Age: 66.0
Sex: F
Vaccine: PPV
Symptoms: Ultrasound abdomen normal, VIIth nerve paralysis, Viral infection
Clinical narrative: Information has been received from a physician concerning an approximately 60 year old female patient who on an unspecified date, was vaccinated IM with a dose of PNEUMOVAX 23 (Lot#: not reported). The physician stated that the patient received PNEUMOVAX 23 and on an unspecified date, the patient developed Guillain-Barre Syndrome. She was hospitalized for an unspecified number of days at an unspecified hospital. She was at the brink of needing a ventilator. She had facial droop. She also had an ascending mixed motor neuropathy. She had difficulty walking. At the time of the report, the patient was recovering from Guillain-Barre Syndrome and was getting treatment. Follow-up information was received from a physician indicating that the 66-year-old patient female was vaccinated IM with a first dose of PNEUMOVAX 23 (Lot# 659485/1715U) in the left arm at 10:02 am on 10-MAY-2008, and the second dose (lot # 662747/1086X, IM). The physician stated that the patient received PNEUMOVAX 23 and in the left deltoid at 10:35 am on 30-APR-2010. The patient also received 2 doses of influenza vaccine, trivalent on 13-NOV-2008 and 29-OCT-2009, 2 doses of influenza virus vaccine on 07-DEC-2005 and 01-NOV-2007, a dose of Td toxoids on 10-NOV-2004, a dose of zoster vaccine live on 04-JUN-2009. It was reported that the female patient who was admitted to Hospital with a symptom complex of intense progressive uncomfortable paresthesias involving her extremities in stocking glove distribution, associated with myalgias, reduced appetite and gait disturbance. The patient was in excellent health on May 18, 2010 at which time she was seen for a comprehensive physical examination. A thorough neurological examination was done at that time and served as a very useful baseline when she was re-examined at the time of admission. The patient was well until nine days later, approximately May 27, 2010. Her initial symptoms were symmetric, proximal myalgias that were moderately severe. There was no rash and no muscle cramping. She was suspected of having a statin induced myopathy or perhaps a viral syndrome. Laboratory studies were sent off and her CRESTOR was discontinued. Her CBC at the time of onset of her symptoms (May 27, 2010) was normal. Attempts at enterovirus identification by PCR was negative. Over the next few days the patient developed the progressive symptoms described above, i.e. the prickling paresthesias, ascending rostrally along with gait imbalance. Furthermore neurological examination in the office on the day of admission was remarkable for dramatic changes in her deep tendon reflexes compared with the exam on May 18, 2010. The patient was admitted to Hospital for further evaluation on 02-JUN-2010. She was seen in the office on the morning of admission and by 7:00 p.m. that evening it was apparent the patient was getting significantly weaker. She had a drawn look to her face and was beginning to develop some ptosis of the left eye. She was getting progressively weaker in the lower extremities. Her initial neurological examination showed her periorbital musculature to be preserved and the masseter muscles were symmetric. The deep tendon reflexes which had been normal three weeks earlier were depressed at the biceps, triceps and brachioradialis but still active. She no longer had deep tendon reflexes in the quadriceps or Achilles tendons. Sensory testing identified the lack of light touch sensation up to the level of the mid forearms and mid calves bilaterally. She had some mild biceps weakness. See admission history and physical. Additional initial laboratory studies identified several areas of concern. Her serum sodium was 122. Her liver function tests were mildly abnormal with an SGOT of 53, SGPT of 132 and an alkaline phosphatase of 199 and a GGT of 121. Although these initial hospital liver function tests were abnormal, there were actually a mild improvement from a set done in the emergency department two days earlier when she was seen at Hospital for approximately the same complaints. The patient's serum osmolality was reduced at 259. Her lipase level was mildly elevated at 73, although she had no GI symptoms. TSH was normal at 3.4. Antibodies for hepatitis At Band C were negative. A CT scan of her head was unremarkable. An ultrasound study of her abdomen did not disclose any abnormalities in the pancreas or spleen. There were no shadowing gallstones seen. The initial impression was the patient had possible Guillain-Barre syndrome. The patient was seen by the doctor in Neurological consultation. He examined the patient and concluded that the patient had an acute immune polyneuropathy that was compatible with Guillain-Barre syndrome. He recommended a number of studies, several of which have been described. A lumbar puncture was done by interventional radiology, and that identified four tubes of clear colorless spinal fluid with only 13 nucleated cells which were 90% mature lymphocytes. Cerebrospinal fluid glucose was normal. Cerebrospinal fluid protein for which normal goes from 15-45, was three times normal at 149 mg. While in the hospital the patient became weaker, and a left facial Bell's palsy developed by the next day. At that point it was decided to administer intravenous immunoglobulin which was given as a test dose on June 4, 2010, following which she had three more doses administered on about that date of 20 grams, 30 grams and again 30 grams respectively. The patient was also started on high dose oral prednisone 60 mg daily on June 4, 2010 and this was reduced to 40 mg on June 9, 2010. Following administration of the corticosteroids and immunoglobulin the patient's neurological symptoms quickly stabilized and the paresthesias reduced. She remained generally quite weak with disproportionate weakness in her lower extremities and left face. The patient continued to have worsening hyponatremia. Serum and urine electrolytes were compatible with inappropriate ADH syndrome, presumably on the basis of her immunologic disorder. At one point her serum sodium got down to 119. During this time she was on intense fluid restriction and was started on DECLOMYCIN 300 mg q8h, which was changed to 150 mg q.i.d. Following that series of steps the patient's serum sodium gradually improved. The patient had some mild hyperglycemia while in the hospital which was simply monitored with Accu-Cheks q.i.d. and a few doses of subcutaneous insulin. Additional testing showed a weakly positive GM-1 IGM antibody with negative IGG antibodies. The patient gradually improved on continued prednisone and DECLOMYCIN. By the time of her discharge her liver function tests had returned to normal as had electrolytes. Her myalgias resolved and her paresthesias were markedly reduced. Post discharge physical therapy will be ordered with the view to help her with her continued weakness and mild sense of imbalance. Initially she had some dysarthria but that had long resolved prior to her discharge, so she did not require speech therapy. Her fluid restriction was lifted and the DECLOMYCIN was discontinued. She was also asked to see her eye care provider in the next two days because of residual incomplete closure of her left eyelid. She was discharged on a tapering course of prednisone, Amlodipine 5 mg daily, Fluticasone nasal spray b.i.d. in each nostril, ASMANEX 220 mg once daily by inhalation, Ranitidine 150 mg b.i.d., resumption of CRESTOR 10 mg daily, losartan potassium (MSD) 100 mg daily, LYRICA 50 mg b.i.d. The patient will see the physician in follow up in the next week or two. Guillain-Barre Syndrome was considered to be an other important medical event, significant disability or incapacity and life threatening by the physician. Bell's palsy, hyponatremia, hyperglycemia, and autoimmune hepatitis were considered to be other important medical event, and life threatening by the physician. A lot check had been initiated. No further information is available. All medical records are available upon request.