Peritoneal Membrane

Clinical Symptoms of Acute Al Encephalopathy and Chronic Al Encephalopathy (also Referred to as Classical Dialysis Dementia ) 

relatively low exposure accumulation of Al over a period of years can lead to a number of clinical manifestations, some of which seem to be bypassed in acute Al encephalopathy due to extremely high exposure to Al. Al encephalopathy is a clinical syndrome and, as can be seen in Table 5, there are similarities and differences in the neurological symptoms of acute and chronic Al encephalopathy. In chronic Al encephalopathy microcytic anemia [41, 93, 95—98] and EEG changes [99-104] can precede clinical symptoms [105]. It is unknown if these symptoms can also precede the clinical symptoms of acute encephalopathy. In contrast to acute Al encephalopathy, where speech disturbances are absent, speech disorders are an important presenting clinical sign of neurotoxicity in chronic Al encephalopathy. The neurological basis of the speech apraxia is obscure but it appears to have elements of dysarthria and dysphasia [33, 73], The initial 

Patients with acute and chronic Al encephalopathy can demonstrate unilateral or bilateral myoclonic jerks of the extremities for several months in the chronic form and days to weeks in the acute form, followed by convulsions and coma even when the exposure is terminated, ft seems as if brain pathology reaches a point of no return which results in frequent epileptic insults and inevitably leads to coma and death, either due to superimposed infections like aspiration pneumonia, or pulmonary edema due to cardiac toxicity. Recovery is exceptional in severe cases. In the past, reports showed that the early stages of chronic Al encephalopathy progressed to death, mainly because the most important source of Al, namely the dialysis fluid contamination, was not recognized as such and the exposure continued for months to years [10-17, 19-42]. 

Fluctuation of neurological symptoms can be seen in relation to dialysis in chronic Al encephalopathy, sometimes provoked by dialysis sessions due to additional exposure with contaminated dialysate superimposed to chronic Al intoxication [28, 29]. 

One of the most confusing features of Al encephalopathy is the lag phase between exposure and clinical symptoms and the subsequent rapid course of the disease. The delay can be months to years in the classical form and several weeks in the acute form. Because patients are generally symptom-free or demonstrate minor symptoms like microcytic anemia, physicians are unaware of the exposure until the development of severe symptoms. Until recently it was not known that a relatively short dialysis related exposure time to Al can be fatal. 

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Peritoneal dialysis (PD) utilizes similar principles as hemodialysis in that blood is exposed to a semipermeable membrane against which a physiologic solution is placed. In the case of PD, however, the semipermeable membrane is the peritoneal membrane, and a sterile dialysate is instilled into the peritoneal cavity. The peritoneal membrane is composed of a continuous single layer of mesothelial cells that covers the abdominal and pelvic walls on one side of the peritoneal cavity, and the visceral organs, including the GI tract, liver, spleen, and diaphragm on the other side. The mesothelial cells are covered by microvilli that increase the surface area of the peritoneal membrane to approximate body surface area (1 to 2 m2). 

Complications associated with PD include mechanical problems related to the PD catheter, metabolic problems associated with the components of the dialysate fluid, damage to the peritoneal membrane, and infections (Table 23-10). Strategies to manage infectious complications of PD are discussed below. 

With regard to capsule transplantation, no ill effect on animal growth or behavior was noted as a result of capsule transplantation. Some capsules were free-floating within the peritoneal cavity and were free of fibrosis on the surface while others were adherent to the peritoneal membrane or to each other. The latter criteria served for further selection and screening of capsule chemistries. Details on the in vivo functioning of encapsulated islets have been presented elsewhere [23]. 

Factors that influence drug dialyzability in chronic ambulatory peritoneal dialysis include drug-specific characteristics (e.g., molecular weight, solubility, degree of ionization, protein binding, and VD) and intrinsic properties of the peritoneal membrane (e.g., blood flow, pore size, and peritoneal membrane surface area). 

Make an incision through the skin and peritoneal membrane to open the abdomen. 

In peritoneal dialysis (PD), sterilisation of the fluid by heat leads to the presence of reactive carbonyl compounds, which have been incriminated in the progressive deterioration of the peritoneal membrane in long-term PD patients.441 Glutathione in conjunction with glyoxalase I, as well as aminoguanidine, counteracted the effect. 

Q12 Irritation and damage to other structures in the abdomen may occur if the diverticulitis is not treated. Abdominal muscles may go into painful spasm and a minority of patients might have rectal bleeding. A major problem could be development of an intestinal obstruction or an abscess in the wall of the intestine. The abscess may eventually cause perforation of the intestinal wall leakage of infected material into the peritoneal cavity and then infection of the peritoneal membranes (peritonitis) may occur. Peritonitis is a very serious condition. 

The adverse effects of peritoneal dialysis fluids on the peritoneum have been succinctly summarized by authors arguing the case for a new, less toxic, and less acidic fluid for peritoneal dialysis (7). A low pH, high osmolality and lactate concentration, and the presence of several toxic contaminants may all contribute to impaired cellular function in the peritoneal membrane. In conventional peritoneal dialysis pH is dehberately lowered to 5.0-5.6... 

