6.06 Food Poisoning - Staphylococcal
The patient is brought to the ED 1 to 6 hours after eating, with
severe nausea, vomiting, and abdominal cramps progressing into
diarrhea. He appears very ill: pale, diaphoretic, tachycardic,
orthostatic, perhaps complaining of paresthesias or feeling as if he
is "going to die." Others may have similar symptoms from eating the
same food. The physical examination, however, is reassuring. There is minimal
abdominal tenderness, localized, if at all, to the epigastrium or to
the rectus abdominus muscle (which is strained by the vomiting)
What to do:
- Completely examine the patient, and perform any tests needed
to rule out myocardial infarction, perforated ulcer, dissecting
aneurysm, or any of the catastrophes which can present in
- In the meantime, infuse 0.9% NaCl or Ringer's lactate
solution intravenously and observe the patient, doing repeated
vital sign checks and physical examination. In younger
patients, who have the renal and cardiovascular reserve to
handle rapid hydration, 1-2 liters infused over an hour often
provides dramatic improvement in all symptoms.
- If the patient is improving, and beginning to tolerate oral
fluids, discharge him with instructions to advance his diet over the next hours, starting with an oral rehydration solution such as
He should expect to be eating and feeling
well in another 1 or 2 days.
- 3/4 teaspoon of table salt
- one teaspoon of baking soda
- one cup of orange juice
- four tablespoons of sugar and
- four cups of water.
- If symptoms resolve more slowly, you may want to discharge
the patient with a single dose of an antiemetic or
antispasmotic such as a prochlorperazine (Compazine) 25mg suppository or a dicyclomine (Bentyl) 20mg tablet.
- If hypotension or other significant symptoms persist; if the
patient cannot tolerate parenteral rehydration, or cannot
resume oral intake; he may have to be admitted.
What not to do:
- Do not immediately resort to medications (e.g., Compazine,
Tigan) for nausea and vomiting. They may interfere with
elimination of toxins, and do not help correct the fluid and
electrolyte imbalances responsible for many of the symptoms.
- Do not immediately resort to medications (e.g., Lomotil,
Imodium) for cramping and diarrhea, for the same reasons.
- Do not skimp on intravenous fluids.
- Do not pursue expensive laboratory investigations on
- Do not presume food poisoning without a good history for it.
Many of the symptoms accompanying any gastroenteritis seem to be
related to electrolyte disturbances and dehydration, which can be
substantial even in the absence of copious vomiting and diarrhea, and
resistant to oral rehydration, because the gut is unable to absorb,
and allows liter after liter to pool in its lumen. Lactated Ringer's
solution is the choice for intravenous rehydration, because it
approximates normal serum electrolytes, and can be infused rapidly.
Lactated Ringer's approximately replaces the electrolytes lost in
diarrhea, but normal saline has more of the chloride lost by
The most common food poisoning seen in most EDs is caused by the
heat-stable toxin of Staphylococcus, which is introduced into food
from infections on handlers, and grows when the food sits warm.
Chemical toxins have a similar presentation, but the onset of
symptoms may be more immediate. Other bacterial food poisonings
usually present with onset of symptoms later than 1-6 hours after
eating, less nausea and vomiting, more cramping and diarrhea, and
longer courses. A clearly implicated food source may give a clue to
the etiology: shellfish suggesting Vibrio parahemolyticus, rice
suggesting Bacillus cereus, meat or eggs suggesting Staphylococcus,
Campylobacter, Clostridium, Salmonella, Shigella, enteropathic E.
Coli, or Yersinia..
Whenever someone suffers any gastrointestinal upset, it is natural,
if not instinctive, to implicate the last food eaten. Caution
patients (especially if they are planning to sue the food supplier)
that the diagnosis of food poisoning cannot be established without a
group outbreak or a sample of tainted food for analysis.
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Craig Feied, MD
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