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The Biology and Practice of Current Nutritional Support
Second Edition Rifat Latifi Digital Instant Download
Author(s): Rifat Latifi
ISBN(s): 9781570595950, 157059595X
Edition: 2ed.
File Details: PDF, 2.47 MB
Year: 2003
Language: english
LANDES LANDES
BIOSCIENCE V ad e me c u m BIOSCIENCE V ad e me c u m
Table of contents (excerpt)
1. Clinical Implications
of Carbohydrate, Proteins,
Lipids, Vitamins and Trace
7. Protein Metabolism in Liver
and Intestine During Sepsis:
Mediators, Molecular Regulation,
The Biology and Practice
Elements in Nutrition Support and Clinical Implications of Current Nutritional
2. Current Nutrient Substrates
3. Biochemistry of Amino Acids:
8. Biochemical Assessment and
Monitoring of Nutritional Status Support
Clinical Implications
4. Acute Phase Proteins
9. Optimizing Drug Therapy
and Enteral Nutrition: Detecting 2nd edition
Drug-Nutrient Interactions
in Critically Ill Patients
10. Techniques and Monitoring
5. Arginine Metabolism of Total Parenteral Nutrition
in Critical Care and Sepsis
11. Radiologic Assessment
6. Wound Healing and the Role of Nutritional and Metabolic
of Nutrient Substrates Status
12. Enteral Nutrition: Indications,
Monitoring and Complications
The Vademecum series includes subjects generally not covered in other handbook
series, especially many technology-driven topics that reflect the increasing
influence of technology in clinical medicine.
The name chosen for this comprehensive medical handbook series is
Vademecum, a Latin word that roughly means “to carry along”. In the Middle
Ages, traveling clerics carried pocket-sized books, excerpts of the carefully
transcribed canons, known as Vademecum. In the 19th century a medical publisher
in Germany, Samuel Karger, called a series of portable medical books
Vademecum.
The Landes Bioscience Vademecum books are intended to be used both in the
training of physicians and the care of patients, by medical students, medical house
staff and practicing physicians. We hope you will find them a valuable resource.
All titles available at

I SBN 1- 57059- 595- X Rifat Latifi
www.landesbioscience.com
Stanley J. Dudrick
v a d e m e c u m
The Biology and Practice

of Current Nutritional Support
2nd Edition
Rifat Latifi, M.D.
Department of Surgery
University of Arizona
Tucson, Arizona, U.S.A.
Stanley J. Dudrick, M.D.

Yale University School of Medicine
St. Mary’s Hospital/Yale Affiliate
Waterbury, Connecticut, U.S.A.
LANDES
BIOSCIENCE
GEORGETOWN, TEXAS
U.S.A.
VADEMECUM
The Biology and Practice of Current Nutritional Support, 2nd Edition
LANDES BIOSCIENCE
Georgetown, Texas U.S.A.
Copyright ©2003 Landes Bioscience

All rights reserved.
No part of this book may be reproduced or transmitted in any form or by any
means, electronic or mechanical, including photocopy, recording, or any
information storage and retrieval system, without permission in writing from the
publisher.
Printed in the U.S.A.
Please address all inquiries to the Publisher:

Landes Bioscience, 810 S. Church Street, Georgetown, Texas, U.S.A. 78626
Phone: 512/ 863 7762; FAX: 512/ 863 0081
ISBN: 1-57059-595-X
Library of Congress Cataloging-in-Publication Data
CIP applied for, but not received at time of printing.
While the authors, editors, sponsor and publisher believe that drug selection and dosage and
the specifications and usage of equipment and devices, as set forth in this book, are in accord
with current recommendations and practice at the time of publication, they make no
warranty, expressed or implied, with respect to material described in this book. In view of the
ongoing research, equipment development, changes in governmental regulations and the
rapid accumulation of information relating to the biomedical sciences, the reader is urged to
carefully review and evaluate the information provided herein.
Dedication
Jonathan Evans Rhoads, M.D.

1907-2002
Dedicated to the surgeon of the century, whose extraordinary personal at-

tributes and countless professional, educational and scientific contributions
serve as the quintessential model that has greatly influenced and inspired the
editors and will continue to endure for future generations.
Rifat Latifi, M.D. and Stanley J. Dudrick, M.D.

Contents
Foreword ....................................................................... xvii
1. Clinical Implications of Carbohydrate, Proteins,
Lipids, Vitamins and Trace Elements
in Nutrition Support ......................................................... 1
Larry H. Bernstein
Overview .................................................................................................... 1
Stress Hypermetabolism and the Nutritionally-Dependent
Adaptive Dichotomy .............................................................................. 2
Energy Requirements of Injured Man ......................................................... 3
Nutritional Requirements ........................................................................... 6
Clinical vs. Laboratory Information ............................................................ 8
Information Model ................................................................................... 10
Length of Stay (LOS) ................................................................................ 11
Improving Correction of Malnutrition ...................................................... 11
Nutrition Support Monitoring .................................................................. 12
Quality Management ................................................................................ 13
2. Current Nutrient Substrates ............................................ 17
Wendy Swails Bollinger, Timothy J. Babineau
and George L. Blackburn
Introduction ............................................................................................. 17
Hepatic Disease and Stress: Branched-Chain Amino Acid
Enriched Diets ..................................................................................... 17
Arginine .................................................................................................... 24
Glutamine ................................................................................................ 27
Nucleotides ............................................................................................... 33
Lipids ....................................................................................................... 35
Conclusion ............................................................................................... 43
3. Biochemistry of Amino Acids:
Clinical Implications ....................................................... 52
Rifat Latifi, Khawaja Aizimuddin
Introduction ............................................................................................. 52
Structure of Amino Acid and Proteins ....................................................... 52
Amino Acid and Protein Synthesis ............................................................ 53
Post-Synthetic Modification ...................................................................... 54
Protein Function ....................................................................................... 54
Classification of Amino Acids ................................................................... 55
Amino Acids in Critical Illness and Injury ................................................ 58
Amino Acids in Circulation ...................................................................... 59
Digestion of Amino Acids ......................................................................... 59
Absorption of Amino Acids ....................................................................... 60
Biochemical Transformation of Amino Acids ............................................ 61
4. Acute Phase Proteins in Critically Ill Patients ................. 63
Khawaja Azimuddin, Rifat Latifi and Rao R. Ivatury
Role of the Acute Phase Response ............................................................. 63
Physiology ................................................................................................ 63
Sequence of Events During Acute Phase Response .................................... 65
Modulation of the Acute Phase Response .................................................. 65
The Acute Phase Proteins .......................................................................... 65
Albumin ................................................................................................... 66
Prealbumin ............................................................................................... 67
Retinol-Binding Protein ............................................................................ 67
Transferrin ................................................................................................ 67
C-Reactive Protein .................................................................................... 67
Ceruloplasmin .......................................................................................... 68
Fibrinogen ................................................................................................ 68
Complement ............................................................................................. 68
Amyloid .................................................................................................... 68
Alpha 1 Acid Glycoprotein ....................................................................... 68
Alpha-1 Protease Inhibitor ........................................................................ 68
Monitoring Nutrition in the Critically Ill Patient ...................................... 69
5. Arginine Metabolism in Critical Care and Sepsis ............ 72
Rima I. Kandalaft, V. Bruce Grossie, Jr.
Pathways of Arginine and Ornithine Metabolism ...................................... 72
Fate of Exogenous Arginine ...................................................................... 80
Nitric Oxide in Critical Care .................................................................... 81
Conclusion ............................................................................................... 83
6. Wound Healing and the Role of Nutrient Substrates ...... 88
David A. Lanning, Rifat Latifi
Basic Principles of Wound Healing ........................................................... 88
Malnutrition and Wound Healing ............................................................ 89
Nutritional Supplementation and Wound Healing ................................... 91
Specific Nutrients, Vitamins, and Trace Elements ..................................... 92
Conclusion ............................................................................................... 98
7. Protein Metabolism in Liver and Intestine
During Sepsis: Mediators, Molecular Regulation,
and Clinical Implications .............................................. 103
Timothy A. Pritts, Eric Hungness and Per-Olof Hasselgren
Introduction ........................................................................................... 103
Liver ....................................................................................................... 103
Intestine .................................................................................................. 113
8. Biochemical Assessment and Monitoring
of Nutritional Status ..................................................... 126
Robert S. DeChicco, Laura E. Matarese, Douglas Seidner and Ezra Steiger
The Incidence of Malnutrition ............................................................... 126
Methods of Nutrition Assessment ........................................................... 126
9. Optimizing Drug Therapy and Enteral Nutrition:
Detecting Drug-Nutrient Interactions .......................... 145
Marcia L. Brackbill, Gretchen M. Brophy
Introduction ........................................................................................... 145
Avoiding Tube Occlusions ...................................................................... 145
Pharmacokinetic Interactions .................................................................. 148
Pharmacodynamic Interactions ............................................................... 150
Influence of Tube Placement on Drug Efficacy ....................................... 151
Optimizing Tolerance to Enteral Nutrition and Drug Therapy ............... 152
Summary ................................................................................................ 153
10. Techniques and Monitoring of Total
Parenteral Nutrition ...................................................... 158
Renee Piazza-Barnett, Laura E. Matarese, Douglas L. Seidner
and Ezra Steiger
Introduction ........................................................................................... 158
Macronutrients ....................................................................................... 158
Micronutrients/Additives ........................................................................ 159
Access/Delivery ....................................................................................... 162
Monitoring Parameters ........................................................................... 163
Complications of Parenteral Nutrition Therapy ...................................... 165
Cycling Total Parenteral Nutrition .......................................................... 177
Conclusion ............................................................................................. 177
11. Radiologic Assessment of Nutritional
and Metabolic Status ..................................................... 181
Diane R. Horowitz, Rifat Latifi
Introduction ........................................................................................... 181
Ultrasound Use in Assessing Body Composition ..................................... 181
Conclusion ............................................................................................. 190
12. Enteral Nutrition: Indications, Monitoring
and Complications ........................................................ 192
Gayle Minard
Introduction ........................................................................................... 192
Indications .............................................................................................. 192
Contraindications ................................................................................... 194
Monitoring ............................................................................................. 194
Complications ........................................................................................ 195
Conclusion ............................................................................................. 198
13. Enteral Access: Open, Endoscopic
& Laparoscopic Techniques .......................................... 199
Keith Zuccala, John M. Porter
Gastrostomy ........................................................................................... 199
Jejunostomy ............................................................................................ 203
Conclusion ............................................................................................. 206
14. Total Parenteral Nutrition: Current Concepts
and Indications ............................................................. 208
Rifat Latifi, Stanley J. Dudrick
Introduction ........................................................................................... 208
General Indications for Use of TPN ........................................................ 209
Specific Indications for Total Parenteral Nutrition .................................. 210
Short Bowel Syndrome ........................................................................... 210
Enterocutaneous Fistula .......................................................................... 211
Inflammatory Bowel Disease ................................................................... 212
Liver Failure ............................................................................................ 212
Acute Pancreatitis .................................................................................... 214
Cancer and TPN: To Feed or Not to Feed? ............................................. 215
15. Intestinal Adaptation: New Insights .............................. 219
Jon S. Thompson
Introduction ........................................................................................... 219
Structural Changes .................................................................................. 219
Functional Adaptation ............................................................................ 220
Summary ................................................................................................ 230
Systemic Factors ...................................................................................... 230
Clinical Implications ............................................................................... 235
16. Intestinal Regeneration and Nutrition .......................... 250
Jon S. Thompson, Shailendra K. Saxena and John G. Sharp
Introduction ........................................................................................... 250
Mechanism ............................................................................................. 250
Clinical Implications ............................................................................... 253
17. Nutritional and Metabolic Management
of Short Bowel Syndrome ............................................. 261
Stanley J. Dudrick, Frizan Abdullah and Rifat Latifi
Introduction ........................................................................................... 261
Pathophysiology ...................................................................................... 263
Nutritional and Metabolic Management ................................................. 265
Immediate Postoperative Period .............................................................. 265
Bowel Adaptation Period ........................................................................ 268
Long-Term Management Period ............................................................. 270
Growth Hormone, Glutamine, and Hormone Modified Diet ................. 270
Surgical Considerations ........................................................................... 271
18. Pharmacologic Aspects of Short Bowel Syndrome ........ 275
Patricia Pecora Fulco, Donald F. Kirby
Physiologic Considerations ..................................................................... 275
Site Specific Contributions ..................................................................... 276
Adaptation .............................................................................................. 278
Intravenous Access in SBS Patients ......................................................... 278
Conclusion ............................................................................................. 296
19. Nutritional Support in Inflammatory Bowel Disease .... 306
John H. Seashore, Melissa F. Perkal
Introduction ........................................................................................... 306
Malnutrition in Inflammatory Bowel Disease ......................................... 306
Nutritional Support in Inflammatory Bowel Disease ............................... 309
Summary ................................................................................................ 314
20. Nutrition Support of Acute Pancreatitis........................ 320
Rifat Latifi, Stanley J. Dudrick
Introduction ........................................................................................... 320
Pathophysiology of Acute Pancreatitis ..................................................... 320
Alcohol and Biliary Disease ..................................................................... 322
Oxygen-Derived Free Radicals ................................................................ 322
Pancreatic Ischemia in Experimental Acute Pancreatitis .......................... 323
Metabolic Changes and Other Complications
in Acute Pancreatitis ........................................................................... 323
Biochemical Abnormalities ..................................................................... 325
Lung Injury ............................................................................................ 326
Nutritional Management in Acute Pancreatitis ....................................... 326
The Effects Of Nutrient Substrates ......................................................... 327
Inhibition of Pancreatic Secretion ........................................................... 328
Rationale for TPN in Acute Pancreatitis ................................................. 329
Dextrose and Amino Acids ..................................................................... 329
Lipids ..................................................................................................... 330
Administration and Monitoring of TPN ................................................. 330
21. Nutritional Management of Chronic Pancreatitis:
Current Concepts .......................................................... 334
Rifat Latifi, Paul G. Perch and Stanley J. Dudrick
Introduction ........................................................................................... 334
Etiologic and Risk Factors of Chronic Pancreatitis .................................. 335
Nutritional Deficiencies in Chronic Pancreatitis ..................................... 335
Pancreatic Diabetes ................................................................................. 336
Diagnosis of Malabsorption in Chronic Pancreatitis ................................ 336
Principles of Clinical Management of Chronic Pancreatitis ..................... 337
Enteral Feeding ....................................................................................... 338
Total Parenteral Nutrition ....................................................................... 339
Nutrient Substrates in Chronic Pancreatitis ............................................ 339
Enzyme Treatment of Exocrine Pancreatic Insufficiency .......................... 340
The Role of Exogenous Pancreatic Enzymes in Pain Management .......... 341
The Effect of Exogenous Enzymes in Gastrointestinal Hormones ........... 342
Conclusion ............................................................................................. 342
22. Nutritional Support in Liver Failure
and Liver Transplantation ............................................. 346
Rifat Latifi
Introduction ........................................................................................... 346
Malnutrition in Patients with Chronic Liver Disease .............................. 347
Hepatic Encephalopathy ......................................................................... 347
Amino Acids in Hepatic Encephalopathy ................................................ 349
Nutritional Assessment ........................................................................... 350
Peritransplant Nutrition: Support ........................................................... 352
Metabolic Changes ................................................................................. 353
Nutrition Status of Donors ..................................................................... 353
How to Feed Liver Transplant Patients .................................................... 354
Conclusion ............................................................................................. 356
23. Nutritional Support in Renal Transplantation .............. 360
Susan T. Crowley, Richard Formica and Antonio Cayco
Introduction ........................................................................................... 360
Protein Malnutrition and Nitrogen Balance ............................................ 360
Dyslipidemia .......................................................................................... 362
Vitamin Supplementation ....................................................................... 364
Bone Metabolism .................................................................................... 365
Summary ................................................................................................ 366
24. Biology of Nutrition Support
in the Critically Ill Patient ............................................ 369
Rifat Latifi, Selman Uranües
Introduction ........................................................................................... 369
Protein and Nitrogen Metabolism in Critically Ill Patients ...................... 370
Amino Acid Metabolism ......................................................................... 370
Branched-Chain Amino Acids (BCAA) ................................................... 372
Nucleotides and Nucleic Acids in Nutritional Support ............................ 372
Omega 3-Fatty Acids .............................................................................. 375
Growth Hormone ................................................................................... 375
Immune-Enhancing Enteral Nutrition: Clinical Evidence ....................... 376
Summary ................................................................................................ 378
Selected References ................................................................................. 379
25. Nutrition Support in Patients with Pulmonary
Failure and ARDS ......................................................... 384
Vanessa Fuchs, A.K. Malhotra and Rifat Latifi
Malnutrition and Lung Functions ........................................................... 384
Anatomy of Respiratory Failure .............................................................. 384
Acute Respiratory Distress Syndrome (ARDS) ........................................ 385
Nutritional Assessment ........................................................................... 387
Molecular Basis Nutritional Management ............................................... 389
Summary ................................................................................................ 392
26. Nutritional Support for the Burned Patient .................. 395
G.J.P Williams, Michael J. Muller and David N. Herndon
Introduction ........................................................................................... 395
Hypermetabolism in Burns ..................................................................... 395
Physiologic Responses to Burn Injury ..................................................... 397
Nutritional Support ................................................................................ 399
Hormonal Manipulation of Burn Hypermetabolism ............................... 406
Summary ................................................................................................ 409
27. Nutritional Support after Small Bowel
Transplantation ............................................................. 418
S. Janes, S.V. Beath
Introduction ........................................................................................... 418
Recovery from Ischemia and Preservation ............................................... 419
Weaning off Parenteral Nutrition ............................................................ 420
Establishment of Normal Diet ................................................................ 424
Monitoring ............................................................................................. 424
Complications after Intestinal Transplant and Implications
for Nutritional Support ...................................................................... 425
Conclusion ............................................................................................. 426
28. Nutritional Support in Patients with Head
and Neck Cancer ........................................................... 430
Matthew E. Cohen, Rosemarie L. Fisher
Introduction ........................................................................................... 430
Risk Factors for Malnutrition .................................................................. 430
Malnutrition and Clinical Outcome ....................................................... 432
Surgery, Nutritional Support and Clinical Outcome ............................... 434
Radiotherapy, Nutritional Support and Clinical Outcome ...................... 439
Chemotherapy, Nutritional Support and Clinical Outcome .................... 440
Enteral Nutrition Delivery ...................................................................... 441
Surgical Gastrostomy or Jejunostomy ...................................................... 444
Conclusion ............................................................................................. 445
29. Nutritional Support in Patients with Gastrointestinal,
Pancreatic and Liver Cancer .......................................... 449
Matthew E. Cohen
Esophageal Cancer .................................................................................. 453
Gastric Cancer ........................................................................................ 455
Colon Cancer ......................................................................................... 456
Pancreatic Cancer ................................................................................... 459
Liver Cancer ........................................................................................... 460
Cost Effectiveness ................................................................................... 463
Conclusion ............................................................................................. 464
30. The Treatment of Obesity ............................................. 473
Souheil Abou-Assi, Rifat Latifi and Stephen J.D. O’Keefe
Epidemiology .......................................................................................... 473
Measurements of Obesity ........................................................................ 473
Health Risks Associated with Obesity ..................................................... 474
Can Obesity and Its Co-Morbid Diseases Be Reversed? .......................... 475
Summary of Interventions, and Results of Randomized
Controlled Trials ................................................................................ 475
Bariatric Surgery ..................................................................................... 481
Current Operations ................................................................................ 481
Nutritional Complications Following Bariatric Surgery ........................... 484
Index ............................................................................. 489
Editors
Rifat Latifi, M.D.
Associate Professor of Clinical Surgery
University of Arizona
Tucson, Arizona, U.S.A.
Chapters 3, 6, 11, 17, 20, 24, 25, 30
Stanley J. Dudrick, M.D.

