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AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 22, Number 5 ■ September 2004
versus nonselective beta blockade on qt dispersion in patients with nonischemic dilated cardiomyopathy. Am J Cardiol 1999;843:350354 5. Abraham WT: Beta-blockers: The new standard of therapy for mild heart failure. Arch Intern Med 2000;160(9):1237-1247
MALIGNANT ASCITES PRESENTING AS ABDOMINAL COMPARTMENT SYNDROME To the Editor:—Shock or hypoperfusion state is a fairly common medical problem, which requires rapid evaluation. However, at times, the cause of the acute hypoperfusion state remains obscure despite extensive diagnostic evaluation. Elevated intra-abdominal pressure and the resulting abdominal compartment syndrome (ACS) is an example of such a rare and easily overlooked cause of shock.1-7 A 67-year-old woman was admitted with a week-long history of mild dyspnea and right-sided pleuritic chest pain. Her past medical history was notable for anterior wall myocardial infarction 7 years previously arterial hypertension, and hypothyroidism. Her medications included levothyroxine, metoprolol, cilazapril, hydrochlorothiazide, and warfarin. On admission to the ED she had no signs of distress, and her vital signs and temperature were normal. The abdomen was obese and somewhat tense. Initial laboratory tests revealed a blood chemistry remarkable for a blood urea nitrogen of 30, serum creatinine of 1.85 mg/dL and LDH of 1,638 U/dL. A chest film revealed small right-sided pleural effusion and elevated hemidiaphragms. Electrocardiogram was normal. While in the ED the patient’s dyspnea worsened and desaturation was noted. Two hours later the patient became acutely agitated; her periphery was cold, systolic blood pressure was 80 mm Hg and saturation was 89% while breathing 100% oxygen through a facemask. The patient was intubated and transferred to the intensive care unit. Hypotension was severe and required continuous infusion of norepinephrine and epinephrine (up to50 g/min each). She became oliguric and a repeated creatinine was 4.3 mg/dL. The peak inspiratory pressure was 50 cm of H2O, and blood gases revealed significant hypoxemia (PO2 of 141 mm Hg with an FIO2 of 1.0). A bedside echocardiogram revealed normal biventricular function without pulmonary hypertension or pericardial effusion. Indirect measurement of the intra-abdominal pressure via instillation of 50 mL of saline into the urinary bladder showed an increased pressure of 45 mm Hg. Bedside abdominal ultrasonography revealed massive ascites, and was followed by paracentesis with removal of 4,500 mL of turbid fluid and a 15 mm Hg reduction in the intra-abdominal pressure measurement. After the parecentesis blood pressure increased, epinephrine was quickly weaned off and norepinephrine was reduced to less than half its previous level. Urinary output increased up to 60 mL per hour, and the peak inspiratory pressure dropped to 35cm of H2O. Despite this improvement, which lasted approximately 12 hours, she continued to deteriorate. Cytologic examination of the ascitic fluid revealed large malignant epithelial cells consistent with pancreatic adenocarcinoma. In view of the nature of the underlying illness a conservative approach was adopted and the patient died 72 hours after her admission. This case shows an important and probably underestimated cause for hypoperfusion and multiorgan failure in the medical patient, ie, ACS. The characteristic coexistence of shock, anuria, and respiratory failure in a patient with distended abdomen and elevated airway pressure should alert the clinician to this medical urgency. In the present case, the excessive abdominal pressure with the accompanying multiorgan failure and the rapid improve-
© 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2205-0006$30.00/0 doi:10.1016/j.ajem.2004.06.005
ment after decompression indicated the existence of ACS. Intraabdominal hypertension (IAH) is defined as an abnormally elevated intra-abdominal pressure, and is generally said to exist when the measured pressure exceeds 20 mm Hg.8,9,10 ACS exists when IAH is accompanied by manifestations of organ dysfunction, with prompt improvement on abdominal decompression.1,2,3,10 Measurement of intra-abdominal pressure can be done indirectly by transudation of pressures from indwelling tubes such as: femoral vein, rectal, gastric, and urinary bladder catheters. The latter, using a standard foley catheter and instillation of 50 ml of saline, is simple, accurate and is usually considered as the procedure of choice.1,2,3,4,11 The adverse physiologic effects of IAH impact multiple organ systems:2,3,6,10 pulmonary dysfunction is characterized by progressive reduction in compliance and total lung capacity manifesting as hypoxemic and hypercarbic respiratory failure. Elevated hemidiaphragms may be seen on chest film. Cardiovascular dysfunction is a consequence of decreased venous return and direct compression of the abdominal veins, as well as reduced preload attributable to increased inthrathoracic pressure. Renal and portosystemic visceral dysfunctions are mainly the result of a direct suppressive effect of IAH on renal and splanchnic blood flow, as well as the diminished cardiac output. Oliguria and metabolic acidosis are the typical manifestations. Patients at risk of developing ACS include those with severe blunt and penetrating abdominal trauma, ruptured abdominal aortic aneurysms, and intra- or retropritoneal hemorrhage. Additional causes include abdominal neoplasm, tense ascites, and pancreatitis.2 The definitive treatment of ACS is abdominal decompression either surgically or by large volume paracentesis, which reverses all of the adverse effects of increased intra-abdominal pressure.3 In summery, ACS is a serious condition, which requires a high index of suspicion to avoid a delay in diagnosis and treatment that may adversely affect outcome. YORAM ETZION, MD, PhD Department of Medicine E LEONID BARSKI, MD Department of Medicine A YANIV ALMOG, MD Medical Intensive Care Unit Soroka University Medical Center Faculty of Health Sciences Ben Gurion University Beer-Sheva, Israel
