Professional Documents
Culture Documents
Pa Tho Physiology of Guillain Barre Syndrome
Pa Tho Physiology of Guillain Barre Syndrome
PRECIPITATING FACTOR
PREDISPOSING FACTOR
Formation of antigen presenting cell in conjunction to histocompatability complex molecules ( homologous or identical amino acids of pathogen and GM1 ganglioside of peripheral myelin sheath)
IgG Activation of CD4 that recognizes antigens from the infectious agent
IgM
molecular mimicry
autoimmunity activation (activated T-cell facilitates opening of the blood brain barrier)
Dull aching pains in the lower back, flank and proximal legs demyelination of nerve segments
IF TREATED EARLY
IF TREATED LATE
IF UNTREATED
bad prognosis
PROGRESSIVE: blurred vision, clumsiness and falling, difficulty moving facial muscles, muscle contraction, palpitations
EARLY: muscle weakness, sensory changes, paresthesia in feet or hands, loss of reflexes begins with the peripheries
EMERGENCY: Breathing temporarily stops, Unable to take a deep breath, DOB, Drooling, Fainting
Respiratory insufficiency
RDS
Dyspnea
Respiratory arrest
Shock
DEATH
Prepared by: Ralph Rhandall R. Espejo Sheana V. Malillin Gretchen I. Maguddayao Rafael C. Palattao
BACK
Post infection to C. Jejuni Hodgkin s Lymphoma Mononucleosis poor hygiene lifestyle/stress food poisoning
BACK
Signs and Symptoms Dull aching pains in the lower back, flank and proximal legs
Clinical History Assessment: Paresthesia, paralysis-(+) CSF findings(+) Electromyogram-detects tiny electrical impulse in the muscle
BACK
CSF examination-unusually protein level of 600 mg/ml Cellular abnormality Nerve conduction test= (-)PTR MRI
Back
Diagnosis diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, hyporeflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis - typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100 1000 mg/dL), without an accompanying increased cell count pleocytosis. A sustained increased white blood cell count may indicate an alternative diagnosis such as infection. Electrodiagnostics Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.
Diagnostic criteria -Required: -Progressive, relatively symmetrical weakness of two or more limbs due to neuropathy -Areflexia -Disorder course < 4 weeks Supportive: -relatively symmetric weakness accompanied by numbness and/or tingling -mild sensory involvement -facial nerve or other cranial nerve involvement -absence of fever -typical CSF findings obtained from lumbar puncture -electrophysiologic evidence of demyelination from electromyogram
Back
Back
Ventilatory support(ventilator)
Back
Campylobacter jejuni is a species of curved, helical-shaped, non-spore forming, Gramnegative, microaerophilic bacteria commonly found in animal feces. It is one of the most common causes of human gastroenteritis in the world. Food poisoning caused by Campylobacter species can be severely debilitating, but is rarely life-threatening. It has been linked with subsequent development of Guillain-Barr syndrome (GBS), which usually develops two to three weeks after the initial illness.
Back
TREATMENT: Patients who are diagnosed with GBS should be admitted to a hospital for close monitoring until it has been determined that the course of the disease has reached a plateau or undergone reversal. Although the weakness may initially be mild and no disabling, symptoms can progress rapidly over just a few days. Continued progression may result in a neuromuscular emergency with profound paralysis, respiratory insufficiency, and/or autonomic dysfunction with cardiovascular complications. Approximately one third of patients require admission to an intensive care unit (ICU), primarily because of respiratory failure. After medical stabilization, patients can be treated on a general medical/neurologic floor, but continued vigilance remains important in preventing respiratory, cardiovascular, and other medical complications. Patients with persistent functional impairments may need to be transferred to an inpatient rehabilitation unit. Continued care also is needed to minimize problems related to immobility, neurogenic bowel and bladder, and pain. Early involvement of allied health staff is recommended. Early recognition and treatment of GBS also may be important in the long-term prognosis, especially in the patient with poor clinical prognostic signs, such as older age, a rapidly progressing course, and antecedent diarrhea. Immuno modulatory treatment has been used to hasten recovery. Intravenous immunoglobulin and plasma exchange have proved equally effective.
MEDICATIONS Immunomodulatory therapy, such as plasmapheresis or the administration of intravenous immunoglobulins (IVIGs), is frequently used in GBS patients.The efficacy of plasmapheresis and IVIGs appears to be about equal in shortening the average duration of disease. Combined treatment has not been shown to produce a further, statistically significant reduction in disability. The decision to use immunomodulatory therapy is based on the disease's severity and rate of progression, as well as on the length of time between the condition's first symptom and its presentation. Risks, such as thrombotic events associated with intravenous immunoglobulin (IVIG), should be taken into consideration. Patients with severe, rapidly progressive disease are most likely to benefit from treatment, with faster functional recovery.
Back