Professor of Surgery
Yale University School of Medicine
St. Mary’s Hospital/Yale Affiliate
Waterbury, Connecticut, U.S.A.
Chapters 14, 17, 20, 21
Contributors
Frizan Abdullah S. V. Beath
Department of Surgery The Birmingham Children's
Yale University Hospital and
New Haven, Connecticut, U.S.A. University of Birmingham
Chapter 17 Birmingham, U.K.
Chapter 27
Souheil Abou-Assi
Section of Nutrition Larry H. Bernstein
Division of Gastroenterology Yale University Pathology
Department of Internal Medicine Bridgeport, Connecticut, U.S.A.
Richmond, Virginia, U.S.A. Chapter 1
Chapter 30
George L. Blackburn
Khawaja Azimuddin Division of Nutrition
University of New Mexico Beth Israel Deaconess Medical
Espanola Hospital Center
Espanola, New Mexico, U.S.A. Harvard Medical School
Chapters 3, 4 Boston, Massachusetts, U.S.A.
Chapter 2
Timothy J. Babineau
Minimally Invasive Surgery Wendy Swails Bollinger
Boston Medical Center Department of Health Matters
Boston University School Pennsylvania State University
of Medicine University Park, Pennsylvania, U.S.A.
Boston, Massachusetts, U.S.A. Chapter 2
Chapter 2
Marcia Brackbill Rosemarie L. Fisher
Department of Pharmacy Section of Digestive Diseases
Shenandoah University Yale University School of Medicine
Winchester, Virginia, U.S.A. New Haven, Connecticut, U.S.A.
Chapter 9 Chapter 28
Gretchen M. Brophy Richard Formica

Department of Pharmacy Section of Nephrology
and Neurosurgery Yale University School of Medicine
Virginia Commonwealth University New Haven, Conneticut, U.S.A.
Medical College of Virginia Chapter 23
Richmond, Virginia, U.S.A.
Chapter 9 Vanessa Fuchs
Hospital General de México
Antonio Cayco The American British Cowdray
Section of Nephrology Medical Center
Yale University School of Medicine México DF, Mexico
New Haven, Connecticut, U.S.A. Chapter 25
Chapter 23
Bruce Grossie
Matthew E. Cohen Department of Nutrition and Food
Section of Digestive Diseases Sciences
Yale University School of Medicine Texas Woman's University
New Haven, Connecticut, U.S.A. Denton, Texas, U.S.A.
Chapters 28, 29 Chapter 5
Susan T. Crowley Per-Olof Hasselgren

Section of Nephrology Department of Surgery
Yale University School of Medicine Beth Israel Medical Center
New Haven, Conneticut, U.S.A. Harvard Medical School
Chapter 23 Boston, Massachusetts, U.S.A.
Chapter 7
John M. Daly
Department of Surgery David N. Herndon
Weill Medical College of Cornell Galveston Shriners Hospital
University Blocker Burn Unit
New York, New York, U.S.A. Galveston, Texas, U.S.A.
Forward Chapter 26
Robert S. Dechicco Diane R. Horowitz

The Cleveland Clinic Foundation Radiologist
Cleveland, Ohio, U.S.A. Private Practice
Chapter 8 Orlando, Florida, U.S.A.
Chapter 11
Eric Hungnness A. K. Malhotra
Department of Surgery Virginia Commonwealth University
University of Cincinnati Department of Surgery
Cincinnati, Ohio, U.S.A. Medical College of Virginia
Chapter 7 Hospitals and Physicians
Rao R. Ivatury Chapter 25
Virginia Commonwealth University
Department of Surgery Laura E. Matarese
Medical College of Virginia The Cleveland Clinic Foundation
Hospitals and Physicians Cleveland, Ohio, U.S.A.
Richmond, Virginia, U.S.A. Chapters 8, 10
Chapter 4
Gayle Minard
S. Janes Department of Surgery
The Birmingham Children's The University of Tennessee
Hospital and Memphis, Tennessee, U.S.A.
University of Birmingham Chapter 12
Birmingham, U.K.
Chapter 27 Michael M. J. Muller
Rima I. Kandalaft South Auckland Burn Service
Department of Nutrition and Food Middlemore Hospital
Sciences Otahuhu, Auckland, New Zealand
Texas Woman's University Chapter 26
Denton, Texas, U.S.A.
Chapter 5 Stephen J. D. O'Keefe
Section of Nutrition
Donald F. Kirby Division of Gastroenterology
Section of Nutrition Department of Internal Medicine
Medical College of Virginia Richmond, Virginia, U.S.A.
Hospitals Chapter 30
Chapter 18 Patricia Pecora Fulco
Medical College of Virginia Hospitals
David A. Lanning Virginia Commonwealth University
Children’s Hospital of Michigan Richmond, Virginia, U.S.A.
Wayne State University Chapter 18
Detroit, Michigan, U.S.A.
Chapter 6 Paul G. Perch
Virginia Commonwealth University
Medical College of Virginia
Hospitals and Physicans
Chapter 21
Melissa F. Perkal John G. Sharp
Department of Surgery Department of Anatomy
Yale University School of Medicine University of Nebraska Medical
New Haven, Connecticut, U.S.A. Center
Chapter 19 Surgical Services at the Omaha VA
Medical Center
Renee Piazza-Barnett Omaha, Nebraska, U.S.A.
The Cleveland Clinic Foundation Chapters 15, 16
Cleveland, Ohio, U.S.A.
Chapter 10 Jon S. Thompson
John M. Porter University of Nebraska Medical
Department of Surgery Center
University of Arizonia Omaha, Nebraska, U.S.A.
Tucson, Arizona Chapter 15, 16
Chapter 13
Selman Uranues
Timothy A. Pritts Department of Surgery
Department of Surgery AustriaGraz University
University of Cincinnati Graz, Austria
Cincinnati, Ohio, U.S.A. Chapter 24
Chapter 7
G.J.P. Williams
Shailendra K. Sazena Clinical Burns Fellow
Department of Surgery Shriners Burns Hospital
University of Nebraska Medical Galveston, Texas, U.S.A.
Center Chapter 26
Omaha, Nebraska, U.S.A.
Chapters 15, 16 Abdulmasih Zarif
St. Mary's Hospital
John H. Seashore Waterberry, Connecticut, U.S.A.
Yale University School of Medicine Chapter 17
New Haven, Connecticut, U.S.A.
Chapter 19 Keith Zuccala
Danbury Hospital
Douglas L Seidner Danbury, Connecticut, U.S.A.
The Cleveland Clinic Foundation Chapter 13
Chapters 8, 10
Ezra Steiger
Cleveland Clinic Hospital
Chapter 8
Foreword
It has been over 35 years since Dudrick et al described the growth of
beagle puppies fed intravenously demonstrating normal weight gain and
normal growth compared to their orally fed counterparts. This major achieve-
ment is worthy of all the accolades that have been heaped on Drs. Dudrick,
Rhoades and Vars for this work done at the University of Pennsylvania.
These studies demonstrated for the very first time that one could grow an
animal from a young age by administration of all nutrients by vein. This
study in animals was followed shortly thereafter in 1967 by the birth of a
young child with intestinal atresia. She was treated for well over a year with
intravenous nutrition demonstrating normal growth. Studies such as these
were replicated in a whole variety of clinical situations such as trauma, can-
cer, inflammatory bowel disease, radiation enteritis, G-I fistula and poor
wound healing.
Major achievements by Dr. Dudrick were not only to initiate a new therapy
and bring it from the laboratory to the clinical bedside but also to refine the
technique such that it could be applied with low morbidity. The develop-
ment of nutrition support teams and the development of the American So-
ciety of Parenteral and Enteral Nutrition were created by the concept of
teaching proper nutritional support throughout the world. Teams of doc-
tors, nurses, dietitians and pharmacists as well as others came together in
hospitals to administer parenteral and enteral nutrition. Utilization of teams
minimized complications and maximized effectiveness.
The decade of the 1970’s was marked by the ever-increasing use of
parenteral nutrition demonstrating its metabolic efficacy in terms of weight
gain, serum protein metabolism, wound healing and improvement in out-
come. Prospective randomized trials were then begun and carried through
into the 1980’s evaluating the use of parenteral nutrition compared with
other modalities in situations of cancer treatment.
The use of crystalline amino acids replaced protein hydrolysates. Fat emul-
sions were refined and brought into general use. Multi-vitamin preparations
were better defined along with micronutrient requirements. These studies
were painstaking occurring in both animal models and in humans, but they
were necessary as new nutrient administration techniques gave rise to vita-
min and mineral deficiencies. Early recognition of these problems led to
their solution.
The decades of the 1980’s and 1990’s demonstrated efficacy of certain
specific amino acids that would provide either metabolic fuels such as
glutamine for the intestinal track and for muscle as well as specific amino
acids such as arginine that might enhance immune effector cell function.
Omega-3 fatty acids, use of RNA and use of specific vitamins and minerals
were demonstrated to enhance immunological cell function. We entered an
age of nutrient pharmacology as noted by Dr. J. Wesley Alexander. Prospec-
tive randomized trials of enteral and parenteral nutrition were carried out in
elective surgery patients as well as critically ill patients in the intensive care
unit. These studies focused not only on clinical outcome measures but also
focused on cost efficiencies. Again, use of nutritional support teams in hos-
pitals minimized morbidity using nutritional support.
Drs. Latifi and Dudrick have superbly put this text, “The Biology and
Practice of Current Nutrition Support”, together. The chapters vary from
methods of assessing and monitoring nutritional status to those of the use of
intravenous and enteral nutritional support. Practical chapters define
laparoscopic placement of feeding tubes as well as the use of a variety of nutri-
tional substrates, which can be administered in different clinical scenarios.
Of particular importance, is the chapter on nutritional metabolic man-
agement of the short bowel syndrome. Dr. Dudrick was the first to propose
the use of long-term intravenous nutritional support for patients with short
gut syndrome and defined quite well the metabolic needs of these patients.
Many were kept alive for long periods of time by their intestinal tract to adapt
and finally giving way to combinations of enteral and parenteral nutrition.
There is no question that the discovery, implementation and utilization of
total parenteral nutritional support have made enormous benefits to our
patients; saving lives and improving clinical outcome. The recent death of
Dr. Jonathan E. Rhoads, former Chairman of the Department of Surgery at
the University of Pennsylvania and mentor to Dr. Stanley J. Dudrick exem-
plifies the value of an inquisitive mind and the strength of working in part-
nership with many others to achieve beneficial outcomes.
John M. Daly, M.D.

Lewis Atterbury Stimson Professor
Chairman, Department of Surgery
Weill Medical College of Cornell University
Surgeon-in-Chief
New York Presbyterian Hospital-Weill Cornell Center
CHAPTER 1
CHAPTER 1
Clinical Implications of Carbohydrate,

Proteins, Lipids, Vitamins and Trace
Elements in Nutrition Support
Larry H. Bernstein
Overview
Malnutrition occurs in 30-50% of hospitalized patients admitted to acute care
hospitals.1 Patients who are malnourished or are at malnutrition risk usually have
risk factors or disease co-morbidities, any and all of which, unattended, may ad-
versely affect the outcomes of the surgical patient. Severe malnutrition is usually
easily recognized merely by extreme or significant weight loss, loss of strength, and
loss of function. Identifying severe malnutrition in a timely manner, then, should
lead to appropriate intervention.1,2 Nevertheless, that is not always the case, and
malnutrition of moderate degree is often unnoticed at the time of admission. It is
especially important for surgeons to be aware of the risk of malnutrition, particu-
larly in the geriatric patient, because of the very strong association between malnu-
trition and postoperative complications.3,4 Malnutrition occurs with co-morbidities
and is a significant co-morbidity. The surgeon also has to be concerned with the
effects of the metabolic requirements for acute injury independent of and interact-
ing with a malnourished state.
The Malnutrition Risk
The problem of unrecognized patient risk is tied to our conception and defini-
tion of the malnutrition risk. Increasingly, the risk of malnutrition is viewed in
terms of unexpected complications, such as, pneumonia, urinary infection, sepsis,
systemic inflammatory response syndrome (SIRS), which lends itself to expression
in statistical terms. That has not always been the case.
Definitions of Malnutrition
We traditionally make a distinction between marasmus, or chronic inanition
and kwashiorkor. Marasmus is starvation with loss of fat stores and skeletal muscle,
but sparing of circulating transport proteins produced by the liver. Kwashiorkor is
defined by the decrease in circulating plasma proteins. These concepts fit neatly into
measurement criteria using anthropometrics and the laboratory, but they don’t em-
body the dynamic changes of the critically-ill patient. We refine our concept of the
high risk surgical patient, in particular, by reviewing the metabolic response to stress
injury.
The Biology and Practice of Current Nutritional Support, 2nd Edition, edited by Rifat Latifi
and Stanley J. Dudrick. ©2003 Landes Bioscience.
2 The Biology and Practice of Current Nutritional Support
Imperative for Nutritional Intervention

