We are reporting a unique case of olmesartan associated severe sprue-like enteropathy in a 52-year-old woman who presented to our hospital complaining of severe abdominal pain and nausea. At the emergency department she suffered from a cardiac arrest and was found to have a colon perforation. The patient was treated conservatively without surgical intervention and olmesartan was discontinued. After one month, she had complete resolution of her symptoms.

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A trauma patient's greatest risk of death after the first 24 hours of injury stems from a combination of 3 conditions: hypothermia, acidosis, and coagulopathy. 1,2Nurses caring for trauma patients must be aware of these factors and how to manage them in an evidence-based manner. This article is focused on seriously injured trauma patients and the coagulopathies that they experience in the acute phase of injury. It provides an overview of coagulation and explores risk factors for trauma-induced coagulopathy. In addition to the coagulopathy induced by trauma, many patients may also be taking medications that interfere with hemostasis. Therefore, medication-induced coagulopathy is reviewed. We briefly review current evidence-based guidelines for blood component and fluid management and the role of thromboelastography (TEG or ROTEM) point-of-care diagnostic tools in the assessment and management of trauma-induced coagulopathies (TIC). Normal Physiological Mechanisms of CoagulationA large body of research has resulted in better defining how coagulation takes place. This cell-based model of coagulation has replaced the traditional version of the intrinsic and extrinsic coagulation cascade system. This cell-based model consists of 3 phases that overlap one another: initiation, amplification, and propagation 3,4 (Figure 1). The initiation phase begins when the blood vessel wall is injured, exposing tissue factor. When plasma containing factor VIIa comes in contact with cells bearing tissue factor, the 2 factors form a complex. 3,4 This complex then activates factors IX and X. Factor Xa complexes with factor Va to form thrombin (factor IIa) in small amounts. Trauma Coagulopathy is the inability of blood to coagulate normally; in trauma patients, it is a multifactorial and complex process. Seriously injured trauma patients experience coagulopathies during the acute injury phase. Risk factors for trauma-induced coagulopathy include hypothermia, metabolic acidosis, hypoperfusion, hemodilution, and fluid replacement. In addition to the coagulopathy induced by trauma, many patients may also be taking medications that interfere with hemostasis. Therefore, medication-induced coagulopathy also is a concern. Traditional laboratory-based methods of assessing coagulation are being supported or even replaced by point-of-care tests. The evidence-based management of trauma-induced coagulopathy should address hypothermia, fluid resuscitation, blood components administration, and, if needed, medications to reverse identified coagulation disorders. (Critical Care Nurse.

INTRODUCCIÓNSe ha señalado recientemente que la enfermedad tromboembólica venosa (ETEV) constituye la cenicienta de las enfermedades cardiovasculares, si se compara con otras manifestaciones más estudiadas de trombosis arterial y presentadas clínicamente como infarto de miocardio (IAM), enfermedad cerebrovascular (ECV) o arteriopatía periférica (1). Sin embargo, la ETEV es una enfermedad frecuente, muchas veces infradiagnosticada y potencialmente mortal, debido a la posibilidad de fragmentación del trombo venoso con producción de un embolismo pulmonar (EP). Este constituye, de [0212-7199 (2005) RESUMENObjetivos: Comparar los costes del tratamiento ambulatorio por una Unidad de Hospitalización a Domicilio (HADO) frente a la hospitalización convencional en el tratamiento agudo de la trombosis venosa profunda (TVP) y embolismo pulmonar (EP).Métodos: Durante el año 2002 se trataron 21 pacientes con TVP en la Unidad de HADO. La mediana de edad fue de 81 años, 11 fueron mujeres (52%) y, excepto uno, todos los pacientes presentaban importante comorbilidad. El diagnóstico se realizó en el hospital por ecografía-doppler. En 13 casos se realizó además una gammagrafía pulmonar, objetivándose EP concomitante en 7 pacientes. El tratamiento se realizó mediante heparinas de bajo peso molecular (HBPM) seguidas de anticoagulantes orales en 3 pacientes. No hubo complicaciones excepto un caso que requirió un ingreso breve debido al pobre control sintomático de la TVP y cuyos costes se imputaron a HADO. El estudio comparativo de costes se realizó con respecto a pacientes con TVP (grupo de diagnóstico relacionado, GDR 131) y EP ingresados (GDR: 78). El coste farmacoló-gico para pacientes de HADO se calculó para 10 días.Resultados: La estancia media hospitalaria de los pacientes ingresados fue de 8,1 días en TVP y 13,1 en TEP frente a 1 día en los pacientes en HADO. El ahorro de costes en HADO para el tratamiento agudo fue estimado en 1.680 € por paciente.Conclusiones: El tratamiento ambulatorio mediante una unidad de HADO de pacientes con TVP (y TEP seleccionados) resultó una estrategia segura, eficaz y coste-efectiva. Tratamiento domiciliario de la trombosis venosa profunda. Comparación de costes con la hospitalización convencional

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Objective To report a case of pseudohyperkalemia due to a pneumatic tube transport system. Case Summary A 75-year-old male presented to the emergency medicine department with chest pain and intermittent vision loss over the previous 2 days. Laboratory studies revealed a potassium value of 9.6 mEq/L and a white blood cell (WBC) count of 262 × 109/L. An electrocardiogram did not reveal changes consistent with hyperkalemia. Emergent treatment for the hyperkalemia was instituted. Repeat plasma potassium values obtained after treatment for the hyperkalemia remained significantly elevated. It was eventually recognized that the hyperkalemia was due to the combination of undiagnosed leukemia causing a significantly elevated WBC count and transport of the patient's specimen to the laboratory via a pneumatic tube transport system. Manual transport of the specimen to the laboratory repeatedly revealed normal or hypokalemic values. Discussion Hyperkalemia is a potentially fatal electrolyte abnormality that must be differentiated from pseudohyperkalemia. Pseudohyperkalemia is defined as a spurious elevation of potassium levels usually due to mechanical trauma during venipuncture resulting in hemolysis and release of potassium from the cellular elements of blood. Pneumatic tube transport systems should be listed in the scientific literature as another potential cause of pseudohyperkalemia, especially in patients with high WBC and/or platelet counts. Conclusion Pharmacists and other health care providers should be aware of pneumatic tube transport systems potentially causing pseudohyperkalemia, because regular treatments for hyperkalemia for this problem may cause patient harm.

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