Abeed H. Chowdhury

A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte® 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers.

Objective: We compared the effects of intravenous infusions of 0.9% saline ([Cl−] 154 mmol/L) and Plasma-Lyte 148 ([Cl−] 98 mmol/L, Baxter Healthcare) on renal blood flow velocity and perfusion in humans using magnetic resonance imaging (MRI). Background: Animal experiments suggest that hyperchloremia resulting from 0.9% saline infusion may affect renal hemodynamics adversely, a phenomenon not studied in humans. Methods: Twelve healthy adult male subjects received 2-L intravenous infusions over 1 hour of 0.9% saline or Plasma-Lyte 148 in a randomized, double-blind manner. Crossover studies were performed 7 to 10 days apart. MRI scanning proceeded for 90 minutes after commencement of infusion to measure renal artery blood flow velocity and renal cortical perfusion. Blood was sampled and weight recorded hourly for 4 hours. Results: Sustained hyperchloremia was seen with saline but not with Plasma-Lyte 148 (P < 0.0001), and fall in strong ion difference was greater with the former (P = 0.025). Blood volume changes were identical (P = 0.867), but there was greater expansion of the extravascular fluid volume after saline (P = 0.029). There was a significant reduction in mean renal artery flow velocity (P = 0.045) and renal cortical tissue perfusion (P = 0.008) from baseline after saline, but not after Plasma-Lyte 148. There was no difference in concentrations of urinary neutrophil gelatinase–associated lipocalin after the 2 infusions (P = 0.917). Conclusions: This is the first human study to demonstrate that intravenous infusion of 0.9% saline results in reductions in renal blood flow velocity and renal cortical tissue perfusion. This has implications for intravenous fluid therapy in perioperative and critically ill patients. NCT01087853

Fluids and gastrointestinal function.

Purpose of reviewTo highlight recent developments relating perioperative fluid therapy to gastrointestinal function by reviewing clinically pertinent English language articles mainly from January 2010 to March 2011. Recent findingsThe control of fluid and electrolyte balance involves multiple processes in which the gastrointestinal tract plays an integral role. Diseases affecting the gastrointestinal tract commonly cause fluid and electrolyte disturbance. Similarly, intravenous fluid therapy in the perioperative period can affect gastrointestinal function and have a bearing on postoperative outcome. Striking a balance, in terms of both fluid composition and volume, is likely to reduce the morbidity associated with interstitial edema, a frequently observed occurrence with contemporary perioperative fluid regimens. This balance may be best achieved using individualized and goal-directed approaches to fluid therapy, in order to provide fluid when it is needed and in the correct quantities. SummaryIn planning strategies of fluid therapy, the possibility of adverse effects on the gastrointestinal tract should be considered, as this is likely to have an impact on fluid and electrolyte balance and postoperative outcome.

Effects of Bolus and Continuous Nasogastric Feeding on Gastric Emptying, Small Bowel Water Content, Superior Mesenteric Artery Blood Flow, and Plasma Hormone Concentrations in Healthy Adults: A Randomized Crossover Study.

Objective:We aimed to demonstrate the effect of continuous or bolus nasogastric feeding on gastric emptying, small bowel water content, and splanchnic blood flow measured by magnetic resonance imaging (MRI) in the context of changes in plasma gastrointestinal hormone secretion. Background:Nasogastric/nasoenteral tube feeding is often complicated by diarrhea but the contribution of feeding strategy to the etiology is unclear. Methods:Twelve healthy adult male participants who underwent nasogastric intubation before a baseline MRI scan, received 400 mL of Resource Energy (Nestle) as a bolus over 5 minutes or continuously over 4 hours via pump in this randomized crossover study. Changes in gastric volume, small bowel water content, and superior mesenteric artery blood flow and velocity were measured over 4 hours using MRI and blood glucose and plasma concentrations of insulin, peptide YY, and ghrelin were assayed every 30 minutes. Results:Bolus nasogastric feeding led to significant elevations in gastric volume (P < 0.0001), superior mesenteric artery blood flow (P < 0.0001), and velocity (P = 0.0011) compared with continuous feeding. Both types of feeding reduced small bowel water content, although there was an increase in small bowel water content with bolus feeding after 90 minutes (P < 0.0068). Similarly, both types of feeding led to a fall in plasma ghrelin concentration although this fall was greater with bolus feeding (P < 0.0001). Bolus feeding also led to an increase in concentrations of insulin (P = 0.0024) and peptide YY (P < 0.0001), not seen with continuous feeding. Conclusion:Continuous nasogastric feeding does not increase small bowel water content, thus fluid flux within the small bowel is not a major contributor to the etiology of tube feeding-related diarrhea.

Temporal assessment of pancreatic blood flow and perfusion following secretin stimulation using noninvasive MRI.

To dynamically quantify pancreatic perfusion and flow within the arteries supplying the pancreas in response to secretin stimulation.