The identification of geriatric surgical patients at high risk for malnutrition and
1 initiating their timely nutritional support is a critical standard of care issue used by
the Joint Commission for Accreditation of Healthcare Organizations. This can be
achieved by a systematized program for identifying patients who might need either
nutritional supplements or aggressive nutritional support. The program has to iden-
tify chronic losses and an acute stress state by both clinical and laboratory charac-
teristics and allow for timely correction of deficits.5,6
Stress Hypermetabolism and the Nutritionally-Dependent
Adaptive Dichotomy
Stress Injury
Stress injury is described in three stages: the ebb phase, the catabolic flow phase,
and the anabolic flow phase.7,8 The ebb phase is dominated by circulatory changes
that requires fluid resuscitation over a period of 8-24 hours. The catabolic flow
phase is dominated by catabolism with initial liver glycogenolysis over the first 24
hours concomitant with skeletal muscle proteolysis to provide gluconeogenic sub-
strates, and lipolysis to provide fatty acid fuel for energy after enzyme induction.
This phase lasts for three to 10 days, but may be extended. The anabolic flow phase
emerges as metabolism shifts to synthetic activities and reparative processes.
Cytokine and Hormonal Events
It is essential to control the hormonal and metabolic balances in these phases for
the metabolic management of the stressed patient. The catabolic flow phase is driven
by cytokine mediators released by lymphocytes and macrophages in the cellular
immune reaction, dominated by interleukin-6 (IL-6).9 The release of these media-
tors is proportionate to the amount of the injury. The release of cytokines is linked
to upregulation of hormonal and humoral events.9 The hormonal events include
the release of glucagon and catecholamines, thyroid hormone, growth hormone,
and cortisol, and their effects—hyperglycemia, metabolic rate, release of free fatty
acids and associated ketosis, insulin growth factor 1 (IGF1), and negative nitrogen
balance from gluconeogenesis.
Catabolic Reactions
The principal action of glucagon is on the conversion of hepatic glycogen to
glucose, thereby, raising the plasma glucose level. Thyroid hormone (T4) has an
effect on target organs through the free hormone (FT4). The catabolic effect of
growth hormone on lipid metabolism is reciprocal to an anabolic effect through
IGF1. An adrenal cortisol secretory response opposes the action of insulin and
promotes a diabetogenic response. Hypercortisolemia results in muscle proteolysis.
Amino acids, especially branch chains amino acids from skeletal muscle, provide
the gluconeogenic precursors through alanine. These hormones are released by the
stress response and drive the metabolic pathways necessary for the use of carbohy-
drate and fatty acid fuels, and necessary to support the repair of damaged tissue.
The humoral events include the changes in and interactions between serum pro-
teins in the inflammatory response. The systemic effects of fever, tachycardia, in-
creased energy expenditure, muscle weakness and wasting are associated with the
elevations of acute phase reactants (APRs) (C-reactive protein, tumor necrosis
factor-alpha, alpha-1 acid glycoprotein) and hormonal changes.7,8
Clinical Implications of Nutrition Elements 3
Suppressed Syntheses
The stress response immediately suppresses synthetic activity by the liver,9 an
organ that has a sole synthetic function with NADP dominated pathways. The se- 1
rum cholesterol decreases as does the production of essential transport proteins,
such as, albumin, transferrin, cortisol-binding globulin (CBG), thyroxine-binding
globulin (TBG), transthyretin or thyroxine-binding prealbumin (TTR), insulin
growth-factor 1 (IGF1).9 While the transport proteins decline abruptly by as much
as 40%, the synthesis of APRs is unaffected. Their essentially controlling and adap-
tive role they exert through their binding to and effects on active ligands.
Nutritionally-Dependent Adaptive Dichotomy (NDAD)
The above relationship, under the influence of cytokines, Ingenbleek refers to as
the nutritionally-dependent adaptive dichotomy (NDAD).9 One has to also con-
sider that this adaptive relationship in stress injury is affected by protein malnutri-
tion prior to the injurious state. Why? Because the basal level of binding proteins is
set low and the adaptive response is blunted.
Free Ligands and the Adaptive State
The metabolic effect of stress injury in the catabolic phase increases the flow of
fuel substrates for energy using processes by its effect on the liver. The decrease in
CBG, TBG, TTR and RBP increases the hypermetabolic effect. The free hormone
hypothesis states that hormonal effect on target tissue is a result of the free hormone.
The adrenal gland is releasing increased cortisol which has an amplified effect with
it’s binding to a lower plasma concentration of CBG. The liver is the repository for
extrathyroidal T4. The extrathyroidal T4 is released with a decreased circulating TBG
and TTR.9 The result is an increased thyroidal activity measured by an increased
free T4 (FT4). This is actually what is referred to as the sick euthyroid syndrome. The
TSH is not affected or slightly decreased, but not in the hyperthyroid range. Vita-
min A is stored in the liver, and it is transported in the circulation in a complex with
TTR and RBP. The vitamin A and RBP are dependent on the level of TTR.
Effect of Stress Injury on Liver Syntheses
The metabolic effect of stress injury on the liver is coupled with the reciprocal
effect of GSH.9 The decreased synthesis of GSH dependent IGF1 occurs with a
high level of GSH. The IGF1 promotes anabolism and protein retention. The result
is an increase of lipid utilization with a breakdown of lean body mass to support
gluconeogenesis. The IGF1 is bound to IGF1 binding protein-3 (IGFBP-3), which
is unaffected by stress. The decreased level of IGF1, which has a short halflife of 8
hours, results in a decrease in the free and active protein, supporting the increased
catabolism.
Energy Requirements of Injured Man
Proteolysis and Nitrogen Loss
The hypermetabolism as it affects protein metabolism is measured by the break-
down of skeletal muscle and the oxidation of amino acids through alanine to
alpha-ketoglutarate in the Krebs cycle.7,8 This results in the release of the amino
group and the production of urea nitrogen through the urea cycle. The somatic
protein loss is also associated with the release of 3-methyl histidine, an amino acid
specific for skeletal muscle that is excreted into the urine with urea nitrogen.
Cuthbertson described the catabolic loss of nitrogen that cccurs with severe
injury and is associated with skeletal muscle wasting, loss of strength, and attrib-
1 uted to extensive breakdown of muscle.7,8 The increased rate of metabolism in stress
injury is measured by the rate of protein oxidation and by the rate of CO2 produc-
tion. The rate of protein oxidation is measured by the rate of nitrogen appearance
in the urine. There is normally 4 grams of unmeasured nitrogen to be accounted for
in 24 hours, so the total nitrogen is calculated from urinary urea nitrogen by adding
4 grams, assuming that the nonurea nitrogen is negligible.
Nitrogen Loss and Gluconeogenesis
The rate of gluconeogenesis is decreased in normal man, a nitrogen sparing
effect, when 6-10 grams of carbohydrate is provided. The rate of gluconeogenesis is
not increased in starvation as the body economy relies on lipolysis and fatty acid
fuels associated with ketogenesis. These patients have a normal or decreased urinary
nitrogen. The rate of gluconeogenesis is accelerated during the acute catabolic state,
even when glucose is provided. This is unabated, though, by providing exogenous
glucose.10 The loss of nitrogen with trauma or sepsis is related to the extent of the
injury.7,8 Nitrogen balance studies measure nitrogen equilibrium, which is the net
loss or gain of protein from the body.11 The nitrogen loss after severe injury is
proportional to the severity and extent of trauma, and it tapers off in days. Indeed,
the nitrogen loss is greatest with severe trauma and delayed refeeding. The net ac-
cretion of body protein in the reparative phase is slow in the post-injury phase and
has been measured by Hill and associates using whole body neutron activation
analysis.12 Anabolism with refeeding occurs at a constant rate of 3 gm of nitrogen
(20 gm protein) per 70 kg body weight per day, but muscle activity is required for
rebuilding the loss.12
Stress Metabolism of Carbohydrate and Fat
Stress injury results in alterations in carbohydrate and fat utilization. Adipose
tissue is converted to fatty acids and glycerol as described above. Fatty acids are
oxidized by non glucose-dependent tissues. The glycerol is and unoxidized ketones
are used as a glucose fuel. As the concentration of plasma glucose rises in severe
injury, the hyperglycemia is related to crude muscle losses with increased urinary
nitrogen loss. The site of injury is supported by the breakdown of whole body
protein to support the immune response. This is not associated with a lack of insu-
lin, but with increased activities of counterregulatory hormones opposing the insu-
lin action.9 Fat is not utilized as the primary fuel in the extensively injured extremity
because of the shift to glycolytic metabolism in the injured tissue associated with
increased production of lactate.7-9 A significant amount of glucose production by
the liver is from lactate and pytuvate as the wound metabolizes glucose.
Measuring Energy Expenditure
Indirect calorimetry and tracer techniques are used to study substrate oxidation
in vivo.10,13,14 The latter requires blood sampling and is only used in the research
setting. CO2 production is used to measure substrate oxidation and energy expen-
diture by indirect calorimetry from measurement of respiratory gas exchange rates.
The method assumes the CO2 expired is proportional to the rate of respiration.
The assumption depends on the O2 disappearing from the inspired air being used
exclusively for biological oxidations so that all the CO2 expired is derived from
combustion of substrates. It is also assumed that all of the nonprotein nitrogen

excreted into the urine is derived only from the oxidation of free amino acids, which
is 16% of the nitrogen content. Indirect calorimetry measures the net loss of sub- 1
strate by oxidation, regardless of cycling that may occur along the way. The method
of indirect calorimetry and the Fick principle both measure the oxygen consump-
tion (VO2) and the carbon dioxide production (VCO2). Indirect calorimetry mea-
sures the oxygen consumption (VO2) and the transpulmonary O2 gradient from the
respiratory gas exchange. Fick proposed to measure the VO2 and VCO2 from gas
exchange and the transpulmonary O2 and CO2 gradient by heart catheterization. In
this idealized model, the O2 input and CO2 output is measured, and the cardiac
output (CO) provides the flow rate. The result is:
VO2 = CO (arterial O2 – mixed venous O2)
VCO2 = CO (arterial CO2 – mixed venous CO2)
Assuming that ambient air is the only source for O2 and the only sink for meta-
bolic CO2, the VO2 and the VCO2 are measured from the fractional concentrations
of O2 and CO2 concentrations in the inspired (FI) and the expired (FE) air flows.
The calculation is:
VO2 = (FIO2 – FEO2)Ve
VCO2 = (FICO2 – FECO2)Ve, where Ve is the ventilatory rate.
The only significant difference between these is that the measures of VCO2 are
12% lower and less accurate with Fick than with indirect calorimetry.13
Energy of Fuels
The respiratory quotient (RQ), defined as VCO 2/VO2, is the measure of
efficiency of respiration.10 The calorimetric RQ is between 0.69 and 1.00. The en-
ergy expenditure being measured by the VO2, a value of less than 1.0 is incomplete
combustion. RQ is important for calculating the nutritional requirements in pro-
viding assisted nutritional support. The RQ for fat is 0.7, whereas the RQ for carbo-
hydrate is 1.0. We have to weigh the advantage of the administration of fat versus
carbohydrate energy sources. Fat has an advantage over carbohydrate because it is a
dense calorie source and it is efficiently oxidized based on it’s low RQ. The effect of
excessive carbohydrate calories is excessive CO2 production, which drives a hyperp-
nea, detrimental to the pulmonary compromized patient. Lipid has a rate of admin-
istration that is rate limited by it’s clearance. Excessive fat administration is
immunosuppressive.
Harris-Benedict Equation
The use of indirect calorimetry is limited in most clinical settings, except for
intensive care units, because of cost requirements for the technology and for the
staffing. The Harris-Benedict equation is most commonly used to calculate the esti-
mated calorie and protein needs with reasonable agreement with actual needs.
Males BEE = 66.47 + 13.75 W + 5.0 H—6.76 A
Females BEE = 655.10 + 9.56 W + 1.85 H—4.68 A, where W is weight in
kg, H is height in cm and A is age in years.
Consideration must be given to existing energy needs that go beyond basal or
resting needs. This basic estimate of energy needs (BEE/REE) is often increased to
reflect the energy required for physical activity and any anticipated hypermetabolic
response to injury or illness.
BEE x (activity factor) x (injury factory) = TEE (total energy expenditure)
Nutritional Requirements
1 Energy Requirements Under Stress
The calorie and protein requirements for stressed patients are shown in Table
1.1. For normal energy needs 100-150 g of CHO must be furnished daily. Glucose
oxidation under normal conditions is at approximately 2-4 mg/kg/min, and in
severe stress is only slightly greater at 3-5 mg/kg/min. Catabolism of peripheral
muscle and lipolysis release carbohydrate and lipid substrates in severe stress (14).
An excess of 400-500 g of glucose per day is not used. However, administration of
carbohydrate as a sole energy source has a calorigenic effect, increasing the utiliza-
tion of fuel by about 20% over REE. Protein sparing by glucose is abrogated by
severe stress.
Protein Requirements
Protein is required for growth, maintenance and repair of tissue. 6.25 grams of
protein has one gram of nitrogen. Nitrogen balance occurs when protein synthesis
and breakdown are in equilibrium. Dietary protein contains 20 common amino
acids of which nine are essential. The recommended dietary allowance of protein
for an adult (non pregnant or lactating) is 0.8 g/kg/day. In the catabolic phase of
acute stress or trauma, protein requirements are increased at 1.5 to 2.0 g/kg/day or
more for wound repair, or to replace protein lost in drainage of exudate. The provi-
sion of adequate calories and protein is mandatory.
Fat Requirements
35% of diet intake as fat is required for energy and for essential fatty acids.
EFAD occurs at a ratio of 0.4 or greater. Linolenic acid deficiency is characterized
by: growth retardation, scaly dermatitis, and alteration of the normal triene:tetrene
ratio. Linoleic acid is derived from linoleic and may be derived exogenously. Oils as
corn, soy and safflower contain 50-70% of their fat as linolenic. Linoleic acid is a
precursor of arachidonic acid, which is needed for prostaglandin and thromboxane
synthesis. Most lipid emulsions presently available are composed for the most part
of long chain triglycerides (LCT). Complications from use of LCTs include com-
promised immune function, hyperlipidemia, impaired alveolar diffusion capacity,
and reduced function of the reticulo-endothelial system.
Minerals and Trace Elements
The macronutrients, water and electrolytes constitute the major part of nutri-
ent intake, regardless of the route of administration. The major minerals—calcium,
phosphorus, and magnesium, and electrolytes—sodium, potassium and chloride
must be provided. They are essential for neuromuscular, cardiac, endocrine and
skeletal function. Potassium is the main intracellular cation and it is in equilibrium
with sodium, divalent cations, and anions. Its intracellular concentration is 140
mmol/L. The total body potassium is 71 mmol/kg. The total body potassium is
depleted in malnourished surgical patients, and it is disproportionately reduced
compared with nitrogen. It is increased with short term TPN without increasing
the total body nitrogen, but long term feeding also increases nitrogen.11 It is impor-
tant to keep in mind the following:
1. glucose infusions increase the need for K+;
2. there is a retention of 3 meq K+ per gm of nitrogen;
Table 1.1. Calorie and protein needs in stress
Stress Clinical Setting CHO% NPC:N Stress 1

0 Simple starvation 28 150:1 1.0
1 Elective Surgery 32 100:1 1.5
2 Polytrauma 40 100:1 2.0
3 Sepsis 50 180:1 2.5
3. infusion of about 80-120 meq K+ per day is required to replenish stores in

patients receiving TPN.
The most important divalent cation is magnesium, important for membrane,
mitochondrial, and nuclear metabolic functions. The extracellular magnesium ac-
counts for only 3% of the total body magnesium. Magnesium becomes depleted
with protein-energy malnutrition, and it has to be increased to about 15 mmol per
day to improve nitrogen balance. Phosphate is the main intracellular anion. It is
critical for buffering systems, energy linked nucleotide reactions, membrane func-
tion, oxygen transfer systems, and neuromuscular function. The majority of phos-
phorus is in bone matrix with calcium. The serum phosphorus falls rapidly during
TPN, and it is extremely sensitive to the administration of glucose and insulin and
less sensitive to use of a mixed substrate. As with magnesium and potassium, phos-
phorus promotes nitrogen retention. The importance of monitoring for adequate
blood levels of magnesium and phosphate is covered later.
Vitamins
Beyond maintenance requirements, little of a definitive nature is known regard-
ing the needs for vitamins and minerals in critical illness or injury, except for the
nutrients involved in wound repair, as Vit A, Vit C and Zinc.11 The most important
trace elements for our consideration include iron, zinc, chromium, copper, manga-
nese, iodide, selenium and molybdenum, and cobalt. These are required for meta-
bolic function and their deficiency is associated with specific biochemical change
and functional abnormality that is relieved by giving these nutrients. Of these, co-
balt is associated with vitamin B12. These are absorbed in bound and elemental
forms, and they circulate as protein-bound complexes or ligands that are not in free
equilibrium with tissue stores. These are usually incorporated as cofactors of en-
zymes or proteins in tissue. In relationship to this dissociation of plasma level and
tissue stores, the plasma concentration is not a measure the total body stores. For
example, zinc plasma concentration is normal in the hypercatabolic state as zinc is
being lost and the patient is in negative zinc balance. The plasma zinc is maintained
by a net outflow from tissue stores. A positive zinc balance occurs with provision of
nutritional support as there is a net inflow of zinc into tissue with anabolism, and
the plasma level falls unless exogenous zinc is given. Vitamins are active in minute
quantities and have to be provided in any regimen of TPN to avoid deficiency.
Patients with steatorrhea, short bowel, and pancreatic insufficiency require increased
fat soluble vitamins, including 10,000-30,000 IU per day of vitamin A. Patients
with chronic liver disease will have reduced vitamin A stores. Those receiving TPN
may need 3300 IU per day.
Clinical vs. Laboratory Information

