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 .
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.
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.
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.
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.
22.
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.
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.
