Panhemispheric infarction: a complication of cuffed catheter. (Case Report).

Abstract

The need for reliable vascular access remains the Achilles heel of hemodialysis. Complications of vascular access are a leading cause of morbidity and mortality in patients who undergo hemodialysis, especially in those patients with end-stage renal disease. Among methods of vascular access, arteriovenous fistulae have the lowest rate of infection and should be the access of choice when vascular anatomy permits. Also, the incidence of staphylococcal infections in patients infected with human immunodeficiency virus is increasing. To emphasize the need to use arteriovenous fistula access for hemodialysis whenever possible, we report the case of a patient with end-stage renal disease and human immunodeficiency virus infection who died as a result of panhemispheric infarction and uncal herniation as a result of fulminant staphylococcal bacteremia caused by central venous catheter sepsis.

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Staphylococcal infections are occurring with increasing frequency in the setting of human immunodeficiency virus (HIV) infection, and they comprise one-third of all cases of bacteremia, with the risk increasing with decrements in cluster designation 4 (CD4) count. Patients with end-stage renal disease (ESRD) who undergo hemodialysis also have a high incidence of catheter-:related complications, such as septicemia, phlebitis, thrombosis, and air embolism. We report the case of a patient with ESRD due to HIV nephropathy who developed fatal panhemispheric infarction and uncal herniation as a result of fulminant staphylococcal bacteremia.

Discussion

The leading cause of morbidity in patients who undergo hemodialysis in the United States is related to vascular access complications. (1,2) The mortality rate due to infection in hemodialysis patients is close to 25%. (3) The incidence of central venous catheter-related bacteremia is reported to be between 2.8 and 18.5% of patients; (4-6) thus, the need for a reliable vascular access remains the Achilles heel of hemodialysis. Because of the increasing incidence of infective complications leading to patient death, the Dialysis Outcomes Quality Initiative (DOQI) guidelines stress the need for increased use of AV fistulae as the access route of choice for hemodialysis. The DOQI guidelines specify that 40% of all chronic hemodialysis patients should be dialyzed through AV fistulae and that no more than 10% of chronic hemodialysis patients should be dialyzed through central venous catheters.7 Despite these recommendations, the 2000 Annual Report: ESRD Clinical Performance Measures Project reports that between Octo ber and December 1999, only 27% of all chronic hemodialysis patients were dialyzed through AV fistulae, and 23% were dialyzed with a catheter. These numbers seem to be much better than the catheter rate reported in 1997 among hemodialysis patients in the U.S. Renal Data System. (8,9)

The use of AV fistulae as the access for hemodialysis presents the lowest rate of infection and should be the access of choice whenever the patient's vascular anatomy permits. (7) Central venous catheters and PTFE synthetic grafts are associated with higher risks for bacteremia than AV fistulae. (10)

Comorbid disease and late referral have perpetuated a need for synthetic PTFE grafts and central venous catheters, however. (11) The likelihood of finding an AV fistula is lower in women, blacks, obese patients, elderly patients, and patients with peripheral vascular disease. (12)

Staphylococcus aureus is one of the most common pathogens involved in endocarditis, accounting for up to 35% of cases, and central venous catheters are a common source of this infection. (13) Among patients with infective endocarditis, approximately 30% develop neurologic complications, with an embolic event being the most common. (14) Embolic complications are more commonly a result of mitral valve vegetation and the native valves than they are of prosthetic valves. (15,16) The risk for developing neurologic complications is increased in patients with Staphylococcus aureus infection and in patients with aortic and mitral valve involvement. (14) Mortality rates tend to be higher in patients with neurologic complications as well as in patients with late-stage HIV infection. (17,18)

Conclusions

Metastatic infections and septic embolizations are recognized complications of line sepsis and endocarditis. Cerebral infarction can occur as a complication of central venous catheter insertion, as Hurwitz and Posner (10) found, possibly because of the dislodging of atheromatous plaque. Panhemispheric infarction in our patient, however, was due to a septic embolus from mitral vegetation occluding the right internal carotid artery, as evidenced by similar microbiologic growth on culture. Our literature search failed to reveal any citation of panhemispheric infarction as a result of infective endocarditis related to central venous catheter sepsis. This case report reemphasizes the dangers of using a cuffed catheter for vascular access for hemodialysis and stresses the need to follow the DOQI recommendations regarding the use of primary AV fistula for hemodialysis whenever feasible.

Accented November 15, 2001.

References

(1.) Windus DW. Permanent vascular access: A nephrologist's view. Am J Kidney Dix 1993;21:457-471.