1 Clinical and Functional Status
The importance of clinical indicators is correlation with functional status and
identification of prior co-morbidities, i.e., cancer, sepsis, major surgical procedure,
prolonged vomiting or diarrhea, fistula, inability to take in or utilize nutrients.15
These are associated with depletion from hypo- and/or hypermetabolism. Clinical
indicators are excellent categorical criteria for risk assessment, but they can by them-
selves, contribute to over- and underutilization (malutilization) of nutritional sup-
port. Table 1.2 lists clinical risk factors for malnutrition.
Laboratory Evaluation
Laboratory indicators are objective and may be used for measuring calorie and
protein needs, for identifying serious clinical risk of malnutrition, for documenting
agreement between clinical criteria and actual deficits, for documenting anabolic
response from nutrient repletion, and for assessing prognosis.5,6 These are shown in
Table 1.3. The finding that the laboratory is no better than subjective global assess-
ment is expected concordance between two types of observations. The sensitivity
and one—specificity of a test is actually fitted to a receiver-operator characteristic
curve to remove, as much as possible, the effect of decision value selection, but it is
affected by the choice of the dependent variable that is used to define the outcome.
We have to put into context additional value provided by the laboratory. Agree-
ment between SGA and severe losses for at least two laboratory measures confirms
correlation between clinical and laboratory tests. On the other hand, there are unique
patient (sub)groups (syndromic classes) that have incongruously depressed serum
proteins either because of early protein depletion or repletion that may or may not
agree with clinical assessment.16
Redundant Laboratory Abnormals
Syndromic classes is treated in the information-based definition of decision-values
proposed by Spiekerman, Rudolph and Bernstein.16 A simple example of this con-
cept is the observation that a patient has an albumin of 2.7 g/dl AND and lympho-
cyte count of 1,080. In a more formal way, one takes the tests and scales them for
intervals, assigning values in the assigned ranges from 1 to k. The test combinations
form pattern classes, which group into the malnourished and nonmalnourished
groups with frequencies related to risk. The existence of three groups (non-disease,
moderate, severe) requires a multivalued logic with at two decision-values for a
laboratory test. In the absence of a gold standard test to use as a supervisory vari-
able, it would be possible to determine the correct assignment of laboratory data to
each group only if sufficient variables are used to form a classification.
Tests to Monitor
Test selection has a basis in pathophysiology. Hypermetabolism increases pro-
teolysis and gluconeogenesis with loss of muscle mass and amino acid oxidation
resulting in urinary loss of nitrogen as 3-methyl histidine, creatinine, and urea.
Nitrogen loss is a primary measure of stress. The greatest nitrogen losses in trauma
occur in the first few days, at a time when total urinary nitrogen reflects the cata-
bolic phase more accurately than urinary urea nitrogen.
Table 1.2. Clinical risk factors

• inadequate nutrient intake for 5 days or more 1
• recent unexplained weight loss
• surgery or disease of the gastrointestinal tract
• unwillingness or inability to eat or eat enough
Table 1.3. Laboratory risk factors

Total lymphocyte count < 1200/mm2
Pre-Albumin < 11 mg/dl
Transferrin < 150 mg/dl
Albumin < 3.0 g/dl
Liver transport proteins are characterized by different rates of production and

degradation, and short halflife is a useful characteristic for following catabolism and
anabolic response. The acute phase proteins, C-reactive protein (CRP) and alpha-1
antitrypsin are elevated with the inflammatory response (ceruloplasmin and trans-
ferrin are also) even when other proteins are severely depressed. CRP is a particularly
good indicator of bacterial infection. CRP and TNF-α are increased associated with
the cytokine mediated response, particularly interleukin-6.
Table 1.4 is a comparison of the plasma proteins that are used to assess protein
energy malnutrition (PEM). The phenomenon of protein depletion is referred to as
an inverted acute phase response. Serum albumin, with a halflife of 21 days, is in-
sensitive for measuring anabolism, and its volume distribution makes it a popula-
tion rather than an individual measure of nutrition. It is unsuitable for the dynamic
evaluation of nutritional repletion. Albumin increases by only 0.2 g/dl a week with
aggressive nutrition support. Transferrin, with a halflife of 8 days, is somewhat bet-
ter than albumin, but it is affected by iron balance. Table 1.5 shows the features of
an ideal nutritional marker.
Rapid Turnover Proteins
Proteins with short halflifes less than 2 days, such as transthyretin (prealbumin,
thyroxine-binding prealbumin, TBPA, TTR), are needed to measure the anabolic
response. TTR increases at an expected rate of 1 g/dl a day, or doubles in a week
with nutrition support.5,16 It may be halved after a week to 10 days NPO. It may be
elevated by corticosteroid therapy after a few days. Retinol-binding protein (RBP),
which has a half-life of 36 hours, circulates bound with vitamin A to TTR in a 1:1:1
molar ratio. The complex is elevated in patients with renal failure on dialysis and
RBP is excreted in the urine. RBP and TTR are both measured easily by nephelom-
etry. Insulin growth-factor 1 (IGF1) or somatomedin C is the best measure of ana-
bolic response because it has the insulin effect without the lipolytic effect of growth
hormone. It is bound to the IGFBP3 receptor and it is difficult to measure because
of an extraction and long incubation time. The method has been improved by an
automated column methodology (Nichols). Arguments have been made for mea-
suring fibronectin, which may have a role in wound healing. Fibronectin is de-
creased in burn patients and appears to be a predictor of sepsis. The most easily
measured of this class of tests is TTR. A TTR of less than 8.5 mg/dl is a critical
Table 1.4. Plasma protein used in nutrition assessment

1 Albumin: limited value for detecting acute changes in nutritional status.
3.0-3.5 g/dl Mild depletion
2.5-2.9 g/dl Moderate depletion
2.4 or less Severe depletion
Transferrin: half-life of 8 days
Affected by iron metabolism
TTR: half-life is 1.9 days
Early predictor of protein malnutrition
Measures response to nutritional support
A serum TTR < 11 mg/dl is protein malnutrition
TTR decreases at a rate of 0.8 to 1.5 mg/dl per day, depending on the level of stress with no
oral feeding. It doubles in a week with nutritional support.
Table 1.5. Features of an ideal marker

• Identify clinically significant depletion
• Reflects severity of deficits
• Indicator of current status and change in status
• Sensitive to decline
• Sensitive to improvement
• Minimal interference
finding for a burn patient because the patient can’t hold a graft. A TTR of less than
5 mg/dl is severe protein depletion. A case study illustrates its advantage.
Case Example
An 88-year old woman with lower GI bleeding associated with perforated di-
verticulitis had a surgical resection and proximal diverting colostomy with a some-
what complicated recovery. She was maintained on PPN initially and changed to
central TPN day 13 when she had an obstruction that resolved by day 20 after the
small bowel was decompressed.
Postoperative Day
Test 1 13 16 26 Reference range
ALB, g/L 27 25 25 27 35-55
TTR, mg/L 72 121 160 205 160-350
Information Model
Getting the Most Out of Information
I previously referred to the concept of syndromic classes.16,17 Even though it is a
formal idea that is measurable, it is not important for surgeons to feel a deficiency
of knowledge with unfamiliarity with this. The truth of the matter is that you use it
often in practice. Clinical decisions are made by observing data from laboratory
and clinical findings together.
The evaluation of nutritional status is somewhat refined by an information model.
The model is derived from the fundamental theory of communication, which uses
redundancy to minimize the effects of noise in message transmission. We use an

information model for medical decision-making by treating disease as a symptom
complex that is a coded-message (each coded-message is a syndromic class). The 1
message transmission can be interpreted from the redundant information (correla-
tion) in the message. Regression is the most common approach to continuous data.
It is a smoothing function and carries a risk of loosing information. It does not
reveal the structure of the data. There are approaches that learn and classify data
(clinical and laboratory) based on analysis of the information content of the data,
such as, recursive partitioning and amalgamation, Rypka’s truth table comprehen-
sion,17 Rudolph’s group-based reference,16 and neural networks. These are based on
classification matrices that are formed by similarities and differences of features that
define data sets. Normal-reference is defined by Rudolph and Bernstein18 as the set
having no information. That is a departure from distance from the center.
Length of Stay (LOS)
Association between Malnutrition and Length of Hospital Stay
Clinical and laboratory indicators of nutritional status are associated with excess
LOS.19 The best predictor of nutritional class is a combination of tests.20 Use of the
chemistry profile can take into account the information in: albumin, total protein,
cholesterol. TTR (prealbumin, transthyretin, thyroxine-binding prealbumin), with
its short halflife (1.9 days), is sensitive to changes in nutrititional status and is an
indication of severity of deficits. It is not affected by hydration status in the way that
albumin is. Serum TTR can be combined with the chemistry panel. These tests may
be scored and used to predict LOS. Although the information model can be used to
examine the relationship between malnutrition and LOS, it can be used to examine
the effects of an implementation program, which includes early feeding, but may
include other measures. In this case LOS becomes an outcome variable and inter-
ventions become inputs.
Improving Correction of Malnutrition
Identify Malnutrition Risk and Intervene
The ability to identify malnourished patients and to implement early interven-
tion has implications for continuous quality improvement.1 Using laboratory as well
as clinical indicators of malnutrition should allow identification of all patients at
risk within 24 hours of admission. Laboratory tests can be triggered by admission
criteria, such as weight loss, decreased food intake, or medical condition, or they can
be added to a standard admission profile. Advanced age over 65 years or serum
albumin concentration below 3.2 g/dl can be used as automatic criteria for obtain-
ing TTR.
Monitoring Effectiveness of Feeding
The greatest value of TTR is its measure of current nutritional status.5,6,21 Thereby,
it allows determination of adequacy of feeding, and it should reduce the discharge of
wasted patients who are at risk of readmission. Its physiological range is 16-35 mg/
dl. Serious malnutrition is reflected by a serum concentration < 11 mg/dl, severe at
< 7 mg/dl. It increases at a rate of 1 mg/dl per day with adequate nutritional sup-
port. A TTR concentration of less than 11 mg/dl after a week of nutrition support
or a daily increase of less than 0.5 mg/dl is a reasonable indication that the feeding is
inadequate or that the patient is unresponsive. Serum TTR concentration is a prog-

nostic indicator.
1 Clinical Processes Incorporating Transthyretin (Prealbumin)
A profile including TTR can be incorporated into a clinical practice guideline
implemented through a critical pathway. Although TTR acts as an acute phase
reactant, it can be used to establish a baseline for nutritional support. Urinary ni-
trogen excretion is often used to assess the amount of protein deficit prior to feed-
ing. Failure to increase TTR is an indication of inability to provide adequate nutrients
by method of feeding. Systematic identification of patients at risk, appropriate tim-
ing and mode of feeding, and monitoring effectiveness are essential elements for
such a guideline.
Nutrition Support Monitoring
TTR a Measure of NDAD
We have seen how the use of a short halflife protein, such as TTR can be used
alone, or in combination with serum albumin and clinical indicators for identify-
ing serious risk. TTR is a measure of the NDAD, so the decrease in TTR is associ-
ated with changes in CRP, TNFalpha, RBP and IGF1.9 In some patients who have
recieved high dose corticosteroids, the TTR is elevated, but it is possible to trend
patients as they receive nutritional support. In these patients it might be argued
that urinary nitrogen excretion is done weekly.
Nitrogen Loss
Nitrogen balance is daily intake of nitrogen minus the excretion. The intake
represents nutritional nitrogen and the excretion consists of measured urinary ni-
trogen plus a factor for unmeasured gastrointestinal and cutaneous losses, usually 2
to 4 grams. Nitrogen balance is calculated as:
N intake—(urinary N + change BUN + 4)
change in BUN (g) = (0.6 weight) (SUNf—SUNi),
where i and f are the initial and final values in the measurement period, SUN is
serum urea nitrogen (g/l), and weight is body weight in kilograms. A positive bal-
ance indicates an anabolic state with an overall gain in body protein for the day. A
negative nitrogen balance indicates a catabolic state with a net loss of protein. Uri-
nary nitrogen excretion may rise to 30-50 g/day with severe stress, which is the
equivalent of 1 to 1.5 kg of lean body mass.
Overfeeding and Monitors
We have already considered the consequence of lipids versus carbohydrate as an
energy source. The effects of excess carbohydrate are hyperglycemia and on driving
pCO2 production with CO2 retention. Carbohydrate also leads to fatty liver. This
necessitates the close monitoring of pCO2 measurement for patients on nutritional
support and less frequent evaluation of liver function, such as the alkaline phos-
phatase. Table 1.6 lists the complications of overfeeding. The electrolytes have to be
monitored because of losses from fluid loss. The fluid associated electrolyte losses
are listed in Table 1.7.
We have to add to the complications the serious effect of hypophosphatemia.
Hypophosphatemia and hypokalemia can both occur as a result of the refeeding
syndrome. They have to be watched as closely as the pCO2, the glucose, and the
TTR. The K+, Mg2+ and H2PO32- are intracellular cations and anion, respectively.
They move into the cell and out of the circulation with refeeding. They are critical
for excitation-contraction coupling, and failure to monitor these can result in sud- 1
den death. In the case of magnesium, the serum level is not an accurate measure of
the total body load. A patient with tetany may have low calcium concentration, but
if the calcium fails to resolve this, than administration of magnesium is the best test.
Table 1.8 lists the requirements for monitoring phosphate levels. The lowering of
serum phosphorus levels leads to a decrease in ATP and other phosphorylated com-
pounds in the tissues and blood. When the serum level falls to 1.0 mg/dl or lower,
leukocyte dysfunction and a potential for sepsis occurs. In addition, reduced nucle-
otide production due to hypophosphatemia can result in hemolytic anemia, neuro-
muscular dysfunction, myocardial depression and respiratory failure. Adequate
treatment of the severely malnourished patient requires adequate nutritional sup-
port with careful monitoring. Repletion must be initiated slowly while monitoring
serum phosphorus, along with serum electrolytes, glucose, and magnesium levels.
Quality Management
Excess LOS variation is a global outcome variable. It is dependent on extended
period after surgery without oral intake (Meguid’s IONIP), initial condition, unex-
pected complication (wound site infection, pneumonia), and malnutrition. The ef-
fect of nutritional status is independent and interacts with the other factors. The
laboratory tests predict outcome by forming severity classes. Mozes et al22 recently
classified surgical and nonsurgical major diagnostic categories into groups homoge-
neous with respect to LOS from seven laboratory values (wbc, Na, K, CO2, BUN,
HCT, ALB) for 73,117 admissions at UCSF and Stanford. Studies have shown that
Hb, cholesterol23 and insulin-like growth factor 1 (IGF1)24 are predictors of mortal-
ity. Nutritional markers are important tests in any analysis.
Quality Management has to focus on medical outcomes of alternative strategies,
i.e., feeding, not feeding, delayed intervention, and the costs of interventions. Policy
considerations are the organizational purview of a Nutrition Committee and the
Nutrition Support Team. The cost of data collection can be significant. The cost of
prevention, with an effect on under- and over-utilization, can be less than the cost of
failure to develop a system. The use of the laboratory has a low cost in supporting a
system of quality management.
The information model has been used to determine optimum decision-values
for tests, and has been used to examine the relationship between tests, malnutrition
and LOS. It can be used to examine differences in the effects of interventions. Not
all interventions can be assumed to be equivalent. Preoperative feeding for five days
before a major procedure assumes utilization costs that have a different significance
for marginally than severely at risk patients. Perioperative interventions, intrave-
nous and enteral, are uniquely identified input variables. In addition to the assign-
ment of treatment effects, it is necessary to identify the initial pretreatment condition
as distinguished from the treatment effects. Therefore, laboratory data need to be
adequate to examine post-treatment status. These can be described in the form of a
truth table with each defining variable as a column and each patient as a row.
It is important to recognize that a quality improvement model for nutritional
interventions has to take into account the expectations of costs to do nothing, the
expected costs of alternative interventions, and the costs reduced by failure avoid-
ance. Traditional cost accounting models are not adequate for the complexity
of the issues.
Table 1.6. Problems of overfeeding

