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Cardiorespiratory physiotherapy performance NO COMMITMENT IN Guillain-BAR CASE
Janice Gomes Barbosa Monteiro Ft Ft Ft Cristina Fernandes Luiza Machado Odete
Hospital Nossa Senhora da Penha in respiratory therapy IMPROVEMENT IN INTENSIVE
Cardiorespiratory physiotherapy performance NO COMMITMENT IN GUILLAIN-BARRE SYND
Monograph presented as as partial requirement for obtaining the title of Improve
ment in Respiratory Therapy in Intensive Care, Hospital Nossa Senhora da Penha,
under the guidance of Vanessa Beasini Ft.
ABSTRACT Guillain-Barre Syndrome is an acute demyelinating polyneuropathy charac
terized by paresis or paralysis, which affects more than one member, associated
with loss of tendon reflexes and increased CSF protein. Presents an acute and pr
ogressive nature, often requiring special care in the Intensive Care Unit (ICU)
due to respiratory failure presented, resulting in muscular weakness. The object
ive of this work is the physical therapy approach in cardiorespiratory complicat
ions, where the degree of impairment varies in severity from mild abnormalities
to disorders that can be potentially fatal. ABSTRACT Guillain-Barre syndrome is
an acute acute dismyelinating polineuropathy, characterized by paresis or paraly
sis, That Affects there limbs, to arreflexed and Associated Increase of cerebros
pinal fluid protein. Lt seams Has to Be the acute and progressive intensive care
unit, because of respiratory failure. The Objective ofthis study is to show how
the physioterapists shouid act in case of cardiorespiratory problems bappen, Wh
ere Can it should vary from bland or Potentially fatal. MATERIALS AND METHODS Th
is study was conducted through a literature review of published literature in th
e last 10 years, with a case report. We selected specific books of neurology, ph
ysiotherapy, research on Medline and Lilacs, some specific sites of neurology jo
urnal articles and healthcare. Preference was given to books, articles and magaz
ines published in Portuguese, English and Spanish. For research we used the foll
owing keywords: polyneuropathy, Guillain-Barre syndrome, respiratory physiothera
SUMMARY - INTRODUCTION PATHOPHYSIOLOGY II-11.1-Commitment cardiorespiratory phys
ical therapy approach III.1 IIIA - Monitoring III.1.1 - ventilometer III.1.2-III
.1.3 mechanical vacuum pump - Ventilatory Mode (SIMV + PS) III.1.4-III.1.5 Ideal
PEEP - Bronchial Hygiene maneuvers (MHB) III.1.6-Weaning IV-V-CASE REPORT DISCU
SSION CONCLUSION VI-VII-REFERENCES 1 3 9 11 11 13 14 15 17 20 22 24 27 29 30
1-INTRODUCTION Guillain-Barre Syndrome or Acute Inflammatory Demyelinating Polyn
europathy is one of the most common diseases of the peripheral nervous system th
at threatens the life, since the advent of polio vaccine, became the most freque
nt cause of acute flaccid paralysis in all the world. It manifests with symmetri
cal motor deficits, with ascending paralysis, with weakness beginning in the dis
tal limbs, but advancing rapidly to affect the functions most proximal (Robbins,
1998; BENNETT & PLUM, 1996), acute onset and progressive nature, often requirin
g special care such as tracheostomy and mechanical ventilation in the Intensive
Care Unit (UTL), due to respiratory failure presented, resulting in muscle weakn
ess (LEVY &
OLIVEIRA, 2003; LIJNDY & EKMAN, 2000), approximately one third of all patients h
ave impairment of respiratory muscles (Scanlan et al, 2001) is identified as a s
yndrome, more for their clinical and laboratory tests, than by a malfunction sta
tes. It occurs in all age groups, although more frequent in the bands between 16
and 25 and between 45 and 60 years, there is a slight predominance in males (LE
VY & OLIVEIRA, 2003; LIJNDY & EKMAN, 2000). Considered medical emergency when th
e patient presents acutely and can sometimes be fatal, although it is often trea
ted as a benign disease, for those who see only the cases that evolve with mild
and recovery in a few weeks (PATTEN, 1985) potential for respiratory failure, as
well as difficulty in swallowing and deregulation unattended, are the basis of
nature as potentially fatal syndrome (Guillain-Barré. The progression can be ala
rmingly rapid, so that critical functions like breathing can be lost in some day
s or even hours.€Involvement of cranial nerves can determine cardiorespiratory d
isorders, manifestations of which can darken the prognosis of the syndrome (PLUM
& BENNETT, 1996; SANVITO, 1997). Because potential for rapid deterioration, pat
ients with a presumptive diagnosis of Guiltain-Barre syndrome in general need to
be hospitalized for observation. The course of the disease and the decline of t
he functions are highly variable (BENNETT & PLUM, 1996). Although uni rare disea
se that affects about 3 people to every 100,000 inhabitants (Díaz et al, 2002),
the mortality rate remains high by 13%, and third of these patients die from car
diovascular complications and ¼ pneumonia and respiratory failure (Tavares et al
, 2000) All data reinforce the need for more research on the disease by health c
are, while the physiotherapists also the approach to these patients. These profe
ssionals should learn on the disease to get an overview, especially about physic
al therapy, the literature is very scarce, to learn how to interact effectively,
both in monitoring as the quality of care so that treatment is the best, but wi
th awareness of their role in preventing and / or minimize the appearance of com
plications, especially cardio, largely responsible for the mortality of this syn
II-PATHOPHYSIOLOGY In 1916, Guillain, Barré and Strohl pointed to an acute radic
uloneurítica syndrome characterized by motor deficits, abolition of tendon refle
xes, paresthesias, minor deterioration of objective sensitivities, pain on compr
ession of muscle mass and protein-cytological dissociation of cerebrospinal flui
d (Read). The table is now known in medical circles as Guillain-Barre syndrome (
5GB) or polyradiculoneuritis (PRN) acute. (SANVITO, 1997). The disease occurs in
almost all parts of the world, at any time of year, affecting adults and childr
en, men and women, regardless of social class and habits
of life. It seems to be more frequent with advancing age and is slightly more co
mmon in men. The incidence is 2-4 cases for every 100,000 in North America. The
epidemiological patterns are similar worldwide (Tavares et al, 2000). Histopatog
ênicos aspects of Guillain-Barre syndrome have been widely debated. Guillain adm
itted the etiology of infectious virus, however, despite the technical refinemen
ts of the virus research today, evidence of the presence of this agent has not y
et been given. The autoimmune hypothesis, now has the most fans seem to occur in
this syndrome and a kind of delayed hypersensitivity. Many confirmed the partic
ipation of nerves in the inflammatory mechanism of lymphocyte T, presumably as a
response to a precipitating infection or other immune stimulus, occurring react
ion of an antigen with myelin (SANVITO, 1997). Is there a structural similarity