(2.) Vanherweghem JL, Dhaene M, Goldman M, Stolear JC, Sabot JP, Waterlot Y, et al. Infections associated with subclavian dialysis catheters: Thc key role of nurse training. Nephron 1986;42:l16-119.

(3.) Keane WF, Shapiro FL, Raij L. Incidence and type of infect ions occurring in 445 chronic hemodialysis patients. Trans Am Soc Artif Intern Organs 1977;23:41-47.

(4.) Schwarzbeck A, Brittinger WD, Henning GE, Strauch M. Cannulation of subclavian vein for hemodialysis using Seldinger's technique. Trans Am Soc Artif Intern Organs 1978;24:27-31.

(5.) Vanholder R, Lameire N, Verbanek J, van Rattinghe R, Kunnen M, Ringoir S. Complications of subclavian catheter hemodialysis: A 5 year prospective study in 257 consecutive patients. Int J Artif Organs 1982; 5:297-303.

(6.) Uldall PR, Merchant N, Woods F, Yarworski U, Vas S. Changing sub-clavian haemodialysis cannulas to reduce infection. Lancet 1981;1:1373.

(7.) National Kidney Foundation Dialysis Outcomes Quality Initiative. NKFDOQI clinical practice guidelines for vascular access: National Kidney Foundation Dialysis Outcomes Quality Initiative. Am J Kidney Dis 1997;30(4 Suppl 3):S150-S191.

(8.) National Institute of Diabetes and Digestive and Kidney Diseases. Vascular access, in United States Renal Data System (USRDS): 1997 Annual Data Report--Dialysis Morbidity and Mortality (Wave 2). Bethesda, MD, National Institutes of Health, 1997, pp 58-61.

(9.) ESRD Clinical Performance Measures Project. Vascular access: 2000 annual report. Am J Kidney Dis 2001;37(1 Suppl 2):S137-S181.

(10.) Robinson DL, Fowler VG, Sexton DJ, Corey RG, Conlon PJ. Bacterial endocarditis in haemodialysis patients. Am J Kidney Dis 1997;30:521-524.

(11.) Butterly DW, Schwab SJ. Dialysis access infections. Curr Opin Nephrol Hypertens 2000;9:631-635.

(12.) Allon M, Ornt DB, Schwab SJ, Rasmussen C, Delmez JA, Greene T, et al. Factors associated with the prevalence of arteriovenous fistulas in hemodialysis patients in the HEMO study: Hemodialysis (HEMO) Study Group. Kidney Int 2000;58:2178-2185.

(13.) Lowy FD. Staphylococcus aureus infections. N Engl J Med 1998;339:520-532.

(14.) Heiro M, Nikoskelainen J, Engblom E, Kotilainen E, Marttila R, Kotilainen P. Neurologic manifestations of infective endocarditis: A 17-year experience in a teaching hospital in Finland. Arch Intern Med 2000;160:2781-2787.

(15.) Sandre RM, Shafran SD. Infective endocarditis: Review of 135 eases over 9 years. Clin Infect Dis 1996;22:276-286.

(16.) Vlessis AA, Hovaguimian H, Jaggers J, Ahmad A, Starr A. Infective endocarditis: Ten-year review of medical and surgical therapy. Ann Thorac Surg 1996;61:1217-1222.

(17.) Rerkpattanapipat P, Wongpraparut N, Jacobs LE, Kotler MN. Cardiac manifestations of acquired immunodeficiency syndrome. Arch Intern Med 2000;160:602-608.

(18.) Tunkel AR, Kayc D. Neurologic complications of infective endocarditis. Neurol Clin 1993;11:419-440.

(19.) Hurwitz BJ, Posner JB. Cerebral infarction complicating subclavian vein catheterization. Ann Neurol 1977;1:253-254.

RELATED ARTICLE: Key Points

* Arteriovenous fistulae are preferred points of access for hemodialysis.

* Central venous catheters are prone to a high incidence of systemic bacterial infections with devastating outcomes.

* Although central nervous system complications secondary to cuffed catheters are described, this may be the first reported case of panhemispheric infarction due to total occlusion of the internal carotid artery by an infected thrombus from mitral vegetation.

