INCREASED INTRACRANIAL PRESSURE

INCREASED INTRACRANIAL PRESSURE

1. INCREASED INTRACRANIAL PRESSURE Mr. Binu Babu M.Sc. Nursing Mrs. Jincy Ealias M.Sc. Nursing

2. Components inside skull Skull is rigid closed structure contains The brain and interstitial fluid - 78%; Intravascular blood-12% The CSF -10%

3. INTRACRANIAL PESSURE ICP is the total pressure exerted by the three components within the skull It is the hydrostatic force measured in the brain CSF compartment Monro-kellie hypothesis states that skull is a rigid structure if the volume of the any three components increases the volume from another component is displaced , the total intracranial volume will not change

4. Norma l compensatory mechanisms Alteration CSF volume – increased absorption decreased production displacement to subarachnoid space Alteration in blood volume vasoconstriction, vasodilation Tissue brain volume-distention of dural space

5. These compensatory mechanisms are to maintain a relatively constant amount of cerebral blood flow to meet the metabolic needs of the brain tissue. Cerebral blood flow is the amount of blood in millimeters passing through 100g of brain tissue in 1 minute Under normal conditions, the cerebral blood flow ranges between 50 and 60mL per 100g brain per minute. It makes approximately 700 to 850mL blood per minute for the whole brain and accounts for about 20% of the total cardiac output. The brain uses 20% of the body’s oxygen and 25% of the glucose

6. Increased ICP is a life threatening situation that results from an increase in any or all of three components within the skull (brain, CSF , blood ) Brain edema is the common cause for elevated intracranial pressure

7. Causes Aneurysm rupture and subarachnoid hemorrhage Brain tumor Encephalitis irritation and swelling, or inflammation, of the brain) Head injury Hydrocephalus (increased fluid around the brain) Hypertensive brain hemorrhage (bleeding in the brain from high blood pressure) Intraventricular hemorrhage (bleeding into the fluid-filled areas, or ventricles, inside the brain) Meningitis (infection of the membranes covering the brain and spinal cord) Subdural hematoma (bleeding between the covering of the brain and the surface of the brain) Epidural hematoma (bleeding between the inside of the skull and the outer covering of the brain) Seizure Stroke

8. Cerebral edema Vasogenic cerebral edema :- It is caused by changes in endothelial lining of cerebral capillaries These changes alllow leakage of macromolecules from the capillaries into surrounding extravascular space Brain tumours , abscesses and ingested toxins common causes Cytotoxic cerebral edema :- It results from local disruption of the functional or morphological integrity of cell membrane. It develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia. Mostly in grey matter of brain Interstitial cerebral edema :- It is the result of periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus

9. Mechanism of elevated ICP - 1

10. Mechanism of elevated ICP - 2

11. Clinical Manifestations Behavior changes Decreased alertness Headache - Compression of other intracranial structures continuous, worse in the morning Lethargy Nervous system symptoms, including weakness, numbness, eye movement problems, and double vision Seizures Vomiting - Projectile vomiting, due to the compression of CTZ

12. Change in vital signs Indicate increased pressure on the thalamus, hypothalamus, pons and medulla Manifested as Cushing's triad Elevated systolic BP Bradycardia Widening of pulse pressure Change in body temperature hypothalamus affected Ocular signs Compression of cranial nerve - pupillary dilation Fixed unilateral dilated pupil – herniation of the brain Optic- blurred vision, diplopia Trochlear, abducens – eye movements

13. Motor function Decrease in motor function Controlateral hemiparesis or hemiplegia Decortication - interruption of voluntary motor cortex Decerebration - disruption of motor fibers in the midbrain and brain stem. Opisthotonus position:- It is a state of severe hyperextension and spasticity in which an individual's head, neck and spinal column enter into a complete "bridging" or "arching" position.

14. Diagnostic studies History collection and physical examination Computed tomography Magnetic resonance imaging Electroencephalogram Positron emission tomography Measurement of ICP Lumbar puncture

15. Measurement of ICP ICP should be monitored in patients admitted with Glasgow coma scale (GCS) 8 or less and an abnormal CT or MRI Normal ICP 5-15 mm hg/10 to 20cm H2O Methods Epidural subdural Subarachnoid Intraparenchymal Ventricular

16. Measurement of ICP Gold standard – ventriculostomy A Specialized catheter is inserted into right lateral ventricle and coupled to an external transducer This technique directly measures pressure inside ventricles, facilitates removal or sampling of CSF for intraventricular drug administration. Direct visualization of the height of the CSF column generated outside the body or through its measurement by an external transducer

17. CSF drainage Using a closed system, elevations in ICP are controlled by removal of CSF by gravity drainage and by adjusting the height of drip chamber and drainage bag relative to ventricular reference point. Typically a point 15 cm above ear canal the drainage bag is placed Raising the height diminishes the drainage and vice versa Normal adult CSF production- 20-30ml/ hr Total CSF volume- 90-150ml

18. Complic a tions Tentorial herniation Mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brain stem Uncal herniation Lateral and downward herniation Cingulate herniation It occurs when there is lateral displacement of brain tissue beneath the falx cerebrai

19. Management Identifying and treating the underlying cause of increased ICP Maintaining adequate perfusion and oxygenation to the brain

