PATHOPHYSIOLOGY OF GUILLAIN BARRE SYNDROME ASSOCIATED WITH CAMPILOBACTER JEJUNI INFECTION

PRECIPITATING FACTOR

PREDISPOSING FACTOR

ETIOLOGY Campilobacter Jejuni

Invasion of C. Jejuni through the GI tract

Activation of Immune Response

Migration to Regional Lymph Nodes

Production of Activated T-cells

Production of Activated B-cells

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)

Production of activated T cells

Production of activated B cells

IgG Activation of CD4 that recognizes antigens from the infectious agent

IgM

activation of complement system

molecular mimicry

failure of the immune system

autoimmunity activation (activated T-cell facilitates opening of the blood brain barrier)

production of antibodies that cross react with peripheral myelin sheath

migration of lymphocyte and macrophage adjacent to the area

macrophage cytokine TNF

cell-mediated activation of C5b-C9 membrane complex attack

attacks GM1 gangliosides of peripheral myelin sheath

edema between myelin lamelae and vesicular disruption

Dull aching pains in the lower back, flank and proximal legs demyelination of nerve segments

disruption in the propagation of electrical nerve impulses

peripheral nerve denrvation and atrophy

Autonomic Nervous System dysfunction

GUILLAIN BARRE SYNDROME

IF TREATED EARLY

IF TREATED LATE

IF UNTREATED

Cell body survives

Cell body dies

extensive axxonal destruction

Regeneration of peripheral nerves

collateral reinnervation from surving axona

bad prognosis

RECOVERY OF MOTOR FUNCTION AXON REGENERATION

ascending weakness progresses

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

Treatment and Medication

Weakening of the diaphragm and respiratory muscles

Respiratory insufficiency

RDS

Dyspnea

Respiratory arrest

Shock

DEATH

Prepared by: Ralph Rhandall R. Espejo Sheana V. Malillin Gretchen I. Maguddayao Rafael C. Palattao

 -Age ( Age 16-25, 45-60y/o) -Sex (more prevalent to men)

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Post infection to C. Jejuni Hodgkin s Lymphoma Mononucleosis poor hygiene lifestyle/stress food poisoning

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 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

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 Signs and Symptoms -Loss of sweating -Sinus tachycardia -Hyper/hypotension

CSF examination-unusually protein level of 600 mg/ml Cellular abnormality Nerve conduction test= (-)PTR MRI

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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

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 SPEECH THERAPY PHYSICAL THERAPY EXCERCISE

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 Ventilatory support(ventilator)

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 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.

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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.
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