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INTRODUCTION

A meaningful analysis of fluid, electrolyte, and acid–base abnormalities is dependent on the history and physical examination of each patient. Although a rigorous appraisal of laboratory parameters often yields the correct differential diagnosis, the clinical characteristics provide an understanding of the extracellular fluid volume (ECFV) and pathophysiology. Thus, the evaluation always begins with an overall assessment of the patient.

INITIAL PATIENT ASSESSMENT

History

The history should be directed toward clinical questions associated with fluid and electrolyte abnormalities. Xenobiotic exposure commonly results in fluid losses through the respiratory system (hyperpnea and tachypnea), gastrointestinal (GI) tract (vomiting and diarrhea), skin (diaphoresis), and kidneys (polyuria). Patients with ECFV depletion often complain of dizziness, thirst, and weakness. Usually the patients can identify the source of fluid loss.

A history of exposure to nonprescription and prescription medications, alternative or complementary therapies, and other xenobiotics can suggest the most likely electrolyte or acid–base abnormality. In addition, patient characteristics (race, gender, age), premorbid medical conditions, and the ambient temperature and humidity should always be considered.

Physical Examination

The vital signs are invariably affected by significant alterations in ECFV. Whereas hypotension and tachycardia often characterize life-threatening ECFV depletion, an increase of the heart rate and a narrowing of the pulse pressure are the earliest findings. Abnormalities are best recognized through an ongoing dynamic evaluation, realizing that the measurement of a single set of supine vital signs offers useful information only when markedly abnormal. Orthostatic pulse and blood pressure measurements provide a more meaningful determination of functional ECFV status (Chaps. 3 and 16).

The respiratory rate and pattern can give clues to the patient’s metabolic status. In the absence of lung disease, hyperventilation (manifested by tachypnea, hyperpnea, or both) is often either caused by a primary respiratory stimulus (respiratory alkalosis) or is a response to the presence of metabolic acidosis. Although hypoventilation (bradypnea or hypopnea or both) is present in patients with metabolic alkalosis, it is rarely clinically significant except in the presence of chronic lung disease or in combination with respiratory depressant xenobiotics. More commonly, hypoventilation is caused by a primary depression of consciousness and respiration with resulting respiratory acidosis. Unless the clinical scenario (eg, nature of the poisoning, presence of renal or pulmonary disease, and findings on physical examination or laboratory testing) is classic, arterial or venous blood gas analysis is recommended to determine the acid–base disorder associated with a change in ventilation.

The skin should be evaluated for turgor, moisture, and the presence or absence of edema. The moisture of the mucous membranes can also provide valuable information. These are nonspecific parameters and often fail to correlate directly with the status of hydration. This dissociation is especially true with xenobiotic exposure because many xenobiotics alter skin and mucous membrane moisture without necessarily altering ECFV status. For example, antimuscarinics commonly ...

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