Dedhia NM, Schmidt LM, Twardowski ZJ, Khanna R, Nolph KD. Long-term increase in peritoneal membrane transport rates following incidental intraperitoneal sodium hypochlorite infusion. Int J Artif Organs 1989 12(11) 711-14. 

At least 11 different mammalian AQP have now been identified, of which seven (AQPl, -2, -3, -4, -6, -7, -8) are expressed in the Iddney. Many of these also have extra-renal expression sites (e.g, AQPl may be unportant in fluid removal across the peritoneal membrane). Two asparagine-prohne-alanine sequences in the molecule are thought to interact in the membrane to form a pathway for water translocation. AQPl is found in the proximal tubule and descending thin limb of the loop of Henle and constitutes almost 3% of total membrane protein in the kidney. It appears to be constitutively expressed and is present in both the apical and basolateral plasma membranes, representing the entry and exit ports for. water transport across the cell, respectively. Approximately 70% of water reabsorption occurs at this site, predominantly via a transcellular (i.e., AQPl) rather than a paracellular route. Water reabsorption in the proximal tubule passively follows sodium reabsorption, so that the fluid entering the loop of Henle is still almost isosmotic with plasma. 

An adjunct to the assessment of adequacy in PD patients is the peritoneal equilibration test (PET). The PET assesses peritoneal membrane transport characteristics in terms of solute clearances and ultrafiltration. The results are used to select a dialysis regimen appropriate to the transport characteristics of the patient (e.g., high transporters may do better on short dwell APD regimens). The PET is typically undertaken at the same time as adequacy assessments in PD patients. 

As in hemodialysis, the clearance of urea, a product of protein catabolism, is measnred with Kt/V. Kt/V is a unitless value that correlates the patient s peritoneal membrane urea clearance (K) with the dnration of dialysis (t) and the volume of distribution (P) of urea. Calculation of Kt/V for PD requires that the total volume of drained effluent per day be determined (this value is the volume instilled plus volume of water ultraflltered). The dialysate to plasma (D/P) urea concentration is determined, and Kt is estimated as ... 

The K/DOQI clinical practice guidelines suggest that the adequacy of PD be assessed by using measured Kt/V and CEj three times in the first 6 months of dialysis (i.e., at months 1, 4, and 6). The reasoning behind this frequency is to accurately establish a baseline creatinine and urea excretion rate. Thereafter the KtA and Clcr should be measured every 4 months, at months 10, 14, and so on. The rationale for this is that it is imperative to detect subtle decreases in residual renal function and noncompliance and to make the necessary alterations to the prescribed PD dose to compensate for them. It is recommended that the first PET be conducted within the first month of treatment. Because solute clearance is dependent on peritoneal membrane transport properties, the guidelines also recommend that a PET be conducted within the first month of treatment. Future PET assessment is only recommended for patients with suspected changes in peritoneal membrane transport function, particularly when usual efforts to increase the PD dose are not successful. 

Intraperitoneal irrigation of antimicrobial agents for treatment of intraabdominal infection has been smdied often with conflicting results. Intraoperative antimicrobial irrigation does not improve patient outcomes in comparison with copious intraoperative irrigation with normal saline. Possibly the most important aspect of peritoneal irrigation is the dilutional effect on bacteria and adjuvants that promotes infection (intestinal contents and hemoglobin). Most system-ically administered antimicrobials easily cross the peritoneal membrane so that peritoneal fluid concentrations are similar to serum. " Confined areas, such as an abscess, can be expected to attain much lower antimicrobial concentrations. 

Membranes suitable for dialysis include vegetable parchment, animal parchment, gold beater s skin (peritoneal membrane of cattle), fish bladders, collodion and cellophane. 

Mesenteric—associated with the mesenteries i.e., double-folded peritoneal membranes connecting the intestines with the dorsal wall of the abdominal cavity... 

With scissors make a vertical incision 13-15 mm long for the Chinese hamster and 8-10 mm long for the Armenian hamster so as to pass through the peritoneal membrane. 

The decreased clearance of waste materials results in a buildup of waste in the blood. Blood urea nitrogen (BUN) and creatinine are two end products of protein and muscle metabolism. In addition to waste buildup, electrolyte and acid buildup and bicarbonate loss may be noted, leading to imbalances. Supplemental cleansing of the Wood through dialysis— use of an artificial kidney (hemodialysis) or the peritoneal membrane (peritoneal dialysis) to filter blood—may be performed until renal function is restored. 

There are two common types of dialysis, the most common being hemodialysis. Hemodialysis removes wastes and water by circulating blood outside the body through an external dialyzer that acts as a filter and contains a semipermeable membrane. Peritoneal dialysis uses a peritoneal membrane inside the body to filter wastes and water from the blood. 

Soak the abdomen in 70% EtOH to sterilize. Dissect the skin but leave the peritoneal membrane intact. 

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