Increased intracranial pressure

Increased intracranial pressure

1. INCREASED INTRACRANIAL PRESSURE PRESENTED BY: MISS.SHWETA SHARMA M.SC. NURSING 2 ND YEAR ROLL NO. 5 AIIMS, JODHPUR

2. INTRODUCTION The central nervous system contents, including brain, spinal cord, blood, and cerebrospinal fluid (CSF), are encased in a noncompliant skull and vertebral canal, constituting a nearly incompressible system. In a normal adult, the skull encloses a total volume of 1450 mL: 1300 mL of brain, 65 mL of CSF, and 110 mL of blood. ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm Hg.

3. MONROE-KELLIE HYPOTHESIS

4. The Monroe- kellie hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others.

5. Cerebral Perfusion Pressure CPP = MAP - ICP (Normal = 70 - 100 mm Hg) MAP = 1/3 Systolic + 2/3 Diastolic BP CEREBRAL BLOOD FLOW (CBF) Flow = Pressure/Resistance Cerebral Blood Flow = Cerebral Perfusion Pressure (systemic pressure – intracranial pressure)/Cerebral Vascular Resistance

6. Because brain tissue has limited space to change, compensation typically is accomplished by displacing or shifting CSF, increasing the absorption of CSF, or decreasing cerebral blood volume. Without such changes, ICP will begin to rise. Under normal circumstances, minor changes in blood volume and CSF volume occur constantly due to alterations in intrathoracic pressure (coughing, sneezing, straining), posture, blood pressure, and systemic oxygen and carbon dioxide levels.

7. Increased ICP is defined as a sustained elevation in pressure above 20mm of Hg.

8. EPIDEMIOLOGY 90% of affected individuals are women of childbearing age. Individuals with chronic hypertension or obesity are also at an increased risk for developing intracranial hypertension. A frequency of occurrence has been established to be 1.0 per 100,000 in the general population, 1.6 to 3.5 per 100,000 in women, and 7.9 to 20 per 100,000 in women who are overweight.

9. INTERRELATIONSHIPS

10. ETIOLOGY Primary or Intracranial Causes Trauma (epidural hematoma, subdural hematoma, intracerebral haemorrhage or contusions) Brain tumours Stroke Nontraumatic intracerebral Haemorrhage (aneurysm rupture) Idiopathic or benign intracranial hypertension Hydrocephalus Meningitis

11. Secondary or Extracranial Causes Hypoventilation (hypoxia or hypercarbia) Hypertension Airway obstruction Metabolic (drug-induced) Seizures Hyperpyrexia High altitude cerebral oedema

12. 1. Decreased cerebral blood flow Increased ICP may significantly reduce cerebral blood flow, resulting in ischemia and cell death. A rise in PaCO2 causes cerebral vasodilatation, leading to increased cerebral blood flow and increased ICP; a fall in PaCO2 has a vasoconstrictive effect. Decreased venous outflow may also increase cerebral blood volume, thus raising ICP.

13. 2. Cerebral edema Cerebral edema or swelling is defined as an abnormal accumulation of water or fluid in the intracellular space, extracellular space, or both, associated with an increase in brain tissue volume. As brain tissue swells within the rigid skull, several mechanisms attempt to compensate for the increasing ICP. These mechanisms include autoregulation and decreasing the production and flow of CSF.

14. 3. Cerebral response to increased ICP As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage. The brain can maintain a steady perfusion pressure when the arterial systolic blood pressure is 50 to 150 mm Hg and ICP is less than 40 mm Hg. At a certain volume or pressure, the brain’s ability to autoregulate becomes ineffective and decompensation (ischemia and infarction) begins. When this occurs, the patient exhibits significant changes in mental status and vital signs.

15. The bradycardia, hypertension, and bradypnea associated with this deterioration are known as Cushing’s triad, a grave sign. At this point, herniation of the brain stem and occlusion of the cerebral blood flow occur if therapeutic intervention is not initiated. Cessation of cerebral blood flow results in cerebral ischemia, infarction and brain death.

16. BRAIN SHIFT – TYPES Unchecked lateral tentorial herniation leads to central tentorial and tonsillar herniation, associated with progressive brain stem dysfunction from midbrain to medulla.

17. Headache – worse in the morning, aggravated by stooping and bending. Vomiting – occurs with an acute rise in ICP. Papilledema – occurs in a proportion of patients with ↑ΙCP. It is related to CSF obstruction and does not necessarily occur with brain shift alone. Restlessness (without apparent cause), confusion, or increasing drowsiness Stuporous , reacting only to loud auditory or painful stimuli

18. When the coma is profound, with the pupils dilated and fixed and respirations impaired, death is usually inevitable. The earliest sign of increasing ICP is a change in LOC. Slowing of speech and delay in response to verbal suggestions are other early indicators.

19. ICP monitoring

20. Lumbar puncture is avoided in patients with increased ICP because the sudden release of pressure can cause the brain to herniate.

