Diarrhea clinical presentation

In general, the clinical presentation of the human diseases associated with the ingestion of marine seafood toxins is similar to that of any other food poisoning disease. However, a number of clinical issues make these diseases particularly difficult to diagnose and treat. For example, the neurotoxic syndromes associated with CFP, PSP, and NSP represent points along a continuum of disease severity rather than clinically exclusive diseases. Even if fish or other seafood is the suspected source of a disease outbreak, diarrhea associated with the outbreak could be misdiagnosed as originating from bacterial rather than from phycotoxin contamination. 

Acute intoxication, either accidental or in attempted suicide, can cause headache, drowsiness, vision disturbance, vomiting and diarrhea, cardiovascular collapse, and respiratory failure. Deaths have been recorded at blood concentrations of 1 pg/ml (SEDA-11, 586) (38,39). Compared with adults, mortality in children after acute chloroquine poisoning is extremely high. Although the clinical presentation is mostly similar to that in adults (apnea, seizures, cardiac dysrhythmias), a single 300 mg chloroquine tablet was enough to kill a 12-month-old female infant (SEDA-16, 302). 

Table 36-1 outlines the clinical presentation of diarrhea while Table 36-2 shows common drug-induced causes of diarrhea. A medication... 

The average incubation period for V. cholerae infection is 1 to 3 days. The clinical presentation can vary from asymptomatic to life-threatening dehydration owing to watery diarrhea. The onset of diarrhea is abrupt and is followed rapidly or sometimes preceded by vomiting. Initial stools generally do not have the rice water appearance that is classically noted with cholera. Fever occurs in less than 5% of patients, and the physical examination correlates weU with the severity of dehydration. In the most severe state, this disease can progress to death in 2 to 4 hours if not treated. In some cases, fluid accumulates within the intestinal lumen causing abdominal distension and ileus and may cause intravascular depletion without diarrhea. Patients may lose up to 1 liter of isotonic fluid every hour. 

As useful as natural PGs may be in principle, they offer almost insurmountable clinical obstacles. As already noted, these obstacles are rapid metabolic degradation, lack of specificity, and other effects. Specifically, uterine effects, which could precipitate abortion in pregnant women, and diarrhea can present problems. Thus by molecular modifications it is hoped to obviate or minimize as many of these shortcomings as possible. 

III. Clinical presentation. After acute oral overdose, most agents cause only nausea, vomiting, and diarrhea. Specific features of toxicity are described in Table 11-4. 

III. Clinical presentation. Most low-concentration antiseptic ingestions are benign, and mild irritation is self-limited. Spontaneous vomiting and diarrhea may occur, especially after a large-volume ingestion. 

III. Clinical presentation. Within minutes to a few hours after ingestion, victims develop profound hypokalemia and skeletal muscle weakness progressing to flaccid paralysis of the limbs and respiratory muscles. Ventricular arrhythmias, hypophosphatemia, rhabdomyolysis, acute renal failure, and coagulopathy may also occur. Gastroenteritis with severe watery diarrhea, mydriasis with impaired visual accommodation, and CNS depression are sometimes present. More often, patients remain conscious even when severely Intoxicated. 

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

III. Clinical presentation. The various clinical presentations are described in Table 11-38. In most cases, the onset of vomiting and diarrhea is rapid. A delay in onset of more than 6-12 hours suggests amatoxin, monomethylhydrazine, ororellanine... 

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