1 • excess CO2 production
• fat deposition
• hyperglycemia
• pulmonary edema
• worsening of existing congestive heart failure
• hepatic complications
Table 1.7. Etiology of common electrolyte deficiencies
Electrolyte Cause of Deficiency

Sodium Loss of skin, GI tract, lungs or kidney
Kidney—diuretic use, renal damage, adrenal insuffic
Potassium Starvation, loss from skin, bile, lower GI tract or fistula.
Renal: diuretics, alkalosis, Amphotericin
Bicarbonate Diarrhea, pancreas or small bowel loss, renal tubular acidosis,
mineralcorticoid deficiency
Chloride Diuretics, gastric loss, intestinal loss, secretory loss, renal
reabsorption due to drug therapy-carbenicillin, sulfate, phosphate
Magnesium starvation, intestinal loss, malabsorption, diarrhea, laxative abuse,
diuretics, cyclosporin
Phosphorus starvation, alkalosis, glucose administration, diabetic keto
acidosis, GI tract losses, aluminum containing antacids.
Table 1.8. Clinical conditions for which phosphorus levels should

be monitored during treatment
• Refeeding phase for the malnourished patient
• Alcohol withdrawal and nutritional support
• Insulin therapy with diabetic keto-acidosis
• Phosphate binding antacid therapy
• Recovery diuretic phase after severe burns
• Severe respiratory alkalosis
The ability to identify malnourished patients and to implement early interven-

tion has implications for continous quality improvement (1). Using laboratory as
well as clinical indicators of malnutrition should allow identification of all patients
at risk within 24 hours of admission. Laboratory tests can be triggered by admis-
sion criteria, such as weight loss, decreased food intake, or medical condition, or
they can be in a standard admission profile.
Transthyretin (prealbumin, thyroxine-binding prealbumin, TBPA, TTR) is a
transport protein with a short halflife (1.9 days) that is sensitive to changes in
nutrititional status and is an indication of severity of deficits. It allows determina-
tion of adequacy of feeding, and it should reduce the discharge of wasted patients
who are at risk of readmission. It has a physiological range of 16-35 mg/dl. Serious
malnutrition is reflected by a serum concentration < 11 mg/dl, severe at < 7 mg/dl.

It increases at a rate of 1 mg/dl per day with adequate nutritional support. The table
of ranges shows the effect of nutrition support on TBPA. Moderately malnourished 1
patients with low ALB have increased TBPA with nutrition support.
A profile including TTR can be incorporated into a clinical practice guideline
implemented through a critical pathway. Although TTR acts as a acute phase reac-
tant, it can be used to establish a baseline for nutritional support. Urinary nitrogen
excretion is often used to assess the amount of protein deficit prior to feeding. Fail-
ure to increase TTR is an indication of inability to provide adequate nutrients by
method of feeding. Systematic identification of patients at risk, appropriate timing
and mode of feeding, and monitoring effectiveness are essential elements for such a
guideline.
Selected References
1. Brugler L, DiPrinzio MJ, Bernstein L. The five-year evolution of a malnutrition
treatment program in a community hospital. J Qual Imp. 1999; 25:191-206.
2. Bernstein LH, Shaw-Stiffel TA, Schorow M et al. Financial implications of malnu-
trition. In: Labbe R, ed. Clinics in laboratory medicine. Nutition support. Vol 13.
Philadelphia: Saunders, June 1993:491-506.
3. Meguid MM, Mughal MM, Meguid V et al. Risk-benefit analysis of malnutrition
and preoperative nutrition support: a review. Nutr Int 1987; 3:25-34.
4. Meguid MM, Campos ACL, Meguid V et al. IONIP: a criterion of surgical out-
come and patient selection for preoperative nutritional support. Br J Clin Pract
1988; 42(suppl 63):8-14.
5. Bernstein LH, Leukhardt-Fairfield CJ, Pleban W et al. Usefulness of data on albu-
min and prealbumin concentrations in determining effectiveness of nutritional
support. Clin Chem 1989; 35:271-274.
6. Bernstein LH. Utilizing laboratory parameters to monitor effectiveness of nutri-
tional support. Nutr Int 1994; 10:58-60.
7. Kinney JM. Metabolic Responses to Injury. Chapter 2. In: Winters RW, Greene
HL, eds. Nutritional Support of the Seriously Ill Patient. New York: Academic
Press, 1983:5-12.
8. Wilmore DW, Black PR, Muhlbacher F. Injured Man: Trauma and Sepsis. Chap-
ter 4. In: Winters RW, Greene HL, eds. Nutritional Support of the Seriously Ill
Patient. New York: Academic Press, 1983:33-52.
9. Ingenbleek Y, Bernstein L. The stressful condition as a nutritionally dependent
adaptive dichotomy. Nutrition 1999; 15:305-320.
10. Kinney JM. Energy Metabolism: Heat, Fuel and Life. Chapter 1. In: Kinney JM,
Jeejeebhoy KN, Hill GL et al, eds. Nutrition and Metabolism in Patient Care.
Philadelphia: W.B. Saunders, Harcourt Brace Jovanovich, 1988:3-34.
11. Jeejeebhoy KN. Nutrient Metabolism. Chapter 3. In: Kinney JM, Jeejeebhoy KN,
Hill GL et al, eds. Nutrition and Metabolism in Patient Care. Philadelphia: W.B.
Saunders, Harcourt Brace Jovanovich, 1988:60-88.
12. Hill GL, King RFGJ, Smith RC et al. Multi-element analysis of the living body by
neutron activaion analysis—application to critically ill patients receiving intrave-
nous nutrition. Br J Surg 1979; 66:868-72.
13. Ferrannini E. Equations and Assumptions of Indirect Calorimetry: Some Special
Problems. In: Kinney JM, Tucker HN, eds. Energy Metabolism: Tissue Determi-
nants and Cellular Corollaries. New York: Raven Press, 1992:1-17.
14. Young VR, Yong-Ming Y, Fukagawa NK. Whole Body Energy and Nitrogen (Pro-
tein) Relationships. In: Kinney JM, Tucker HN, eds. Energy Metabolism: Tissue
Determinants and Cellular Corollaries. New York: Raven Press, 1992:139-161.
15. Jeejeebhoy KN, Baker JP, Wolman SL et al. Critical evaluation of the role of clini-
cal assessment and body composition studies in patients with malnutrition after
total parenteral nutrition. Am J Clin Nutr 1982;35:1117-27.
1 16. Spiekerman AM, Rudolph RA, Bernstein LH. Determination of malnutrition in
hospitalized patients with the use of group-based reference. Arch Path Lab Med
1993; 117:184.
17. Rypka EW. Methods to evaluate and develop the decision process in the selection
of tests. In: McPherson RA, Nakamura RM, eds. Clinics in laboratory medicine.
Laboratory immunology II. Strategies for clinical laboratory management. Vol 12.
Philadelphia: Saunders, June 1992:351.
18. Rudolph RA, Bernstein LH, Babb J. Information-Induction for the diagnosis of
myocardial infarction. Clin Chem 1988; 34:2031-2038.
19. Shaw-Stiffel TA, Zarny LA, Pleban WE et al. Effect of nutrition status and other
factors on length of hospital stay after major gastrointestinal surgery. Nutr Int
1993; 9:140-145.
20. Bernstein LH, Shaw-Stiffel T, Zarny L et al. An information approach to likeli-
hood of malnutrition. Nutrition 1996; 12(9/10):772-776.
21. Bernstein LH (Chairman). Prealbumin in Nutritional Care Consensus Group. Mea-
surement of visceral protein status in assessing protein and energy malnutrition:
Standard of care. Nutrition 1995; 11:169-171.
22. Mozes B, Easterling MJ, Sheiner LB et al. Case-mix adjustment using objective
measures of severity: The case for laboratory data. Health Services Research 1994;
28[6]:689-712.
23. Verdery RB, Goldberg AP. Hypocholesterolemia as a predictor of death: a prospec-
tive study of 224 nursing home residents. J Gerontol:Med Sci 1991; 46:M84-M90.
24. Sullivan DH. The role of nutrition in increased morbidity and mortality. (Review)
Clin Geriatric Med 1995; 11:661-74.
CHAPTER 1
CHAPTER 2
Current Nutrient Substrates

Wendy Swails Bollinger, Timothy J. Babineau and George L. Blackburn
Introduction
Traditionally, nutrition support was simply the provision of calories and protein.
More recently, however, we have discovered that manipulation of certain nutrients
may significantly alter the response to illness and facilitate the healing process. These
findings suggest that patient-specific feeding with nutrient-specific formulas may
hold promise for improved patient outcome. This chapter discusses some of the
advantages and disadvantages of administering certain nutrient substrates, specifically
branched-chain amino acids, arginine, glutamine, nucleotides, and lipids.
Hepatic Disease and Stress: Branched-Chain Amino Acid
Enriched Diets
Hepatic Disease
The discovery of altered plasma amino acid concentrations (low branched-chain
amino acids and high aromatic and sulfur- containing amino acids) in patients with
hepatic encephalopathy prompted the development of branched-chain enriched
parenteral and enteral formulas. These formulas differ from conventional amino
acid formulas in that they contain a greater concentration of the branched-chain
amino acids (BCAA) leucine, valine, isoleucine and a lower amount (or none) of the
aromatic amino acids (AAA) phenylalanine, tyrosine, tryptophan and the
sulfur-containing amino acid methionine. The modified amino acid profile in these
solutions is thought to counterbalance the altered plasma amino acid concentra-
tions seen in patients with hepatic encephalopathy. These plasma amino acid alter-
ations are a result of an increased utilization of BCAA by the peripheral muscles and
a decreased metabolism of the AAA by the failing liver.
The use of BCAA-enriched formulas in patients with encephalopathy is based
predominantly upon the AAA/false neurotransmitter theory.1 Fischer postulated that
the decrease in BCAA and increase AAA plasma concentrations seen in patients
with hepatic dysfunction allows a disproportionate amount of AAA to cross the
blood brain barrier. As a result, there is an increase in serum levels of “false neu-
rotransmitters” (octopamine and phenyethylanine) and a concomitant decrease in
the levels of normal neurotransmitters (dopamine and norepinephrine). In addition,
there is an increased serum serotonin concentration (physiologic neuroinhibitor)
due to excess tryptophan. This altered ratio of BCAA to AAA is believed to contribute,
in part, to the development of encephalopathy. It was Fisher and colleagues who
first noted that the administration of BCAA-enriched, low AAA solutions to animals
The Biology and Practice of Current Nutritional Support, 2nd Edition, edited by Rifat Latifi
and Stanley J. Dudrick. ©2003 Landes Bioscience.
and humans with hepatic encephalopathy resulted in more normal patterns of plasma
amino acid concentrations and an improvement in encephalopathy.2,3
A number of prospective, randomized clinical trials have investigated the use of
parenteral BCAA solutions when hepatic encephalopathy is present.3,4-6 Most of
these trials have shown no significant change in mental status. It is important to
2 note, however, that many of the early trials used solutions containing only BCAA as
opposed to the BCAA-enriched, low AAA formulas typically used today. In an early
multicenter, prospective, randomized trial, 34 patients with cirrhosis of the liver
(predominantly cryptogenic) and grade III to IV hepatic encephalopathy received
either an intravenous solution containing 60 g of BCAA only in 20% dextrose or
lactulose (30-40 g every 4 hours via a nasogastric tube or 200-300 g/day via in-
termittent rectal enemas) plus 20% dextrose.4 Seventy percent of the patients
receiving the BCAA solution regained consciousness (defined as grade 0 hepatic
encephalopathy) within 48 hours compared to only 47% in the lactulose group.
Although this difference was not statistically significant, the authors concluded that
parenteral administration of BCAA is at least as effective as lactulose in ameliorating
the symptoms of hepatic encephalopathy. Interestingly, these authors found no cor-
relation between the modifications in plasma amino acid levels and an improvement
in the patient’s mental status. Instead, they noted a significant decrease in plasma
ammonia levels in both groups at the time of mental recovery. Since lactulose is
believed to work by binding excess ammonia, these results suggest that BCAA may
favorably impact on hepatic encephalopathy, at least in part, by decreasing free
plasma ammonia levels.
Wahran, et al5 also noted a slight improvement in responsiveness in patients
with hepatic encephalopathy who received a BCAA parenteral solution. In this
prospective, double-blind trial, 50 cirrhotic patients with acute hepatic encephal-
opathy (grade II to IV) were randomized to receive either an amino acid free
parenteral solution consisting of dextrose and lipids or the same solution with the
addition of 40 g of a 100% BCAA solution. The carbohydrate and fat portions of
each parenteral solution were isocaloric and provided 30 kcal/kg. In addition, all
patients were prohibited from taking any food by mouth. Although the patients in
the BCAA-treated group showed a statistically significant improvement in their
plasma BCAA to AAA ratios (1.10 ± 0.08 to 1.96 ± 0.22), this ratio never returned
to a normal ratio of 3.0 to 3.5. Fifty-six percent of the patients receiving the BCAA
solution demonstrated an improvement in encephalopathy compared to 48% in
the control group. This difference, however, was not statistically significant. As the
authors readily pointed out, this study had two major shortcomings. First, patients
with active gastrointestinal bleeds were not excluded from the study; a complication
that may worsen encephalopathy. Second, twice as many patients in the control
group received systemic antibiotics which would theoretically decrease the amount
of enteric bacteria and their byproducts and subsequently ameliorate hepatic en-
cephalopathy.
The largest and most complete prospective, double-blind trial was a multicenter
study done by Cerra and colleagues.6 Seventy-five patients with acute hepatic en-
cephalopathy (grade II or higher; average grade 2.65) due to chronic hepatic disease
(85% alcoholic cirrhosis) were randomized to receive either oral neomycin or a
branched-chain enriched (36%) parenteral solution low in AAA and methionine.
Patients with acute viral hepatitis, acute fulminant hepatitis, hepatorenal syndrome,
significant gastrointestinal bleeding, nonhepatic coma and patients requiring
Current Nutrient Substrates 19
severe fluid restriction were excluded from the study. The control group received
25% dextrose intravenously plus oral neomycin (4 g daily divided into 4 doses)
whereas the treatment group received a daily infusion of the branched-chain en-
riched parenteral solution plus placebo tablets. Oral intake was restricted in both
groups until the encephalopathy had resolved. A maximum daily protein intake of
1.1 g/kg was reached by day 3 and was well tolerated in the group receiving the 2
BCAA-enriched solution. Despite receiving what some clinicians would consider a
high protein load for this patient population, 53% of the patients in the BCAA
group demonstrated complete resolution of their encephalopathy compared to only
17% of the patients in the control group (p<0.05). Not suprisingly, net protein
catabolism was decreased in the group being fed as evidenced by a positive nitrogen
balance by day 4. The group not being fed protein remained in negative nitrogen
balance throughout the study. Moreover, 55% of the patients in the control group
died whereas only 17% of the patients receiving the BCAA-enriched solution died
(p<0.01). These results suggest that administration of BCAA-enriched parenteral
solutions in amounts that provide at least 1 g protein/kg/day is well tolerated in
cirrhotic patients with hepatic encephalopathy, and may improve mental status and
survival. There are, however, some researchers who contend that the improved sur-
vival may have been a result of providing nutritional support in these critically ill
patients rather than due to the BCAA-enriched solution itself.7
The disparity between the results of these clinical trials may be partially due to
differences in experimental design, patient population, type and amount of BCAA
solution administered, as well as diversity of the control group (Table 2.1). It has
been suggested that because Cerra and collegues6 excluded patients with serious
complications (i.e., fulminant hepatitis, hepatorenal syndrome, etc.) that would not
be expected to improve by changing the serum BCAA to AAA ratio that this may
explain why the results of their study differed from others.8 Interestingly, none of
the studies shown in Table 2.1 compared a BCAA solution to a conventional parenteral
amino acid solution. There are, however, several enteral studies that have addressed
this issue.
Eriksson and collegues9 were among the first to investigate the use of a BCAA
formula delivered orally. Seven patients with liver cirrhosis and chronic hepatic en-
cephalopathy (grade I to II) participated in a 28 day study with a cross-over design.
Patients received each of the following oral supplements, in addition to their regular
diet, for a 14 day period: a BCAA solution containing BCAA only (30 g protein/
day) or a placebo solution devoid of amino acids. The results failed to demonstrate
a significant improvement in mental status when patients consumed the BCAA
solution instead of the placebo (43% vs 29%, respectively). These findings have
been substantiated by several other small, prospective cross-over studies.10,11
In contrast, Horst, et al12 noted a significant worsening of mental status in cir-
rhotic patients with encephalopathy receiving a standard oral diet containing a maxi-
mum of 80 g protein/day compared to those receiving a standard oral diet, restricted
to 20 g protein/day, supplemented with an oral BCAA-enriched (35% BCAA) solu-
tion, low in AAA that provided up to a maximum of 60 g protein/day.
Most of the clinical trials using oral BCAA examined the efficacy of using these
formulas over a short time period (i.e. less than one month). Thus, in an attempt to
evaluate the long-term effects of using BCAA during hepatic encephalopathy,
Marchesini, et al13 conducted a multicenter prospective, randomized, double-blind
trial in which patients were followed for a three-month period. Sixty-four cirrhotic
2
20
Table 2.1. Parenteral BCAA clinical trials
The Biology and Practice of Current Nutritional Support