21. COMPLICATIONS Brain stem herniation Diabetes insipidus Syndrome of inappropriate antidiuretic hormone (SIADH) Seizures Stroke Death

22. MEDICAL MANAGEMENT Invasive monitoring of ICP Immediate management to relieve increased ICP - decreasing cerebral edema, lowering the volume of CSF, or decreasing cerebral blood volume while maintaining cerebral perfusion. Administering osmotic diuretics and corticosteroids Restricting fluids and draining CSF Controlling fever Maintaining systemic blood pressure and oxygenation Reducing cellular metabolic demands

23. Monitoring ICP The purposes of ICP monitoring are: to identify increased pressure early in its course (before cerebral damage occurs) to quantify the degree of elevation to initiate appropriate treatment to provide access to CSF for sampling and drainage to evaluate the effectiveness of treatment

24. An intraventricular catheter (ventriculostomy), a subarachnoid bolt, an epidural or subdural catheter, or a fiberoptic transducer-tipped catheter placed in the subdural space or the ventricle can be used to monitor ICP.

25. Complications of ICP monitoring: Infection Intracranial hemorrhage or haematoma CSF Leakage Mechanical failure or blockage Over drainage of CSF

26. METHODS OF REDUCING INTRACRANIAL PRESSURE Mannitol infusion: An IV bolus of 100 ml of 20% mannitol infused over 15 minutes reduces intracranial pressure by establishing an osmotic gradient between the plasma and brain tissue. This method ‘buys’ time prior to craniotomy in a patient deteriorating from a mass lesion. Mannitol is also used 6-hourly for a 24–48-hour period in an attempt to reduce raised ICP.

27. CSF withdrawal: Removal of a few ml of CSF from the ventricle immediately reduces the intracranial pressure. Within minutes, however, the pressure will rise and further CSF withdrawal will be required. In practice, this method is of limited value, since CSF outflow to the lumbar theca results in a diminished intracranial CSF volume and the lateral ventricles are often collapsed. Continuous CSF drainage may make most advantage of this method.

28. Sedatives: If intracranial pressure fails to respond to standard measures then sedation may help under carefully controlled conditions. - Propofol, a short acting anaesthetic agent, reduces intracranial pressure but causes systemic vasodilatation. If this occurs pressor agents may be required to prevent a fall in blood pressure and a reduction in cerebral perfusion. - Barbiturates (thiopentone) reduce neuronal activity and depress cerebral metabolism; a fall in energy requirements theoretically protects ischemic areas.

29. Controlled hyperventilation: Bringing the PCo2 down by hyperventilating the sedated or paralyzed patient causes vasoconstriction. Although this reduces intracranial pressure, the resultant reduction in cerebral blood flow may aggravate ischemic brain damage and do more harm than good. Maintaining the blood pressure and the cerebral perfusion pressure (CPP) (>60 mmHg) appears to be as important as lowering intracranial pressure.

30. Hypothermia: Cooling to 34°C lowers ICP. Hypothermia after cardiac arrest with slow rewarming has been reported to improve outcome. Steroids: By stabilising cell membranes, steroids play an important role in treating patients with oedema surrounding intracranial tumours. Dexamethasone is given 4-6 mg every 6 hours.

31. SURGICAL MANAGEMENT

32. Decompressive craniectomy is performed on victims of traumatic brain injury, stroke, Chiari Malformation, and other conditions associated with raised intracranial pressure. Resection of intracranial mass lesions producing elevated ICP.

33. Nursing assessment History collection - it may be necessary to obtain this information from family or friends. Neurologic examination - evaluation of mental status, LOC, cranial nerve function, cerebellar function (balance and coordination), reflexes, and motor and sensory function. Because the patient is critically ill, ongoing assessment will be more focused, including pupil checks, assessment of selected cranial nerves, frequent measurements of vital signs and intracranial pressure, and use of the Glasgow Coma Scale.

34. Nursing diagnosis Ineffective airway clearance related to diminished protective reflexes (cough, gag) as evidenced by presence of secretions. Goal- Patient will maintain a patent airway. Interventions- Assess the airway for patency. Secretions obstructing the airway must be suctioned with care, because transient elevations of ICP occur with suctioning. Coughing is discouraged because coughing and straining also increase ICP. The lung fields are auscultated at least every 8 hours to determine the presence of adventitious sounds or any areas of congestion. Elevating the head of the bed may aid in clearing secretions as well as improving venous drainage of the brain.

35. Ineffective breathing pattern related to neurologic dysfunction (brain stem compression, structural displacement) as evidenced by altered respiratory rate. Goal- Patient will have normalization of respiration. Interventions- Assess the respiratory pattern and monitor constantly for respiratory irregularities. Monitor arterial blood gas values. Place patient with proper body alignment for maximum breathing pattern. Suction secretions, as necessary. Provide oxygen as prescribed.

36. Ineffective cerebral tissue perfusion related to the effects of increased ICP as evidenced by reduced saturation. Goal- Patient will maintain adequate cerebral tissue perfusion through reduction in ICP. Interventions- Assess and monitor the intracranial pressure. The head is kept in a neutral (midline) position, maintained with the use of a cervical collar if necessary, to promote venous drainage. Elevation of the head is maintained at 0 to 30 o to aid in venous drainage unless otherwise prescribed. Extreme rotation of the neck and flexion of the neck are avoided because compression or distortion of the jugular veins increases ICP. Extreme hip flexion is also avoided because this position causes an increase in intra-abdominal and intrathoracic pressures, which can produce a rise in ICP. The Valsalva maneuver, which can be produced by straining at defecation or even moving in bed, raises ICP and is to be avoided.

