Pretreatment testing in the emergency department

96

AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 15, Number 1 • January 1997

9. Krentz A J, Boyle PJ, Justice KM, et al: Successful treatment of severe refractory sulfonylurea-induced hypoglycemia with octreotide. Diabetes Care 1993;16:184-186

PRETREATMENT TESTING IN THE EMERGENCY DEPARTMENT To the Editor:--The care given by emergency physicians has benefited many patients, especially those severely ill from illness or accident. However, emergency physicians sometimes forget that not all of their patients require immediate treatment. Abnormal laboratory findings sometimes prompt overly hasty treatment, before other information needed to elucidate the diagnosis and perhaps lead to more appropriate therapy is obtained. From my own area of interest, I will cite some examples of patients with metabolic disorders who often do need urgent therapy, but seldom so quickly that there is not enough time to first obtain pretreatment blood or urine specimens. It may not be necessary to learn the results of the additional tests before treatment is given: what is important is to obtain the specimens and be certain they will be analyzed. The following are some laboratory abnormalities that too often trigger quick intravenous therapy before a urine or another blood specimen is obtained. Hypoglycemia. Unless this is found in a clinical setting that validates and explains the finding (eg, a diabetic receiving hypoglycemic therapy), another blood specimen should be obtained for a repeat measurement of glucose, as well as serum insulin, Cpeptide, and perhaps, cortisol concentrations, before intravenous glucose is given. The results of those assays will help identify individuals who may have injected insulin surreptitiously (who will have very high insulin but normal C-peptide levels), individuals who may have an insulinoma (in which case both of those measurements will be high), and those who may have hypoadrenalism. Some serum can be saved (or retrieved) for subsequent assay for oral hypoglycemic drugs, if that analysis should be needed. Hyponatremia. Obtaining the urine concentrations of sodium and creatinine, as well as the osmolality, before initiating administration of saline can help evaluate whether the individual may have sodium deficiency and how the kidneys are responding to the state of hydration. Too often, urine specimens in such patients are obtained only after saline has been infused and urinary sodium excretion has increased. Hypokalemia. The explanation for this abnormality could often be elucidated sooner with knowledge of the pretreatment urine potassium and creatinine concentrations. The normal renal response to potassium deficiency owing to extrarenal losses (eg, gastrointestinal) results in low urinary K + excretion and concentration (usually <10 retool/L). A higher urinary K + concentration suggests a renal basis for the deficit, as might be found in patients taking a kaliuretic drug or those with some variety of hyperaldosteronism. Hyperkalemia. Unless confirmed by characteristic electrocardiographic abnormalities, or when found in an expected clinical setting (eg, a patient with known renal failure), the analysis should be repeated in serum and plasma before starting treatment. Otherwise, if the hyperkalemia is spurious, owing to in vitro release of K + from fragile erythrocytes, or from platelets (in patients with severe thrombocytosis) or leucocytes (in patients with striking leucocytosis), treatment to reduce serum K + may cause hypokalemia. Adrenocortical insufficiency. Unless suspected in a typical clinical setting (eg, a patient with known adrenal or pituitary failure, or one who has received glucocorficoid therapy), a blood specimen should be obtained to measure cortisol, and perhaps also aldosterone, gonadotropin, thyroid-stimulating hormone, and thyroxine concentrations, before giving intravenous hydrocortisone. The results of these assays will help distinguish between "pri-

mary" adrenal failure (ie, Addison's disease) and secondary failure owing to hypopituitarism. Physicians in other fields have their own lists of similar problems. Infectious disease specialists complain about patients with acute systemic infections who are given intravenous antibiotic therapy before specimens for stain and culture have been obtained. Rheumatologists despair about joint fluids not examined for urate or calcium pyrophosphate crystals. Hematologists worry about confusing laboratory findings in anemic patients who are transfused before additional specimens have been obtained. Not every patient who wants or needs emergency care must have immediate treatment. Some first require additional examinations to clarify the diagnosis. MILFORDFULOP,MD

Department of Medicine Albert Einstein College of Medicine Bronx, NY

AN UNUSUAL CAUSE OF SMALL BOWEL OBSTRUCTION: STRANGULATED OBTURATOR HERNIA To the Editor:--Obturator hernia was first described in 1724 by Arnaud de Ronsil. 1 This rare type of hernia mostly affects elderly emaciated women, with the peak incidence found in the seventh and eighth decades of life. 1,2 The clinical presentation is usually recurrent intestinal obstruction with thigh or knee pain on the affected side, the so called Howship-Romberg sign. Delayed diagnosis and surgical intervention have contributed to high mortality in the past. Recently however, a high index of suspicion in older patients presenting with intestinal obstruction of no obvious cause, combined with advances in diagnostic imaging techniques, has resulted in early diagnosis and treatment before the onset of bowel necrosis. Report of a case. An 84-year-old woman presented with 7 days of anorexia and intermittent lower abdominal pain followed by 2 days of vomiting and abdominal fullness. The patient denied systemic medical or pelvic surgical history. Physical examination revealed decreased bowel sounds with abdominal distension, no focal tenderness or rebounding pain, and no fever. Digital rectal examination showed no significant abnormality. The laboratory data, including complete blood counts and blood urea nitrogen, creatinine, amylase, and creatine phosphokinase levels, were within normal limits. Plain abdominal film showed multiple dilated loops of small bowel with air-fluid levels, consistent with small bowel obstruction. Undergoing conservative management with nasogastric decompression and intravenous fluids, the patient's condition became better with less abdominal fullness on the second hospital day. One day later, mild focal tenderness developed over the right lower quadrant of the abdomen accompanied by abdominal fullness. In addition, the typical Howship-Romberg sign developed, characterized by pain over the right thigh that was exacerbated by extension, abduction, or inward rotation of the thigh and relieved by flexion. A follow-up plain abdominal film showed air distension of the small bowel with no obvious improvement. The barium enema study disclosed no gross abnormality of the colon and patency of the ileocecal valve. The mucosa of terminal ileum was normal but there was an abrupt interruption of barium filling at the right obturator foramen region. The presumptive diagnosis of obmrator hernia was made and was soon confirmed by pelvic computed tomography scanning (Figure 1). The patient underwent an emergency exploratory laparotomy. The terminal ileum was found entrapped in the Richter's type of right obturator hernia. The strangulated gangrenous terminal ileum, 6 cm in length, was resected followed by a primary end-to-end anastomosis. As the hernia was reduced, the obturator fossa was