NEUROLOGICAL CONDITIONS FOR CRITICAL CARE AND TRAUMA.pptx

critical care nurse specialities

1. NEUROLOGICAL CONDITIONS Dr. Lakshmi Rajeswaran , RN, PhD. Nurse educator/ Training specialist Rory Meyers College of Nursing New York university, USA. College of Nursing and Midwifery University of Rwanda . 09.03.2021 2/20/2021 Dr. Lakshmi Rajeswaran 1

2. NEUROLOGICAL CONDITIONS Learning outcomes: At the end of this session, the learner will be able to: Recap of anatomy & physiology of central nervous system Define different neurological conditions Explain cerebral edema ,different types, s igns and symptoms, and investigations. Apply critical care principles in managing cerebral e dema. Explain hydrocephalus, Subarachnoid hemorrhage, space occupying lesions, cerebral aneurysms, signs and symptoms, investigations and management in critical care units. Explain the role of collaborative, multidisciplinary care relevant to these conditions in critical care units. 2/20/2021 Dr. Lakshmi Rajeswaran 2

3. BRAIN 2/20/2021 Dr. Lakshmi Rajeswaran 3

4. TERMINOLOGIES RELATED TO NERVOUS SYSTEM Aneurysm Berry aneurysm Blood Brain Barrier (BBB) Cerebrospinal fluid ( CSF) Cerebral Perfusion Pressure (CPP) Craniotomy Delayed cerebral Ischemia (DCI) Diplopia Early Brain Injury (EBI) Electro Encephalography (EEG) External Ventricular Drain (EVD) Glasgow Coma Scale (GCS) Hydrocephalus Herniation Intra Cranial Pressure (ICP) Neuroma Papilledema Saccular aneurysm Schwannoma Seizure Space Occupying Lesion (SOL) Stroke Subarachnoid hemorrhage (SAH) Traumatic Brain Injury (TBI) Vasospasm 2/20/2021 Dr. Lakshmi Rajeswaran 4

5. CONDITIONS FOR DISCUSSION Cerebral edema Hydrocephalus Intra cranial hypertension Sub arachnoid hemorrhage Cerebral Aneyrysm Cerebral vaso spasm Space occupying lesion 2/20/2021 Dr. Lakshmi Rajeswaran 5

6. CEREBRAL OEDEMA Cerebral oedema is not a disease. Pathological state due to increased water content Occurs in response to brain insult both in neurological & non neurological conditions Causes increased intra cranial pressure (ICP) Increased ICP decreases cerebral perfusion, ischemia Mass effect causes herniation. 2/20/2021 Dr. Lakshmi Rajeswaran 6

7. FLUID COMPARTMENTS (BRAIN FLUID COMPARTMENTS LOCATION QUANTITY FUNCTION Brain – blood Inside the cerebral vessels Approximately 70 ml These compartments are inter linked and control the fluid & solutes from one compartment to other. Cerebro spinal fluid Ventricular system Approximately 150 ml Interstitial fluid Brain parenchyma > 250 ml Intra cellular fluid Neurons & Glial cells Amount not known 2/20/2021 Dr. Lakshmi Rajeswaran 7

8. CLASSIFICATION Vasogenic oedema Cytotoxic /ionic/cellular oedema Hydrostatic oedema Osmotic/hypostatic oedema Interstitial /hydrocephalus oedema 2/20/2021 Dr. Lakshmi Rajeswaran 8

9. VASOGENIC EDEMA Vasogenic edema ( common form of cerebral edema) Caused by brain trauma, acute malignant hypertension, radiation, tumors, inflammation & infection Involvement of the blood brain barrier (BBB) causing accumulation of protein rich fluid in the extra cellular space. Vasogenic edema produces Localized swelling around contusions or hematoma 2/20/2021 Dr. Lakshmi Rajeswaran 9

10. CYTOTOXIC OEDEMA BBB is intact. Beyond 6 minutes of ischemia causes irreversible damage to the brain cells. Occurs when there is hypoxic ischemia damage when there is an ionic gradient disturbance leading to accumulation of Intracellular fluid. 2/20/2021 Dr. Lakshmi Rajeswaran 10