between the antigens of the pathogens involved and peripheral nerve. Thus a cros
s-reaction, involving the production of antibodies, on the cellular immune respo
nse, with consequent attack on peripheral nerves and spinal roots. Since it is c
onsidered an autoimmune disease, is frequently associated with viral infection (
Levy & Oliveira, 2003; Lundy & Ekman, 2000) that often precede the onset of neur
opathy in 1-3 weeks. Infections well documented history include: Campylobacter g
astroenteritis jejunio, viruses respiratpórias and gastrointestinal infections w
ith herpes viruses, cytomegalovirus (CMV), Mycoplasma sp, 111V, Epstein-Barr vir
us and spirochete (Lyme disease). There is a report of a case of this syndrome a
fter infection with Haemophilus influenza, and the report of 11 cases after 1-2
weeks of acute infection by Plasmodium sp. Other previous events include surgica
l procedures, vaccinations, diseases lifomatosas (particularly Hodgkin lymphoma)
, autoimmune diseases like lupus erythematosus (SLE) (Tavares et al, 2000). The
pathological changes are located in the nerve roots and ganglia rachidian as wel
l as cranial and peripheral nerves rachidian. Pathological, dependent inflammato
ry lesions, characterized by congestion, edema and infiltration of mononuclear c
ells, also occurring inflammatory segmental demyelination of nerve fibers, axona
l degeneration can also occur, depending on the intensity of the process (SANVIT
O, 1997) Once the primary process is the loss of myelin,€more myelinated periphe
ral nerves (motor and sensorioestereotáxico) are more severely affected than non
-myelinated nerves or poorly myelinated (pain and temperature) The Guillain-Barr
e syndrome can occur in different clinical forms: 1. forms paraplegic and tetrap
legic 2. forms with multiple cranial nerve involvement;
3. forms with edemas of Papua 4. pseudomiopáticas forms (predominance of motor d
eficit in the proximal muscles of the limbs);
5. 6, 7. 8. 9.
ataxic forms, forms with ascending paralysis (Landry-type Guillain-Barre syndrom
e); hiperágicas forms, forms with ophthalmoplegia-ataxia-areflexia (Miller-Fisch
er type); forms dysautonomia;
10. forms with hyponatremia, 11. relapsing forms (type Natrass) 12. forms of a p
rolonged course (chronic) (Parsons et al, 2003) The early neurological symptoms
are due to the usually symmetric weakness in the extremities, often associated w
ith paresthesias, in contrast to most other neuropathies, sometimes the proximal
muscles are affected initially more than the distal muscles (Rowland, 1997). Th
e paresthesias are usually the first sign, and if the legs are the most affected
, this change heralds the onset of sensory muscle weakness that occurs in all ca
ses and the pain can be prominent in a small group (NITRINL & Bacheschi, 1991 ).
Initial symptoms of the syndrome usually consist of tingling and "pins and need
les sensations" in the legs, and may be associated with low back pain continues.
At the presentation, which usually occurs a few hours or days after the first s
ymptoms there is already weak. It is generally more prominent in the legs but th
e arms and cranial muscles may be compromised first. Tendon reflexes are also so
on lost, even in body regions where the force is maintained. As the spinal roots
tend to be very committed, the Guillain-Barre syndrome can involve short nerves
, such as axial and intercostal nerves as well as cranial nerves and long (BENNE
TT & PLUM, 1996) The respiratory function is often compromised by the involvemen
t intercostal and phrenic nerves. Deficits may occur in the cranial nerves affec
ting speech and swallowing (Parsons et al, 2003) The involvement of cranial nerv
es can determine dysphagia, dysarthria and dystonia due to impairment of facial
muscles, ocular and oropharyngeal, and cardiopulmonary disorders, manifestations
of which may darken the prognosis of the syndrome. Sphincter disturbances are n
ot common, although they may occur in the early stages difficulty urinating. Neu
rodegenerative disorders may also occur: hipendrose, vasomotor instability, Dyst
hermic, tachycardia, bradycardia, hypotension (SANVITO, 1997). The loss of tendo
n reflexes in Guillain-Barre is joint and several mechanisms may be involved, as
loss of afferent fibers of muscle spindles, denervation of muscle fibers intraf
usais, temporal dispersion of nerve conduction
(Asynchronous impulse conduction in peripheral nerve). The paresis is aggravated
with the nadir being reached in 30 days, and usually lasts 14 days. The progres
sion can be alarmingly rapid, so that critical functions like breathing can be l
ost in a few days or even a few hours (BENNETT & PLUM, 1996) From the evolutiona
ry point of view we are witnessing an initial deployment phase of the neurologic
al (7 to 10 days), a state period (2 to 4 weeks) and a third phase of resolution
of symptoms (two to three weeks). The syndrome is of course self-limited and re
covery is usually complete in most cases. However, sequelae such as motor defici
ts and muscle atrophy can occur in a few cases. The recovery phase begins with t
he remyelination of injured nerves. Most patients recover excellent recovery of
muscle strength over time, usually returning to normal. A small percentage has v
arious levels of paralysis, which can be persistent (PARSONS EI AL, 2003) The di
agnosis must be based on the combination of several clinical and laboratory find
ings, since no observation is isolated and no pathognomonic laboratory test is s
pecific for the disease . The tests include: Blood: (basic biochemistry, blood c
ount, CK, ESR, liver function tests and acute phase proteins). Liver enzymes are
elevated in one third of patients on admission, usually normalizing the first w
eeks. Probably this is due to liver involvement in the preceding infection. The
blood count may reveal leukocytosis. Immunology: (search serum anti-glucoside)€a
re found antibodies to GMI glycoside in 25% of patients. Examination of CSF: (ce
rebrospinal fluid - RSI). The CSF usually presents with normal pressure, WBC unc
hanged and increased proteins, this elevation without pleocytosis is characteris
tic of the disease. The peaks of high protein are given 4-6 weeks of symptom ons
et, probably a reflection of the inflammatory process, the level of nerve roots,
breaking the barrier. The leukocyte count may be slightly elevated in 12% patie
nts. Neurophysiological studies: These studies reveal within the first two weeks
: 69% of demyelination and axonal involvement 3%, 3% unexcitability nervosa and
22% inconclusive results. About 3% of patients present neurophysiology unchanged
TAVARES E 'AL, 2000). The EMG confirms the involvement of myelin, characterized
by decreased conduction velocity (PRADO, RAMOS & VALLE, 1999). The nerve conduc
tion tests are important for the prognosis: a low amplitude in the distal evoked
potential, indicating a possible trend bad for the patient. An electrophysiolog
y detecting denervation also indicates a poor prognosis.