Immune dysfunction in patients with obstructive jaundice before and after endoscopic retrograde cholangiopancreatography

This prospective observational study investigated monocyte cytokine responses to lipopolysaccharide (LPS) in patients with obstructive jaundice (OJ) before and after endoscopic biliary drainage. Dendritic cell (DC) subsets and their expression of co-stimulatory molecules were also studied. Forty patients with OJ and ten non-jaundiced patients with normal gastroscopy findings were recruited. Ten healthy volunteers provided control blood samples for immunological assays. Patients with OJ had blood and duodenal mucosa sampled at the time of endoscopic retrograde cholangiopancreatography (ERCP) and further blood sampled during the recovery phase. Monocyte cytokine responses to LPS, DC subsets and co-stimulatory molecule expression were compared with controls. Duodenal morphology and occludin expression were also assessed. Monocytes obtained before ERCP from jaundiced patients demonstrated reduced cytokine responses to endotoxin compared with controls (IL-1β: 2678 compared with 4631 pg/ml, P=0.04 and IL-6: 3442 compared with 6157 pg/ml, P=0.002). Monocytes from patients with malignancy had poorer responses to endotoxin than from those with benign OJ (IL-1β: 2025 compared with 3332 pg/ml, P=0.001). After ERCP, the secretion of inflammatory cytokines by monocytes obtained from jaundiced patients increased (IL-1β: 2150 compared with 2520 pg/ml, P=0.03 and IL-6: 2488 compared with 3250 pg/ml, P=0.01). Occludin expression (85 compared with 95%, P=0.004) and mean duodenal villus height (334 compared with 404 μm, P=0.03) were lower in jaundiced patients. Before biliary drainage, patients with OJ had a higher percentage of myeloid dendritic cells (mDCs) and greater mDC expression of CD40 (P=0.04) and CD86 (P=0.04). Monocytes from patients with OJ had lower proinflammatory cytokine secretion in response to LPS, an effect reversed following biliary drainage.

Education and imaging. Gastrointestinal: Duodenal duplication cyst causing recurrent acute pancreatitis.

A 17-year-old male student presented with recurrent attacks of acute pancreatitis over a 3-month period. There was no history of alcohol consumption. His liver function tests, lipid profile and serum calcium concentrations were normal. An abdominal ultrasound did not reveal gallstones or biliary dilatation. Abdominal CT (Fig. 1A) revealed a 3 ¥ 2 cm thin-walled cyst (arrow) projecting into the contrast-filled lumen of the second part of the duodenum. A coronal MRCP reconstruction (Fig. 1B) confirmed the presence of the cyst (arrow) and its relationship to the medial wall of the duodenum, with an absence of pancreaticobiliary ductal dilatation or choledocholithiasis. Side viewing endoscopy showed an intraluminal bulge arising from the periampullary region. Ductal cannunaltion was not possible as the papilla could not be located. These appearances are consistent with a diagnosis of a duodenal duplication cyst arising at the level of the ampulla of Vater. A type III choledochal cyst (choledochocele) or a Wirsungocele were unlikely as the cyst was confined to the duodenum and did not involve the intrapancreatic portion of the common bile duct or the pancreatic duct. This patient underwent a laparotomy and transduodenal excision of the cyst following identification of the major papilla (Fig. 2Aand B). A transduodenal sphincteroplasty of both the biliary and pancreatic orifices was also performed to ensure ductal patency. Histological examination of the resected specimen stained with haematoxylin and eosin confirmed the absence of malignancy and the presence of smooth muscle between layers of duodenal mucosa (Fig. 2C). The muscle layer within the duplication cyst can be clearly visualised following immunostaining with antibody to alpha smooth muscle actin (Fig. 2D). The patient has not had another episode of pancreatitis for over six months after the operation. Congenital duodenal duplication cysts are a rare cause of recurrent pancreatitis. Abdominal pain and distension are typical features but gastrointestinal bleeding can occur due to the presence of ectopic gastric mucosa, allowing subsequent diagnosis during endoscopy. Pancreatitis, secondary to pancreatic ductal outflow obstruction is usually the result of pancreatic duct compression involving the cyst, or stone disease if there is direct communication with the pancreaticobiliary tract. Although endoscopic drainage and snare resection is considered safe, surgical excision is accepted as the treatment of choice with the intention to alleviate symptoms, prevent pancreatitis and eliminate the risk of malignant transformation, a development reported in only a small number of cases.