11. INTERSTITIAL OEDEMA Interstitial oedema caused by extravasation of fluid as a result of high pressure obstructive hydrocephalus. Also known as hydrocephalus oedema Common causes: Meningitis Subarachnoid hemorrhage Congenital hydrocephalus 2/20/2021 Dr. Lakshmi Rajeswaran 11

12. OSMOTIC BRAIN OEDEMA Caused by critical reduction in serum osmolality resulting in increased intra cellular water. Conditions which either decrease serum osmolality or increase brain tissue will produce abnormal osmotic pressure gradient. Caused by iatrogenic dextrose/ water E.g. Syndrome of in appropriate antidiuretic hormone (SIADH) causes brain oedema. Traumatic Brain Injury (TBI). 2/20/2021 Dr. Lakshmi Rajeswaran 12

13. HYDROSTATIC OEDEMA Results from sudden increase in intra vascular in an intact vascular bed causing extra cellular accumulation of protein poor fluid. Hydro static may follow the sudden decompression of a mass lesion. E.g Head injury 2/20/2021 Dr. Lakshmi Rajeswaran 13

14. BLOOD BRAIN BARRIER Blood – brain barrier (BBB) is a term used to describe the unique properties of the microvasculature of the CNS. CNS vessels have additional properties that tightly regulate the movement of molecules, ions, cells between the blood and CNS. BBB regulates the neuronal function as well as protect the CNS from pathogens, toxins, inflammation , injury and disease. Multiple sclerosis, brain trauma, stroke, neurodegenerative disorders , Parkinson's, Alzimers , epilepsy, brain tumor affects BBB 2/20/2021 Dr. Lakshmi Rajeswaran 14

15. PHYSIOLOGICAL FUNCTION BBB dysfunction can lead to ion dysregulation , altering homeostasis lead to neuronal dysfunction and degeneration. Maintain ionic homeostasis and brain nutrition Regulate level of neuro transmitters Limit plasma macromolecules leak into the brain Protect the brain against neurotoxins 2/20/2021 Dr. Lakshmi Rajeswaran 15

16. PATHOPHYSIOLOGY ( CEREBRAL OEDEMA) Due to the injury or different pathogenesis, damaged brain cell swell, injured blood vessel leak and block the absorption pathways force fluid to enter brain tissues. Inside the skull, brain 1400 ml, CSF- 150 ml and blood 150ml is constantly located. Skull is a rigid box which can not be stretched. If the volume of one of these components increases, it will force reduction of volume of the other compartments. As the brain, blood or CSF volume continues to increase, the accommodative mechanism fails and increase ICP. It leads to reduced blood flow and causes cerebral ischemia. 2/20/2021 Dr. Lakshmi Rajeswaran 16

17. CLINICAL MANIFESTATIONS Clinical manifestations are secondary to ICP. Head ache Projectile vomiting Lethargy Altered level of sensorium Plantar extension Hypertension Bradycardia , Altered respiratory pattern Coma & death. 2/20/2021 Dr. Lakshmi Rajeswaran 17

18. MEDICAL MANAGEMENT General measures : Optimal head and neck position Adequate oxygenation Maintenance of normotension Specific measures: Short term hyperventilation Osmotic agents ( Mannitol) Hypertonic saline Surgical management: De-compressive craniotomy High dose barbiturates 2/20/2021 Dr. Lakshmi Rajeswaran 18

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20. NURSING MANAGEMENT 2/20/2021 Dr. Lakshmi Rajeswaran 20

21. NURSING MANAGEMENT Airway, breathing, circulation, position Monitoring of ICP ( 20 mm of Hg causes high mortality) Normal ICP- 0-15 mmHg. Glasgow Coma scale Cerebral oxygenation monitor Microdialysis Electroencephalogram Induced hyperventilation Hyperosmolar therapy (Mannitol, hypertonic saline). Corticosteroids Temperature management ( normo-thermia , antipyretics, surface cooling) 2/20/2021 Dr. Lakshmi Rajeswaran 21

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23. BRAIN HERNIATION Brain herniation is the displacement of brain tissue through the rigid dural folds (i.e., falx and tentorium) or skull openings (e.g. foramen magnum). Five types: 1. Subfalcine 2. Transtentorial 3. Central herniation 4. Tonsillar herniation 5. Upward herniation 2/20/2021 Dr. Lakshmi Rajeswaran 23