Other complementary tests: Depending on the patient's condition and its comorbid
ities may require the request of the electrocardiogram (ECG), urinalysis, stool
culture, chest radiography (Tavares et al, 2000) The differential diagnosis shou
ld be considered especially with the Polio Acute anterior (in children and young
people) and the nervous manifestations of acute intermittent porphyria (SANVITO
, 1997) The prognosis of Guiilian-Barré syndrome is considered good, with over 9
0% of patients achieving a complete or nearly complete recovery, in the short te
rm. However, about 5-15% of patients may experience severe disturbances for a lo
ng time, preventing the return to work and other activities by two or more years
(Tavares et al, 2000). This is reserved in the "bulbar forms" as well as forms
that evolve with ascending paralysis quick installation; fatal cases, though rar
e in modern intensive care services may occur (KNOBEL, 1998 & SANVITO, 1997) bet
ter prognosis and shorter hospitalization time in ICU are related to the use of
Plasmapheresis (plasma exchange of a patient by Albumin - 14 sessions with excha
nge of 1.5 plasma volume per session) or hyperimmune immunoglobulin Intravenous
(400mg/kg/day - 5 days) (Prado, Ramos & Valle, 1999). Both treatments are effect
ive, and your choice should be individualized. The isolated use of corticosteroi
ds is not beneficial (BENETTI & PLUM, 1996). During the acute onset of symptoms,
the patient should be under intensive care. The prognosis in general and good,
with complete reversibility of the neurological deficit by approximately 60% of
those affected (PRADO et al, 1999). Virtually all deaths are due to complication
s of prolonged hospitalization. The main complications are sepsis secondary to p
ulmonary or urinary infection, pulmonary embolism, delayed treatment of respirat
ory failure and dysautonomia, comp1icações These can be minimized by the excelle
nt medical care and nursing in an ICU (Parsons et al, 2003)-II.1 COMMITMENT Card
iorespiratory The respiratory weakness caused by neuromuscular dysfunction is pa
rticularly dangerous because it develops insidiously and remain silent without o
bvious clinical signs of pulmonary insufficiency. Vital capacity may fall to a l
ow level before hypoxemia develop. Some factors contributing to the development
of respiratory impairment, such as: lack of protection of the upper airway, the
respiratory muscle weakness and pulmonary complication secondary. Facial and oro
pharyngeal weakness may impair swallowing and prevent adequate removal of secret
ions, leading to pulmonary aspiration. This risk is increased further by weaknes
s of the muscles of the larynx and upper airway problems. In addition, weakness
of muscles of the tongue and retropharyngeal can cause intermittent obstruction
of the airways. Bankruptcy bulbar only can justify intubation. Weakness and para
lysis of the diaphragm and intercostal muscles results in the progressive failur
e of mechanical ventilation, but also in decreased strength and effectiveness of
cough inadequate. These abnormalities change with micro pulmonary atelectasis i
n the suburbs, with decreased pulmonary compliance and increased pulmonary shunt
. (LAWN ET AL, 2001).
With progressive weakness, atelectasis increases and results in hypoxemia, incre
ased respiratory rate and respiratory effort,€leading to fatigue of respiratory
muscles weakened, particularly the diaphragm, and finally culminates in hypoxia,
hypercapnia and acute respiratory failure. Occurs frequently, decompensation at
night during sleep, when the diaphragm performs all the work of breathing. Pulm
onary complications, atelectasis, with or without lobar collapse, aspirations an
d pulmonary infiltrates may worsen the situation. The autonomic nervous system d
ysfunction is usually present if the disease is severe enough to require mechani
cal ventilation. The dysautonomia may result from any combination of excess or d
eficiency of sympathetic activity. Additionally, a variety of arrhythmias can oc
cur in such patients and constitute a major cause of mortality (Parsons et al, 2
003). Autonomic changes are more frequent: orthostatic hypotension, cardiac arrh
ythmias, transient hypertension, anhidrosis, and often constitute the main frame
work of the neuropathy. Other changes are small or medium-sized pupils, halter,
impotence, urinary and fecal incontinence, dilation of the esophagus and colon (
NITRINI & Bacheschi, 1991). Postural hypotension is one of the most significant
effects of prolonged bed rest due to impairment of the ability of the circulator
y system to adjust the position, the circulatory system is unable to maintain a
stable blood pressure for longer periods and, for unknown reasons, not maintains
an adequate sympathetic response (HALAR & BELL, 2001). To prevent the drop in b
lood pressure when going from lying to standing position Ø, and quickly restore
normal blood pressure and blood volume, central sympathetic reflexes are activat
ed guards. These reflexes adrenergic derivatives of the major thoracic veins and
right atrium (acting as baroreceptor low pressure), cause an increase in plasma
levels of norepinephrine. The adrenergic system influences the release of renin
and angiotensin II, which potentiates the sympathetic response. The end result
is a transient increase in pulse of up to 15 bpm and a more prolonged vasoconstr
iction of the vessels of the lower limbs and the mesenteric blood supply, thus m
aintaining blood pressure (HALAR & BELL, 2001) Signs and symptoms of postural hy
potension are paresthesias, burning of the lower limbs, dizziness, fainting, diz
ziness, increased pulse (over 2übpm), reduced systolic pressure (greater than 20
mmHg) and decreased pulse pressure and systolic volume, which depends on the di
astolic filling may not be sufficient to maintain adequate cerebral perfusion. A
ny patient with significant respiratory muscle weakness or bulbar should be tran
sferred to the ICU for observation. Likewise, patients with significant autonomi
c dysfunction or rapidly progressive generalized weakness should be closely moni
tored in an ICU (Parsons et al, 2003) The treatment of dysautonomia consists of
hydration and use of laxatives to prevent vagal stimulation, but if is necessary
to use drugs to treat arrhythmias, or dysautonomia, small doses of drugs titrat
able short-acting and are recommended (Parsons et al, 2003).
