Acid-Base, Fluid, and Electrolytes
Joshua Dilday DO
Search for more papers by this authorAsser Youssef MD
Search for more papers by this authorNicholas Thiessen MD
Search for more papers by this authorJoshua Dilday DO
Search for more papers by this authorAsser Youssef MD
Search for more papers by this authorNicholas Thiessen MD
Search for more papers by this authorForrest “Dell” Moore MD, FACS
Vice Chief of Surgery Associate Trauma Medical Director
John Peter Smith Health Network/Acclaim Physician Group, Fort Worth, TX, USA
Search for more papers by this authorPeter Rhee MD, MPH, FACS, FCCM, DMCC
Professor of Surgery at USUHS, Emory
Morehouse Chief of Surgery and Senior Vice President of Grady, Atlanta, GA, USA
Search for more papers by this authorGerard J. Fulda MD, FACS, FCCM
Associate Professor Chairman Department of Surgery
Department of Surgery, Jefferson Medical College, Philadelphia, PA
Physician Leader Surgical Service Line, Christiana Care Health Systems, Newark, DE, USA
Search for more papers by this authorSummary
This is a unique question-and-answer chapter for surgical residents and trainees, concentrating on the acid-base, fluid, and electrolytes. Central diabetes insipidus (DI) is a failure of anti-diuretic hormone (ADH) released from the posterior pituitary gland. Central DI manifests as polyuria with dilute urine in setting of hypertonic plasma. Failure of the urine osmolarity to increase after fluid restriction is diagnostic confirmation. Treatment is aimed at replacing free water deficits and vasopressin, an ADH analogue. Acidosis is from the loss of bicarbonate and not the addition of an acid, a normal anion gap is expected. A widened anion gap would be expected from an etiology that caused the addition of an acid. The loss of bicarbonate causes a gain of chloride ions to maintain electrical neutrality. Because of this, normal gap metabolic acidosis has also been referenced as “hyperchloremic metabolic acidosis”. The treatment in this setting would be to replace fluids and electrolytes.
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