24. BRAIN HERNIATION 2/20/2021 Dr. Lakshmi Rajeswaran 24

25. PREDISPOSING FACTORS Hematoma ( trauma, epidural, subdural hematoma, contusion, intra cerebral hemorrhage) 2. Tumors 3. Malignant infarction 4. Infections (abscess, empyema, hydatid cyst) 5. Hydrocephalus 6. Subarachnoid hemorrhage 7. CSF over drainage 8. Metabolic hepatic encephalopathy 2/20/2021 Dr. Lakshmi Rajeswaran 25 Munakomi , S., & Das, J.K. (2021). Brain herniation. StarPearls Publishing LLC. www.nci.nlm.gov//books/NBK542246

26. SIGNS OF HERNIATION Depends on the type of herniation. Central herniation : Cushing triad: hypertension, bradycardia and irregular respiration. Raised ICP Motor weakness Altered sensorium Loss of brainstem reflexes Cheyne stroke breathing De cerebrate and decorticate position 2/20/2021 Dr. Lakshmi Rajeswaran 26

27. TREATMENT/MANAGEMENT ICP monitoring GCS monitoring Management of intracranial hypertension De-compressive hemi- craniectomy CSF drainage Osmotherapy Physiological neuro protection Sedation, analgesics, ventilation Hyperventilation Hypothermia Barbiturate coma 2/20/2021 Dr. Lakshmi Rajeswaran 27

28. ICU MANAGEMENT Mechanical ventilation Sedation to avoid agitation and strain Hyperventilation: cause vaso constriction and lowers the ICP Fluids must be restricted but patient must not be dehydrated Diuretics (mannitol) Blood pressure control Corticosteriods Hypothermia Pentobarbital coma can lower cerebral blood flow. Monitor urine output, DVT observation, prevention of stress ulcer. Patient centered inter-professional care bundle 2/20/2021 Dr. Lakshmi Rajeswaran 28

29. ASSIGNMENT ICP – assignment – Cushing’s Triad Identify three priority nursing diagnoses for the patient suffering with cerebral edema & develop a nursing care plan. 2/20/2021 Dr. Lakshmi Rajeswaran 29

30. HYDROCEPHALUS Hydrocephalus is defined as a disturbance of formation, flow or absorption of cerebrospinal fluid (CSF), leads to increase in volume occupied by the fluid in the CNS. Acute hydrocephalus occurs over days Sub acute hydrocephalus occurs over weeks Chronic hydrocephalus occurs over months/years. Communicating hydrocephalus: full communication occurs between the ventricles and subarachnoid space. Caused by over production/ defective absorption of CSF. Seen in intra cranial hemorrhage, meningitis resulting in the damage to the arachnoid granulation 2/20/2021 Dr. Lakshmi Rajeswaran 30

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32. TYPES OF HYDROCEPHALUS Non communicating hydrocephalus occurs when CSF flow is obstructed within the ventricular system or in the arachnoid space, Caused by intra ventricular or extra ventricular mass occupying lesion Congenital hydrocephalus occurs due to ventriculomegally develops in the fetal & infancy period, Associated with macroce p haly. 2/20/2021 Dr. Lakshmi Rajeswaran 32

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36. PATHOPHYSIOLOGY Normal CSF production is : 0.20-0.35 mL/minute Secreted by chroid plexus located in ventricles (lateral & 4 th ventricle) Total volume of CSF in an adult is : 120 ml. ICP rises if production of CSF exceeds absorption. This occurs if CSF is overproduce, resistance to CSF flow is increased, CSF reabsorption is decreased. 2/20/2021 Dr. Lakshmi Rajeswaran 36

37. EPIDEMIOLOGY Untreated hydrocephalus, death may occur due to herniation secondary to ICP. Incidence is equal in males and females. Infancy hydrocephalus related to various forms of congenital malformations and premature birth. Adult hydrocephalus represents 40% of total cases (USA). 2/20/2021 Dr. Lakshmi Rajeswaran 37