APPROACH III-Physical therapy Respiratory therapy is a very broad area of profes
sional practice that deals with the evaluation and treatment of patients of all
ages with acute or chronic cardiopulmonary disorders. Employs a variety of thera
peutic exercises and techniques relating to evaluate and effectively treat patie
nts with cardiopulmonary dysfunction. Since the main goals of cardiorespiratory
physiotherapy: the prevention of obstruction and accumulation of secretions in t
he airways, which interfere with normal expiration, to improve the cleanliness a
nd ventilation of the airways through the mobilization and drainage of secretion
s, to improve fatigue resistance and tolerance the general exercise, reduce the
cost of energy during respiration through the reeducation of breath, prevent or
correct postural deformities associated with respiratory disorders, promote rela
xation, maintaining and / or improve chest mobility and improve the effectivenes
s of cough (Kisner & Kolby, 1998) III.1 - Monitoring Due deterionzação potential
for rapid, patients with a presumed diagnosis of Guillain-Barre syndrome in gen
eral need to be hospitalized for observation (Bennett & Plum, 1996). During the
evolution phase intense and progressive disease in the first 2-4 weeks, monitori
ng should include frequent measurement of vital capacity and ability to swallow.
The failures of respiratory function has to be anticipated and should be recogn
ized. (Lawn et al, 2001).€Intensive treatment and insertion of a cannula should
be started early, before the decline of ventilatory strength, loss of autonomic
regulation or fatigue unproductive coughing in a situation of acute emergency. T
his early intervention prevents many potentially fatal seizures. Much of the red
uction of mortality rate in Guillain-Barré place in intensive care today. (BENNE
TT & PLUM, 1996). Between 10 and 23% of patients eventually require mechanical v
entilation. The best way to monitor respiratory function is with frequent pulmon
ary function tests at the bedside, vital capacity and maximal inspiratory and ex
piratory pressure. Arterial blood gas analysis often remains normal until the re
spiratory failure is severe, so they lead to a false sense of security regarding
the respiratory status (Parsons et al, 2003). In acute axonal form, which can b
e explosively rapid, so that the ventilator support is required within hours aft
er admission to hospital (BENNETT & PLUM, 1996) The respiratory failure is a con
sequence of the combination of respiratory muscle failure with hypercapnia and s
econdary pneumonia inability to cough or protect the airway. Clinically, neuromu
scular respiratory failure is characterized by rapid shallow breathing, fatigue,
sweating, speech short, greater use of accessory muscles, tachycardia, and para
doxical breathing. Since the main indications: when the vital capacity is less t
han 15 ml / kg body weight, and when the inspiratory pressure is less than -25 t
o -30 cmH2O, when patients have severe bulbar impairment, to the point they can
not eliminate secretions or protect the airway, and when patients do not
can keep the PaCO2 and pH in arterial blood gases. The rapidity of disease progr
ession should be considered. The more rapid the development of motor impairment
early intubation should be (Parsons et al, 2003) the careful guidance of the pat
ient regarding the possibility of rapid deterioration and the prognosis is favor
able uni important first step. While they can breathe and speak, patients should
be instructed in a communication system in order to be able to make himself und
erstood if there is a need for respiratory support and intubation (BENNETT & PLU
M, 1996). Assessing the need for support of ventilatory support should be repeat
ed every 6 hours. Especially during sleep, for the early detection of oxygen des
aturation, patients should be monitored by pulse oximetry (LAWN ET AL, 2001) The
treatment of dysautonomia is to prevent the change of position (Parsons et al,
2003), but early mobilization is the most effective way of making opposition to
postural hypotension and should include mobilization of range of motion, stretch
ing exercises, walking and calisthenics, as tolerated by the patient, the pillow
s to elevate your feet and recline the backs can be used to assist during the re
conditioning process may occasionally be necessary orthostatic board, elastic st
ockings full extension and a variety of abdominal belts are regularly used (DeLi
si et al, 2002) In patients with coronary artery disease, symptoms of angina, ma
y also be prominent now the coronary blood flow decreased diastolic filling inad
equate follow the process of restoring normal postural cardiovascular responses
may vary 20-72 days (DeLisi et al, 2002).
Evolution of respiratory failure in patients with Guillian-Barre Syndrome Normal
Oxygen Saturation 02> 97% to a. PaO2> 75 mmHg at a. Chest x-ray course Integrit
y Oropharynx Swallowing difficulty Breathing Without Unobstructed ventilation in
spiratory force> 50 CVmI / kg> 15 PaCO2 (mmHg) 40 <97% with 02 PaO2/FiO2 <100% A
telectasis Asp. Weakness occasional oral language <50 10-15 40-48> 95% with 02 P
aO2 <55mmHg Vacuum infiltration Obst. Positional <30 <10> 48 Borderline Failure
aa: ambient air; Fi02: fraction of inspired 02, PaO2: partial pressure of oxygen
in arterial blood; PaCO2: partial pressure of CO2 in arterial blood; VC: vital
capacity. (Diaz et al, 2002).
III.1.1 - ventilometer The measurement of lung volumes, among them the tidal vol
ume, minute volume and vital capacity can be done through the use ventilometer.
