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1. To possess optical activity, a compound must be:
A) a carbohydrate.
B) a hexose.
C) asymmetric.
D) colored.
E) D-glucose.

2. Which of the following monosaccharides is not an aldose?

A) Erythrose
B) Fructose
C) Glucose
D) Glyceraldehyde
E) Ribose

3. The reference compound for naming D and L isomers of sugars is:

A) fructose.
B) glucose.
C) glyceraldehyde.
D) ribose.
E) sucrose.

4. When two carbohydrates are epimers:

A) one is a pyranose, the other a furanose.
B) one is an aldose, the other a ketose.
C) they differ in length by one carbon.
D) they differ only in the configuration around one carbon atom.
E) they rotate plane-polarized light in the same direction.

5. Which of the following is an epimeric pair?

A) D-glucose and D-glucosamine
B) D-glucose and D-mannose
C) D-glucose and L-glucose
D) D-lactose and D-sucrose
E) L-mannose and L-fructose

Page 1
 6. Which of following is an anomeric pair?
A) D-glucose and D-fructose
B) D-glucose and L-fructose
C) D-glucose and L-glucose
D) -D-glucose and -D-glucose
E) -D-glucose and -L-glucose

7. When the linear form of glucose cyclizes, the product is a(n):

A) anhydride.
B) glycoside.
C) hemiacetal.
D) lactone.
E) oligosaccharide.

8. Which of the following pairs is interconverted in the process of mutarotation?

A) D-glucose and D-fructose
B) D-glucose and D-galactose
C) D-glucose and D-glucosamine
D) D-glucose and L-glucose
E) -D-glucose and -D-glucose

9. Which of the following is not a reducing sugar?

A) Fructose
B) Glucose
C) Glyceraldehyde
D) Ribose
E) Sucrose

10. Which of the following monosaccharides is not a carboxylic acid?

A) 6-Phospho-gluconate
B) Gluconate
C) Glucose
D) Glucuronate
E) Muramic acid

Page 2
11. D-Glucose is called a reducing sugar because it undergoes an oxidation-reduction
reaction at the anomeric carbon. One of the products of this reaction is:
A) D-galactose.
B) D-gluconate.
C) D-glucuronate.
D) D-ribose.
E) muramic acid.

12. Hemoglobin glycation is a process where __________ is __________ attached to

hemoglobin.
A) glycerol; covalently
B) glucose; enzymatically
C) glucose; non-enzymatically
D) N-acetyl-galactosamine; enzymatically
E) galactose; non-enzymatically

13. When forming the disaccharide maltose from two glucose monosaccharides:
A) water is eliminated.
B) a hemiacetal is converted to an acetal.
C) the resulting dissacharide is no longer a reducing sugar.
D) Both A and B
E) A, B, and C above

14. From the abbreviated name of the compound Gal(1  4)Glc, we know that:
A) C-4 of glucose is joined to C-1 of galactose by a glycosidic bond.
B) the compound is a D-enantiomer.
C) the galactose residue is at the reducing end.
D) the glucose is in its pyranose form.
E) the glucose residue is the  anomer.

15. Starch and glycogen are both polymers of:

A) fructose.
B) glucose1-phosphate.
C) sucrose.
D) -D-glucose.
E) -D-glucose.

Page 3
16. Which of the following statements about starch and glycogen is false?
A) Amylose is unbranched; amylopectin and glycogen contain many (1  6)
branches.
B) Both are homopolymers of glucose.
C) Both serve primarily as structural elements in cell walls.
D) Both starch and glycogen are stored intracellularly as insoluble granules.
E) Glycogen is more extensively branched than starch.

17. Which of the following statements about hydrogen bonding in glycogen and cellulose is
true?
A) Glycogen forms more internal H-bonds than cellulose.
B) Extensive internal hydrogen bonding makes cellulose more water soluble than
glycogen.
C) Extensive hydrogen bonding with water makes cellulose more soluble than
glycogen.
D) Glycogen primarily forms hydrogen bonds within a single chain.
E) The hydrogen bonding in cellulose favors a helical conformation.