38. CLINICAL MANIFESTATIONS Influenced by the following: Age Cause Location of obstruction Duration Rapidity of onset Symptoms in infants Poor feeding Irritability Reduced activity Vomiting Symptoms in children: Slowing mental capacity Head ache, blurred vision Neck pain, vomiting Stunted growth, spasticity, drowsiness 2/20/2021 Dr. Lakshmi Rajeswaran 38

39. CLINICAL MANIFESTATIONS Symptoms in adults: Cognitive deterioration Head ache ( usually during morning hours) Neck pain Nausea Vomiting Blurred vision Double vision ( diplopia) Difficulty in walking Drowsiness Incontinence Symptoms of Normal pressure Hydrocephalus (NPH) Gait disturbance Dementia Urine incontinence Personality changes Parkinsonism. 2/20/2021 Dr. Lakshmi Rajeswaran 39

40. PHYSICAL SYMPTOMS Discussion by the students : D iscuss the physical symptoms exhibited by Infant Children Adult Person with normal pressure hydrocephalus 2/20/2021 Dr. Lakshmi Rajeswaran 40

41. CAUSES Infants & children : brainstem malformation, causing stenosis of the aqueduct of Sylvius . Congenital toxoplasmosis Acquired causes in infants: Mass lesion ( medulloblastoma,astrocytoma ) Intra ventricular hemorrhage, head injury, rupture of a vascular Malformation Meningitis Increased venous pressure related to venous thrombosis Iatrogenic: In adults: Subarachnoid hemorrhage Head injury Tumors Idiopathic Meningitis 2/20/2021 Dr. Lakshmi Rajeswaran 41

42. INVESTIGATIONS CSF analysis Genetic testing ( X-linked hydrocephalus is suspected) CT scan MRI Skull X-Ray R adionuclide Cistenography EEG 2/20/2021 Dr. Lakshmi Rajeswaran 42

43. MEDICAL MANAGEMENT Intermittent lumbar puncture Continuous CSF drainage Decreasing CSF secretion at the chroid plexus ( acetazolamide) Increasing CSF reabsorption ( Isosorbide ) 2/20/2021 Dr. Lakshmi Rajeswaran 43

44. PHARMACOLOGIC THERAPY Diuretics Acetazolamide (ACZ) Furosemide ( helpful in treating post hemorrhagic hydrocephalus by decreasing the secretion of CSF. Anticonvulsants – interfere impulse transmission of cerebral cortex & prevent seizures. Antibiotics: Prevents shunt infection, meningitis. 2/20/2021 Dr. Lakshmi Rajeswaran 44

45. SURGICAL MANAGEMENT Shunts are performed in most patients. The principle of shunt is to establish a communication between the CSF ( Lumbar or ventricular) and a drainage cavity ( peritoneum, right atrium & pleural cavity). 2/20/2021 Dr. Lakshmi Rajeswaran 45

46. TYPES OF SHUNT A ventriculo peritoneal (VP) shunt is used most commonly. The lateral ventricle is the usual proximal location . The advantage of this shunt is the length of the catheter may be obviated with growth by using a long peritoneal catheter. Ventriculo atrial (VA) shunt is also called a “ vascular shunt”. It shunts the cerebral ventricles through the jugular vein and superior vena cava into the right atrium. Mostly used in patients with peritonitis, morbid obesity, after abdominal surgery. 2/20/2021 Dr. Lakshmi Rajeswaran 46

47. TYPES OF SHUNT Lumbiperitoneal shunt: Ventriculopleural shunt ( second line therapy) Torkildsen shunt ( Rare) Only used for communicating hydrocephalus, CSF fistula or pseudo tumor cerebri . Used if other type of shunt is contra indicated. Effective only in acquired obstructive hydrocephalus. 2/20/2021 Dr. Lakshmi Rajeswaran 47

48. COMPLICATIONS VP shunt: Shunt malfunction Infection Over drainage Under drainage Peritonitis Hernia Bowel perforation CSF leakage Subdural hematoma ( Rinker et al: 2015). VA shunt Pulmonary hypertension Infection Blockage Catheter thrombosis Malposition 2/20/2021 Dr. Lakshmi Rajeswaran 48

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53. NURSING ASSESSMENT Head circumference Neurological and vital signs Check the fontanelle ( for infant & child) Monitor the signs of ICP History taking Assess the motor and cognitive functions 2/20/2021 Dr. Lakshmi Rajeswaran 53

