neurological alterations
- 1. Abeer Radwan
- 2. Objectives By the end of this presentation we will be able to :- 1- identify Guillain Barre syndrome pathophysiology, assessment methods, and management. 2- Introduce craniotomy types, and care ( pre, intra, and post operative ). 3- identify Intracranial hypertension pathophysiology, diagnostic methods and management.
- 4. Guillain-Barre Syndrome (GBS) May be described as a collection of clinical syndromes that manifests as an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes. Single entity characterized by inflammatory peripheral neuropathy, its a combination of clinical features with various forms of presentations and multiple pathologic processes. The Prototype of GBS is AIDP, which involve rapidly progressive ascending peripheral nerve dysfunction which lead to paralysis.
- 5. Most cases don’t require admission to an intensive care unit, but those whom in need those with respiratory failure. After medical stabilization, patients can be treated on a general medical/neurologic floor. - Occur in 1.8 case / 100,000 persons. - More often in men. Sometimes clusters of cases are reported ( 1977, swine flow vaccination ).
- 6. Etiology - Still unknown cause. - It include an immune- mediated response involving cell mediated immunity and development of IgG antibodies. - Most patients report a viral infection 1-3 weeks before manifestations, usually involve upper respiratory tract .
- 7. - Triggering events :- 1- viral infections. 2- Bacterial infections. 3- vaccines. 4- lymphoma 5- surgery. 6- Trauma
- 8. Pathophysiology GBS affect the motor and sensory pathway of peripheral nervous system, as well as autonomic nervous system functions of cranial nerves. Major findings is segmental demyelination process of peripheral nerves. It thought to be autoimmune response to antibodies formed in response to a recent physiologic event. T- cells cause edema and inflammation, then Macrophages break down the myelin. Inflammation around demylinated area cause dysfunction. Thickly myelinated fibers of motor pathways and the cranial nerves are more severely affected than the thinly mylinated sensory fibers do.
- 9. Pathophysiology After inflammatory process stops, myelinproduction cells begin. When remyelination occurs, normal neurological functions return. ** in some cases axonal damage occur, so recovery degree depend on degree of axonal damage. GBS course :- Ascending paralysis advance over 1-3 weeks. Plateau from 2-4 weeks. Descending paralysis followed by normalization.
- 10. Assessment and diagnosis Diagnoses of GBS depend on :- A- Clinical findings. B- CSF analysis. C- nerve conduction studies.
- 11. Assessment and diagnosis A- Clinical findings. 1 – motor weakness 2- paresthesias. 3- sensory changes. 4- cranial dysfunction. 5- autonomic dysfunction. ** assessment start from symptoms recognition, which start as lower extremity weakness. Motor loss usually symmetric, bilateral, and ascending.
- 12. Assessment and diagnosis Admission to hospital occur when weakness prevent mobility. ICU admission occur when respiration became difficult. As condition progress closer monitoring needed, specially respiratory monitoring ( Tv and inspiratory force) ** continuous respiratory and neurological assessment should be maintained for ongoing assessment.
- 13. Assessment and diagnosis B- CSF analysis. -Elevated CSF protein with normal cell count. - Increase in protein usually occurs after the first week, but doesn’t occur in 10% of all cases. C- nerve conduction studies. - Test the velocity at which nerve impulses are conducted show significant reduction, as the demyelinating process of the disease suggests.
- 14. Management recovery take time 1- Medical. * no curative treatment, just supporting body functions and prevent any complications. ** Plasmapheresis (4 to 6 changes/ 5-8 days) , and IV immune globulin used as treatment. 2- nursing. *maintain surveillance for complications. * initiate rehabilitation. * facilitate nutritional support. * providing comfort and emotional support. * patient education.
- 15. Craniotomy
- 16. Craniotomy Is a surgery that performed to gain access to portions of the central nervous system (CNS) inside the cranium. Common procedures include tumor or removal , cerebral decompression , evacuation of hematoma or abscess , and clipping or removal of an aneurysm or AVM.
- 17. Craniotomy Most patients who undergo craniotomy for tumor resection or removal do not require care in a critical care unit . Patients who do usually need intensive monitoring or are at greater risk for complications because of underlying cardiopulmonary dysfunction or the surgical approach used.
- 18. Operative terms - Burr hole - Infratentorial. - Craniotomy. - Craniectomy. - Cranioplasty. - Supratentorial.
- 19. Pre-operative care - Major priority in caring for preoperative patient, is protection the integrity of CNS. - Care :- 1- Maintaining adequate cerebral oxygenation. ( optimal oxygenation, hemodynamic stability, cerebral perfusion). 2- Seizure activity management is essential for controlling metabolic needs. 3- Assessment and documentation of the patients preoperative neurological status. Focusing on the deficits. 4- laboratory test required ( CBC, KFT, LFT, BUN, Endocrine test, fasting blood sugar, chest radiography, ECG, cross match, MRI, MRA). 5- Shaving of hair occur in operation room.
- 20. Pre-operative care 6- preoperative education. 7- Most patients experience some degree of post operative eye or facial swelling and periorbital ecchymosis. 8-instruct the patient about avoiding activities that provoke sudden ICP changes. 9- breathing exercise. 10- transsphenoidal surgery, need to be prepared for the sensation associated with nasal packing, mouth breathing instructions and coughing and sneezing avoidance important part of preoperative education. 11- patient and family psychosocial support is a major concern.
- 21. Surgical consideration - Surgical approach depend on surgical site, and to give surgeon ability to gain adequate exposure to the site. - Site selected in manner where it cause least amount of disruption to the intracranial content. - Surgical approach:- A- Transcranial. B- Transsphenoidal.