This device can be used in the patient breathing spontaneously, connecting to a
mouthpiece (IV INTERNATIONAL SYMPOSIUM VM - HOSP. Lebanese Syrian, 2002). Indica
tions respirometry are: pre-operative control of mechanical ventilation, patient
s with neurological or neuromuscular diseases and weaning.€Tidal volume is the a
mount of air that enters and leaves the lungs with each respiratory cycle, with
approximate values in normal individuals, 400-500 ml. The respiratory rate in no
rmal adult at rest is 12-20 bpm. Patients on mechanical ventilation with Vt <300
ml and f <25 1pm, are less likely to succeed in weaning (IV International Sympo
sium on VM - HOSP. Lebanese Syrian, 2002) Volume minutes can be expressed by the
product (VC xf), and its largest utility the measure of its isolated components
. Healthy subjects submitted to the home, guaranteeing a minute ventilation of a
bout 6 liters, and those in weaning should have Vmin <10 liters to be able to ma
intain spontaneous breathing. Taking into account the relationships between alve
olar ventilation and CO2 production, values of Vmin> 10 liters in the presence o
f hypercapnia (PaCO2> 45 mm Hg), raise the suspicion of increased dead space, wh
ich decreases the chances of weaning. Already high levels of PaCO2 Vmin normal o
r low, reflect reduced respiratory drive. The CV is defined as the maximum volum
e exhaled after a maximum inspiration, effortlessly. Its normal value is 65-75 m
l / kg, but values> 10 ml / kg are considered favorable for weaning ventilatório
.Está reduced under conditions that damage to muscle contraction or conduction o
f nerve pathways. Its measurement is true only when performed with the cooperati
on of the patient, who must inhale air through the ventilometer to total lung ca
pacity (TLC), and exhale the air until the residual volume (RV) (VI INTERNATIONA
L SYMPOSIUM VM - HOSP. Lebanese Syrian, SAO PAULO, 2002). III.1.2 - Manovacuomet
er The simplest test for assessment of respiratory muscle strength is a measure
of the maximum pressure that can be generated during inspiration and expiration
with values measured by mechanical vacuum pump (VI INTERNATIONAL SYMPOSIUM VM, H
OSP. Lebanese Syrian, 2002 ) The MIP is obtained at residual volume (RV), but th
e inclusion of union-way valve to the gauge, ensures that the inspiratory effort
is initiated close to functional residual capacity (FRC), which increases the p
erformance of the test (eliminates the factor of elastic recoil of the lungs and
chest cavity), and its validity as the maximum expiratory pressure is obtained
from the total lung capacity (TLC), based on the maximum muscle stretching, gene
rating greater force. Some factors may affect these pressures, including age, se
x and the variability between individuals and the adaptation of oral perioral, a
nd that the technique requires patient cooperation.
The maximum pressure uni reflect global index of respiratory muscle strength and
must be interpreted in relation to lung volumes, given their close relationship
. The MIP and MEP indicates decreased when muscle weakness, when there is a decr
ease of MIP with normal MEP thought to be at a mechanical disadvantage, as in ca
ses of hyperinflation, when there is a decrease of MEP will present the patient
coughing ineffective, having, for example, difficulty expectoration of secretion
s (VI International Symposium on VM, HOSP. Lebanese Syrian, 2002). The approxima
te normal values in young adults are: MIP = Men -111 + - 34 cm H2O, MIP female =
-72 + - 26cmH20, MEP male = +151 + - 68cmH20, MEP female +93 + - 3OcmH2O. Just
note that the test should be performed after lung emptying most, and how far to
take the greater of three attempts, each one of them should not exceed 25 second
s duration. The main indications for assessing respiratory muscle strength are:
respiratory failure, weaning and aid in determining muscle training (if MIP is g
reater than 14 crnH2O) use the Threshold for training. Measures should be taken
daily (VI International Symposium on VM, HOSP. Sirl LEBANON, 2002). III.1.3 - sy
nchronized intermittent mandatory ventilation - (VLMS + PS) This ventilatory mod
e, the fan cycles provide controlled, assisted and spontaneous, using time windo
ws where the duration remains fixed (CARVALHO, 2000). The fan sends a cycle cont
rolled by starting the counting of time windows, to detect the first effort of t
he patient before the end of the window and after a controlled cycle, initiate a
cycle seen in this interval remaining after one cycle, assisted, if the patient
displays other inspiratory efforts, the fan provide spontaneous cycles. If you
have been assisted cycles and / or spontaneous in the previous window, the fan w
ill not start the window with a cycle controlled, but will await the patient's e
ffort. If the patient exhibited no effort in the previous window,€the new window
is started with a controlled cycle, ie cycles controlled only occur after an ap
nea or a window after a window where there was only one cycle controlled (CARVAL
HO, 2002). Like for SIMV + PS fan prioritizes the patient's effort may occur ove
r relatively long periods of apnea to respiratory rates low. In spontaneous cycl
es for the assistance of pressure support, which consists in offering pre-determ
ined levels of positive pressure and constant in the patient's airway during ins
piration (CARVALHO, 2002). The fan should be able to generate an inspiratory flo
w slightly greater than or equal to that requested by the patient at each moment
(VI INTERNATIONAL SYMPOSIUM VM, HOSP. Lebanese Syrian, 2002) The goal of this p
ressure would only "relieve" an inspiration very laborious , "saving" the respir
atory muscles, but still getting over the sick time control, inspiratory flow an
d volume, a consequence of four variables, pressure level
support employee, level of self-peep, respiratory system impedance (compliance a
nd resistance) and muscular effort of the patient. The fan "recognizes" the begi
nning of a spontaneous inspiration to activate the pressure support, typically t
hrough detection of a small decrease in base pressure in the airways (triggers p
ressure) or by detecting a slight air flow direction of the patient's airway, sh
oots per stream. For the fan is able to generate an inspiratory pressure constan
t, it is necessary to almost instantaneous release of a high inspiratory flow, s
ufficient not only to meet the patient's inspiratory demand, but also to keep th
e ventilator circuit pressurized at the pressure Support (VI INTERNATIONAL SYMPO
SIUM VM, HOSP. Lebanese Syrian, 2002). The type of control exercised over the sp
ontaneous cycles is the pressure, controlled parameter (fixed) and the resulting
flow is a parameter (free and descending). However, the fan continually monitor
s the value of the inspiratory flow and end the cycle when it reaches a certain
value (CARVALHO, 2002) For the fan "recognize" that the patient ends his spontan
eous inspiration, disabling the inspiratory muscles, he agreed to stop pressure
support so that the inspiratory flow drops below certain critical levels. In som
e fans, this interruption is made when the inspiratory flow falls below 25% of m
aximum flow rate achieved at the beginning of inspiration or 5% of maximum flow
(Servo 300). In others, the disruption occurs when inspiratory flow falls below
a preset value set, for example 4 A or 10 A (VI INTERNATIONAL SYMPOSIUM VM HOSP.