Author Patients Experimental Group Control Group Results/Conclusions
Rossi-Fanelli, et al4 34 patients with liver 100% BCAA (57 g protein/day) Lactulose No significant change in
cirrhosis/grade III to + 20% dextrose + 20% dextrose encephalopathy. BCAA
IV encephalopathy are as effective as lactulose
in reversing hepatic
encephalopathy.
Wahran, et al5 50 patients with liver 100% BCAA (40 g protein/day) Dextrose + lipid No significant change in
cirrhosis/grade II to + dextrose + lipid encephalopathy.
IV encephalopathy
Cerra, et al6 75 patients with liver 35% BCAA-enriched (maximum 25% dextrose + Significant improvement in
cirrhosis/grade II to of 85 g protein/day) oral neomycin encephalopathy and survival
IV encephalopathy + placebo tablets in BCAA-enriched group.
Current Nutrient Substrates 21
patients (66% alcoholic) with hepatic encephalopathy were randomized to receive

either a 100% BCAA oral supplement or a casein-based oral supplement in addition
to an oral diet containing 45-65 g protein daily. Patients were randomized to receive
either one packet of BCAA/kg body weight (0.24 g 100% BCAA/packet) or one
packet of casein/kg body weight (0.17 g casein/packet: 22% BCAA). Since all pa-
tients weighed between 60 and 80 kg, the oral supplements provided between 14 to 2
19 g BCAA or 10 to 14 g casein daily. After three months, twice as many patients
receiving the BCAA supplement demonstrated an improvement in mental status
(defined by the portal-systemic encephalopathy index) when compared to those
patients receiving the casein-based supplement (p<0.01). In addition, when the ten
casein-treated patients who showed no improvement in mental status were given the
BCAA supplement, eight of them demonstrated a rapid improvement in their
neuropsychologic function. These results suggest that long-term supplementation
(i.e., 3 months or more) of oral BCAA is superior to casein in terms of improving
mental status in cirrhotic patients with chronic encephalopathy.
The results of these enteral BCAA studies are summarized in Table 2.2. As was
the case with the parenteral BCAA studies, there are several factors which may ac-
count for the different results seen in the enteral studies. First, of the studies re-
ported here, those which failed to demonstrate any difference between BCAA and
standard amino acid solutions had a sample size of less than ten patients. Thus, they
may have been unable to detect any significant differences due to a Type II error.
Second, not all of the studies used the same experimental design (i.e., cross-over
design versus parrallel group comparison) nor did they administer the diets in the
same fashion. Several of the studies gradually increased the daily protein intake until
encephalopathy developed, whereas others adminstered a constant amount of protein
throughout the study. Finally, all of the diets differed in regard to the total percentage
of BCAA, as well as the ratio of each BCAA. Taken together, therefore, it is difficult
to compare the studies or to draw any definite conclusion.
The primary goal of nutrition support during hepatic dysfunction is to provide
sufficient protein in order to support protein synthesis and to promote regeneration
of liver cells. In view of this, perhaps the most important finding of these clinical
trials is that BCAA formulas can be safely administered to this patient population in
amounts that provide 1.0 to 1.5 g protein/kg/day without exacerbating preexisting
encephalopathy. Thus, encephalopathic, cirrhotic patients who are unable to tolerate
low to moderate intakes of standard protein sources may benefit from receiving
BCAA-enriched solutions. In 1997 the European Society for Parenteral and enteral
nutrition published guidelines recommending the aforementioned.14 In addition,
there is evidence to suggest that administration of BCAA-enriched solutions are
better utilized by cirrhotic patients and can improve hepatic protein synthesis.15
Stress
The metabolic response to injury is characterized, in part, by an increase in lean
body mass catabolism, a reduction in total body protein synthesis, and an increase
in the use of BCAA by the skeletal muscle. The result is an obligatory negative
nitrogen balance. In view of this, numerous investigators have examined the
protein-sparing effects of administering BCAA-enriched formulas in the setting of
stress, sepsis or trauma. The results of these clinical trials suggest that administration
of BCAA-enriched solutions can reduce nitrogen loss and support protein synthesis
better than standard amino acid solutions in critically ill patients.
Exploring the Variety of Random
Documents with Different Content
apparent to the throne of Persia. Sinnimâr was the architect.
There was a stone, so the story runs, which, if removed, the
whole building would fall. The secret was known to Sinnimâr
alone; and Nomân dashed him from the top, that the secret might
perish with him. (Life of Mahomet, vol. i. p. clxxi.)
[122] The treaty is given as follows:—‘This is the Treaty of
Khâlid with the son of Adi, Amr son of Abd al Masîh, and Iyâs ibn
Cabîsa, empowered in that behalf by the citizens of Hîra. They
shall pay, year by year, 190,000 dirhems, to be levied on clergy
and laity, saving mendicants who have abjured the world. The
Mussulmans on their side shall protect the city, otherwise there
will be no obligation to pay the tribute. If the city be disloyal in
word or deed, the treaty shall be void.’ The terms are given alike
in two independent traditions; but the rising, which shortly after
swept over the land, cancelled it.
[123] Showeil was an old dotard. When Kerâmat said to him,
‘What carest thou for an old creature like me?’ he replied, ‘I am
not my mother’s son if I take less for thee than a thousand
dirhems.’ She feigned to think it much, but paid it down. When
she had gone, his companions laughed at him for asking such a
trifling sum for so distinguished a captive. He went to Khâlid: ‘I
meant,’ he said, ‘to ask the highest figure that there was; but now
they tell me that numbers go beyond a thousand, and that I did
not ask enough. Give me, therefore, a fitting ransom.’ Khâlid said:
‘Thou purposedst one thing, my friend, and the Lord purposed
another. I judge by what appeareth, and leave thy purposes
alone.’ I give the story as I find it, absurd as it appears, for the
lady is said to have been fourscore years of age. The romance of
early love, at any rate, was soon changed into a more sordid
passion. The tale, though surrounded by marvels (e.g. Mahomet’s
foretelling the conquest of Hîra), is, no doubt, founded on some
slight substratum of fact. The lady’s age must be exaggerated as
well as the simplicity of Showeil, since she was the daughter of
Abd al Masîh who headed the deputation from the city.
[124] Tradition gives with considerable zest a somewhat
coarse and childish conversation between Khâlid and the aged
Abd al Masîh (called Ibn Backîla, ‘son of the bean-stalk,’ from his
green dress), who headed the deputation. ‘Whence comest thou?’
asked the conqueror. ‘From my mother’s womb.’ ‘And where art
thou now?’ ‘In my clothes,’ and so on. Asked what was the most
wonderful thing he had ever seen, he said, ‘The road from Hîra to
Damascus, which was lined in my early days with villages all
along, so that a woman could travel on it alone, taking with her a
single cake; but that time hath long passed by.’ His attendant
carried a little bag containing a quick poison, which his master
was prepared to swallow if any indignity had been shown him.
Khâlid took and swallowed it, saying that no soul could die before
its time. As no ill effect followed, the chief was lost in amazement,
and declared that Khâlid must be irresistible. Marvellous tales of
this sort are, however, very rare now. Some touching verses are
recorded as sung by Ibn Backîla on the fall of Hîra. Here is a
specimen:—
Now that the Princes of the house of Mundzir are gone,

shall I ever again behold the royal herd of camels
returning at eve from the pastures of Khawarnac and
Sedîr?
Now that the horsemen of Nomân are passed away, shall
I ever again feed the young she-camel on the
pastures between Mecca and Hafîr?
Like a flock of goats on a stormy day, we are scattered by
the Beni Maád (the invading Moslems), even as
pieces of camels slaughtered for the feast.
Heretofore our homes were sacred, and we like the teats
of a well-filled udder,
Yielding tribute at the appointed times to the Chosroes,
and imposts in cattle and gold.
Alas! even so is the changeful wheel (bucket) of the well
of fortune. Now the day brightens with joy and
gladness, and now it is dark with sorrow and grief.
Masûdi speaks of the Ibâdites (the Christian aborigines of

Hîra) as still in his time inhabiting this neighbourhood.
[125] For the field of Mûta, where Khâlid rallied the fragments
of the Moslem army broken by the Roman legions, see Life of
Mahomet, chap. xxiii.
[126] The ‘Service of Victory’ consisted of eight continuous
Rakâats, or series of prostrations, with the appointed Sura of
Victory.
In this first campaign there is no mention of any Moslems
killed. There were, no doubt, casualties among the rank and file of
the Bedouin tribes, but these are taken little account of. If any
‘Companion,’ or leader of eminence, had been slain, the fact
would, no doubt, have been mentioned. We must remember that
most of the soldiers from Medîna had returned to their homes
from Yemâma, so that there may not have been many
Companions present with Khâlid at this time.
With reference to Khâlid’s speech, I should notice that it was
the tendency of the Kûfa and Bussora schools to magnify the
difficulties of the conquest of Irâc in their own interest, as
enhancing their claims upon the revenues of the Sawâd, or
surrounding province. In this sense there is a fragment from the
Arab warrior Amr ibn Cacâa:—
The Lord water the ground where lie buried the heroes of
Irâc
Upon the dusty plain and beneath the sandy mounds!
And then he mentions in verse the various fields in which they