- 23. B- Transsphenoidal. - The approach for pituitary lesions. -Inter through nasal cavity sphenoid sinus entered to reach the anterior wall of the sella turcica. -Then sphenoid bone and dura opened to gain intracranial access. When tumor removed, surgical bed packed with small section of grafted adipose tissue. When intranasal structures closed nasal splint and soft packing or nasal tampons are placed in nasal cavity.
- 24. Surgical consideration - Position :- 1- supine. 2- prone. 3- sitting. - Arterial and central line placement. - Head fixation is a must ( skull pins). - Position with minimal stress over skin to prevent pressure ulcer. - Continuous monitoring all through surgery to prevent any complication or deterioration ( Air embolism ‘ removal’ ).- - Clipping skin edges and continuously irrigate site to prevent air embolism.
- 25. Post operative management A- Medical :- *** management depend on underlying cause, but direct management after surgery focus on complication prevention. *** complications :- 1- Intracranial HTN. ( edema expected post 48-72 hr) manage through :- CSF drainage, positioning, steroid. 2- Surgical hemorrhage. need surgical re-exploration 3- fluid imbalance.( due to disturbance in ADH production, or SIADH) Self limiting condition, only fluid replacement needed, and some times vasopressin used. 4- CSF leak. ( through subarachnoid opening, if transnasal leak use glucose content) Manage through head elevation and rest, lumber puncture or placement of lumber subarachnoid catheter. If risk for meningitis opening reseal needed. 5- DVT ( patients in risk ). manage through prophylactic measures, such as pneumatic device, LMWH
- 26. Post operative management B- nursing management :- Primary goal of post craniotomy nursing management is protection of CNS integrity. 1-preserving adequate cerebral perfusion pressure. 2- promote arterial oxygenation. 3- provide comfort and emotional support. 4- maintaining surveillance for complications. 5- enhance early rehabilitation. 6- patient education.
- 27. What else !!!
- 29. Intracranial hypertension * Pathophysiology Normal ICP under normal conditions, under 15mmHg. Intracranial space composed of :- 1- brain tissue 80% 2- CSF 10% 3- blood 10 % As Monro- kellie hypothesis say :- Any increase in volume of one of intracranial component must be compensated by a decrease in one or more of the other components so that the total volume remains fixed. Brain compliance help it to tolerate significant increase in volume without increase in ICP. But this compliance limited.
- 30. Intracranial hypertension Brain compliance limited to a certain level where ICP start to increase. When decompensation state start even small increase in volume could cause major elevation in ICP . Intracranial hypertension occur when ICP >20mmHg.
- 31. Cerebral blood flow (CBF) It correspond to metabolic demands. Normal = 50 ml/ 100g of brain tissue / min. Normal brain has a complex capacity to maintain constant CBF, effect known as auto regulation. MAP of 50- 150 mmHg does not alter CBF when auto regulation is functioning. Out side the limit of this auto regulation CBF become passively dependent on perfusion pressure.
- 32. Cerebral blood flow (CBF) - Factors affect CBF :_ 1- arterial blood pressure. 2- changes in metabolic rate. *Acidosis; cause cerebrovascular dilatation. Alkalosis; cause cerebrovascular constriction. ** reduction in metabolic rate decrease CBF where increase in it cause increase in CBF. 3- ABG’s exert profound effect on CBF. * where hypercapnia cause cerebral vasodilation. Where hypocapnia lead to vasoconstriction. ** prolong hypocapnia ( <20mmHg) lead to cerebral ischemia. *** low PaO2 (<40 mmHg) lead to vasodilation; but low PaO2 have not been shown to affect CBF in any direction.
- 33. Assessment and diagnosis 1- Signs and symptoms { LOC, Cushing's triad “bradycardia, widening blood pressure, systolic hypertension), diminished brainstem reflexes, papilledema, decerebrate and decorticate posturing, unequal pupil size, projectile vomiting, decreased pupillary reaction to light, altered breathing patterns, and hedach.} ** earliest and most important sign is the decrease in LOC.
- 34. Assessment and diagnosis Continuous monitoring needed for patient suspected to have intracranial HTN. * Monitor could be used to drain excessive CSF also. * Sites for ICP monitoring :- 1- intraventricular. 2- sub arachnoid space. 3- epidural space. 4- parenchma. Type of monitoring chosen depend on the suspected pathologic condition and physician preference “ table 27-6 “
- 35. Management A- Medical :- started to prevent any secondary insult. Exact ICP that need intervention remains uncertain but current evidence suggest treatment begin when ICP >20 mmHg. All therapies focus on reducing volume of one or more components. Major goal is to determine the cause of the elevated pressure and remove the cause if possible.
- 36. Management B- Nursing :- 1- position. 2- PEEP >20mmH2O, coughing, suction, tight trachystomy tube tie, and valsalva maneuver have been associated with increased ICP. 3-Family contact and gentle touch associated with decrease ICP. 4- Hyperventilation. (??? ) 5- temperature control. 6- BP control. 7- seizure control 8- CSF drainage. 9- Diuretics ( osmotic, non osmotic, Volume maintenance). 10- Control metabolic demand ( avoid noxious stimulations, medication use ).
- 37. Herniation syndromes * ICP monitoring aim to prevent herniation. * Herniation if occur could cause shifting of tissue from compartment to another and place pressure on vessels and vital functions center of brain. * If unchecked it could rapidly cause death.
- 39. Types :- A- supratentorial herniation 1- uncal herniation 2- central herniation 3- cingulate herniation 4- transcalvarial herniation B- infratentorial herniation. 1- upward transtentorial herniation. 2- downward cerebellar herniation
- 40. Any questions ?