54. NURSING DIAGNOSES Knowledge deficit Anxiety Risk for infection Risk for impaired skin integrity Risk / delayed growth and development Risk for aspiration 2/20/2021 Dr. Lakshmi Rajeswaran 54

55. NURSING CARE Assessment and complete health history Elicit clinical presentations Neurological status Vital signs, cognitive functions Periodical checking of the shunt site for infection ( redness) Implement seizure precautions Minimizing external stimuli Observe complications of shunt Observe for: ICP Tenderness, redness Pain or swelling ( along the length of the tube or incision). Irritability, drowsiness Nausea, vomiting, headache, double vision Fever, abdominal pain Rehabilitation 2/20/2021 Dr. Lakshmi Rajeswaran 55

56. INTRACRANIAL HYPERTENSION Increased pressure around the brain Causes: Acute IH : Severe head injury Brain abscess Stroke. Idiopathic : Obesity- especially with women, hyperthyroidism, oral contraceptives, CKD, Lupus Chronic IH : Chronic subdural hematoma Brain tumor, encephalitis, hydrcephalus . Arterio -venous malformation Venous sinus thrombosis Vasculitis 2/20/2021 Dr. Lakshmi Rajeswaran 56

57. PATHOPHYSIOLOGY OF INTRA CRANIAL HYPERTENSION Acute intra cranial hypertension is a medical emergency. Cerebral homeostatic mechanism is affected causing rapid increase in ICP. Management: CSF drainage by external ventricular drain or Lumbar drain. Sedation/ analgesia: control pain, agitation, & excessive muscular activity. ( due to delirium). Hydration with isotonic fluids Osmotic diuretics ( monitor fluid & electrolytes) 2/20/2021 Dr. Lakshmi Rajeswaran 57

58. MANAGEMENT Blood pressure control ( MAP need to be high to cerebral perfusion pressure (CPP) & ICP. Corticosteroids ( Dexamethasone) Hyperventilation c auses vaso constriction decreasing cerebral blood flow. ( PaCo2 – 25- 35 mmHg) is short term temporary measure). De compressive craniotomy. Adjust the ventilator settings ( ABG ) Fluid & nutritional support Multidisciplinary care ( nationalist, respiratory therapist, occupational therapist). ICP monitoring & CSF drainage are corner stone of the treatment. 2/20/2021 Dr. Lakshmi Rajeswaran 58

59. ICP MONITORING Nursing interventions causing > ICP Bed bath Patient positioning Oral & bronchial hygiene Suctioning 2/20/2021 Dr. Lakshmi Rajeswaran 59

60. ICP MONITORING Two common devices: 1. Intra paraenchymal monitoring. 2. Intra-ventricular monitoring using v entriculostomy or external ventricular drain (EVD). 2/20/2021 Dr. Lakshmi Rajeswaran 60

61. SIGNS AND SYMPTOMS Acute sustained elevations in ICP will result in < cerebral perfusion , leads to cerebral ischemia. Head ache Visual loss Diplopia Nausea, vomiting Papilledema Widening pulse pressure 2/20/2021 Dr. Lakshmi Rajeswaran 61

62. NURSING CARE Provide physical care gently ( bathing, oral hygiene, touching and suctioning) Avoid head rotation and flexion Reduce the environmental external stimuli Elevate the head of the bed to 30 degree, Maintain the neck in neutral position Maintain normal body temperature Monitor the fluid intake & prevent volume overload Notify the physician if the ICP> 20mmHg or CPP < 50-70 mmHg range. 2/20/2021 Dr. Lakshmi Rajeswaran 62

63. SUBARACHNOID HAEMORRHAGE SAH occurs when blood vessel on/or inside the brain rupture and begins to leak. SAH interferes with normal circulation and reabsorption of Precipitating hydrocephalus and leads to intracranial hypertension and develop as a space occupying lesions . The blood may form thick layers or clots intra ventricular , m ay extend to intra parenchymal and sub- durally . 2/20/2021 Dr. Lakshmi Rajeswaran 63

