Age: 2.0
Sex: M
Vaccine: HEPA, HEPA
Symptoms: Laboratory test abnormal, Nausea, Nervous system disorder, Psychomotor hyperactivity, Pyrexia
Clinical narrative: Information has been received from a physician concerning a 2 year old male who on approximately 03/25/2002 was vaccinated with one dose of hep A virus vaccine inactivated. Within days, the pt experienced "significant neurological impairment." The physician noted that he considered hospitalizing the pt. The pt sought medical attention. Upon internal review, the pt's "significant neurological impairment" was considered to be an other important medical event. Additional info has been requested. Follow up info from the physician noted that the pt was a healthy, normal child with no neurological symptoms who was immunized with the vaccine to go on vacation with his family. Within five hours post vaccination, the pt became unsteady on his feet. His condition worsened and within three days he had developed ataxia. The child became totally disabled and was unable to speak, eat or walk. The pt was hospitalized and had a work-up was done. He had two MRI, a CAT scan and some genetic testing. All of the tests were normal. The pt did have oligoclonal bands, which were producing, antibodies within the central nervous system. The pt was treated with intervenous immunoglobulins to clear the antibodies. He was seen one week after discharge from the hospital and was showing some mild improvement. The physician reported that he has sent blood and spinal fluid for PCR analysis for hep A. He reported that he hopes that the condition is self-limited and that it will run the course and the child will recover. Additional info has been requested.  A 15-day follow up report received 8/11/2003 adds: On 09/09/2002, additional follow-up info was received from the physician stating that the pt has severe acute cerebellar ataxia. The pt has completely lost the ability to feed himself and to walk. He has fallen and broken an arm due to the ataxia. The pt had been admitted twice to the hospital for IVIG treatments.  On 12/19/2002, additional follow-up info was received from the physician stating that the pt's medical condition was improving. The child was now feeding himself, walking 10-20 steps, and sleeping through the night. The physician also reported that he was "very comfortable with the pt's diagnosis of cerebellar ataxia, based on the clinical findings and that the ataxia was far out of proportion to the other symptoms. Ruling against a diagnosis of encephalitis are the results of the pt's tests including the fact that his CSF was negative, and an elevation in the oligoclonal bands." The physician feels that this case is vaccine related. On 12/20/2002 it was reported that there was an insufficient amount of specimen to receive results of the PCR analysis for Hepatitis A. Follow up info indicated that the pt's cerebellar ataxia has significantly improved. The nurse reported that the pt "only sometimes walks with an unsteadiness on his feet". She also reported that the pt recovered completely from difficulties with speech and the broken arm. Please see the laboratory sectin for all relevant lab results. The pt's events were considered to be disabling. Additional info is not expected. A 15-day follow up report received 10/22/2003 adds: Info has been received regarding a case in litigation concerning a minor male pt who was born a healthy, normal child, and who reached his developmental milestones at appropriate stages, who in late March 2002, was vaccinated with a dose of hepatitis A virus vaccine inactivated. The alleged result of the vaccination was that diagnostic studies revealed that the pt was experiencing serious side-effects including cerebellar ataxia due to the vaccine. Said defective condition of the vaccine caused the pt to suffer brain damage. Upon internal review, experiencing serious side-effects, cerebellar ataxia, and brain damage were considered to be other important medical events. No further info is available. It has been determined that WAES #0309USA01849 is a duplicate report of WAES #0205USA02619. Therefore, WAES #0309USA01849 is being deleted from our files and the reports consolidated into WAES #0205USA02619. A 15-day follow up report received 12/31/2003 adds: Additional follow up from medical records indicated that the child fell from his bed injuring his right forearm on 08/21/2002. He was splinted and found to have a "both bone forearm fracture". The child presented to the office for evaluation. It was reported that the child was on an oral antibiotic at that time for a new onset of a right ear infection that began on 08/21/2002. The extremity exam revealed mild deformity with some ecchymosis over the mid and ulnar aspect of the forearm. There was a good palpable pulse and he had spontaneous motion of his digits. There was no elbow or shoulder tenderness. The remainder of his musculoskeletal exam and all other physical exams were normal. X-rays were taken of the right arm and showed "both bone forearm fracture" with about 20 degrees of angulation. The radial fracture is more proximal than the ulna. There was no significant displacement and the left forearm films were negative. The child was placed in a long arm splint and was scheduled for closed reduction and casting under