Age: 68.0
Sex: F
Vaccine: FLU3
Symptoms: Electromyogram abnormal, Electrophoresis protein normal, Fatigue, Guillain-Barre syndrome, Haematocrit normal
Clinical narrative: Case number PHEH2012US022408 is a spontaneous report received initially from a pharmacist on 12 Nov 2012 with a follow up report from pharmacist received on 30 Nov 2012 and 12 Feb 2013. This case refers to a 69-year-old female patient. The patient's medical history included hypothyroidism and penicillin allergy. The patient denied alcohol, tobacco or illicit drug use. This polymedicated patient was vaccinated with FLUVIRIN (batch number: not reported) intramuscularly in left deltoid on 13 Mar 2012. On 21 Apr 2012, the patient was hospitalized for chronic debilitating demyelinating polyneuropathy. She was admitted in emergency room. The patient was noted to have weakness in her muscles of her bilateral lower extremities but normal function of the distal muscles. The patient denied upper extremity weakness, changes in sensation, changes in sensation to the lower extremities, problems controlling her bowels or bladder and other neuro deficits with the exception of possible difficulty swallowing and increased fatigue with chewing. She also denied visual symptoms, tinnitus and sensation changes. Physical examination was done and was found to be normal. Laboratory tests hemoglobin, hematocrit, platelets, white blood cell count, sodium, potassium, chloride, CO2, blood urea nitrogen (BUN), creatinine, glucose were found to be normal. The patient experienced bilateral lower extremity weakness progressive over the previous 3 weeks. Differential diagnosis included Guillain Barre syndrome, transverse myelitis, vascular spinal lesion or other spinal pathology. MRI (magnetic resonance imaging) to date had been unremarkable for any causes that would match the patient's present symptoms but the timeline and progressive nature would make Guillain Barre high on the differential. The patient had received a small dose of steroids during these 3 weeks but she was no longer taking them. Repetition of the lumbar MRI scan was planned since it was dated over 2 weeks ago to see if any new lesions have recurred. She consulted neurologist, who had encouraged checking LFT's (liver function test) in the morning before and PT (prothrombin time) and INR (International Normalized Ratio) in case a lumbar puncture is required. Planned to start the patient on DVT (deep vein thrombosis) prophylaxis and consult physiotherapist and occupational therapist to assist with movement. The patient had negative antibodies for acetylcholine receptors which has made this diagnosis very unlikely. TSH (thyroid stimulating hormone) was planned to be performed to ignore "euthyroid status" (as reported). Pain was controlled with oxycodone and acetaminophen. On 19 Jun 2012, prothrombin time, creatinine, BUN, calcium, electrolytes, CK-MB, prealbumin, western sedimentation rate, protein electrophoresis serum and some miscellaneous tests were found to be normal. On 19 Jun 2012, the acetylcholine receptor (AChR) antibody titer was found to be borderline and negative for muscle specific receptor tyrosine kinase (MuSK) antibody titer. It was commented that the low level of AChR antibodies cannot be categorized as either positive or negative, due to their uncertain clinical significance. Repeat test with AChR and MuSK was done and results found to be same. On 20 Jun 2012, CK (creatine kinase), lupus panel, cortisol total, neutrophil cytoplasmic antibody, protein electro random, cryoglobulins were found to be normal. During the follow-up visit to physician on 19 Jun 2012, the patient had been out of the rehabilitation for 2-3 weeks, treated and admitted for a dominant lower extremity presumed inflammatory neuropathy. The patient had profound proximal weakness in the hip flexors, adductors, abductors, quadriceps in the lower extremity, relatively preserved in the upper extremity although she was areflexic. The patient had severe neuropathic pain that was relentless. She presented to the office after a second gammaglobulin infusion. Physician believed the 5-6 week mark, due to what appeared to be subjective decline in strength. A recent EMG (electromyogram) had shown diffuse axonal components to a neuropathy even in the para spinal muscles in the lower extremities, not in the upper extremities. The patient points to pain in the lower thoracic region. Today she was unable to swallow and food was coming out her nose. Physical examination was found to be normal. The patient's facies and cranial nerves appear to be intact. The patient needs help extending her legs but can lock her knees. Distally the motor power was greater than 3+. There was no sensory level on her abdomen or distally to pinprick and cold. The physician interpreted that the patient had progressive weakness with now dysphasia, presumed inflammatory neuropathy with predominance in the lower extremity, relentless neuropathic pain and wasting. Physician planned to admit her to the hospital where she would be placed on IV fluids and then a swallow study would be done as soon as possible. Inflammatory markers would be repeated including a serum protein. Immunoelectrophoresis and urine protein electrophoresis and Bence Jones. It was reported that the patient may benefit from repeat neuroimaging of the thoracic lumbar spine and differential relentless pain with neuropathic qualities. Further recommendations and potential lumbar puncture would be performed. The seriousness of the event chronic debilitating demyelinating polyneuropathy was reported as hospitalization and disability by the pharmacist. Outcome of the event of chronic debilitating demyelinating polyneuropathy was condition unchanged. Causality of the events was not reported. Follow up report from pharmacist received on 30 Nov 2012: Updated route of administration of vaccine, event (chronic debilitating demyelinating polyneuropathy), its outcome and seriousness. Follow up report from pharmacist received on 12 Feb 2013: Updated new events (muscle weakness, dysphagia, fatigue, myelitis transverse, spinal vascular disorder, nerve pain, thoracic pain, dysphasia, pain, and muscle atrophy), concomitant medications, treatment medications, medical history, clinical course of the events, laboratory data and narrative updated.