18. Following complete hydrolysis of a sample of glycogen and a sample of cellulose,

which of the following must be true?
A) The glycogen sample is more soluble than the cellulose sample.
B) The cellulose sample is more soluble than the glycogen sample.
C) Both samples consist of a mixture of -D-glucose and -D-glucose.
D) The glycogen sample has a higher ratio of -D-glucose than the cellulose sample.
E) The cellulose sample contains only -D-glucose.

19. Which of the following is a heteropolysaccharide?

A) Cellulose
B) Chitin
C) Glycogen
D) Hyaluronate
E) Starch

20. The basic structure of a proteoglycan consists of a core protein and a:

A) glycolipid.
B) glycosaminoglycan.
C) lectin.
D) lipopolysaccharide.
E) peptidoglycan.

Page 4
21. Which of the following statements about heparan sulfate is not true?
A) Sulfation of heparan sulfate to form NS domains is important for its role as an
anti-coagulant.
B) Heparan sulfate can promote protein-protein interactions via the NS domains.
C) The secondary structure of heparan sulfate is completely random.
D) The NA domains of heparan sulfate contain no sulfation.
E) The core repeating structure of heparan sulfate is made up of alternating GlcNAc
and GlcA.

22. In glycoproteins, the carbohydrate moiety is always attached through the amino acid
residues:
A) asparagine, serine, or threonine.
B) aspartate or glutamate.
C) glutamine or arginine.
D) glycine, alanine, or aspartate.
E) tryptophan, aspartate, or cysteine.

23. Which of the following is a dominant feature of the outer membrane of the cell wall of
gram negative bacteria?
A) Amylose
B) Cellulose
C) Glycoproteins
D) Lipopolysaccharides
E) Lipoproteins

24. The biochemical property of lectins that is the basis for most of their biological effects
is their ability to bind to:
A) amphipathic molecules.
B) hydrophobic molecules.
C) specific lipids.
D) specific oligosaccharides.
E) specific peptides.

Page 5
25. Which of the following statements concerning sialic acid residues on glycoproteins is
true?
A) Sialic residues on erythrocytes are recognized by lectins, leading to removal of the
erythrocytes.
B) Sialic residues on ceruloplasmin are recognized by lectins, leading to removal of
ceruloplasmin.
C) Sialic residues are removed by neuraminidases.
D) The anti-viral drug oseltamavir accelerates the removal of sialic acid residues.
E) Both A and B above

26. Why is it surprising that the side chains of tryptophan residues in lectins can interact
with sugars?
A) Because the side chain of tryptophan is hydrophilic and sugars are hydrophobic
B) Because the side chain of tryptophan is (–) charged and sugars are generally (+)
charged or neutral
C) Because the side chain of tryptophan can make hydrogen bonds and sugars cannot.
D) Because the side chain of tryptophan is hydrophobic and sugars are generally
hydrophilic
E) None of the above

27. Which of the following is not a reason that it is difficult to study oligosaccharide
composition from biological systems?
A) Oligosaccharides are often branched.
B) Oligosaccharides often have a high negative charge density.
C) Oligosaccharides have a variety of linkages (e.g., 16 or 14).
D) Oligosaccharides have too much conformational flexibility.
E) There are no specific glycosidase enzymes that can be used to selectively digest
oligosaccharides.

28. Which of the following techniques is not commonly used to study oligosaccharide
structures?
A) X-ray crystallography
B) Matrix-assisted laser desorption/ionization mass spectroscopy (MALDI-MS)
C) Nuclear magnetic resonance (NMR)
D) Complete chemical synthesis
E) Oligosaccharide microarrays

29. Explain why all mono- and disaccharides are soluble in water.

Page 6
30. This compound is L-glyceraldehyde. Draw a stereochemically correct representation of
C-1 and C-2 of D-glucose.

31. Categorize each of the following as an aldose, a ketose, or neither.

H H H H H

H C OH O C H C OH HO C H C

C O H C OH HO C H H C OH H C

H C OH HO C H HO C H C O H C

H H H H H

(a) (b) (c) (d) (e

32. Define each in 20 words or fewer:

(a) anomeric carbon
(b) enantiomers
(c) furanose
(d) pyranose
(e) glycoside
(f) epimers
(g) aldose
(h) ketose

33. (a) Draw the structures of both anomers of glucose in the pyranose ring form. (b) How
many asymmetric carbons (chiral centers) does each of these structures have? (c) How
many stereoisomers of the glucose are theoretically possible?