anesthesia. The procedure was at day surgery on 08/23/2002. They performed a "closed reduction casting of right forearm fracture". The report indicated that the child never broke bones before, never wore a cast or brace and never had problems or complications with surgery, anesthesia, infection, bleeding or other surgical complications. Additional follow up info was received from medical records on 11/18/2003. Additional follow up information was received from medical records. On 01-Apr-2002, the patient was notd to be significantly more impaired than on previous days. He stumbled after every few steps. He ahd tremors in his hand whenever he would reach for an object which improved over 2-3 hours, but still persisted. On 04/08/2002, the child was seen for his acute onset ataxia. An MRI with contrast was obtained and was completely normal. There was no evidence of cerebellar lesions or any mass lesions. Given the MRI at that time, the physician thought that the "overwhelming likelihood remains that this is acute cerebellar ataxia on a postinfectious basis". On 04/18/2003, the ataxia was no better, and was, in fact, somewhat worse. The child was having difficulty walking independently. His mental status continued to be perfect. He had little trouble using his hands, but his gait was the main problem. He had an intercurrently illness the week prior resulting in high fevers, and during this his ataxia worsened. The illness abated. At that time, he had no fevers but he had not really recovered his neruologic function. The illness appeared to have been an upper respiratory infection for which he was seen in the ER and was presumed viral. On 05/02/2002, the child appeared to make some significant improvement. He went to daycare for a full week and was ambulating well if he could hold on to walls or furniture. However, after that point he developed an intercurrently viral infection which he apparently caught from his father. This consisted of mild respiratory symptoms. However, there was an immediate worsening of his ataxia back to its worst level. It has never gotten worse than its current level, and it appeared to be making very mild improvement as he is getting over this infection. Routine chemistries, liver functions, and CBC were normal. An alpha fetoprotein to screen for ataxia telangiectasia was normal at 2.0. At the follow up visit on 05/21/2002, the physician noted progressive deterioration in function over the last month. He was completely non-ambulatory. He was able to sit up unassisted but was unsteady in doing so. He was able to manipulate objects with his hands, but clearly had decreased fine motor skills. He had regression of his speech, although he was still able to communicate effectively. He was fully alert and interactive and followed commands, and there did not appear to be a depression of his mental status. The parents initially attributed his worsening to an intercurrent illness, but he had been completely afebrile for the last several weeks with no improvement noted. At this point, the physician still believed the child had acute cerebellar ataxia. However, he noted it to be much more severe than cases seen following varicella infections. Colleagues of the physician agreed that acute cerebellar ataxia was "the most likely diagnosis and believe that the child was recently admitted for intravenous immunoglobulin treatment (IVIG) (2 grams/kg). The child had no significant adverse reactions to the intravenous immunoglobulin. At the time of discharge, there was no change, better or worse. However, over the following week, he had shown slow but steady improvement. He was able to reach and grasp for objects with more precision and consistency. He was not able to walk independently, but he was requiring significantly less support when he did attempt to walk. More strikingly, the child had significant improvements in his mental status. He was less agitated. He continued to have occasional tantrums, but they were less intense and long acting and he was more responsive to his parent's management. On 06/21/2002, more than 3 weeks since the IVIG treatment, the pt was seen again for followup. There did initially appear to be significant improvement particularly in the area of his mental status and speech. However, his ataxia did not show any further benefits. In fact, it has had a bit of a relapse in terms of the amplitude and strength of the tremor that he had. At the followup appointment on 07/19/2002, the physician indicated that the pt had "essentially plateaued". He maintained much of the benefit he received after the IVIG treatments. On 08/16/2002, it was noted that the child had his last dose of IVIG "just over 3 weeks ago". The parents reported no initial response to the IVIG, but, after about 10 days, there was a persistent and dramatic improvement in the child's motor function. They showed a video from 08/06/2002, which showed: the child walking 5 to 6 steps and much further when holding onto an object for support; the child feeding himself without any difficulty and no dysmetria; and his head tremors were completely resolved. Unfortunately, the child developed an intercurrent viral infection, and since that infection began on approx 08/12/2002, there had been a steady worsening of the child's function again. He is still improving