64. SUBARACHNOID HAEMORRHAGE Subarachnoid hemorrhage (SAH) is commonly associated with: Rupture of aneurysms (80%) Arterio venous malformations Traumatic brain injury Intra cranial aneurysm ( usually occurs in Circle of Willis) Infection High blood pressure / CVA A strong blow to the head from an accident or fall Genetic disorders ( rare) 2/20/2021 Dr. Lakshmi Rajeswaran 64

65. RISK FACTORS Family history Age & gender – 55% SAH victims are women Risk increases with age. Polycystic kidneys Connective tissue disorders Cigarette smoking Alcohol High blood pressure Sickle cell disease Cocaine & amphetamines abuse. 2/20/2021 Dr. Lakshmi Rajeswaran 65

66. PATHOLOGICAL MECHANISM In SAH, neuronal death occurs within first 72 hours termed as early brain injury (EBI). After 72 hours delayed cerebral ischemia (DCI) occurs leads to cerebral atrophy. Reduced cerebral perfusion due to > ICP.> intracranial hypertension. Cerebral edema and loss of blood brain barrier integrity, Cerebral loss of auto-regulation and hydrocephalus 2/20/2021 Dr. Lakshmi Rajeswaran 66

67. SYMPTOMS Patients usually describe “ the worst headache of my life”. Dizziness Weakness Speech changes Neck stiffness Nausea & vomiting Confusion Drowsiness. epilepsy Loss of consciousness 2/20/2021 Dr. Lakshmi Rajeswaran 67

68. DIAGNOSIS OF SAH Physical examination : Look for partial or complete nerve palsy, monocular blindness CT scan & MRI Lumbar puncture after 6- 12 hours of complaining of head ache. CT angiography Trans-cranial Doppler test Routine blood investigations 2/20/2021 Dr. Lakshmi Rajeswaran 68

69. NURSING CARE ( SAH) Continuous observation ( GCS, temperature, ECG monitoring, pupils, any focal deficits. Nutrition : oral route preferred only with intact cough & swallowing reflex). Head position Prevention of aspiration by feeding in sitting position IV fluids Intake output chart Pain management Prevention of DVT Medical treatment to prevent cerebral ischemia ( Nimodipine – 60 mg orally) 2/20/2021 Dr. Lakshmi Rajeswaran 69

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71. CURRENT MANAGEMENT CSF - lumbar drains Active clearing of blood done by instilling thrombolytic into Lumbar or basal cisterns. Calcium channel blocker ( Nimodipine ) to reduce the vaso spasm. Corticosteroids 2/20/2021 Dr. Lakshmi Rajeswaran 71

72. CEREBRAL ANEYRUSMS Cerebral aneurysms are usually found at the base of the brain In sub arachnoid space. Causes: Hypertension Cigarette smoking Congenital Injury or trauma to the blood vessel Complications of some type of blood infection Polycystic kidney disease Types: Cerebral aneurysm Intra cranial aneurysm 2/20/2021 Dr. Lakshmi Rajeswaran 72

73. SYMPTOMS ASSOCIATED ANEURYSM Sudden severe headache Nausea Vomiting Visual disturbance Loss of consciousness Facial pain Numbness Weakness Paralysis Double vision Stiff neck Photophobia Seizure Cardiac arrest 2/20/2021 Dr. Lakshmi Rajeswaran 73

74. TYPES OF ANEURYSMS Saccular aneurysms‘ Berry aneurysms Fusiform aneurysms 2/20/2021 Dr. Lakshmi Rajeswaran 74

75. INVESTIGATIONS MRI scan Angiogram CSF analysis 2/20/2021 Dr. Lakshmi Rajeswaran 75

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79. SURGICAL MANAGEMENT C lipping of the aneurysm Done by brain surgery. Neuro surgeon applies a small metal clip to the base of the aneurysm. This clip cuts off the blood flow to the wakened area and cause the aneurysm to form a clot. The clip is MRI compatible. 2/20/2021 Dr. Lakshmi Rajeswaran 79

80. ANEURYSM COILING Aneurysm coiling : Done with a method of endo vascular therapy. The surgeon insert a very thin flexible tube catheterer in the artery , usually in the groin & threads it through the arteries until it reaches the aneurysm. At the tip of the catheter is a tiny platinum coil that is deposited in the pocket of the aneurysm. These coils reduce the blood flow and cause a clot form the seal inside the aneurysm. 2/20/2021 Dr. Lakshmi Rajeswaran 80

