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Abstrak :
Background Prodromal factors of Guillain-Barre syndrome (GBS) are often associated with previous viral infection (60%). The ailment supported by the acquired immunomediated disorder concept. Viral hepatitis is very rarely found in GBS, preceded by cytomegalovirus (15-18%), Campylobacter jejuni (28%), and Epstein-Barr virus (5%). There is no specific etiology of GBS because those viruses usually appear sporadically (subclinically). All hepatitis virus infection can cause neurological complications, including GBS. Case Report We report two cases of hepatitis A virus infection (HAV) in GBS patients in Dr. Sardjito General Hospital during 5 years of observation (1996-2000) from 92 GBS patients. The diagnosis of HAV was based on more than 2 times increment of transaminase enzyme, positive IgM anti HAV, negative HbsAg, and negative IgM ami HCV. The diagnosis of GBS was based on clinical symptoms of acute generalized paralysis, cerebrospinal fluid examination, and electromyelography. In both cases, sub-clinical and sporadic symptoms appeared several days before paralysis, which makes it more likely that the prodromal period of GBS occurred at the same time of HAV incubation period. Discussion The incidence of HAV in GBS patients during 5 years of observation was 2%. This corresponds with the case reported by Verona et al, 1996 and Pelletier et al, 1985, i.e. the presence of peripheral neuropathy (n. facialis and n. occulomotorius). Possible alternative pathways for hepatitis virus complicating as GBS are perivascular and endometrial peripheral nerve infiltration by mononuclear cells, T cell sensitization, stimulation of IL-2 growth factor surface receptor, and B cell stimulation. All of the conditions mentioned above causes necrotizing arteritis, vascular occlusion, and at the end, segmental demyelinization. Hepatitis virus may replicate in the central nervous system or peripheral nervous system, subsequently developing into multiple neuropathy disorder and poly arteritis. Conclusion The diagnoses of HAV and GBS in both cases were established. HAV is one of several viruses that may trigger GBS. In both cases, HAV infection was sub-clinical and sporadic. Symptoms of hepatitis infection subsided along with improvements in the patient's neurological status. Acute viral hepatitis has a wide clinical spectrum and laboratory manifestation that is in accordance with the severity, varying from unclear symptom (anicteric) to jaundice. Acute hepatitis A, B, C infections have the same symptoms in general. However, hepatitis B and C tend to be more severe. The mildest symptoms are transaminase enzyme level increment, no jaundice, gastrointestinal symptoms, flu-like symptoms, and sometimes it can not be diagnosed. The more severe symptoms are jaundice with obvious generalized symptoms.' The incidence of hepatitis A is difficult to be determined accurately because of its characters, i.e. sporadic, endemic, and has a high rate of asymptomatic infection.23-4

Abstrak :
Latar Belakang : Sindroma Guillain Barre SGB , menyebabkan pasien gagal napas dan memerlukan perawatan dan pengawasan di unit ruang rawat intensif. Beberapa faktor risiko dipikirkan terhadap terjadinya gagal napas pada SGB, berdasarkan gejala klinis yang timbul saat pasien masuk rumah sakit. Metode : Penelitian ini berdesain potong lintang dengan mengambil data sekunder dari pasien SGB yang menjalani perawatan inap di RSUPNCM sejak Januari 2010-Mei 2018. Data dianalisa dan dilakukan penghitungan dengan multivariat regresi logistik. Hasil : Sebanyak 59 pasien memenuhi kriteria inklusi. Insiden terjadinya gagal napas pada pasien SGB sebesar 25. Kelemahan bulbar OR 26,964; IK 95 2,050-354,616 , disotonomia OR 71,646;IK 3,039-1689,312, dan total skor Medical Research Council MRC OR 0,871; IK 95 0,776-0,978 merupakan 3 variabel yang secara independen berisiko tinggi untuk terjadinya gagal napas pada SGB. Faktor risiko yang tidak berhubungan secara bermakna terhadap kejadian gagal napas adalah usia, riwayat antesenden infeksi, durasi awitan hingga admisi, arefleksia, kelemahan fasial, oftalmopegia, dan tipe patologi SGB. Kesimpulan : Kelemahan bulbar, disotonomia dan total skor MRC merupakan faktor risiko untuk terjadinya gagal napas pada pasien SGB dan disarankan agar mendapatkan perawatan di Intensive Care Unit ICU.

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Background Guillain Barre Syndrome GBS may cause respiratory insufficiency and requires care and supervision in the Intensive Care Unit. Several risk factors are thought to be the occurrence of respiratory failure in GBS, based on clinical characteristics at hospital admission. Methods: A cross sectional study was conducted by taking secondary data from GBS patients who were admitted to the Cipto Mangunkusumo hospital from January 2010 to May 2018. Data were analyzed and calculated by multivariate logistic regression. Results: A total of 59 patients met the inclusion criteria. The incidence of respiratory failure in GBS patients was 25 . Bulbar weakness OR 26,964 95 CI 2,050 354,616 , dysotonomia OR 71,646 95 CI 3,039 1689,312 , and total score of Medical Research Council MRC OR 0,871 95 CI 0,776 0,978 are 3 variables that are independently high risk for the occurrence of respiratory failure in GBS. Risk factors that are not significantly associated with respiratory failure are age, antecedent infection history, duration of onset to admission, areflexia, facial weakness, ophthalmopegia, and type of GBS pathology. Conclusions: Bulbar weakness, dysotonomia and total MRC score were risk factors for respiratory failure in GBS patients and were advised to receive treatment in the Intensive Care Unit ICU.

Abstrak :
A 46-year-old man was admitted to ICU with a diagnosis at the time of admission of Guillain Barre Syndrome (GBS) and sepsis due to suspected Ventilator-Associated Pneumoniae (VAP). Specimens for the following laboratory workup were inquired, i.e. complete blood count, culture and resistance workup using specimens obtained from the tip of suction pipe, urinalysis and urine culture, blood culture and resistance, procalcitonin and lactate levels. Neutrophilia was found along with increased procalcitonin and lactate levels, which supported the sepsis diagnosis. Moreover, the result of culture from suction pipe demonstrated colonies of Pseudomonas luteola MDRO, which might be originated from the oropharyngeal colonization of the patients due to poor oral hygiene and ineffective oral hygiene nursing; therefore, the colonies of the microorganism were swabbed away when obtaining the specimens. Ineffective oral hygiene nursing may have a potency to cause VAP and recurrent VAP.