over where he was before the 2nd dose of IVIG, but he has lost significant skills. The child continued to take amitriptyline hydrochloride (Elavil) 10mg q hs. The urine catecholamine sent in the hospital last admission were normal, ruling out a neuroblastoma as a cause for autoimmune ataxia. On 12/18/2002, the physician indicated that the ataxia showed striking improvement over the previous 4 months. The child was seen again for follow up in 07/15/2003 for his ataxia. Since the December visit, the child has made very slow, but very consistent, progress: he was fully ambulatory; he can run; he can throw a ball, though he has trouble catching; he feeds himself indepenently, although he still spills a great deal when he uses silverware; he has had no more falls or injuries due to his ataxia. The child remains behind in speech, but he is beginning to express himself more. He is saying many single words and word combinations. His symptoms continue to fluctuate, both with intercurrently illnesses and interestingly with animal bites. Whenever he has a cold or fever there is a significant worsening of his ataxia that lasts several days. On the other hand, the child was stung by a wasp and both parents noted a dramatic improvement in his symptoms, also lasting several days around that time. On 04/04/2002, an MRI of the brain with and without contrast was unremarkable. On 05/01/2002, blood glucose was 121 mg/dl (elevated), BUN/Creatinine was 30.0 (elevated), glutamine was 393 umol/L (low), and methionine was 16 umol/L (low). On 05/22/2002, a MRI of the brain was unremarkable without abnormal signal or mass effect. On 05/22/2002, enterovirus detection by RT-PCR was negative. On 05/28/2002, a CT chest, abdoment, and pelvis were normal. All other laboratory results are listed below. The cerebellar ataxia, upper limb fracture, fall, impaired self care, speech disorder and physical disability were considered to be disabling. The brain damage and serious side effects were considered other medical events. The follow up info received on 11/12/2003 contained the following adverse experiences: ear infection (08/20/2003). The follow up info received on 11/18/2003 contained the following adverse experiences: upper respiratory infection (04/18/2002); viral infection (04/18/2002, 05/02/2002 and 08/12/2002). Additional info is not expected.  Follow upon 01/08/04: "Follow up information received on 12/22/03 contained the following adverse experiences: croup(02/18/03); nausea(02/14/03); vomiting(02/14/03); diarrhea(02/14/03); Hyperactivity(05/12/03) and left earache(02/18/03).  No further information is available."  Follow up information received on 01/16/2004 states. On 14-Feb-2003 the patient develope nausea, vomiting and diarrhea. At that time, the patient was also noted to have left ear pain, but was afebrile. On 18-Feb-2003, the patient had a cough and a clear runny nose and was not sleeping well. A diagnosis of croup was made. At that time, the patient was still noted to have an earache. On 13-May-2003, his hyperactivity increased as he "can't keep stil" and kicked classmates. He complained of losing his balance more. On 29-Aug-2003, the patient developed ear pain. No further information is available. On 11-Nov-2003, at a well check-up, the patient had markedly decreased speech. He could put 3-4 words together, but it was hard for the physician to understand some of his sentences. The patient was noted to walk unsteady by better than previously. He was also able to run better than at his last visit, but stumbled when stopping. A finger-nose-finger test was noted to be off some. The cerebellar ataxia, upper limb fracture, fail, impaired self care, speech disorder and physical disability were considered to be disabling. The brain damage and serious side effects were considered other important medical events. The follow up information received on 12-Nov-2003 contained the following adverse experiences: ear infection (20-Aug-2003). The follow up information received on 18-Nov-2003 contained the following adverse experiences: upper respiratory infection (18 Apr 2003) and viral infection (02-May-2004 & 12 Aug-2002). Follwo up information received on 22-Dec-2003 contained the following adverse experiences: croup (18-Feb-2003), nausea (14-Feb-2003), vomiting (14-Feb-2003), diarrhea (14-Feb-2003); hyperactivity (12-May-2003) and left earache (18-Feb-2003). The follow-up information received on 19-Feb-2004 contained the following adverse experience: trouble sleeping (?-Jul-2002). No further information is available. (OMIC)  Follow up on 07/28/04 states: "The follow up information received on 11/12/03 contained the following adverse experiences: ear infection (07/20/03). The follow up information received on 11/18/03 contained the following adverse experiences: upper respiratory infection (04/18/02) and viral infection (05/02/04 and 08/12/02). Follow up information received on 12/22/03 contained the following adverse experiences: croup (02/18/03); nausea (02/14/03); vomiting (02/14/03); diarrhea (02/14/03); hyperactivity (05/12/03) and left earache (02/18/03). The follow up information received on 02/19/04 contained the following adverse experience: trouble sleeping (07/00/02). No further information is available. All medical records will be provided upon request."