multiple septic complications of peripheral intravenous cannulation. These included staphylococcal septicemia, tricuspid valve endocarditis, septic thrombosis adherent to the left pulmonary artery, pulmonary emboli, infarction, and abscess formation. Proximal embolization to the right atrium, and later to the left pulmonary artery, of a fragment of a peripheral intravenous cannula must account largely for the extent of cardiorespiratory sepsis. This is an uncommon complication and has been reported to occur from a central venous cathetenv' but to our knowledge, this patient represents the first reported case of this complication from a peripheral intravenous cannula. It is unlikely that this will occur without forceful removal of a cannula, a common occurrence in patients in confusional states. To avoid this, cannulas should be secured as firmly as possible in uncooperative patients. In the event of extraction, the cannula should be inspected and a report of this should be clearly recorded. If the cannula is found to be incomplete, a chest roentgenogram should be performed. Visualization of a fragment on the chest roentgenogram should be followed initially by an attempt at percutaneous removal. To aid detection of cannula fragments, we suggest a radiopaque marker along the length of all cannulas in routine use. Staphylococcus aureus is one of the most common isolates grown from intravenous devices, and it has been postulated that for such growth to occur, microorganisms migrate from the catheter skin entry site. 5 In view of staphylococcal infection manifesting six months after cannulation in this patient, an alternative explanation would be colonization of the foreign body fragment with a bacteremia, possibly resulting from a respiratory tract infection. Appropriate antibiotic therapy and removal of the infected cannula fragment did not prevent a fatal outcome in this patient. This is consistent with the known high mortality rates associated with serious S aureus infections, even with adequate antimicrobial therapy 6 This case reinforces the need to implement recommended practices' to minimize cannula-associated sepsis, and this should include careful inspection of all cannulas forcefully removed. REFERENCES 1 Maki OG, Goldman OA, Rhame FS. Infection control in intravenous therapy Ann Intern Med 1973; 79:867-87 2 Balbi M, Bertero G, Bellotti S, Rolandelli ML, Caponneto S. Right-sided valvular endocarditis supported by an unexpected intracardiac foreign body. Chest 1990; 97:1486-88 3 Cervia JS, Caputo TA, Davis SO, Murray HW Septic pulmonary embolism complicating a central venous catheter. Chest 1990; 98:1526 4 Richardson JO, Grover FL, Trinkle JK. Intravenous catheter emboli. Am J Surg 1974; 128:722-27 5 ReDoJ, GateD JM, Almirall J, Campistol JM, Gonzalez J, Puig de Ia BeUacasaJ. Evaluation of culture techniques for identification of catheter-related infection in hemodialysis patients. Eur J Clin Microbiol Infect Dis 1989; 8:620-22 6 Kaye MG, Fox MJ, Bartlett JG, Braman SS, Glassroth J. The clinical spectrum of Staphylococcus aumu pulmonary infection. Chest 1990; 97:788-92
Critical Mitral Stenosis Causing Ischemic Hepatic Fallure* Successful Treatment by Percutaneous Balloon Mitral Valvotomy Michael B. Harding, M.D.;}. Kevin Harrison, M.D.; Charles}. Davidson, M.D.; Katherine B. Kisslo; R.D.M.S.; and 1fwmas M. Bashore, M.D.
We report a 52-year-old patient with severe mitral stenosis who developed new onset atrial 6brillation, low output congestive heart failure and fulminant ischemic hepatic failure with subsequent severe coagulopatb~ Percutaneous mitral valvotomy resulted in dramatic clinical improvement with complete resolution of liver function. This case illustrates the potentialliEe-saving role for percutaneous balloon mitral valvotomy in treating critically ill patients who are unable to undergo thoracotomy due to coexisting medical (Chat 1992; 101:866-69) illness.
I schemic hepatic failure and coagulopathy due to critical mitral stenosis and low output cardiac failure are
uncommon' and an attempt at surgical correction of the underlying mitral stenosis in this situation may carry a prohibitive surgical risk. Our patient developed fulminant ischemic hepatic failure with new onset atrial fibrillation and critical mitral stenosis. The role of percutaneous balloon mitral valvotomy in this situation is described. CASE REPORT
History and Findings A 52-y~ld white man was transferred to this institution for the evaluation of severe mitral stenosis, heart failure, and hepatic failure. Two years earlier, mitral stenosis had been incidentally diagnosed and mitral valve replacement was recommended but declined. In the interim, the patient developed progressive dyspnea on exertion, orthopnea and pedal edema. Six weeks prior to admission, he became anorectic and developed resting dyspnea. After developing hemoptysis, he sought medical attention. There was no history of alcohol use or exposure to hepatotoxins. On admission to the community hospital, the patient was hemodynamically stable in normal sinus rhythm. His condition dramatically worsened on the third hospital day with the development of atrial6brillation and a ventricular response of 170 beats per minute. Metabolic acidosis with a lactate level of 9.6 mg/L was noted. Hepatic transaminases reflected acute hepatocellular necrosis. Failure of synthetic hepatic function and coagulopathy developed. No episode of hypotension or hypoxemia was documented. Upon transfer, the blood pressure was 110110 mm Hg, the resting pulse was 100 beats per minute and irregularly irregular, and the respiratory rate was 28. The patient was confused, lethargic and deeply icteric. Jugular venous pressure was above the angle of the jaw upright. The carotid upstroke was of low volume. Hales were noted in the midlung fields bilaterally. A right ventricular heave was obvious. The SI and PI were accentuated. A faint opening snap and a grade 116 diastolic rumble were audible. No regurgitant murmur was heard. The liver was enlarged and tender, and ascites *From the Department of Medicine, Division of Cardiology, Duke University Medical Center, Durham. ' Reprint requests: Dr. Bashore, Duke North, Rm 7436 MedicaIJ Cardlac Cath LAboratories, Durham, North Carolina 27710 MiIraJ StenosIs Causing Ischemic Hepatic Failure (Harding et aI)
Table I-Liver and Renal Function TeBtI 119*
SGOT (IV) 97 19 3710 919 27 SGPT(IU) 13 1610 987 176 42. Alkaline phosphatase (I V) lOB 117 87 142 150 2.7 2.7 NA Albumin (w'dl) 3.1 1.8 5.3 12.0 26.6 1.9 Bilirubin (mg/dl) 2.3 19.9 19.5 14.1 11.3 PT (s) (control 10.6-12.5) 14.9 47 25 BVN (mg/dl) 71 29 93 Creatinine (mg/dl) 1.7 2.5 1.8 1.4 1.8
Table 2-Hemodynamic RaultI o/Balloon Valvotomy 3124 Pre-BMV BMV
92 2.8 0.5 10.8 15 1.2
*Admission to community hospital.
t Admission data to our institution, mitral valvotomy performed 1/16. SGOT = serum glutamic oxaloacetic transaminase; SGPT = serum glutamic pyruvic transaminase; PT = prothrombin time; NA = not available; BVN = blood urea nitrogen. was present. The extremities were cold and mottled with 2 + pitting edema to the knees. The toes of his left foot were gangrenous. There was no asterixis. Prerenal azotemia (BUN 93 mg/dl; creatinine 1.8 mg/dl) and mild thrombocytopenia (103,000 per cu mm) were noted. Plasma fibrinogen was normal with an elevated D-dimer of 20 g/ml (normal