had fallen in this first campaign from Hafîr to the siege of Hîra.
[127] These treaties were mostly abrogated by the rebellion
that shortly after swept over the land. But some of the chieftains
remained steadfast, as Salûba ibn Nestûba, ‘the lord of Coss
Nâtick.’ His treaty is given verbatim by Tabari, with the witnesses,
&c., copied, probably, from the original. He had to pay a tribute of
10,000 dirhems, to be contributed rateably by his people
according to each man’s means, besides a tax of four dirhems per
head (apparently a Persian tax, as it is called harazat Chosra).
The terms of these treaties were made by Khâlid, with the
consent and approval of the army, showing how Khâlid
recognised the dominancy of the democratic element.
[128] The terms of the discharge are given by Tabari, who also
mentions nine of the Moslem chiefs employed to attest the
receipts.
[129] One of the great channels drawn above Babylon from
the Euphrates, which flows across the peninsula and falls into the
Tigris.
[130] P. 68.
[131] His name was Shîrazâd, for we come now constantly on
Persian names. The story is that the Moslems were told to shoot
at the eyes of the garrison. And so a thousand of the enemy had
their eyes transfixed; whence the siege was called ‘The action of
the Eyes.’ I give the tradition as I find it—not pretending to offer
an explanation—excepting that the same word stands for eyes
and fountains.
[132] Still called by that name (pl. Felâlij), meaning the district
about Anbâr irrigated by channels from the Euphrates. The army
is said to have passed by the plain of Kerbala, which, however, is
a good deal south of the position I assign to Ain Tamar (‘The
Fountain of Date-palms’).
[133] See above, p. 31. The Beni Taghlib, it will be
remembered, retired into Mesopotamia with Sajâh after her
marriage with Moseilama.
[134] The Companion was Omeir. He had been one of the
refugees to Abyssinia in the persecution of the Coreish, and was
therefore a very early convert. A citizen (Ansâr) was also buried
here; it is not distinctly stated, but I infer, that he too was killed in
the action. This is the first mention of anyone killed on the Moslem
side in the Irâc campaign, though, as said before, loss in the rank
and file of the Bedouin levies was not of such importance as
necessarily to require distinct notice.
[135] Another of these youths was Hemrân, who became the
Mowla, or freedman, of Othman. When surprised in their cloister,
they declared themselves to be ‘hostages,’ perhaps strangers
from a distance, detained to complete their education there.
[136] Welîd was the son of that Ocba who had been put to
death by Mahomet after the battle of Bedr (Life of Mahomet, p.
239). We shall hear more of him by and by.
[137] The distance must have been over 300 miles, besides
the detour rendered necessary by the intervening desert (the
Nefûd of red sand, see Lady Blount’s Pilgrimage to Nejd); and
must have taken, C. de Perceval says, not less than ten days;
with any other than Khâlid, I should have said a good deal more.
[138] Jabala VI. See Life of Mahomet, vol. i. p. clxxxix.
[139] So the ordinary narrative. But there is another account
that Okeidar was sent a prisoner to Medîna; and being
subsequently released by Omar, settled near Ain Tamar, at a
place which, in memory of his former home, he named Dûma.
The name may have given rise to the tradition; though, on the
other hand, the execution of Okeidar is in keeping with Khâlid’s
sanguinary character. For his first encounter with Khâlid, see Life
of Mahomet, p. 458.
[140] Acra was chief of the Beni Temîm, old allies of the Beni
Kelb, who otherwise would have shared the common fate.
[141] The demonstration was probably forced. The citizens,
we are told, murmured secretly,—‘We thought that they had
passed by, like other Arab raiders; their return is the breaking out
of a fresh calamity;’ and so, before long, they found it.
[142] The girl’s name was Sahba. Aly had recently received
into his harem another maiden taken captive at Yemâma; being of
the Beni Hanifa, the son, Mohammed, whom she bore to him,
was called the Hanifite. Thus, though he sat inactive at home, Aly
took his full share of the captive ladies. He also married in this
year Omâma, a granddaughter of the Prophet (being a child of
Abul Aâs and Zeinab) and niece of his deceased wife Fâtima.
I have noticed these expeditions very briefly, as the similarity
of detail becomes tedious. The Persian generals Zermihr and
Rozaba, were attacked by Cacâa and slain before they could
form a junction with the Beni Taghlib, but the fugitives joined the
Bedouin camp at Modeya in the desert. Thereupon, Khâlid
organised three parties to converge at a set time by night upon
the Arab encampment, which was surprised, and left covered with
the dead, ‘like a field of slaughtered sheep.’ The chief, Hodzeil,
escaped.
Among the slain were two Bedouin chiefs who, having
embraced Islam, held an amnesty from the Caliph. Omar took the
occasion again to blame Khâlid for his indiscriminating
vengeance; but Abu Bekr, as before, justified him; ‘for those,’ he
said, ‘who dwell in the encampment of an enemy must take their
chance with him.’ As, however, they were both said to have called
aloud the Moslem shibboleth, their families were set free and
taken care of, and blood-money paid. Omar treasured up these
things against Khâlid.
The similar stratagem of a convergent night attack was
repeatedly resorted to at Thinia, Zomeil, and Bishr, not a soul
escaping the sword but the women and children. Horcus, a
famous chief of the desert, was surprised and slain while drinking
his last draught of wine with his daughters, who were carried
away captive. The subject is a favourite one, and the
bacchanalian verses sung by Horcus in his last cups, with a
swan-like anticipation of impending fate, are assigned to several
different occasions.
[143] Ramadhan fell in December, a.d. 633.
[144] No details are given of this great battle, excepting the
fabulous number of 100,000 slain.
[145] In the troublous times that followed, almost all the
country rose and committed acts of disloyalty which, with one or
two exceptions, cancelled the treaties and engagements now
entered into by Khâlid with the Dihcâns.
[146] According to some traditions, Abu Bekr deputed Omar to
preside at the pilgrimage this year. But the general opinion is that
Abu Bekr did so himself, leaving Othmân during his absence in
charge of Medîna. This is the more likely, as, owing to the
troubled state of the peninsula, he had been unable to go on
pilgrimage the previous year.
[147] See above, p. 53.
[148] Near to Castal (which C. de Perceval makes Callirhoe)
and towards Abila but probably not so far north; the advance on
Syria being made (as always) on the coast of the Dead Sea.
[149] Dzul Kelâa, with his immediate clan, remained firm in the
rebellion of Yemen, and aided Ikrima in its suppression: see
above, p. 54. Ikrima’s column was called ‘the brigade of
substitutes,’ because on his return from the long campaign in the
south, his soldiers were allowed furlough to their homes, on
condition of their giving substitutes for the new expedition in the
north.
[150] Amru is said to have had the promise of the command
over the tribes of Odzra and Sád-Hodzeim (branches of the Beni
Codhâa) from Mahomet when he deputed him to Omân, and Abu
Bekr fulfilled the promise. His present mission must have been
subsequent to the affair at Dûma, as Welîd, on his return to
Medîna from Irâc, was sent to help Iyâdh at Dûma. This further
appears from the notice that Welîd, on joining the Syrian force,
left as his locum tenens over the Beni Codhâa, Imral Cays ‘from
Dûma’; implying that Dûma was by this time a Mahometan
possession.
[151] Marj al Soffar is to the north of the Yermûk on the road to
Damascus, and is frequently mentioned in the subsequent
campaign. It was not far from Jâbia in the Jaulân (Gaulonitis)
which became the grand rendezvous for the Moslem armies, and
the point of departure both for northern Syria and Palestine. The
journey from Medîna to Syria was always, as now, by the country
to the east of the Dead Sea, very much what is the present
pilgrim route from Damascus to Mecca.
Some accounts say that Khâlid himself was killed in the
engagement, which, according to the wont of Saracen defeats, is
slurred over with a few unsatisfactory and garbled words.
According to other traditions, Khâlid was degraded because, in
returning from Yemen, he delayed to swear allegiance to Abu
Bekr, and abused Aly and Othmân for allowing the government to
pass out of the house of Abd Menâf. This is altogether
improbable. The account in the text is the received one and also
the most consistent. But the dates are all uncertain, for none are
reliable till after the battle of Ajnadein.
[152] Shorahbîl had fought under the great Khâlid at Yemâma,
and thence accompanied him to Irâc. Deputed at this crisis to
Medîna with despatches or booty, he there obtained this
command.
[153] The Scriptural expressions of ‘the Promised Land,’ ‘the
Land of Blessing,’ &c., are applied in the Corân to Palestine; and
it remained long the most coveted destination of the Bedouin
levies.
[154] The strength of the four columns is usually given as
27,000, some authorities adding 3,000 rallied from Khâlid’s force,
and some not. Tradition represents Abu Bekr as sending them
forth each to reduce a given district in Syria—Abu Obeida, Hims;
Yezîd, Damascus; Shorahbîl, the Jordan; Amru, Palestine. A
palpable anticipation. Abu Bekr’s vision was yet bounded by the
Roman army, and the issue doubtful.
[155] Ar, or Rabbah of Moab.
[156] The Dothan of Joseph’s story is placed by Robinson
north of Nablûs, near the plain of Megiddo. If this be the same,
Yezîd must have penetrated into the centre of Palestine, which at
this early period of the campaign is not likely. But the whole
account is very brief and confused. It seems, also, improbable
that Abu Obeida should have advanced quite so far as Jâbia,
while as yet the Roman battalions dominated the country north of
the Yermûk.
[157] The names of the Roman commanders are given as
Jâreja (George?), Cayear ibn Nestûs, Darâckis, and Tadzâric
(Theodoric). Tradition pretends that Heraclius, half persuaded of
the truth of Islam, was desirous to cede to the Moslems the plain
of Syria up to the mountains of Asia Minor, but was hindered by
the perversity of his grandees.
[158] The way out, however, could have been only partially
closed, for reinforcements reached the Romans without
hindrance. The ravine was probably passable at some points,
though, on the whole, a sufficient defence against the Arabs.
[159] The country is well described by Laurence Oliphant in
his Land of Gilead, and the picture at p. 87 gives an admirable
idea of the gorge surrounding our battle-field. ‘The Yermûk,’ he
says, ‘at this point is just sinking below the level of the plain
through which it has been meandering, and in the course of the
next mile plunges down, a series of cascades, into the
stupendous gorges through which it winds, until it ultimately falls
into the Jordan below Gadara.’ The grand old military road, still
bearing traces of wheeled carriages, bifurcates five and twenty
miles south of Damascus. The right branch leads S.W. to
Palestine, crossing the Yermûk at Gadara; the other continues to
run south towards Jerash and Bostra, and so onward till it is lost
in the Hajj or pilgrim-route into Arabia. The latter was the road
always traversed by the Saracen armies as they marched into
Syria and Palestine; and I assume that the battle was fought at a
point some 30 miles east of Gadara where this road crosses the
Yermûk. The same road northward leads to Jâbia (Tell Jâbieh);
and Jâbieh became the grand base of operations both for Syria
and for Palestine; for Palestine was never approached from
Arabia but by this circuitous route. The Arabs, we are told, do not
use the Roman road, because probably it is in so rugged and
ruinous a condition. But they always use the bridges when
passable; and Mr. Oliphant tells us of an ‘old Roman bridge of
nine arches, one of which has fallen and has not been repaired,’
over the Yermûk in this vicinity, p. 87. The researches now being
prosecuted to the east of the Jordan may throw farther light on
this great battle-field, the site of which it may be possible yet to
identify.
[160] Some authorities represent the transfer as a punishment
for the surreptitious visit to Mecca; but this is at variance with the
terms of the order, as well as opposed to the whole tenor of Abu
Bekr’s forbearing treatment of Khâlid.
[161] The numbers of Khâlid’s column are variously stated at
9,000 and 6,000; and again as low as 800, 600, and 500. But the
smaller numbers are probably intended to indicate only that part
of his force which formed the flying column in his adventurous
march across the desert: the rest, I assume, followed more
leisurely and by an easier route. In point of fact, 6,000 returned
the following year to Irâc, though they had been thinned by the
Syrian campaign.
Some put the march of Khâlid a month earlier. Ibn Ishâc says
that before leaving, Khâlid despatched the sick and infirm, with
the women and children, to Medîna, with the last consignment of
royal prize, as if he apprehended insecurity during his absence.
[162] The great sea of red sand has been spiritedly described
by Lady Anne Blount in her Pilgrimage to Nejd; her route
(reversed) was the same as Khâlid’s, from Irâc as far as Corâcar,
only her circuit led her farther south to Hâil, and nearer the
mountain range of Ajâ and Selma.
[163] Such is the received account of this extraordinary march,
the memory of which is also preserved in contemporary verse. Ibn
Ishâc speaks of twenty camels, which would have gone but a little
way. Other accounts give the number of camels at so many per
hundred lances, without mentioning the strength of the column.
As before explained, Khâlid probably took the perilous route with
only the lighter part of his force, leaving the bulky and heavy
portion to follow by the ordinary road, along the Wady Sirhân,
after he had cleared the Bostra approach. The lips of the camels
were slit or cut off (according to other accounts bound up) to
prevent their ruminating and the consequent digestion and
assimilation of the water in their stomachs.
[164] They emerged at Suwâ near Tadmor, and forthwith fell
upon the Beni Bahra, a Christian tribe, a portion of which was
engaged in the defence of Dûma the year before. Here again we
have the bacchanalian death-song of Horcûs mentioned before.
We must receive the account of Khâlid’s circuit even after the
passage of the desert, with some reserve. He is said to have
plundered Cariatein and Huwarein on the way from Tadmor; to
have made terms with the Beni Codhâa at Cussum; then to have
passed over the ‘Mount of the Eagle’ (so called from his halting
on it with the Prophet’s black flag), within sight of Damascus; to
have plundered Marj Râhat, and a convent in the Ghûta or plain
of Damascus, killing the men and taking the females prisoners;
and so on to Bostra, which, after some opposition, came to terms.
If this be all true, he may have at Bostra formed a junction with
the body of his column left behind at Corâcar. But it is all very
vague, and with a dash of the marvellous.
Ibn Ishâc gives a somewhat different account. He mixes up
former victories (e.g. the capture of the forty Christian youths, of
Aly’s slave-girl, &c.) with this campaign; and he makes the
storming of Bostra to follow the junction with Abu Obeida. I find no
authority whatever for the romance of the taking of Bostra as
given by Ockley and followed by Gibbon.
[165] In the silence of Byzantine chroniclers we must make the
best of the figures. 80,000 were ‘prisoners,’ either simply so or in
chains; 40,000 were ‘chained together to fight to the death;’
40,000 were ‘tied by their turbans;’ and 80,000 free and
unencumbered. In the Armenian general Bahân we recognise the
Βάαν of Theophanes; a rare (one might say a unique)
coincidence.
[166] The imagination of the crusading army was inflamed by
tales and visions of the dying soldiers each tended by two black-
eyed girls of Paradise, who, wiping the sweat and dust of battle
from the face of their spouse, welcomed and clasped him in their
fond embrace.
[167] It is doubtful whether Abu Bekr’s commission to Khâlid
on his transfer did not at the same time nominate him to the
supreme command of the Syrian forces. Ibn Khaldûn reads so;
and likewise the tradition that Omar, in eventually deposing him,
appointed Abu Obeida similarly to the supreme command. If so,
Khâlid may have chosen not to excite jealousy by assuming the
supremacy at once, but rather to have obtained it by consent. But
our information is, at this early period, vague and incomplete.
[168] The tale is full of childish matter. The following is an
outline from which the reader may draw his own conclusion.
When the two armies were drawn up for battle, Jâreja, riding forth
from the Roman ranks, called out to Khâlid as if challenging him
to single combat. They drew so near to one another, midway
between the two armies, that their horses’ necks touched. Having
pledged their word to each other, a conversation ensued. Jâreja
asked Khâlid why he was called the ‘Sword of God,’ and whether
a sword had really been sent down to him from heaven. Khâlid
smiled, and expounded to him the basis and practice of Islam.
The ingenuous Roman, convinced, forthwith reversed his shield;
whereupon Khâlid, leading him away to his tent, sprinkled clean
water upon him and taught him to pray,—Jâreja following him,
with the prescribed prostrations and words, in two Rakáats.
Meanwhile his followers, supposing that he had attacked Khâlid
and been decoyed away by him, advanced rapidly on the Moslem
line, which at first gave way, and both sides became
promiscuously engaged. Then Khâlid, with Jâreja now upon his
side, issued forth and at the head of their troops charged the
Romans and drove them back; Jâreja fought by the side of Khâlid
all day long, and in the evening was slain, dying a faithful martyr,
though he had prayed but once. The tale is probably founded on
fact, and framed so as to cover the defection of some Roman
general—perhaps a Bedouin,—who, by previous arrangement,
came over to Khâlid on the day of battle, with a following,
perhaps, of Syrians from the Roman camp. Jâreja may be the
Arab rendering here for George.
[169] Battalion or Kardûs. The number of battalions now
formed is variously given at from thirty to forty. The leader of each
is named; but probably tradition has merely selected the most
likely names, for in other respects there is a great want of detail in
the narrative.
[170] The person performing this duty was called Al Cass, the
Declaimer. The following is a specimen of the address by which
Abu Sofiân stirred up each battalion. ‘Lord! these be the
champions of Arabia, the defenders of the Faith. Those yonder
are the champions of Rome, the defenders of Idolatry. O Lord!
this is a day to be held in remembrance among Thy great days.
Wherefore send down help upon Thy servants and succour them.’
[171] Dhirâr is a favourite hero with the pseudo-Wackidy and
other romancers, who represent him as performing the most
marvellous feats in the field. Ikrima’s war-song was:—
A noble maid, both fair and tender,

Knows that her knight can well defend her.
[172] Abu Sofiân himself lost an eye; it was pierced by an