SIRIO LLBANES, 2002) III.1.4 - Ideal PEEP PEEP is not ideal a method of ventila
tion per se, but the application of positive pressure should not be initiated un
til the initial assessment is complete and the condition of lung inflation, the
gas exchange and hemodynamics is determined. (CONSENSUS BRAZILIAN VM, 2000) The
high PEEP is used mainly to improve oxygenation in patients with hypoxemia, resp
iratory failure and aims to open collapsed alveoli, results in higher alveolar v
olume produced by PEEP allows for a more Fi02 low and other parameters such as p
ulmonary compliance and ventilation / perfusion ratio (CIV) can also improve whe
n properly applied. The calculation of optimal PEEP is the patient is sedated an
d effects of anesthesia, through methods such as compliance curve x (Suter metho
d of increasing or PEEP), superseringa, random values, continuous flow (1 to Oct
ober 1), chest CT and evaluating to oxygenation by pulse oximetry (CONSENSUS BRA
ZILIAN VM, 2000) The level of pressure corresponds to the point where the parame
ters indicate a better oxygenation in the safer level of pressure associated wit
h the increase in FRC and pulmonary compliance and PaO2. This phenomenon is due
to additional recruitment of alveoli. The principle is reached a point at which
lung compliance is
maximized, since the blood pressure remains stable, the best compliance point re
presents an estimate of the optimal level of PEEP which must always be assessed
for the safety of lung inflation, the adequacy of pulmonary circulation and oxyg
enation of the acceptability (SCALAN et ai, 2001) values obtained in the calcula
tion of PEEP should not be used in a fixed form, as the lung undergoes continuou
s changes with each observation. The contraindications of PEEP include hypotensi
on, pneumothorax, untreated,€intracranial pressure and high pressure of inflatio
n and the pressures to sustain the maximum inflation, ie,> 35 cm H2O excessive.
The physiological effects of PEEP may be beneficial or harmful depending on its
application. The beneficial effects of PEEP are appropriate: restoration of func
tional residual capacity (FRC), alveolar recruitment, decreased shunt fraction,
increased lung compliance, decreased respiratory effort, increased PaO2 for a gi
ven Fi02, whereas the harmful effects an inadequate PEEP are: increased incidenc
e of pulmonary barotrauma, decreased venous retum and cardiac output, increased
respiratory effort (with hypertension), increased pulmonary vascular resistance,
decreased renal blood flow and portal, increased dead space and increased the m
ean airway pressure. Usually, using a PEEP of 15 cm H2O, although some patients
may require PEEP levels greater than or equal to 50 cm H2O to maintain adequate
oxygenation. Recent evidence suggests that a PEEP greater than 15 cm H2O can be
effective in improving oxygenation and reduction in mortality (SCALAN et al, 200
Parameters of a study including data on PEEP ventilation, oxygenation and hemody
namics. Parameters PEEP = 0 Time (min) Vt (1) F (per min) FiO2 (%) PEEP (cm H2O)
I: E ratio Pmax (cmH2O) Pplat (cmH2O) Pmed. Airways Cs (ml/cmH2O) PaCO2 (mmHg)
PH SaO2 (%) SvO2 (%) PA (%) CO (llmin) to2 (mllmin) The 16 0.8 1:27 80 0 35 30 4
.8 25 43 7.38 5.9 86 61 131/78 989 PEEP = 5 20 0.8 16 80 5 1:27 39 33 9.7 27 42
7.37 92 76 133 / 2 5.7 1022 10 40 PEEP = 0, August 16 1:27 80 10 42 35 30 43 14.
5 7.39 5.9 1105 96 71 130 / 79 PEEP = 15 60 16 80 15 1:27 0.8 48 42 19.7 28 42 7
.35 97 125 / 74 69 5.4 1021 PEEP = 0.8 20 80 16 80 20 1:27 56 49 25 25 44 7.32 9
8 64 4.8 917 110 / 69
Airway pressure (Paw), blood pressure (BP), arterial oxygen saturation (SaO2), o
xygen saturation of mixed venous blood (SvO2), oxygen transport (to2). Note that
with increases in PEEP, PaO2 and saturation increase; the airway pressures incr
ease, compliance improves and then decreases at higher levels of PEEP, and oxyge
n transport (to2) increases, and then declines, the optimal level of PEEP for th
is patient is 10 cm H2O because it provides better oxygenation in the safer leve
l of airway pressure (SCALAN et al, 2001) III.1.5 - Maneuver bronchial hygiene t
herapy hygiene bronchial involves the use of noninvasive techniques for airway c
learance. Several diseases affect airway patency, composition and production of
mucus, ciliary structure and function and normal reflex cough causing retention
of secretions, leading to obstruction and atelectasis (SCALAN et al, 2001). The
main objective of bronchial hygiene therapy is to assist in mobilizing and remov
ing secretions retained with the ultimate purpose of improving gas exchange gas
and reduce work of breathing. For the bronchial hygiene therapy to be effective
requires an initial evaluation and continuation training to the patient. Among t
he conditions in which the bronchial hygiene therapy may be indicated, are the s
eriously ill patients with copious secretions, patients with acute respiratory f
ailure with clinical signs of secretion retention, respiratory sounds audible de
terioration of arterial blood gases, changes chest X-ray, atelectasis, change in
V / Q due to infiltrates or pulmonary condensation. The bronchial hygiene thera
py has proven effective in removing secretions and improving lung function. The
preventive uses are mostly used in patients with neuromuscular disorders, chroni
c diseases and immobilized patients. The most common conditions affecting the co
ugh reflex are musculoskeletal disorders and neurological. Several methods for b
ronchial hygiene, which can be used alone or in combination. These approaches in
clude: therapy, postural drainage, percussion and vibration, vibro, cough and te
chniques relating to expulsion, accessories positive airway pressure and mobiliz
ation, and exercises, the proper use of these techniques requires an understandi
ng of basic principles, its efficiency and application methods (SCALAN et al, 20
01). Most bronchial hygiene therapies help move secretions to the central airway
s, clearance of these secretions requires real cough or aspiration. The cough is
rarely contraindicated, however, the risks and complications may be due to decr
eased perfusion pressure, incontinence, fatigue, rib fracture, headache, broncho
spasm, muscle injury or discomfort,€spontaneous pneumothorax, chest pain, displa
cement of the center line and paresthesia. Immobility is the main factor that co
ntributes to the retention of secretions. Currently, early mobilization and freq
uent change of position are preventive interventions against pneumonia and atele
ctasis (SCALAN et al, 2001). The addition of the exercises the mobilization and
coughing, further increase the removal of mucus. The exercises also improve the
aeration and overall ventilation perfusion (V / Q), besides increasing the produ
ction of sputum and improving lung function. Moreover, the exercises can be stre
nuous and may cause oxygen desaturation in patients with pulmonary involvement.
