Scandinavian Journal of Infectious Diseases

ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19

Fulminant Meningococcemia Starting as an Acute Gastroenteritis Helge L. Waldum & Jan E. Fuglesang To cite this article: Helge L. Waldum & Jan E. Fuglesang (1977) Fulminant Meningococcemia Starting as an Acute Gastroenteritis, Scandinavian Journal of Infectious Diseases, 9:4, 309-310, DOI: 10.3109/inf.1977.9.issue-4.10 To link to this article: http://dx.doi.org/10.3109/inf.1977.9.issue-4.10

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Date: 28 April 2016, At: 02:17

Scand J Infect Dis 9: 309-310, 1977

Case Report

Fulminant Meningococcemia Starting as an Acute Gastroenteritis

Downloaded by [University of California Santa Barbara] at 02:17 28 April 2016

HELGE L. WALDUM and JAN E. FUGLESANG From the Departments of Medicine and Microbiology, University Hospital of Tromss, Norway

ABSTRACT. A 61-year-old man with fulminant meningococcemia starting as an acute gastroenteritis is presented. This is a rare presentation in children and extremely unusal in adults. However, the possibility of meningococcemia should be considered in any seriously ill patient with gastroenteritis.

INTRODUCTION Meningococcal infections usually present clinical pictures that are readily identified either as meningitis or meningococcemia with a haemorrhagic rash. Sometimes, however, the symptoms and signs are unspecific, and the correct diagnosis might therefore be delayed. Here we report a case with acute meningococcemia mimicking an acute gastroenteritis.

CASE REPORT The patient was a 61-year-old man who for many years had used a small dose of corticosteroids because of moderate bronchial asthma. Otherwise, he had been in good health until the morning he was admitted to the hospital. He then had abdominal cramps and profuse diarrhoea. During the following hours he passed large volumes of watery stools. In the afternoon he was found awake with involuntary bowel movements. He subsequently lost consciousness and was taken to hospital. On admission, 12 h after initiation of symptoms, he was deeply shocked with peripheral circulatory failure and hypotension. At that time, however, there was no petechial rash and no stiffness of the neck. The rectal temperature was normal. Laboratory examination revealed normal hemoglobin (15 g/dl), and an erythrocyte sedimentation rate of 1 mm/ h. His WBC count was 1500/pI. A severe thrombocytopenia (12 500/pI)was detected. Arterial blood gas determinations showed a pC0, of 61 mmHg and an oxygen saturation of 60%. The blood pH was reduced to 7.15 with a base excess of -8 mmol/l. The blood glucose concentration was 49 mg/dl. Serum amylase was elevated to 740

u/l (normal 100-350). The serum urea concentration was normal. Blood drawn for determination of serum electrolytes and ethanol test was unfortunately not analysed because of the final outcome. An ECG was normal at admission. Likewise, plain X-ray films of the chest and the abdomen did not show any abnormalities. Lumbar puncture was not done. Immediately after admission, intravenous fluids, antibiotics (penicillin G , sulphonamide and chloramphenicol) and corticosteroids were administered. About half an hour after admission, the patient developed a haemorrhagic rash and respiratory arrest. He was taken into a respirator, but cardiac arrest occurred 1 h later. Autopsy revealed haemorrhagic necrosis of the adrenals and marked gastroenteritis. The meninges were normal. However, a blood culture drawn before death yielded growth of Neisseria meningitidis, type B.

DISCUSSION In this patient meningococcemia presented itself as an acute gastroenteritis. This is a rare clinical presentation, occasionally observed in children (1) and, to our knowledge, only once described in adults (2). The reason why meningococcemia followed this course in our patient is unknown. The longterm corticosteroid medication in addition to an overwhelming infection might have induced an acute adrenal insufficiency. However, the dosage of prednisone used (5 mg per day), would usually not induce any serious suppression of the suprarenal glands. Another possiblity is that the gastroenteritis was secondary to adrenal insufficiency due to haemorrhagic necrosis as demonstrated at autopsy. Scand J Infect Dis 9

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H . L . Waldiim and J . E . Firglesang

The reduced blood glucose concentration at admission might support this. However, the symptoms started at least 12 h before any other signs of bleeding tendency. We therefore think that the haemorrhagic necrosis of the suprarenals was a late event, and we suggest that the gastroenteritis most likely was due to a direct effect of liberated endotoxins. Nevertheless, the possibility of septicemia, and particularly meningococcemia, must be considered in any seriously ill patient with gastroenteritis.

REFERENCES 1. Hoyne, A. L. & Brown, R. H.: 727 nieningococcic cases: an analysis. Ann Intern Med 28: 248, 1948. 2. Weintraub, M. I. & Gordon, B.: “Acute abdomen” with meningococcal meningitis. N Engl J Med 290: 808, 1974.

Address for reprints:

H . L . Waldum, M . D . , Med. avd., Regionsykehuset, N-9012 T r o m s ~ , Norway

Scand J Infect Dis 9

Fulminant meningococcemia starting as an acute gastroenteritis.

Scandinavian Journal of Infectious Diseases ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19 Fulmi...
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