Vomiting clinical presentation

The clinical presentation of nausea and vomiting is given in Table 27-4. Nausea and vomiting may be classified as either simple or complex. 

Hypertensive encephalopathy is a classic feature of malignanthypertension. Its clinical presentation consists of severe headache, mental confusion, and apprehension. Blurred vision, nausea and vomiting, and focal neurologic deficits are common. If untreated, the syndrome may progress over a period of 12-48 hours to convulsions, stupor, coma, and even death. 

In a retrospective analysis of all cases of hyponatremia associated with ecstasy (SEDA-25, 37) at the London Centre of the National Poisons Information Service from December 1993 to March 1996,17 patients were identified with a serum sodium concentration under 130 (range 107-128 mmol/1) (96). In 10, ecstasy was identified analytically, and six of them had SIADH. The clinical presentation was very consistent, with initial vomiting and delirium, and 11 had seizures. There was complete recovery in 14, but two died of cerebral edema 5 hours after ingestion. 

The classic presentation of a patient with acute ACG includes complaints of eye pain, headache, blurred vision, photophobia, the perception of halos around lights, nausea, and vomiting. Clinical signs include an edematous cornea, a fixed mid-dilated pupil, ciliary injection, high lOP, convex iris (iris bombe), and cells and flare in the anterior chamber. There may also be evidence of previous episodes such as peripheral anterior synechiae, anterior subcapsular lens opacities (glaukomflecken), sector iris atrophy, an irregular pupil, and a narrow angle in the contralateral eye. 

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). 

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. 

The clinical presentations included a generalized rash or urticaria sometimes accompanied by nausea, malaise, vomiting, fever, arthralgias, and angioedema. 

T-2 is one of the more stable toxins, retaining its bioactivity even when heated to high temperatures. High concentrations of sodium hydroxide and sodium hypochlorite are required to detoxify it. Aerosol toxicities are generally too low to make this class of toxins useful to an aggressor as an MCBW as defined in Figure 30-1 however, unlike most toxins, these are dermally active. Clinical presentation includes nausea, vomiting, weakness, low blood pressure, and burns in exposed areas. 

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. Shortly after acute ingestion, nausea and vomiting occur, followed by paresthesias of the tongue, lips, and face confusion tremor obtundation coma seizures and respiratory depression. Because chlorinated hydrocarbons are highly lipid soluble, the duration of toxicity may be prolonged. 

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. 

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