References 1. Kron IL, Hartman PK, Nolan SP: The measurement of intraabdominal pressure as a criterion for abdominal re-exploration. Ann Surg 1984;199:28-30 2. Bailey J, Shapiro MJ: Abdominal compartment syndrome. Crit Care 2000;4:23-29 3. Schein M, Wittmann DH, Aprahamain CC, et al: The abdominal compartment syndrome: The physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg 1995;180:745-753 4. Sugrue M: Intra-abdominal pressure: time for clinical practice guidelines? Intensive Care Med 2002;28:389-391 5. Sugerman HJ, Bloomfield GL, Saggi BW: Multisystem organ failure secondary to increased intraabdominal pressure. Infection 1999;27:61-66 6. Morken J, West MA: Abdominal compartment syndrome in the intensive care unit. Curr Opin Crit Care 2001;7:268-274 7. Malbrain ML: Abdominal pressure in the critically ill: measurement and clinical relevance. Intensive Care Med 1999;25:1453-1458 8. Fusco MA, Martin RS, Chang MC: Estimation of intra-abdominal pressure by bladder pressure measurement: validity and methodology. J Trauma 2001;50:297-302 9. Meldrum DR, Cleveland JC Jr, Moore EE, et al: Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 1997;174:667-673
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10. Ivatuury RR, Diebel L, Porter JM, et al: Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 1997;77:783-801 11. Gudmundsson FF, Viste A, Gislason H, et al: Comparing of different methods for measuring intra-abdominal pressure. Intensive Care Med 2002;28:389-391
SPONTANEOUS BASILICA VEIN RUPTURE To the Editor:—Here we report spontaneous vein rupture in a thoracic limb. Vein rupture is a rare event and most reported cases involve the iliac vein. An 81-year-old Caucasian woman with a family history of pulmonary thrombosis embolism (father), that reported an intestinal resection at age 71 because of diverticulitis, arrived in the ED 16 hours after her symptoms started. She had a progressive hematoma in the dorsal region of her left hand without any apparent cause (Fig 1) that showed edema, pain, impaired flexion and extension of the fingers, as well as distal hypothermia. The patient denied any trauma. Her pulse was 78 beats/min and her blood pressure was 140/100 mmHg. Hemoglobin was 12.2 g and hematocrit 31. Fasciotomy was performed 30 minutes after arrival at the ED (Fig 2), approximately 70 mL of blood was drained and intensity of the median, radial, and cubital nerves and of arterial pulse as well as temperature became normal. She was treated with antibiotics and heparin at 5,000 U every 12 hours for 3 days. Exploration of the area under local anesthesia did not suggest thrombosis inside the basilica vein. A single stitch was used to close the fasciotomy 48 hours later (Fig 3) before dismissal of the patient, who continued experiencing hipoasthesia of the middle finger for 3 months. Oral anticoagulants were prescribed for 6 months. The patient did not have any reoccurrence at 4 years later. Spontaneous rupture of a vein is a rare but well-documented event that may occur as a result of a sudden increase of the venous blood pressure that exceeds the resistance of the vascular wall and inflammatory changes, or it can be associated with thrombosis or obstruction.1-5 There are few reports of iliac vein rupture,1-3,6 which happens more frequently in healthy women older than 40 years and of caucasian origin1,3,6 as was the case presented here, although the rupture took place in the basilica vein, being this the first report implying the basilica vein. The clinical picture of vascular events depends on the site of rupture, for example, at the abdominal level it is common to find shock, acute pain and distention in absence of trauma.1-3,7 Martorell described a syn-
FIGURE 2.
drome in the limbs that he named “the throw of a stone” secondary to the spontaneous rupture of calf muscle veins, which appear as a sudden sharp pain on the back side of the leg, associated to edema and Homan’s sign, ecchymosis and decrease in local temperature.8,9 All these clinical data suggest arterial embolism,9,10 as occurred in our case, although the finding was the rupture of the basilica vein. As far as the treatment is concerned, immediate intervention is vital.1-3,6,7 We considered a priority to decompress the affected hand. Furthermore, it is generally recommended to repair rather than ligate the damaged vessel,2,3,6 in our case, after exploring the patient’s vein it was repaired. The outcome will depend also on the location of the event, while in the lower limbs symptoms will recede in about 2 to 3 weeks, but can recur,9 in our case, that took place in the upper limb, it was a single event that did not repeat itself after 4 years. Finally, it is worthwhile to mention that since spontaneous rupture of a vein, as the basilica, is considered a vascular emergency, it has to be treated immediately and continuity of the vein is highly recommended. The authors thank Dr. Simon Kawa for support in the elaboration of the manuscript. ALEJANDRA RANERO, MD MARTIN FREGOSO, MD Departments of Cardiovascular Surgery and Orthopedics Hospital General “Dr. Manuel Gea Gonzalez”, SSA Mexico City, Mexico
© 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2205-0007$30.00/0 doi:10.1016/j.ajem.2004.06.006
FIGURE 1.
The left hand of the patient at admission to the hospital.
The fasciotomy performed 30 minutes after admission.
FIGURE 3.
The left hand of the patient at dismissal of the hospital.