Nutritional Suppor in an Aids Patient

Abstract

HIV infection can cause malnutrition through a wide variety of mechanisms.'-' For example, invasion of glial cells in the central nervous system leading to dementia (AIDS dementia) or neuropathy can interfere with self-feeding. Direct HIV attack on intestinal mucosal cells (AIDS enteropathy) impairs nutrient absorption.',' Recurrent, often multiple, opportunistic infections can lead to rapid nutritional depletion by increasing metabolic' demands while at the same time reducing intake through anorexia, dysphagia, or malabsorption.' Malnutrition in the AIDS patient can also be caused by non-HIV related factors, such as socioeconomic difficulties, fad diets,&dquo; alcohol-induced pancreas or liver disease,l() and various drug therapies (medically as well as self-prescribed).&dquo; Finally, inappropriately chosen or administered nutritional therapy can lead to further exacerbation of the malnutrition. 12The following case report describes a malnourished AIDS patient in whom the primary physician thought total parenteral nutrition (TPN) was required, but where a careful, non-invasive nutritional/ medical reassessment obviated the need for parenteral nutrition or even tube-feeding. CASE REPORTA 32-year-old HIV-positive white man with extrapulmonary tuberculosis, hepatitis, anemia, falling albumin (1.8 g/dL) and &dquo;continuous diarrhea&dquo; was referred to the Nutrition Support Service for TPN.A review of his medical chart revealed the follow-ing pertinent information. With a background of alcohol abuse and intravenous drug abuse, he had initially presented with PneurrLOCystis carinii pneumonia and oral candidiasis 3 months earlier, at which time he was found to be HIV-antibody positive. A month later, tuberculous lymphadenitis was noted on lymph node biopsy, and the patient was placed on antituberculous therapy, although compliance was subsequently questioned. The following month he was again readmitted for fever, headaches, vomiting, and mental status change. A work-up including head CT scan (with contrast), lumbar puncture, cerebrospinal fluid cryptococcal antigen test, serum toxoplasmosis titer, sinus roentgenograms, and drug toxicology screening was unrevealing. An electroencephalogram showed slow wave activity suggestive of diffuse encephalopathy. A diagnosis of progressive HIV encephalopathy was made, and the patient was discharged on codeine and prochlorperazine in addition to his antituberculous therapy (which then included rifampin, pyrazinamide, and ethambutol, but not isoniazid due to resistance of the original mycobacterium isolate).The current hospitalization began 4 days after his last discharge, when he returned complaining of worsening bifrontal, bitemporal headaches, unrelieved by ibuprofen tablets, which he may have taken as many as 30 200-mg of during the previous 24 hours. He also complained of nausea and vomiting and had noted increasing memory loss and inability to concentrate. He denied diarrhea. On admission he was described as a cachectic man &dquo;writhing in bed&dquo; due to the headache b...