Patients with neuromuscular diseases are not good candidates for airway clearanc
e through exercise (SCALAN et al, 2001) Endotracheal Aspiration Endotracheal Asp
iration is a procedure needed for patients on mechanical ventilation and air pro
bes. This procedure is performed to prevent airway obstruction caused by retaine
d secretions, foreign bodies and structural changes such as edema, tumors and tr
auma (SCALAN et al, 2001)
The retained secretions increase airway resistance and respiratory work, which m
ay cause hypoxia, hypercarbia, atelectasis and infection. The difficulty in remo
ving secretions may be due to its thickness, quantity, or the patient's inabilit
y to produce an effective cough. Aspiration involves the application of negative
pressure (vacuum) in the airways through a collector tube (catheter tip or flex
ible duct). The careful execution of the procedure is the best way to avoid or m
inimize the incidence of hypoxemia during suction, when combined with hyperinfla
tion provides even greater protection and help prevent atelectasis. However, the
hyperinflation can shake some patients. The insertion of the catheter via an ad
apter that does not require disconnecting the ventilator can also be useful in p
reventing hypoxemia prevent cardiac arrhythmias. Must use this technique for pat
ients who are receiving high levels of support, especially levels of PEEP above
10 cm H2O. Mechanical stimulation of the airways can cause arrhythmias, bradycar
dia or asystole due to vagal stimulation. Tachycardia may be a result of agitati
on and hypoxemia of the patient. If you observed any major change, you should im
mediately cease the procedure and administer oxygen to the patient, performing m
anual ventilation when needed (SCALAN et al, 2001) Atelectasis due to excessive
air removal of air from the lungs, which can be avoided by limiting the amount o
f negative pressure used, keeping the duration of aspiration as short as possibl
e and hyperinflation before and after the procedure. To avoid mucosal trauma, li
mited the amount of negative pressure, removing the catheter by performing a rot
ation movement (SCALAN et al, 2001). 111.1.6 - Weaning is the process of transit
ion from mechanical ventilation to spontaneous ventilation. The concept of gradu
al transition from mechanical ventilation to spontaneous ventilation is linked t
o techniques that allow patients to gradually upgrading to spontaneous ventilati
on (COSTA, 1999) The weaning process begins when the patient begins to breathe s
pontaneously, as the clinical stabilizes and the factors responsible for respira
tory failure are controlled. Initially, the patient explained the purpose of the
work that will be imposed. Being patient with stable and breathing spontaneousl
y, we can make weaning in different ways (pipe "T", CPAP, SIMV, PS, and VPN) (CO
STA, 1999) Some criteria and clinical conditions must be present at the time of
Start weaning: • Control • VM determinant of cardiovascular stability
• Stability of gas exchange - Sat> 90% Fi02 = or <40%, pH between 7.35 to 7.45,
PaO2> 8OmmHg, PEEP = or <5 cmH2O, PaO2/FiO2> 200. • Stability of respiratory mec
hanics - bronchospasms, pulmonary edema, atelectasis, and pulmonary secretions,
should be under control. • hydrolytic stability - must obey the normal electroly
te concentrations of K (3.6 to 5.0 mmol / l), Ca (2.12 to 2.61 mmol / l), Na (13
5-145 mmol / 1) and Mg (0.7 to 1.0 mmol. • Stability of the respiratory center -
the neurologic and metabolic must be stable. • Hemoglobin (Hb) - minimum fee fo
r promoting weaning - lOg / dl. Anemia results in decreased uptake O2 for Hb. •
Control of cardiac arrhythmias - can increase the process of weaning. • Control
calorie depletion.ۥ Control of infection and fever - can interfere with the bul
let between supply and O2 consumption. • Sleep deprivation and pain - opiates an
d tranquilizers can lead to depression of the respiratory center (COSTA, 1999).
Weaning from mechanical ventilation, and the final withdrawal of ventilatory sup
port, depends on several indices that aims to estimate the ability of the patien
t's ventilatory reserve. The indexes commonly used are the following: • Indices
of oxygenation - a PaO2> 60 mmHg for the patient breathing Fi02 or <40% and a PE
EP = or <5 cm H2O, compared FiO2/FiO2> 200, = 5% pulmonary shunt , • • • • MIP>-
25cmH20, CV above 10-15 ml / kg, breathing patterns - VC between 4:05 ml / kh f
<30 rpm; Tobin index f / VC <rpm / 1, Complacency chest - must be> 25 ml/cmH2O (
COSTA, 1999).
Some factors leading to unsuccessful weaning as, hypoxemia, respiratory muscle f
atigue, pulmonary hyperinflation, muscle atrophy, endocrine, respiratory acidosi
s, diaphragmatic dysfunction by phrenic nerve injury and emotional factors (COST
A, 1999).
IV - CASE REPORT MFP, male, white, unmarried, 26 years, was admitted to the emer
gency room of the Hospital Nossa Senhora da Penha, 18 September 2002, at 11:25 h
ours, with a history of cough, fever, shortness of breath and pain in the body.
