1. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chapter 35: Common Neurosurgical and Neurological Disorders

2. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Care of the Neurosurgical Patient All of the following patient problems require some type of cranial surgery to reduce cerebral edema and/or hemorrhage: –Brain tumors –Aneurysm –Arteriovenous malformation (AVM)

3. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Brain Tumors: Expansion in a Space That’s Too Tight Etiology/Incidence Neoplasm of cranium; some are from metastasis Pathophysiology: Increase in brain tissue causes: Blood and CSF to be shunted from the brain, affecting CPP Disruption in the blood-brain barrier Increased ICP from vasogenic edema

4. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Brain Tumors Signs/Symptoms (clinical manifestations of increased ICP) –Headache –Seizures –Change in level of consciousness (LOC) - Focal neurological deficits Diagnosis based on history –CT initially but MRI preferred –MRA shows vascularity of tumor

5. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management and Nursing Care of Brain Tumors Pharmacology –Steroids if increased ICP –Acid blockers –Anticonvulsants Surgical Management –Biopsy –Craniotomy –Complications Radiation Therapy –Used after biopsy –External beam –Stereotactic –Bradytherapy Chemotherapy –Multiple modalities

6. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A patient admitted to the ICU with an intracerebral tumor has been on long-term steroids to reduce intracranial pressure. Which of the following findings would be a side effect of this therapy? A. Potassium 2.5 mEq/L B. Blood glucose 250mg/dL C. Serum sodium 135 mEq/L D. Creatinine 0.5 mg/dL

7. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer B. Blood glucose 250 mg/dL Rationale: Long-term steroid use can increase the serum glucose level and can cause a steroid-induced diabetes. All of the other lab values would not be related to steroids.

8. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nursing Care Monitor for side effects of steroids Care after craniotomy –Watch for cerebral edema, infection, hyponatremia, hemorrhage, thromboembolism, seizures Care during radiation/chemotherapy Patient education Hospice and family support for malignant gliomas

9. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Aneurysms: Weakening of the Artery Wall Etiology/Incidence –Associated with congenital and degenerative processes –Risk groups are female, smokers, and older –High risk in age group 35 to 60 Pathophysiology –Defect in the media leading to arterial wall weakness –Berry (saccular) aneurysm –Subarachnoid hemorrhage (SAH)

10. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question One of the most common complications of an aneurysm is a subarachnoid hemorrhage. If this occurs, patients will state they are having “the worse headache of my life.” A. True B. False

11. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer A. True Rationale: Bleeding into the subarachnoid space causes a severe headache associated with SAH. This bleeding also causes an increased ICP.

12. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Aneurysms Signs/Symptoms (clinical manifestations) –Half of patients have warning symptoms –Headache, lethargy, neck pain –Cranial nerve deficits of 2-4 –Rupture: “worst headache in my life” –If SAH, then nuchal rigidity, photophobia, blurred vision

13. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Subarachnoid Hemorrhage Complication Bleeding stops when the ICP = MAP; clot forms a seal around the aneurysm Blood in subarachnoid space can stimulate the autonomic nervous system to create hypertension, therefore decreasing CPP Hydrocephalus can result if blood clogs the CSF in the ventricles or arachnoid villi (where reabsorbed)

14. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Diagnosis and Patient Care Diagnosis –History, physical exam, lumbar puncture, cerebral angiogram –CT shows hemorrhage in 92% of cases Management and Nursing Care –Minimal stimulation and quiet environment –Observe for vasospasm

15. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Surgical Care Cerebral aneurysm clipping/excision –Only if area is accessible –Done in first 48 hours –Critical care monitoring postop for airway, vasospasm, LOC changes Endovascular thrombosis (coil) –Thrombogenic platinum alloy that conforms to aneurysm –Complications are hemorrhage, rehemorrhage, and stroke

16. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A patient is admitted to the ICU for vasospasm after aneurysm clipping. VS are 100 – 70 – 22, BP 140/90. Hgb and Hct are 14 and 40%. “Triple H” therapy is instituted to decrease vasospasm. Which of the following is an expected outcome after instituting this therapy? A. BP 120/60 B. BP 160/88 C. Hct 30% D. Hct 50%

17. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer B. BP 160/88 Rationale: The BP needs to be higher than normal by 20 mm Hg to ensure cerebral perfusion pressure (CPP). Lowering the BP too quickly would decrease CPP. Hct is generally kept below normal by 15%, which in this case would be 36%.

18. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Care and Treatment Before Surgery Vasospasm in injured areas –May be due to calcium released from blood cells. Calcium channel blocker, nimodipine are given to prevent this. “Triple H” therapy –Hypervolemia: Give IV colloids/crystalloids to cause cerebrodilatation. Use pulmonary artery catheter to monitor MAP and CO. –Hemodilution: Decrease blood viscosity to increase CBF. Keep HCT < 15% normal. –Hypertension (induced): To keep BP > 20 mm Hg above normal. Ensures CPP. Balloon angioplasty

19. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Arteriovenous Malformations (AVMs) Etiology/Incidence –A tangled mass of arteries and veins without a capillary system –Usually congenital –90% in cerebrum Pathophysiology –Can develop aneurysms and rupture, creating a cerebral hemorrhage (50-60% of cases) –Can cause hydrocephalus and seizures (unresponsive to drug therapy)

20. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins AVM (cont.) Signs/Symptoms (clinical manifestations) –Asymptomatic unless hemorrhage –Headache, seizures, and increased ICP –Cerebral steal: blood flows from viable tissue into AVM Diagnosis –MRI, CT –Can see hemosiderin ring around lesion

21. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management and Nursing Care of AVMs Surgery preferred to decrease the risk of complications –Stereotactic biopsy: with creation of burr holes; done with MRI, CT contrast –Craniotomy: incision and resection –Transsphenoid surgery: sphenoid sinus opened, CSF leak sealed with abdominal fat

22. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Care of Patients with Neurological Disorders Stroke Seizures Guillain-Barré syndrome (GBS) Myasthenia gravis

23. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Stroke: Brain Attack Etiology/Incidence –Medical emergency to decrease neuron death! –75% due to vascular obstruction (thrombi, emboli) –25% due to hemorrhage –TIA (transient ischemic attack) if symptoms last <24 hrs Pathophysiology –Blood flow is blocked by a clot forming on top of atherosclerotic plaque or blood clot formed in the heart or body –Decreases oxygen supply and creates ischemic areas (ischemic penumbra) that can become infarcted –Penumbra can be saved if thrombolytic therapy is instituted early –Ischemic areas cause cerebral edema and increase ICP

24. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Identifying and Treating Stroke Signs/Symptoms (clinical manifestations) –Sudden onset that doesn’t resolve –Use of NIHSS stroke scale –Neurological deficits include: Numbness, tingling Visual changes, difficulty talking Weakness on opposite side of the body as stroke Deficits last for >24 hrs. Diagnosis –CT without contrast ASAP (3 hour critical window) to rule out intracerebral bleed –ECG to see if atrial fibrillation or flutter is the cause

25. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A CT scan of the brain is critical in identifying a vascular obstructive stroke. A. True B. False

26. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer B. False Rationale: A CT scan is vitally important, but the purpose is to rule out hemorrhagic stroke so the patient can be considered for thrombolytic therapy. The nurse must have the CT results that rule out a stroke BEFORE therapy with “clot busters” is started.

27. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management and Nursing Care Assessment for thrombolytic therapy –An infarction may not show up for 24 hrs –The 3-hour window begins from the time the patient was last seen (not presentation time in the ECU) –Bolus dose and drip of tPA (tissue plasminogen activator) –Contraindications for thrombolytic therapy

28. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A patient is admitted to the Emergency Care Unit with stroke symptoms. Which of the following would exclude this patient from thrombolytic therapy? A. Atrial fibrillation, new onset B. An elevated BP of 140/90 C. An INR of 2.5 D. Head trauma over 1 year previous

29. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer C. An INR of 2.5 Rationale: An INR of greater than 1.7 would increase a patient’s chance of an intracerebral bleed. Atrial fibrillation of new onset can cause a stroke. Head trauma that is relatively new (within 2 months) is a contraindication, as is a BP over 185/110.

30. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nursing Management and Care Assessments: initial and ongoing Hazards of immobility Possible preparation for carotid endarderectomy –Removal of plaque that forms a bed for the clot Communication –Emotional lability of patient –Family support and education Patient education Rehabilitation

31. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Seizures Etiology/Incidence –Abnormal excessive neuronal discharge –Sudden, usually without warning (can have aura) –Epilepsy –Non-epileptic seizures ETOH withdrawal Fever Hypoxia Drug intoxication Poisoning

32. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Seizures (cont.) Pathophysiology –Increased permeability makes neurons highly excited –60% of seizures have no known cause Signs/Symptoms (clinical manifestations) –Generalized seizures: affect both hemispheres; affect whole brain from onset to completion Grand mal, tonic, clonic, ataxic, myoclonic and absence –Focal: only specific part of brain is affected; motor responses can travel to whole brain Jacksonian, sensory, autonomic

33. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Seizures (cont.) Diagnosis –Identifying high-risk non-epileptic groups –CT/MRI to see if lesion is cause –EEG –PET to evaluate cerebral perfusion and blood flow –Epilepsy monitoring unit with scalp electrodes

34. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management and Nursing Care for the Seizure Patient Treatment for status epilepticus (medical emergency) –Diazepam –Lorazepam –Phenobarbital –Propofol Surgical treatment Discharge teaching

35. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Care of the Patient With Guillain-Barré Syndrome (GBS) Etiology/Incidence –Inflammation of the peripheral nerves Pathophysiology –Triggered by autoimmune system Signs/Symptoms (clinical manifestations) –Ascending symmetrical lower motor weakness –Ascends to muscles of respiration

36. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Diagnosis and Treatment of GBS Diagnosis –Lumbar puncture: elevated protein levels –Positive serum immunoglobins –Diminished pulmonary function tests Management and nursing care –Airway and breathing management; possible ventilatory support –Plasmapheresis –IV immunoglobin –Supportive care

37. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Myasthenia Gravis Etiology/Incidence –Affects younger women and older men –50% have thymus hyperplasia Pathophysiology –Motor weakness from antibodies impairing nerve function at the myoneural junction Signs/Symptoms (clinical manifestations) –Ocular muscles are first affected (diplopia, ptosis) –Difficulty swallowing (risk for aspiration) –Respiratory muscles are affected; possible need for ventilatory support

38. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Diagnosis and Treatment of Myasthenia Gravis Diagnosis –Blood for acetylcholine receptor antibodies –EMG –Tensilon tests Management and nursing care –Pyridostigmine (Mestinon) –Steroids –Immunosuppressants –Plasmapheresis –Thymectomy