81. ANEURYSM COILING 2/20/2021 Dr. Lakshmi Rajeswaran 81

82. CEREBRAL VASO SPASM Cerebral vaso spasm is a condition where the artery’s wall react to the original bleeding and tightens the space inside the artery and reduce the amount of blood flow , causing Impaired oxygenation , nutrition leads to stroke. 2/20/2021 Dr. Lakshmi Rajeswaran 82

83. CEREBRAL VASO SPASM Early signs: Drowsiness Confusion Change in speech Change in strength Severe head ache Complications: Ischemic stroke Cerebral infarction Permanent neurological deficit. 2/20/2021 Dr. Lakshmi Rajeswaran 83

84. INVESTIGATIONS Cerebral angiography Trans cranial Doppler test CT scan Digital subtraction angiography Magnetic resonance angiography EEG 2/20/2021 Dr. Lakshmi Rajeswaran 84

85. TREATMENT Cerebral angioplasty: A catheter is inserted in the narrow part of the artery. At the end of the catheter, a tiny soft , tough balloon which inflates the narrowed artery. Medical treatment: Calcium channel blocker, Vaso pressors, statins HHH therapy- Hypertension, hypervolemia, & hemo -dilution 2/20/2021 Dr. Lakshmi Rajeswaran 85

86. HEALTH EDUCATION Prevention pneumonia : Deep breathing exercises Deep vein thrombosis : inflatable calf wraps Prevention of constipation: Stool softeners Neurological check: confusion, change in the speech, drowsiness. Head position Adherence to the medications Fluid restriction if required Multi disciplinary care. Seek medical care if there is any change in the neurological status. 2/20/2021 Dr. Lakshmi Rajeswaran 86

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88. SPACE OCCUPYING LEISON ( BRAIN TUMORS) Space occupying is defines as any lesion whether vascular, neoplasms or inflammatory in origin which increases the volume of the intracranial contents and thus rise the ICP. Primary brain tumors' in adults occur above tentorium cerebelli considered as malignant. Brain tumors are commonly found in males & affects 3 rd decade of their life. 2/20/2021 Dr. Lakshmi Rajeswaran 88

89. TYPES OF SPACE OCCUPYING LESIONS 1. Primary brain tumor/lesion ( non- neoplastic cysts, congenital) 2. Metastatic lesion ( Lung, kidney, breast) 3. Trauma ( subdural, extradural hematoma Parasitic ( hydratid cyst, amebic abscess) 5. Vascular ( aneurysms, AVM, stroke) 6. Inflammatory ( abscess, tuberculoma, syphilitic fungal granulomas) 2/20/2021 Dr. Lakshmi Rajeswaran 89

90. WHO (2016) CLASSIFICATION OF BRAIN TUMORS TUMORS OF NEUROEPITHELIAL TISSUE • Astrocyclic tumors (grades I-IV) Oligodendroglial tumors Mixed gliomas Ependymal tumors Choroid plexus tumors Neuronal and mixed Neuronal-glial tumors Neuroblastic tumors Pineal parenchymal tumors Embryonal tumors TUMORS OF THE MENIGINGES Tumors of meningepthelial cells Meningioma Atypical meningioma Anaplastic meningioma Mesenchymal , N onmeningothelial tumors Primary melanocytic lesions 2/20/2021 Dr. Lakshmi Rajeswaran 90

91. WHO (2016) CLASSIFICATION OF BRAIN TUMORS LYMPHOMAS AND HEMATOPOIETIC • Malignant lymphomas • Plasmacytoma • Granulocytic sarcoma GERM CELL TUMORS • Germinoma • Embryonal carcinoma • Yolk sac tumor • Choriocarcinoma • Teratoma • Mixed germ cell tumors TUMORS OF PERIPHERAL NERVES • Schwannoma (neuroma) • Neurofibroma • Perineuroma • Malignant peripheral nerve sheath tumor TUMORS OF THE CELLAR REGION • Craniopharyngioma • Granular cell tumor METASTATIC TUMORS 2/20/2021 Dr. Lakshmi Rajeswaran 91

