increase in vol produce moderate increase in pre,
PATHOPHYSIOLOGY AND ETIOLOGY
• BRAIN COMPENSATE BY
• V)steady state achieved by
Systemic BP
VENTILLATION AND OXYGENATION
METABOLIC RATE AND OXYGEN CONSUMPTION
REGIONAL CEREBRAL VASOSPASM
OXYGEN SATURATION AND HEMATOCRIT
PATHOPHYSIOLOGY AND ETIOLOGY
• BRAIN COMPENSATE BY
• Vi) inability to achieve steady state results in increased ICP
• ETIOLOGIES
• TBI
• CEREBRAL EDEMA
• INTRACEREBRAL HEMORRHAGE
• ISCHEMIA
• STROKE
• ABSCESS
• INFECTIONS
• LESIONS
• INTRACRANIAL SURGERY
PATHOPHYSIOLOGY AND ETIOLOGY
• BRAIN COMPENSATE BY
• Vii) emergency require prompt rx
ICP MONITORING-INTRAVENOUS CATHETER
ALTERATIONS OR COMPROMISE IN CEREBRAL BLOOD
FLOW-TCD STUDY
INCREASED VELOCITIES –VASOSPASM
DECREASED VELOCITY-LOW BLOOD FLOW
ABSENT VELOCITIES-NOFLOW OR BRAIN DEATH
NURSING ASSESSMENT
1.CHANGE IN LOC-
• Awareness-drowsiness, lethargy
• Early behavioral changes-restlessness irritability, confusion and
apathy.
• Falling score on GCS
• Change in orientation
• Difficulty/inability to follow commands
• Difficulty/inability in verbalization or in responsiveness to auditory
stimuli.
• Change in response to painful stimuli
• Posturing (abnormal flexion or extension)
NURSING ASSESSMENT
2.CHANGE IN VITAL SIGNS
• Caused by pressure on brainstem
i)Rising BP or widening pulse pressure (dif b/w systolic and
diastolic BP)
• FOLLOWED BY HYPOTENSION and labile vital signs
indicating further brainstem compromise
• CUSHINGS TRIAD-NEUROLOGIC MEDICAL EMERGENCY
• UNCOMPENSATED INCREASED ICP
• TRIAD-BRADYCARDIA, HYPERTENSION,WIDENING
PULSE PRESSURE
NURSING ASSESSMENT
2.CHANGE IN VITAL SIGNS
• CUSHINGS TRIAD-
• NEUROLOGIC MEDICAL EMERGENCY
• UNCOMPENSATED INCREASED ICP
• TRIAD-BRADYCARDIA, HYPERTENSION,
• WIDENING PULSE PRESSURE
NURSING ASSESSMENT
2.CHANGE IN VITAL SIGNS
ii)Pulse change frm bradycardia to tachycardia as ICP
rises
iii) Respiratory irregularities- tachypnea(early sign),
slowing of rate with lengthening periods of apnea
(CHEYENE –STOKES (rhythmic pattern of increasing and
decreasing depth of respiration with periods of apnea or
KUSSMAUL –paroxysms of difficult breathing
Central neurogenic hyperventilation -prolonged deep
breathing
Ataxic breathing-in coordinated and spasmodic