Case Report

A 44-year-old white woman presented with complaints of fever, chills, nausea, and vomiting for 3 days. She had been diagnosed with HIV secondary to intravenous drug abuse 9 years before this hospitalization, and at the time of admission her CD4 count was 181/[micro]1 and her viral load was 35,000 copies/ml. She also had HIV nephropathy leading to ESRD, for which she had been receiving maintenance hemodialysis for 3 years through a cuffed catheter in the right internal jugular vein. Damage to the peripheral veins caused by chronic intravenous drug abuse prevented the construction of permanent vascular access in the form of an arteriovenous (AV) fistula or polytetrafluoroethylene (PTFE) graft. Her medical history was also significant for hypertension, chronic hepatitis C infection, hypothyroidism, depression, calculous cholecystitis resulting in cholecystectomy, Pneumocystis carinii pneumonia, and HIV-induced dementia. Her medications included azithromycin for the treatment of Mycobacterium avium intracellulare infection, and trimethoprim and sul-famethoxazole (Bactrim; Roche Pharmaceuticals, Nutley, NJ) for Pneumocystis carinii pneumonia prophylaxis. The physical examination revealed a thin, cachectic, middleaged female with a temperature of 39.1[degrees]C. Her pulse rate was 117 beats/mm, her blood pressure level was 140/70 mm Hg, and her respiratory rate was 30 breaths/min. Head and neck examination was significant for the presence of a cuffed dialysis catheter inserted in the right internal jugular vein. The exit site was clean and without any evidence of erythema, swelling, or discharge, and was not tender to palpation. The cardiac examination was unremarkable, except for a Grade II/VI soft, localized, systolic murmur at the apex. There were no peripheral signs of endocarditis. The chest examination was normal, and the abdominal examination revealed a nontender abdomen with no organomegaly. The neurologic examination was significant for echolalia, which was attributed to HIV dementia. She did not have neck sti ffness. Kernig's and Brudzinski's signs were absent.

The initial laboratory examination revealed a white blood cell (WBC) count of 10,000/[micro]1 with 86% neutrophils and 7% lymphocytes, hemoglobin value of 10.3 g/dl, and a platelet count of 191,000/[micro]1. Serum chemistry tests revealed the following values: sodium, 131 mmol/L; potassium, 4.8 mmol/L; chloride, 97 mmol/L, bicarbonate, 20 mmol/L; blood urea nitrogen, 50 mg/dl; creatinine, 7.58 mg/dl; and glucose, 94 mg/dl. Her serum calcium level was 8.5 mg/dl, her phosphorus level was 4.4 mg/dl, and her magnesium level was 2.5 mg/dl. The thyroid-stimulating hormone level was 4.4 mU/L. Blood cultures and swabs cultured from the catheter insertion site were positive for the growth of methicillinresistant Staphylococcus aureus. The initial chest x-ray was unremarkable.

The patient was empirically treated with intravenous vancomycin and gentamicin. Despite intravenous antibiotic treatment for 24 hours, her fever persisted; therefore, her catheter was changed over a guidewire. Three days later, she became acutely tachycardic (heart rate, 156 beats! min), tachypneic (respiratory rate, 50 breaths/min), and hypoxic (partial pressure of oxygen, 45 mm Hg), and she developed a high fever (40.3 [degrees]C). She also became incoherent and noncommunicative. A lumbar puncture was performed, and the results showed normal cerebrospinal fluid pressure and a total WBC count of 9 WBC/ml (all lymphocytes). Computed tomographic scans of the chest showed an area of low attenuation in the left parietal region. A ventilation/perfusion scan of the lungs revealed a low probability of pulmonary embolism. A transthoracic echocardiogram revealed mitral and tricuspid regurgitation with evidence of vegetation over the mitral valve and a probable thrombus in the left ventricular cavity. The same antibiotics and supportive measures were continued. She became hypotensive, necessitating the application of vasopressors and ventilatory support. Surgical treatment was not offered because of the patient's hemodynamic instability. Despite this aggressive medical treatment, she died on the ninth day of hospitalization.

The autopsy revealed multiple patchy areas of myocardial fibrosis and calcifications with thickening of the mitral valve. There were large vegetations on the mitral valve, with two small perforations on the posterior leaflet (Fig. 1). Examination of the brain revealed significant asymmetry, illustrated by narrowed cerebral sulci due to cerebral edema in the right hemisphere (Fig. 2). Uncal transtentorial herniation secondary to increased intracranial pressure was thought to be the cause of death. An examination of the right internal carotid artery (Fig. 3) revealed total occlusion by a thrombus, causing massive cerebral edema and leading to panhemispheric infarction. Cultures from the vegetation on the mitral valve as well as from the thrombus occluding the right internal carotid artery revealed similar growth of methicillin-resistant Staphylococcus aureus. The spleen (Fig. 4), liver, and kidney showed ischemic infarcts suggestive of thromboembolic events.

From the Departments of Medicine and Pathology, University of Texas Medical Branch at Galveston, Galveston, TX.

Reprint requests to Mahendra Agraharkar, MD, Nephrology Division, Department of Medicine, University of Texas Medical Branch at Galveston, 4.200 John Sealy Annex, 301 University Blvd., Galveston, TX 77555-0562. Email: [e-mail]

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