Gastrointestinal: Duodenal duplication cyst causing recurrent acute pancreatitis: Images of Interest

A 17-year-old male student presented with recurrent attacks of acute pancreatitis over a 3-month period. There was no history of alcohol consumption. His liver function tests, lipid profile and serum calcium concentrations were normal. An abdominal ultrasound did not reveal gallstones or biliary dilatation. Abdominal CT (Fig. 1A) revealed a 3 ¥ 2 cm thin-walled cyst (arrow) projecting into the contrast-filled lumen of the second part of the duodenum. A coronal MRCP reconstruction (Fig. 1B) confirmed the presence of the cyst (arrow) and its relationship to the medial wall of the duodenum, with an absence of pancreaticobiliary ductal dilatation or choledocholithiasis. Side viewing endoscopy showed an intraluminal bulge arising from the periampullary region. Ductal cannunaltion was not possible as the papilla could not be located. These appearances are consistent with a diagnosis of a duodenal duplication cyst arising at the level of the ampulla of Vater. A type III choledochal cyst (choledochocele) or a Wirsungocele were unlikely as the cyst was confined to the duodenum and did not involve the intrapancreatic portion of the common bile duct or the pancreatic duct. This patient underwent a laparotomy and transduodenal excision of the cyst following identification of the major papilla (Fig. 2Aand B). A transduodenal sphincteroplasty of both the biliary and pancreatic orifices was also performed to ensure ductal patency. Histological examination of the resected specimen stained with haematoxylin and eosin confirmed the absence of malignancy and the presence of smooth muscle between layers of duodenal mucosa (Fig. 2C). The muscle layer within the duplication cyst can be clearly visualised following immunostaining with antibody to alpha smooth muscle actin (Fig. 2D). The patient has not had another episode of pancreatitis for over six months after the operation. Congenital duodenal duplication cysts are a rare cause of recurrent pancreatitis. Abdominal pain and distension are typical features but gastrointestinal bleeding can occur due to the presence of ectopic gastric mucosa, allowing subsequent diagnosis during endoscopy. Pancreatitis, secondary to pancreatic ductal outflow obstruction is usually the result of pancreatic duct compression involving the cyst, or stone disease if there is direct communication with the pancreaticobiliary tract. Although endoscopic drainage and snare resection is considered safe, surgical excision is accepted as the treatment of choice with the intention to alleviate symptoms, prevent pancreatitis and eliminate the risk of malignant transformation, a development reported in only a small number of cases.

Gastrointestinal: Duodenal duplication cyst causing recurrent acute pancreatitis

A 17-year-old male student presented with recurrent attacks of acute pancreatitis over a 3-month period. There was no history of alcohol consumption. His liver function tests, lipid profile and serum calcium concentrations were normal. An abdominal ultrasound did not reveal gallstones or biliary dilatation. Abdominal CT (Fig. 1A) revealed a 3 ¥ 2 cm thin-walled cyst (arrow) projecting into the contrast-filled lumen of the second part of the duodenum. A coronal MRCP reconstruction (Fig. 1B) confirmed the presence of the cyst (arrow) and its relationship to the medial wall of the duodenum, with an absence of pancreaticobiliary ductal dilatation or choledocholithiasis. Side viewing endoscopy showed an intraluminal bulge arising from the periampullary region. Ductal cannunaltion was not possible as the papilla could not be located. These appearances are consistent with a diagnosis of a duodenal duplication cyst arising at the level of the ampulla of Vater. A type III choledochal cyst (choledochocele) or a Wirsungocele were unlikely as the cyst was confined to the duodenum and did not involve the intrapancreatic portion of the common bile duct or the pancreatic duct. This patient underwent a laparotomy and transduodenal excision of the cyst following identification of the major papilla (Fig. 2Aand B). A transduodenal sphincteroplasty of both the biliary and pancreatic orifices was also performed to ensure ductal patency. Histological examination of the resected specimen stained with haematoxylin and eosin confirmed the absence of malignancy and the presence of smooth muscle between layers of duodenal mucosa (Fig. 2C). The muscle layer within the duplication cyst can be clearly visualised following immunostaining with antibody to alpha smooth muscle actin (Fig. 2D). The patient has not had another episode of pancreatitis for over six months after the operation. Congenital duodenal duplication cysts are a rare cause of recurrent pancreatitis. Abdominal pain and distension are typical features but gastrointestinal bleeding can occur due to the presence of ectopic gastric mucosa, allowing subsequent diagnosis during endoscopy. Pancreatitis, secondary to pancreatic ductal outflow obstruction is usually the result of pancreatic duct compression involving the cyst, or stone disease if there is direct communication with the pancreaticobiliary tract. Although endoscopic drainage and snare resection is considered safe, surgical excision is accepted as the treatment of choice with the intention to alleviate symptoms, prevent pancreatitis and eliminate the risk of malignant transformation, a development reported in only a small number of cases.

Water and Electrolytes

It has been found that the performance of the strongest and fittest people will deteriorate rapidly with dehydration. The present paper is concerned with the anatomy of the fluid spaces in the body, taking into account also the fluid shifts and losses during exercise and their effects on performance. Total body water is arbitrarily divided into that contained within cells (cellular) and that located outside the cells (extracellular). The anatomy of body fluid compartments is considered along with the effects of exercise on body water, fluid shifts with exercise, the consequences of sweating, dehydration and exercise, heat acclimatization and endurance training, the adverse effects of dehydration, thirst and drinking during exercise, stimuli for drinking, and water, electrolyte, and carbohydrate replacement during exercise. It is found that the deterioration of physical exercise performance due to dehydration begins when body weight decreases by about 1 percent.