92. CLASSIFICATION OF CEREBRAL TUMOURS STUDENT ASSIGNMENT: Please read about the different types of tumors: Glioma Metastses Meningioma Micorglioma primary lymphoma Pituatory adenoma Acoustic neuroma Epidermoid Medulloblastoma Papilloma Prolactinoma Craniopharyngioma Pinealoma 2/20/2021 Dr. Lakshmi Rajeswaran 92

93. PRIMARY BRAIN TUMOR 2/20/2021 Dr. Lakshmi Rajeswaran 93

94. METASTIC BRAIN TUMOR 2/20/2021 Dr. Lakshmi Rajeswaran 94

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96. SUBDURAL HAEMATOMA 2/20/2021 Dr. Lakshmi Rajeswaran 96

97. MENINIOMA AND GLIOMA 2/20/2021 Dr. Lakshmi Rajeswaran 97

98. CLINICAL MANIFESTATIONS Head ache Nausea & vomiting Vision changes Changes in the muscle or nerve control Loss of motor function Emotional variability & mood swings Sudden personality changes Papilledema 2/20/2021 Dr. Lakshmi Rajeswaran 98

99. 2/20/2021 Dr. Lakshmi Rajeswaran 99 MECHANISMS LEADING TO SYMPTOMS Mass effect CSF obstruction Irritation of cortex Compression Interruption with the circulation Invasion by the tumor Increased ICP Seizures Focal neurological deficit

100. INVESTIGATIONS Physical examination CT scan brain MRI brain MR angiography Positron emission tomography (PET) Laboratory studies ( CBC, ESR, LFT. Tumor markers) Biopsy 2/20/2021 Dr. Lakshmi Rajeswaran 100

101. TREATMENT Gliomas : Benign: surgical excision Malignant: Surgical excision + Radiotherapy Meningioma: Surgical resection+ Radiotherapy Schwannoma : Surgical resection > 3 cm Pituitary : Pharmacological treatment + Radiotherapy Pineal: Depend on the histology Resection & radiotherapy Craniotomy biopsy Craniotomy excision Radiotherapy Chemotherapy Palliative care 2/20/2021 Dr. Lakshmi Rajeswaran 101

102. ROLE OF CRITICAL CARE NURSE The main goals are: Alleviate neurological symptoms Improve quality of life Achieve a cure where possible. Surgery Radiotherapy Chemotherapy Palliative care Chemotherapy has a limited role due to the mechanism of BBB. 2/20/2021 Dr. Lakshmi Rajeswaran 102

103. ROLE OF CRITICAL CARE NURSE Airway, breathing, circulation Haemo -dynamic & fluid management Monitor signs of ICP. Seizure precautions Observe of CSF leak ( from ears & nose). Observe for venous thrombo embolism Maintain quality of life Provide family centered care. Alternative therapies with palliative care. 2/20/2021 Dr. Lakshmi Rajeswaran 103

104. REFERENCES Carlson, K.K. American Association of Critical Care Nurses (AACN). (2009). Advanced Critical Care Nursing, Saunders Elsevier. St. Louis. Missouri. www.aacn.org American Association of Neurosciences Nurses. (2012). Care of the patient undergoing intracranial pressure monitoring/ External ventricular drainage or Lumbar drainage. AANN Clinical Practice Guideline Series. www.AANN.org . Bauer, A.M., & Rasmussen, P.A. (2014). Treatment of intracranial vasospasm following subarachnoid hemorrhage. 5(72): 1-7. www.frontiersin.org Daiwai , M., Mcnett , M., Lisa, S. et al. (2015).Effects of nursing interventions on itracranial pressure. American Journal of Critical Care. 22(5):432-438. Kadry , H., Noorani , B., & Cucullo , L. (2020). A blood brain barrier overview\on structure, impairment, and biomarkers of integrity. British Medical Central. 17 (1): 2-24. https://doi.org/10.1186/s12987-020-00230-3 . Mahajan , S., & Bhagat , H. (2016). Cerebral edema: Pathophysiological mechanisms and experimental therapies. Journal of Neuroanesthesiology and Critical Care. 3(1): S22-26. www.jnaccjournal.org 2/20/2021 Dr. Lakshmi Rajeswaran 104