A man with laboured breathing, abdominal pain and vomiting

A man in his 40s was hospitalised with suspected gastroenteritis and dehydration. The patient had asthma and an autism spectrum disorder. He lived in his own house and was self-sufficient, and his general condition had been normal prior to his admission.

His medical history was somewhat unclear, as his next of kin had been away for a week, and he could not be expected to give a full account of his situation. He had allegedly been vomiting for about two days, and had a cough with gagging. He also indicated pain in the throat, chest and abdomen. His next of kin stated that he found food in waste containers and that he had a lot of old food in the house.

On admission he was somnolent and weak and was mobilised into a sitting position with a great deal of help. His mucous membranes were dry, and he had diffuse abdominal tenderness. His blood pressure was 124/68 mm Hg, and fell to 92/51 while his medical details were being taken, but was stabilised by administering intravenous fluid. His urine was dark, he was afebrile and his pulse was regular at 70 beats/minute. His breathing was rapid and shallow, with a frequency of 26 per minute, employing accessory respiratory muscles. There was muffling bilaterally over the lungs.

An exploratory neurological examination revealed weakness of the extremities, equal bilaterally. It was noted that his pupils were dilated and did not react to light. There were no focal neurological deficits. His reflexes were equal bilaterally but were not graded.

Arterial blood gases showed pH 7.33 (7.36–7.44), pCO₂ 6.41 kPa (4.7–5.9 kPa), pO₂ 9.91 kPa (10.4–13.2 kPa), O₂ saturation 92.9 % (94–100 %) and lactate 0.9 mmol/l (0.5–1.6 mmol/l). Exploratory blood tests revealed CRP 9 mg/l (< 5 mg/l), leukocytes 12.8 giga/l (3.5–10.0 giga/l), haemoglobin 14.1 g/100 ml (13.4–17.0 g/100 ml), D-dimer < 0.4 mg/l (< 0.5 mg/l), creatinine 94 µmol/l (60–105 µmol/l), urea 13.5 mmol/l (3.2–8.1 mmol/l).

Chest X-ray was perceived as normal, but the radiologist later described veiling and opacities basally on the left side of the image. Abdominal overview X-ray might suggest obstipation. Because of the report of a possible fall, headache and vomiting, a head CT was also taken, but revealed no pathology.

About seven hours after the man had been examined in Acute Admissions, a ward nurse contacted a doctor because the patient was sluggish and his oxygen saturation had fallen to 85 %. While the doctor was present, the patient experienced respiratory and circulatory failure.

Advanced cardiopulmonary resuscitation was started. The initial rhythm was pulseless electrical activity (PEA). After four cycles of CPR, spontaneous circulation was re-established, but 20 minutes later the patient was still not conscious. He was intubated and moved to the Intensive Care Department, where targeted temperature management was started.

These scans provided no clarification. The head CT revealed no pathology. There were no signs on the CT thorax, abdomen and pelvis of pulmonary embolism or aortic dissection.

There were extensive opacities in the lower lobes of the lungs – possibly atelectasis, but infectious opacities had to be suspected. Echocardiography revealed an ejection fraction (EF) of 47 % and good contractions in all sections. No valve faults were found. A lumbar puncture was performed, and findings were normal.

Sedation was discontinued the next day, and the patient was extubated. Lack of swallowing movements and weakness in both lower extremities were noted. In the course of the day he suffered increasing respiratory failure and had to be reintubated. Because of these findings, a neurological consultation was requested.

A clinical neurological examination revealed a reduced level of consciousness. It was not possible to communicate with him, but he showed aversive responses to pain stimuli proximally of the umbilicus.

The patient lay with half-open eyes, possible bilateral ptosis and neither opened nor closed his eyes on request. An examination of the cranial nerves revealed bilaterally equal, dilated pupils without reaction to light. Conjugated eye movements were observed, with no signs of nystagmus. There was no information as to whether he had had double vision, and no signs of facial paresis.

The patient did not squeeze hands when requested to do so, but had spontaneous, bilaterally equal movements of the upper extremities. Attempts at testing gave the impression of generally limited strength in the upper extremities. There were no signs of spontaneous movement in the lower extremities. Sensibility could not be tested because of his reduced level of consciousness. There were no signs of ataxia, no triggerable reflexes in the upper or lower extremities, and no plantar inversion.

The neurologist contacted the Infectious Diseases Control on-duty medical officer at the Norwegian Institute of Public Health because of the suspicion of botulism. Later the same evening the patient received botulism antitoxin. It was decided also to administer immunoglobulin because of the possibility of Guillain-Barré syndrome. Antitoxin treatment consists of a single dose, immunoglobulin therapy must be administered daily while awaiting clarification.

A stool sample was obtained from the patient. PCR analysis of faeces for Campylobacter was positive, but the bacteria could not be cultured. A further lumbar puncture was performed after five days, but the results were still normal. Samples for botulism diagnostics were sent to the Institute for Food Safety and Infection Biology, the Norwegian University of Life Sciences, Oslo Branch. Four days later, the botulism diagnosis was confirmed – after two mice that had been injected with serum from the patient developed clear symptoms of botulism and died.

The immunoglobulin treatment was discontinued. In view of expected long-term respirator treatment, the patient was given a tracheostomy. Piperacillin/tazobactam treatment continued because of assumed aspiration pneumonia.

The patient rapidly improved – respirator treatment was discontinued and the tracheostomy tube removed only four days later. After 11 days in Intensive Care, the patient was moved to an ordinary ward. He was mobilised with a walker and able to eat and drink independently. Two days later he was reported to the local authority as having completed treatment.

However, he remained in the department for a while, waiting for a rehabilitation place. A further neurological examination 18 days after the antitoxin was administered found him virtually restored to his habitual condition.

He is now ambulant without aids and has no focal neurological deficits. He has a slight limp after earlier sciatica.