37. Deficient fluid volume related to fluid restriction as evidenced by dry skin and poor turgor. Goal- Patient will have restoration of fluid balance. Interventions- Assess the fluid volume by measuring intake and output. Monitor skin turgor, mucous membranes, and serum and urine osmolality to assess fluid status. If fluids are given intravenously, ensure that they are administered at a slow to moderate rate with an intravenous infusion pump to prevent too-rapid administration and avoid overhydration. Monitor vital signs, including blood pressure to assess fluid volume status. An indwelling urinary catheter is inserted to permit assessment of renal function and fluid status. Monitor urine output every hour in acute phase, provide oral hygiene and apply emollient to keep skin moist.

38. Risk for infection related to ICP monitoring system ( fibreoptic or intraventricular catheter). Goal- Patient will be free from risk of infections. Interventions- Assess the risk factors of infection. The dressing over the ventricular catheter must be kept dry because a wet dressing is conducive to bacterial growth. Aseptic technique must be used when managing the system and changing the ventricular drainage bag. The drainage system is also checked for loose connections because they cause leakage and contamination of the CSF as well as inaccurate readings of ICP. Observe the character of the CSF drainage and report observations of increasing cloudiness or blood. Monitor the patient for signs and symptoms of meningitis: fever, chills, nuchal (neck) rigidity, and increasing or persisting headache.

39. PROGNOSIS Sudden increased intracranial pressure is a serious and often life-threatening condition. Prompt treatment results in better prognosis. If the increased pressure pushes on important brain structures and blood vessels, it can lead to serious, permanent problems or even death.

40. PREVENTION Increase in ICP cannot be prevented, but head injury can be prevented. Always wear a helmet when driving a bike or playing contact sports. Wear seatbelt when driving and keep seat back as far as possible from the dashboard or the seat in front. Always buckle children into a child safety seat. Falling at home is a common cause of head injury, especially in older adults. Avoid falls at home by keeping floors dry and uncluttered. If necessary, install handrails.

41. Hypertonic saline and mannitol in patients with traumatic brain injury A systematic review and meta-analysis were done by Shi, Jiamin ; Tan, Linhua ; Ye, Jing; Hu, Lei in 2020 to compare the effects of 3% hypertonic saline solution and 20% mannitol solution on intracranial hypertension. Relevant literatures of randomized controlled trials comparing 3% hypertonic saline solution with mannitol in reducing intracranial hypertension from 2010 to October 2019 were collected. As a result, 10 articles that met the inclusion criteria were finally included. A total of 544 patients were enrolled in the study, 270 in the hypertonic saline group and 274 in the mannitol group. There was no significant difference in the decrease of intracranial pressure and the onset time of drug between the 2 groups after intervention. There was a statistically significant difference between the hypertonic saline group and the mannitol group in terms of duration of effect in reducing intracranial pressure and cerebral perfusion pressure after intervention. The study concluded that both 3% hypertonic saline and mannitol can effectively reduce intracranial pressure, but 3% hypertonic saline has a more sustained effect on intracranial pressure and can effectively increase cerebral perfusion pressure.

42. Bedside ultrasonographic assessment of optic nerve sheath diameter as a means of detecting raised intracranial pressure in neuro-trauma patients: A cross-sectional study A cross-sectional study was conducted by Amandeep Kaur, Parshotam L Gautam, Shruti Sharma, Vikram P Singh, Sarit Sharma in 2020 to determine whether the bedside sonographic measurement of Optic nerve sheath diameter (ONSD) can reliably predict elevated ICP in neuro-trauma patients. It is helpful in situations where imaging of brain or direct ICP monitoring is not available or feasible. All patients underwent ONSD sonography of the eye and CT scan subsequently. ONSD of ≥5.0 mm was considered as a benchmark of raised ICP. Mean ONSD of the study group with ONSD ≥5.0 mm was 5.6 ± 0.3 mm. ONSD was raised in 46% of patients, more so in patients with low GCS (3-6). The relationship of ONSD with GCS, CT scan findings, and RTS was highly significant. The sensitivity of the bedside sonographic measurement ONSD to detect raised ICP was 93.2% and specificity was 91.1% when compared with CT scan. Positive Predictive Value of the ONSD measurement was 89.1% and the negative predictive value was 94.4%. The study concluded that ultrasonographic assessment of ONSD is a reliable modality to detect raised ICP in neurotrauma patients. It can be helpful in the early initiation of treatment of elevated ICP, thus preventing secondary brain damage.

43. SUMMARY AND CONCLUSION As discussed throughout the presentation, learning about increased intracranial pressure and its management will help nurses to care for a patient with increased ICP. Nurses can do assessment of such patient, observe the sign and symptoms, provide the necessary nursing care and support the patient psychologically. Nurses can also counsel the patients and their family.