Because the state was admitted to the ward with diagnosis (HD) of interstitial p
neumonia, for monitoring and appropriate treatment, which was observed in the me
dical evaluation that the patient had a severe generalized muscle weakness, due
to which he could not move the rib cage. The RX performed in the emergency depar
tment showed atelectasis on the right, with elevated hemi-diaphragm side, sugges
ting a neurological or pulmonary disease. The blood count showed a leucopenia an
d neutropenia with left shift. Magnetic resonance imaging showed an important of
maxillary sinus with evidence of repetitions. The patient developed high fever
and unstable blood pressure. Due to worsening of clinical status, was transferre
d to the ICU, therefore, submitted to tracheal intubation (TI) and mechanical ve
ntilation (MV). After the procedure, according to medical evaluation, the patien
t was alert, oriented, ruddy, hydrated, acyanotic and anicteric. On auscultation
, breath sounds present bilaterally without adventitious sounds. On physical exa
mination, abdomen showed soft, painless, and isochoric pupils fotorreagentes. Bl
ood gas analysis showed respiratory acidosis and hypoxemia, and the RX showed co
ndensation basal Right to increase the plot, with the HD current acute respirato
ry insufficiency and pneumocystis cariine HIV and interrogated. In discussing th
e case history with the team rose to HD From: Vasculitis, Wegner • • • Polymyosi
tis Polirradiculoneunte • Guillain-Barre Syndrome • Endocarditis Due to suspicio
n was prompted additional tests: ANA, Anti-native DNA, Anti SN, P. Anco, Aldalas
e, blood cultures, urine, echocardiogram. It has been suggested as a treatment s
olumedrol pulse therapy. According to information gathered with family, the pati
ent had been experiencing shortness of breath for a week before admission, the p
rinciples, the great efforts and, after the exertion, accompanied by diarrhea an
d progressive muscle weakness, up to prevent the patient leaves the bed, suggest
ing a flaccid tetraparesis with evolution of approximately two weeks with two fo
rms of HD: 1 - (Guillain-Barre syndrome or severe 2 + Sinusitis - Sinusitis seri
ous + Thrombophlebitis of stamps. What justifies the departure of the patient to
the operating room for drainage stamps sinuses. Complementary exams
Guillain-Barré show were not found because they were returned to family after de
ath of the patient. Patient arrived at the surgery center saturating 90% with ma
nual ventilation (Ambu bag), cyanotic + + + / 4 +, with mydriatic pupils. In des
cribing the surgery, the patient received general anesthesia, where he made an i
ncision with opening of mucosa on the left maxillary sinus with removal of mater
ial, with suture. During surgery, vital signs were worsening with saturation rea
ching 79% to 80%, even with manual ventilation and Fi02 100%. The patient develo
ped cardiac and respiratory arrest (PCR), with saturation below 75%. Resuscitati
on was carried out maneuvers without success, progressing to death. Throughout t
he ICU stay, from 18/08/2002 to 27/09/2002, the patient received follow-up physi
cal therapy, with three sessions daily physiotherapy team, and conduct daily: Ma
neuvers Bronchial Hygiene (MHB), Vacuum the tracheal tube (ACOT), lung re-expans
ion maneuvers (MRP)€calculus of PEEP when necessary, beyond the maintenance of m
echanical ventilation adequate for blood gas and RX The patient remained on mech
anical ventilator Bird 6400, Mode SIMV + PS, keeping tidal volume (VT) from 460
ml to 480 ml, PEEP of 5 and 13 cmH2O, Fi02 between 40 and 65%, remaining comfort
able. Before the arterial blood gases analyzed by the physiotherapy team, it was
observed that the patient has remained constantly in respiratory acidosis with
hypoxemia The data presented in this case report were collected from medical rec
ords filed in the Hospital Nossa Senhora da Penha, with permission from Dr. Paul
Antonácio, clinical director of this service. V - DISCUSSION Virtually all deat
hs are due to complications of prolonged hospitalization and major complications
with sepsis secondary to pulmonary or urinary infection, pulmonary embolism, de
layed treatment of respiratory insufficiency and disautonomias.Essas complicatio
ns can be minimized with appropriate care by all staff approach for patients (Pa
rsons et al, 2003). For Parsons, 2003, complications of hospitalization can be m
inimized with proper care performed by doctors and nurses, but the author fails
to cite any multidisciplinary team working in an ICU. The occupational therapist
, this enabled, is shown to act at all stages of disease, especially during the
progressive period, in which monitoring of respiratory function should not allow
failures to anticipate and recognize the deterioration of the system (LAWN, DN
ET AL, 2001). By consensus, Sanvito 1997; Lawn, DN et al, 2001; Levy et al, 2003
, describe that q disease progression can be alarmingly rapid, so that the criti
cal functions like breathing can be lost in a few days or hours, developments in
MFP in the patient who was admitted to the OS on the morning of September 18, 2
002, being transferred to the ICU the next day, where he was subjected to MV ..
The rapid evolution of the patient M.F.P. prevented the proper initial monitorin
g. However, under the Sixth Symposium on MV Syrian Lebanese Hospital, in 2002, t
he measurement of lung volumes performed with a spirometer, and the verification
of MIP and MEP performed with the mechanical vacuum pump is indicated for patie
nts with neuromuscular diseases, to assess if the patient is able to maintain sp
ontaneous respiration and when necessary to evaluate the success of weaning. Acc
ording to Lawn, DN, et al, 2001, the progressive weakness of respiratory muscles
leads to increased atelectasis and hypoxemia result in increasing the frequency
and the work of breathing, leading to fatigue of respiratory muscles weakened,
particularly the diaphragm, and finally culminating in hypoxia , hypercapnia and
acute respiratory failure. These changes were observed in the patient MFP by mo
nitoring physical therapy, Rx and blood gases. Respiratory acidosis was observed
in blood gases during the patient's stay in ICU, due to the impairment of respi
ratory muscles, resulting in an increased metabolic demand, hypoventilation, lea
ding to decreased lung compliance and hence to a hypercapnia. Because the patien
t is not being continuously sedated, there was no possibility of correcting this
disorder. Although that literature does not report the need for sedation contin
ues (to adjust the mechanical ventilation), and neither the ventilatory mode tha
t the patient should be ventilated, based on Carlos Carvalho, it was decided to
ventilate the patient in SIMV mode + PS, where the fan calls the patient's effor
t, but offers courses controlled and assisted where needed. During the procedure
of endotracheal aspiration, according to Scala 2001 mechanical stimulation of t
he airways can cause arrhythmias, bradycardia or asystole due to stimulation job
!, And tachycardia may be due to the agitation and hypoxemia of the patient, add
ing to the fact that postural hypotension tachycardia, arrhythmias and hypertens
ion are transient autonomic changes as Diaz, TA et al. Nitrini 2002 and 1991. Th
e physiotherapist must evaluate the need to perform the procedure because the se
cretions increase airway resistance and respiratory work can lead to hypoxemia,
hypercapnia, atelectasis and infections. According Thonson et al., 1994, the pos
itioning and support right to sit, lie down and move the patient with (ILB. are
important to prevent bedsores and contractures, but Parsons et al. 2002, mention
ing that the treatment of dysautonomia are to avoid the change in position. Beca
use of this change and 'the main complication of the disease accounts for one th
ird of deaths so during the patient's care MFP, We aspire to prevent change of p
osition, posture drainage] and conducting exercises, knowing the importance that
this work was discussed by Scalan et al, 2001.
VI-CONCLUSION Through this work, it was concluded that the physical therapy appr
oach to the patient with Guillain-Barre syndrome should be special from the mome
nt that you already have a diagnosis, and it confirmed or just a suspicion. All
data reinforce the need for more research on the disease by health care, while a
lso to the physiotherapists, the approach to these patients. These professionals
should interact on the disease to get an overview, in order to offer this patie
nt a better quality of life. Because of the paucity of the literature on physiot
herapy performance in patients suffering from Guillain-Barre syndrome, we conclu
de that there is need to establish clinical protocols, to ensure a targeted appr
oach to physiotherapy every stage of the disease, interacting whole multidiscipl
inary team, with the goal of minimize and reduce the persistence of this patient
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