20. Osmotic Diuretics Mannitol MOA : reduces the water content of the brain due to the establishment of an osmotic gradient between the brain and the intravascular compartment. Mannitol is a large molecule and will not cross the BBB. Dosage : 50 – 200 Gm (1 Gm/kg) IV over 24 hours, titrated to maintain urine output at 30 – 50cc/hr. Contraindications : Patients with anuria related to renal disease, pulmonary edema , severe dehydration, or active intracranial bleeding. Usually used with Lasix 0.5mg/kg . Nursing Implications: Assure foley patency Preassessment of patients cardiovascular status Monitor electrolytes frequently : serum and urine osmolarity , serum and urine electrolytes Always use a filtered needle due to crystallization of the drug An administration set with a 0.22 micron filter must be used Available iv as 20% solution (100 gm in 500 ml of d5w) Must be kept warm or will precipitate Adverse effects: chf , pulmonary edema , kidney failure

21. Glycerol MOA: reduces CSF production along with osmotic effects Dose: 0.5 to 1.0 gm/kg Q 4-6 hours; do not exceed 0.2-1.0 gm/kg/hours give IV as a 10-20% solution in 0.45% or 0.9% saline over several hours (3-5 hours) Side Effects: rate-related; reduced with slow infusion Nursing Implications: Slow acting can be used long-term Metabolized by the body producing energy Mix with iced lemon or juice Monitor electrolytes due to diuresis Loop Diuretics - Furosemide, Ethacrynic Acid MOA: inhibit sodium and chloride reabsorption in the loop of Henle resulting in contraction of the blood volume which may mobilize cerebral edema usually administered with mannitol to increase the therapeutic effect Dose: 0.5 to 1.0 mg/kg prn Side Effects: hypokalemia, dehydration, hypotension, glucose intolerance

22. Corticosteriods (dexamethasone, dexona ) It will help to improve the neuronal function Inhibit the synthesis of prostaglandins thereby preventing formation of inflammatory mediators MOA: exact mechanism unknown; may decrease CSF production and stablize brain cell membranes Dose: dexamethasone most commonly used; 10 mg IV/IM followed by 4 mg IV/IM Q 6 hrs Side Effects: hyperglycemia , GI bleeding, increased infection risk

23. Barbiturates ( Thiopental, pentobarbital ) It will decrease in cerebral metaabolism and subsequent decrease in ICP Antiepileptics ( phenytoin) As seizure prophylaxis H 2 receptor antagonists or proton pump inhibitors Prevent gastric ulcers and bleeding

24. Specific Treatment Surgical removal of intracranial masses. Placement of extraventricular drain (temporary). Placement of VP shunt (usually permanent).

25. Hyperventilation therapy In the past aggressive hyperventilation was one of the important treatment modality It will decrease the C0 2 level in the blood PaCO 2 less than 25 mm Hg Brief periods of less aggressive hyperventilation therapy is useful PaCO 2 30-35 mm Hg

26. Reducing CSF and intracranial blood volume CSF drainage is frequently performed because the removal of CSF with a ventriculostomy drain may dramatically reduce ICP and restore cerebral perfusion pressure.

27. Nutritiona l therapy All patients must have their nutritional needs met regardless of their state of consciousness or health Adequate fluid volume should be maintained

28. Positi o ning Head position: Maintain head in midline position at above 30 degrees to improve cerebral venous drainage; lower cerebral blood volume (CBV) will lower ICP.

29. Surgical decompression Surgical decompression is indicated for clear-cut mass lesions amenable to removal, i.e. tumor, epidural bleed, large contusion. For refractory elevated ICP without a surgical lesion, there may be a role for a decompressive craniectomy . Especially if done early after the initial insult, it may improve functional outcomes of patients.

30. Nursing Management Assessment neurological assessment Glasgow coma scale min score- 3 max score- 15 GCS below 8 - indicative of coma. Maintain cerebral perfusion pressure. Prevent focal or global cerebral ischemia and focal brain compression Maintain the patients head midline to facilitate blood flow. Maintain the head of the bed at 30 - 45 degrees to facilitate venous drainage. Avoid activities that can increase ICP such as suctioning or gagging. Treat hyperthermia as it increases the metabolic needs of the brain. Decrease environmental stimuli which can increase ICP.

31. Dim all lights Speak softly Touch gently and only when needed Space all interventions Limit noxious stimuli such as suctioning to only as needed Maintain fluid balance via accurate I & O. Over hydration will lead to cerebral edema . Monitor electrolytes as these patients are prone to hypernatremia, hypoglycemia , and hypokalemia with diuretic usage. Monitor hyperventilation to maintain CO2 levels at 25 - 35mm Hg to prevent vasodilation.

32. Nursing Diagnosis Ineffective tissue perfusion (cerebral) related to reduction of arterial blood flow and cerebral edema . Interventions Maintain hemodynamic parameters within normal range Calculate and monitor CPP Monitor neurologic status Maintain input and output chart Administer medication Administer oxygen

33. Decreased intracranial adaptive capacity related to decreased cerebral perfusion. Interventions Monitor vital signs, ICP and neurologic status Position the head end of the bed Maintain normothermia Give sedatives Administer osmotic diuretics Decrease stimuli in patients environment

34. THANK YOU