arrow, which was with difficulty withdrawn. There is a foolish tale
that Abdallah, son of Zobeir, then a boy, overheard Abu Sofiân,
who, with a company of the Coreish, stood upon a knoll,
applauding the Romans when they advanced, and crying, ‘Out
upon you,’ when they fell back, as if siding with them. He ran and
told his father, who laughed, saying, ‘It is mere spite, for we are a
deal better than the Romans.’ This is a manifest anti-Omeyyad
tale, for tradition is almost unanimous that Abu Sofiân,
notwithstanding his age, distinguished himself that day by his
valour and his ardour in stirring up the troops (Ibn Khaldûn, p. 85);
and indeed it would have been altogether against his interest to
have done otherwise.
[173] The disaster, making every allowance for exaggeration,
must have been appalling. We are told that there were driven over
the precipice 80,000 ‘chained’ and 40,000 free soldiers, besides
those that perished by the sword.
[174] The order given by Omar is couched in terms which
would appear to imply that Khâlid was in supreme command in
Syria, from which command he was now deposed, and Abu
Obeida substituted in his room. This is not consistent with the
previous narrative. It is possible, indeed, to construe the order as
deposing Khâlid simply from his command over his own Irâc
contingent, and transferring it to Abu Obeida. But it is certain that
Abu Obeida from this time became in permanence the Ameer, or
governor-general and commander-in-chief of Syria. See Ibn
Khaldûn, p. 86, and previous note p. 106.
[175] The date is fixed by that of Abu Bekr’s death (August
22); twenty days after which we are told that the battle was
fought. But the messenger bringing the news of the Caliph’s death
could hardly have taken more than half that time for so urgent a
journey. We may safely, therefore, place the action about the end
of August (Jumâd II.); or, rather, following other traditions, early in
Rajab, that is, the beginning of September.
[176] The new king is called otherwise Shahrîzân and
Shahrîzâz, son of Ardshîr. His commander is called Hormuz
Jâdzoweih.
[177] The poet Farazdac (who flourished shortly after),
enumerating the various families of the Beni Bekr ibn Wâil, when
he comes to the clan of Mothanna, describes him as ‘the hero
who slew the elephant at the battle of Babylon.’ So also Abda, a
Bedouin poet, who, being in search of his mistress, chanced to be
present as a wayfarer at the battle, makes a similar reference to
the slaughter of the elephant.
[178] The delay may have been occasioned by Abu Bekr’s
sickness, or the proposal to employ the apostate Arabs in the
campaign may have been difficult to answer.
[179] The Council House (Dar ul Nadwâ) built by Cossaí. Life
of Mahomet, Introduction.
[180] From this account it would appear that Abu Bekr did not
perform the full pilgrimage to Mina and Arafât. Some authorities
make Omar to preside at this pilgrimage, others Abd al Rahmân.
Possibly Abu Bekr performed only the Omra or Lesser Pilgrimage
(Ibid. p. xii.), and left Omar to fulfil the other rites.
There is a curious incident quoted by an early writer as an
authority to prove that Abu Bekr was himself present. Some one
bit the ear of a man at the pilgrimage in play. Abu Bekr sent the
case to Omar as judge, and he summoned a surgeon. Thereupon
Abu Bekr recited, as in point, a story of the Prophet, who, having
made the gift of a slave to his aunt, bade her not to bring him up
as a surgeon, lest in the discharge of his profession he should be
subject to reprisals for injuries done in surgical operations.
[181] That is, the year in which the Viceroy of Yemen besieged
Mecca. He had in his train an elephant; and the year, a.d. 570, is
therefore called ‘the year of the Elephant.’ Ibid. p. xxvi.
[182] There is a tradition that Abu Bekr’s illness was owing to
poison, given to him and to Attâb and another, which, being a
slow but deadly drug, did not take effect till a year after. No details
are given; the tale is evidently apocryphal, and based on the
desire (common in those early days) to give to Abu Bekr the
honour of martyrdom.
[183] Meaning the Divine physician.
[184] The tradition proceeds: Abu Bekr answered, ‘The Lord
bless thee, Othmân! If I had not chosen Omar, then I had not
passed thee over; and I know not whether Omar will accept the
office. As for myself, I could wish that I had never borne the
burden of the Caliphate, but had been of those who departed this
life in times that are past.’
This would imply that Abu Bekr had thought of Othmân as his
successor in default of Omar. The conversation, however, is
professedly secret and confidential. It rests solely on the authority
of Othmân himself, and we need not give too much heed to it.
[185] It is not stated on what day this occurred. It may have
been only a day or two before his death; for his interview with
Mothanna shows that even on the last day of his life, he was able
to gather up his strength.
The ordinance ran in these words: ‘In the name of the Lord
most Merciful! This is the covenant of Abu Bekr, son of Abu
Cohâfa, with the Moslems:’ (here he swooned away)—‘I have
appointed, as my Successor over you, Omar, son of Khattâb. I
have not in anywise spared myself in this matter; but have striven
to the utmost to do the best for you.’ Ibn Khaldûn adds: ‘I know
that he will do judgment and justice amongst you; but if he commit
tyranny or injustice, verily the future is hidden from mine eyes.’
Asma had been the wife of Jáfar; and again, after Abu Bekr’s
death, became one of Aly’s numerous wives. The Arab women
still tattoo their breasts and arms with elaborate and beautiful
designs.
The reader will remark the freedom with which women of the
highest rank appeared in public even at this period, their habits
partaking still of the freedom of the desert. But this was not long
to last.
[186] Sura, v. 18. Some make this to have been said in reply
to Ayesha, who had been repeating the few lines just given as
recited by Abu Bekr himself.
[187] The prayer is somewhat similar to the last words of
Mahomet. See Life of Mahomet, p. 509.
[188] The 21st Jumâd II. He reigned two years, three months,
and ten days. He died on the same day of the week (Monday) as
Mahomet, and at the same age, 63 lunar years.
[189] Abu Bekr told Asma that he wished her alone to wash
his body and lay it out. On her replying that her strength was not
equal to the task, he said that she might ask Abd al Rahmân to
help her. He desired to be buried in the same two garments he
had on, with a new piece over them; and when those around
objected, he made use of the words in the text.
[190] It was opposite the house of Othmân, which adjoined the
apartments of Ayesha and the other widows of Mahomet. The
cortège would thus pass across the open court of the mosque.
The grave was dug after the same fashion as Mahomet’s (Life, p.
517). Talha, and Abd al Rahmân the Caliph’s son, were the two
who descended to adjust the body in the grave.
A curious incident illustrates the rude manners of the time.
When her father died, Ayesha, with her sister Omm Farwa
(Asháth’s wife), and a party of female friends, began to wail.
Omar forbade it, as a work of Satan, but they persisted. Omar, on
this, ordered Hishâm to bring forth Omm Farwa. Ayesha
screamed and said, ‘Who is Omar? I forbid thee my house.’ But
Omm Farwa was brought forth and beaten with a whip, on which
the mourning women dispersed. The story is probably
exaggerated; but that it should have been preserved at all is a
proof of the rough notions prevalent as to the treatment of ladies
of rank and birth at this early period.
[191] Some say 8,000 dirhems; others, that he had no fixed
allowance, but took only what sufficed for the maintenance of his
family. In support of the latter statement, a tradition is given that
his wife, having a longing for some sweetmeats, saved up a little
money for the purpose. Abu Bekr finding it out, took the whole
sum and put it back into the treasury, as more than absolutely
needed for the maintenance of his household. Many of these
traditions are evidently exaggerated with the view of enhancing
the hardness and thrift of Abu Bekr’s life, and his conscientious
use of the public money, in contrast with the luxury and
extravagance of later Caliphs. Thus we are told that at his death
he desired that whatever property was found in his house should
be sent to Omar, in repayment of what he had received; there
was only a camel, a cutler-slave, and a carpet worth five dirhems.
They were sent to Omar with the deceased Caliph’s message,
whereat Omar wept, but carried out the request to the letter. All
these stories, the feeding and milking of the goats, engaging in
merchandise, &c., must be received dubiously.
[192] Mines were worked in the lands of the Beni Suleim.
[193] In the general distribution, each soul received ten
dirhems the first year, and twenty the second, besides what was
spent in the public service. Warm clothing was purchased from
the Bedouin tribes, and distributed among the destitute in the
winter. In all, they estimate that 200,000 dirhems (say 10,000l.)
were received in Abu Bekr’s reign—but a poor forecast of what
was to come! A woman was employed to weigh the treasure as it
came in.
[194] The three things are variously related: e.g. that he did
not himself go forth with the expeditions against the apostate
tribes; others, of weak authority, relate chiefly to the succession to
the Caliphate, and some are clearly of an Alyite stamp.
[195] It does not, however, by any means follow that he had
none. Slave-girls, as part of the harem, are rarely mentioned,
unless one happened to bear issue to her master, when she
became free, as his Omm walad.
[196] It seems he had a presentiment it would be a girl, for he
said to Ayesha: ‘Thy brothers and sisters must all share equally.’
‘What sisters?’ she asked in surprise; ‘there is only Asma.’ ‘The
one,’ he answered, ‘that Habîba bint Khârija is big with.’ One of
his sons, Abdallah, was only three years old at his death; and his
mother, Coteila, was probably alive when he died. When Omm
Rumân, Ayesha’s mother, died, is nowhere stated.
[197] The old blind man, hearing a commotion at Mecca,
asked what it might be, and being told that his son had died
—‘Alas!’ he cried, ‘glory hath departed from us; and who
succeedeth him?’ They answered, Omar. ‘It is well,’ he replied;
‘for he was his worthy fellow.’ As the Caliph’s father, he inherited a
sixth part of his son’s estate.
[198]
[199] This is almost the only mention made of Aly during Abu
Bekr’s Caliphate, excepting when he gives advice in the Caliph’s
Council, marries a new wife, or purchases some attractive bond-
maid. In such a self-indulgent life, he was becoming portly and
inactive.
[200] I.e. of the Muhâjerîn or Ansâr; that is, the Coreish, on the
one hand, and the natives of Medîna on the other.
[201] The following is an outline of the narrative, as given by
the Arab historians. On Shahrîrân’s death, after the battle of
Babylon (summer of a.d. 634), Dokht Zenân, daughter of
Chosroes (Perwîz), for a brief period, and then Sapor, son of
Shahrîrân, occupied the throne. The latter gave the hand of
Azarmîdokht, another daughter of Chosroes, to his favourite
minister Furrukhzâd. But she resented the alliance; and, at her
call, the hero Siâwaksh slew the intended husband on the
marriage night, besieged the palace, and, putting Sapor to death,
proclaimed Azarmîdokht queen. Such was the state of things
when Mothanna, in August, went to Medîna. During his absence,
Burân, another daughter of Chosroes, having great influence with
the nobles, summoned the warrior Rustem from Khorasan to
avenge the death of his father, Furrukhzâd, which he did most
effectually—defeating the royal troops, killing Siâwaksh, and
putting out Azarmîdokht’s eyes; and then he set Burân upon the
throne. Her regency (such was the ordinance) should continue
ten years, in default of any prince being discovered of the royal
blood; after which, the male line being proved extinct, the dynasty
would be confirmed in the female line. Burân then appointed
Rustem her minister, with supreme powers, and the nobles rallied
round him. This was just before Abu Obeid’s appearance on the
stage.
The chronology, however, is utterly confused and uncertain.
This Burân is said to have opposed Shîra (Siroes) for a year; and,
when he finally succumbed to have retained her authority as
arbiter (àdil) in the State. She is also said to have sent gifts to
Mahomet, &c. But so much we may assume as certain that
between Perwîz (a.d. 628) and Yezdegird there was an interval of
four and a half years. See Weil’s Chalifen, vol. i. p. 64, and Tabari,
vol. ii. p. 178.
[202] The Persian campaign begins now to assume greater
consistency and detail; but, partly from alteration of the river beds,
and partly from the sites of towns, &c., being no longer known, it
is not always easy to follow the course of the campaign.
Namârick, the scene of Abu Obeid’s first victory, was on the
Bâdacla, or western branch of the Euphrates. Jabân was there
taken prisoner; but the captors, not recognising his rank,
ransomed him in exchange for two skilled artisans. Mothanna,
discovering his quality, would have put him to death for the
deception, but Abu Obeid stood by the ransom. ‘The faithful are
one body,’ he said, ‘and quarter given by any one of them must be
sustained by all; it would be perfidy to put him to death.’ He was
therefore let go; but being again laid hold of after the battle of the
Bridge, was then executed. The second engagement took place
at the royal date-preserve of Sakatia, near Kaskar (subsequently
the site of Wâsit). Abu Obeid, hearing that Jalenûs was on his
way with supports, hurried on and gave battle to Narsa before he
came up. Expeditions were then sent to Barôsama and the
country around.
[203] Called also Dzú Hâjib.
[204] It was twelve cubits long and eight broad.
[205] The common tradition is that Ibn Salûba, Chief of Hîra
(as a kind of neutral), constructed the bridge for both sides. The
account given by Belâdzori is more probable, that it was a
standing bridge belonging to Hîra, as it would be chiefly for its
use. The Moslems crossed at Marwaha, near Babylon. The action
must therefore have been fought on the banks of the main river,
and not on the western channel.
[206] Dates now begin to be given, but the chronology is still
very doubtful. One authority places the battle forty days after that
of Wacûsa on the Yermûk—that is to say, seven or eight weeks
after Abu Bekr’s death. But in the interval between that event and
the present battle, there took place Abu Obeid’s protracted march,
the battle of Namârick and the expeditions following it, the
gathering of Jabân’s army and its march, all which must have
occupied at the least two months, and probably a good deal
more.
[207] A marvellous vision was seen by the wife of Abu Obeid.
A man descended out of heaven, having a pitcher in his hand, out
of which he gave drink first to her husband, and then, one after
another, to several warriors of his tribe. She told Abu Obeid, who
answered that he wished it might be a token of impending
martyrdom to him and them. He then appointed each of the
warriors, in turn, whom she had named, to succeed him if he fell;
and so it turned out. Abu Obeid cut at the lip of the elephant,
being told (erroneously) that it was the part where a mortal blow
could most easily be struck.
[208] The same clan as Abu Obeid’s.
[209] The depth is as much as fifteen feet, and it runs at the
rate of one and a half to three knots an hour. (Rich’s Travels.) The
banks, however, are not so high, nor is the current so rapid, as of
the Tigris.
[210] The remarkable fact of a Christian chief, Abu Zobeid, of
the Beni Tay, being, not only on the Moslem side, but taking so
prominent and brave a part in the defence of the broken force, is
noticed both by Ibn Athîr and Belâdzori. We shall see how largely
Mothanna was indebted to Christian help in the next decisive
battle.
[211] Firuzân was the name of the insurgent. But, with the
exception that the nobles sacrificed the empire to intrigue and
jealousies, we are much in the dark as to the inner history of
Persia at this time. There were two parties, we are told, the
Persians proper, or the national faction, which supported Firuzân;
and the other nationalities, Rustem. But they soon coalesced.
[212] See above, pp. 128, 129.
[213] Sura, viii. v. 14.
[214] The names of the tribes now flocking to the war are,
many of them familiar to the reader of the Prophet’s life; as the
Beni Hantzala, Khátham, Abd al Cays, Dhabha. The Beni Azd
were 700 strong, under Arfaja.
These levies are represented as the response to the present
summons of Omar, now made afresh after the battle of the
Bridge; but erroneously so, for they reached Mothanna at once,
and fought under his banner within a month of that disaster. It
took some time for the fresh levies to gather, as we shall see.
[215] The history of this contingent is interesting. Mahomet
had promised Jarîr that he should have a commission to gather
the scattered members of the Beni Bajîla into a fighting column.
Jarîr followed Khâlid into Irâc, and then returned to Medîna,
where he found Abu Bekr sick, or too much occupied to attend to
his claim. But after his death, Omar, in fulfilment of the Prophet’s
promise, gave him letters to the various governors to search out
everywhere those who, before Islam, belonged to the Bajîla tribe,
and still desired to be associated with it. A great rendezvous of
these was accordingly made, at a spot between the Hejâz and
Irâc, whither, yielding to the persuasion of Omar, they now bent
their steps. There was rivalry between Jarîr and Arfaja as to the
command of this tribe; but the levy had some grudge against
Arfaja, who therefore left them and took the command of his own
tribe, the Beni Azd. Arfaja is also said, by another tradition, to
have led the Beni Bajîla into Syria; but that (if true) must have
been a different body of men, and at a different time.
[216] The tradition runs: ‘Among those who joined Mothanna
was Anis ibn Hilâl, with an immense following of the Beni Namr
(Christians); for they said, We shall surely fight on the side of our
own people.’
[217] Rustem and the insurgent Firuzân had come to a
compromise, and agreed, we are told, to a division of power.
[218] Mehrân is called Hamadâny, because he was a native of
that province. He is said, as on the former occasion, to have
given Mothanna the option of crossing by the bridge.
The channel was the Bâdacla, which is here described as a
spill canal to pass off the surplus waters of the Euphrates when in
flood, into the Jowf or sea of Najaf—the same as the western
branch of the river taken off (as already described) by the cut at
Museyib, above Babylon. Boweib was not far from Hîra, the
inhabitants of which must have been in much excitement during
this and other great battles in the vicinity, on which their
alternating fate depended.
[219] ‘Mothanna was an example,’ we are told, ‘in word and
deed. The people trusted and obeyed him both in what they liked
and what they disliked’—a noble, single-minded commander,
whose repeated supersession had no effect upon his loyalty and
zeal.
[220] ‘I brought the army,’ Mothanna said, ‘to an evil pass by
getting before the enemy and closing the bridge upon him; but the
Lord graciously warded off the danger. Beware, therefore, of
following my example, for verily it was a grievous lapse. It
becometh us not to bar the escape of those who have nothing to
fall back upon.’ It will be observed that the compunction was not
at all for any unnecessary bloodshed among the helpless enemy
(an idea altogether foreign to the thoughts of a Moslem crusader),
but of gratuitous loss and risk to the Moslems. It may have added
to Mothanna’s grief that in repelling this last charge he lost his
brother. The slain are put at 100,000. ‘Years after, even in the
time of the civil wars, you could not walk across the plain without
stumbling on the bones strewed all around.’
[221] The horse and spoil of Mehrân were awarded to the
column in which this youth was fighting. Jarîr and another had a
quarrel over them. Had the youth been a Mussulman, no doubt he
would have obtained the whole as a prize.
[222] His own tribe, the Beni Bekr ibn Wâil.
[223] Amr went on with supplies to Hîra, where the rest of the
families were in hiding. The female defenders of their camp
remind one of Layard’s description of a similar occasion on which
the women of an Arab encampment rushed out to repel an attack,
armed with tent-poles and pitchforks. (Nineveh and Babylon, p.
168.)
[224] It would unnecessarily weary the reader to detail these
raids at any length. Some of them were against other and hostile
branches of the very Christian tribes that had fought at the Bridge
and at Boweib on the Moslem side; some were to obtain supplies
for the army, which was reduced at one time to great extremities
for food; but most were for the double purpose of striking terror
into the people, and at the same time gaining plunder. On one
occasion the Beni Bekr ransomed a great company of prisoners
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The Biology and Practice

Stanley J. Dudrick, M.D.

Copyright ©2003 Landes Bioscience

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Jonathan Evans Rhoads, M.D.

Dedicated to the surgeon of the century, whose extraordinary personal at-

Rifat Latifi, M.D. and Stanley J. Dudrick, M.D.

Stanley J. Dudrick, M.D.

Gretchen M. Brophy Richard Formica

Susan T. Crowley Per-Olof Hasselgren

Robert S. Dechicco Diane R. Horowitz

John M. Daly, M.D.

Clinical Implications of Carbohydrate,

Imperative for Nutritional Intervention

combustion of substrates. It is also assumed that all of the nonprotein nitrogen

Table 1.1. Calorie and protein needs in stress

Stress Clinical Setting CHO% NPC:N Stress 1

3. infusion of about 80-120 meq K+ per day is required to replenish stores in

Clinical vs. Laboratory Information

Table 1.2. Clinical risk factors

Table 1.3. Laboratory risk factors

Liver transport proteins are characterized by different rates of production and

Table 1.4. Plasma protein used in nutrition assessment

Table 1.5. Features of an ideal marker

redundancy to minimize the effects of noise in message transmission. We use an

inadequate or that the patient is unresponsive. Serum TTR concentration is a prog-

Table 1.6. Problems of overfeeding

Table 1.7. Etiology of common electrolyte deficiencies

Electrolyte Cause of Deficiency

Table 1.8. Clinical conditions for which phosphorus levels should

The ability to identify malnourished patients and to implement early interven-

malnutrition is reflected by a serum concentration < 11 mg/dl, severe at < 7 mg/dl.

Current Nutrient Substrates

The Biology and Practice of Current Nutritional Support

patients (66% alcoholic) with hepatic encephalopathy were randomized to receive

Now that the Princes of the house of Mundzir are gone,

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And then he mentions in verse the various fields in which they

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[172] Abu Sofiân himself lost an eye; it was pierced by an

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