Friday, April 5, 2019
Meningitis Due To Intravenous Immunoglobulin Therapy
Meningitis Due To Intravenous Immunoglobulin Therapy dandy Aseptic Meningitis Due To High Dose Intravenous Immunoglobulin Therapy for Guillain-Barr SyndromeAbs footpathThe absolute majority of unseemly reactions of endovenous immunoglobulin (IVIG) therapy are mild, transient and self-limiting however, potentially serious complications are rare and occur in little than 5% of forbearings receiving IVIG therapy. IVIG associated transient unfertile meningitis is an uncommon adverse effect and this phenomenon has been seldom described in literature. We advertise a case of aseptic meningitis due to high back breaker IVIG therapy in a Guillain-Barr syndrome (GBS) patient. The cerebrospinal precarious (CSF) analysis revealed high cell counts with predominance of lymphocytic cells, raised protein, conventionality glucose level and no developing of the organism on elaboration. He was managed symptomatically with adequate hydration and analgesic. Our patient improved without neurol ogic complications. This case emphasizes the brilliance of recognizing IVIG associated neurological complications in GBS patients.KeywordsAseptic meningitis Guillain-Barr syndrome Intravenous immunoglobulinIntroductionIntravenous immunoglobulin (IVIG) therapy is recommended in Guillain-Barr syndrome (GBS) patients. The majority of adverse reactions of IVIG therapy are mild, transient and self-limiting however, potentially serious complications are rare and occur in less(prenominal) than 5% of patients receiving IVIG therapy. According to Kemmotsu et al., IVIG associated transient aseptic meningitis is an uncommon phenomenon occurring in about 1% of patient.The common adverse effects are headache, nausea and vomiting, myalgia, low backache, tachycardia, mild grade fever and flushing. The serious complications are aseptic meningitis, thromboembolism, transverse venous sinus thrombosis, myocardial infarction, acute stroke, acute brain disease, posterior reversible encephalopathy synd rome, anaphylactic reaction, acute renal failure and serum sickness. IVIG associated transient aseptic meningitis is a very rare complication. Our patient developed aseptic meningitis following intravenous immunoglobulin therapy.Case PresentationA 14 days old boy presented with dickens days history of acute incursion pure motor, progressive, symmetric, areflexic, flaccid quadriparesis without bladder/bowel, bulbar, respiratory symptoms or autonomic dysfunction. He had no history of fever, preceding illness of diarrhea, respiratory tract infection or any toxin exposure. A clinical diagnosing of Guillain-Barr syndrome (GBS) was made with Hughes Disability Scale 4. sum conduction study was suggestive of pure motor, predominantly demyelinating affection of right ulnar, bilateral median, bilateral tibial and bilateral peroneal nerves. Electrocardiogram (ECG) and serum potassium level were normal and urinary porphobilinogen was negative. Clinical compose and electrophysiological para meters fulfilled the Asbury criteria of GBS.Intravenous immunoglobulin was given according to the recommended dose (0.4 mg/kg/day). His weight was 45 kg and total 90 gm IVIG was planned over five days in divided doses. On the fourth day, after receiving 72 grams of IVIG excerpt, the patient developed progressive worsening headache, neck put out and recurrent vomiting. There was no history of fever, loss of consciousness or visual symptoms.His temperature was normal. On neurological examination, meningeal signs neck rigidity, Kernig signs and Brudzinski signs were positive. Bilateral fundi were normal. There were no other focal neurological signs.InvestigationsHemogram and blood biochemistry were at heart the normal range. Blood culture was sterile. X-ray chest was normal and Mantoux test was negative. Lumbar puncture showed normal opening pressure and cerebrospinal fluid (CSF) analysis revealed pleocytosis (Total cell counts 180 cell/dl) with lymphocytic predominance (85%), rais ed protein (110 mg/dl), normal sugar (56 mg/dl) and normal chloride (111 mEq/L) levels. CSF gram stain, AFB stain, KOH preparation, India ink and CSF culture for bacteria and fungi were negative. CSF TB PCR and HSV PCR were negative. MRI brain with gadolinium contrast was normal (Figure 1).Differential diagnosingDiagnosis of acute aseptic meningitis was based on clinical features, CSF findings, negative viral markers and negative culture. The diagnosis of IVIG associated aseptic meningitis was made as there was a strong temporal relationship between onset of aseptic meningitis and high dose IVIG therapy the extensive search for other causes of meningitis was negative and the improvement of symptoms deep down some days. However, possibility of viral meningitis was also thought, but absence of prodromal symptoms, no identifiable rise in serum viral titres and self-improvement of symptoms ruled out the possibility of viral meningitis.TreatmentHis symptoms were managed with hydration and analgesics. No antibiotic drug or antiviral therapy was given. A very slow infusion of IVIG was continued under strict inadvertence until completion of full dose therapy on the next day. The signs of meningeal irritation-neck rigidity, Kernigs signs and Brudzinski signs disappeared over next two days.OutcomeThe patient was discharged in stable condition with Hughes GBS Disability Scale 1. He find completely without any neurological sequelae. He was asymptomatic after three months of followup.DiscussionThe exact pathophysiology of IVIG generate aseptic meningitis is not clear. The various postulated mechanisms of IVIG associated aseptic meningitis are direct toxic effect, immunologic drug hypersensitized reaction, allogenic immunologic reaction, hypersensitivity reaction to various stabilizing agents and cytokine release triggered by the therapy. Wada et al. showed the excitotoxic effect of IVIG in acute encephalopathy following IVIG therapy.The IgG is an active ingredient o f intravenous immunoglobulin capable of crossing the blood-brain barrier, penetrates the meninges, and enters the brain parenchyma.In our patient, aseptic meningitis developed after 72 hours of initiation of IVIG. However, in literature, most patients developed aseptic meningitis within 48 hours of beginning IVIG therapy. According to Jarius et al., aseptic meningitis was frequently associated with polymorphic pleocytosis in the CSF examination however, our patient had lymphocytic pleocytosis.Most of the side effects associated with IVIG are mild, self-limited and related to the infusion rate and no special therapy is ask. Risk factors for IVIG associated aseptic meningitis are history of migraine and rapid, high dose infusion of IVIG. Slower infusion rate, proper hydration, antihistamines and analgesics may help to prevent mild reactions. Systemic steroid may be required in severe cases. Our patient was under strict supervision and no medical treatment was given. He improved with out any neurological complications.Headache and fever are well-recognized side effects of high dose IVIG, aseptic meningitis has rarely been reported in the literature in GBS patients. A high index of clinical suspicion should be kept for IVIG induced aseptic meningitis and should be confirmed by careful neurological examination and CSF analysis.Take-Home MessageAcute aseptic meningitis may develop as a transient, self-limiting complication of high dose IVIG therapy in GBS patient.Early recognition and management is required to prevent permanent neurological sequelae.IVIG therapy should be continued in mild aseptic meningitis as the IVIG infusion is a life thriftiness drug for GBS patient, at a slow infusion rate, with proper hydration, histamines and analgesics.This case emphasizes the importance of recognizing IVIG associated neurological complications in IVIG treated GBS patient.ReferencesFigure LegendsFigure 1. Normal MRI brain with gadolinium contrast
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