Page 7
34. Identify all the epimeric pairs in the structures shown below.

35. In the following structure:

(a) How many of the monosaccharide units are furanoses and how may are pyranoses?
(b) What is the linkage between the two monosaccharide units? (c) Is this a reducing
sugar?
Explain.

36. In measuring long-term glucose levels in the bloodstream, glycated hemoglobin must be
separated from unmodified hemoglobin to determine the percentage of glycated
hemoglobin. Suggest a simple chromatographic method by which this separation can
be performed.

37. (a) Define “reducing sugar.” (b) Show the reaction product of glucose after it is used
as a reducing sugar. (c) Explain why fructose is also considered a reducing sugar.
(Hint: It must first undergo a chemical conversion.) (d) Sucrose is a disaccharide
composed of glucose and fructose
(Glc(1  2)Fru). Explain why sucrose is not a reducing sugar, even though both
glucose and fructose are.

Page 8
38. Match these molecules with their biological roles.
(a) glycogen __ viscosity, lubrication of extracellular secretions
(b) starch __ carbohydrate storage in plants
(c) trehalose __ transport/storage in insects
(d) chitin __ exoskeleton of insects
(e) cellulose __ structural component of bacterial cell wall
(f) peptidoglycan __ structural component of plant cell walls
(g) hyaluronate __ extracellular matrix of animal tissues
(h) proteoglycan __ carbohydrate storage in animal liver

39. The number of structurally different polysaccharides that can be made with 20 different
monosaccharides is far greater than the number of different polypeptides that can be
made with 20 different amino acids if both polymers contain an equal number (say 100)
of total residues. Explain why.

40. Describe one biological advantage of storing glucose units in branched polymers
(glycogen, amylopectin) rather than in linear polymers.

41. Explain how it is possible that a polysaccharide molecule, such as glycogen, may have
only one reducing end, and yet have many nonreducing ends.

42. What is the biological advantage to an organism that stores its carbohydrate reserves as
starch or glycogen rather than as an equivalent amount of free glucose?

43. Draw the structure of the repeating basic unit of (a) amylose and (b) cellulose.

44. Explain in molecular terms why humans cannot use cellulose as a nutrient, but goats and
cattle can.

45. The glycosaminoglycans are negatively charged at neutral pH. What components of
these polymers confer the negative charge?

46. Sketch the principal components of a typical proteoglycan, showing their relationships
and connections to one another.

Page 9
47. Describe the differences between a proteoglycan and a glycoprotein.

48. Describe the structure of a proteoglycan aggregate such as is found in the extracellular
matrix.

49. How do oligosaccharide portions of glycoproteins change the properties of the proteins?

50. Describe the process by which “old” serum glycoproteins are removed from the
mammalian circulatory system.

51. What are lectins? What are some biological processes that involve lectins?

52. Briefly explain how the drugs Tamiflu and Relenza work to prevent the flu.

53. Briefly explain the procedure involved in using an oligosaccharide microarray to

identify the binding specificity for a potential lectin.

Page 10
Answer Key
1. C
2. B
3. C
4. D
5. B
6. D
7. C
8. E
9. E
10. C
11. B
12. C
13. D
14. A
15. D
16. C
17. D
18. C
19. D
20. B
21. C
22. A
23. D
24. D
25. C
26. D
27. D
28. A
29. These compounds have many hydroxyl groups, each of which can hydrogen bond with
water. (See Chapter 4.)
30. In D-glucose, the positions of the —H and —OH on C-2 are the reverse of those for C-2
of L-glyceraldehyde. (Compare Fig. 7-1, p. 236, with Fig. 7-2, p. 236.)
31. Molecules (b) and (d) are aldoses; (a) is a ketose; (c) and (e) are neither.
32. (a) The anomeric carbon is the carbonyl carbon atom of a sugar, which is involved in
ring formation. Once the anomeric carbon is involved in a glycosidic bond it is the
only carbon with more than one oxygen. (b) Enantiomers are stereoisomers that are
nonsuperimposable mirror images of each other. (c) Furanose is a sugar with a
five-membered ring. (d) Pyranose is a sugar with a six-membered ring. (e) A glycoside
is an acetal formed between a sugar anomeric carbon hemi-acetal and an alcohol, which
may be part of a second sugar. (f) Epimers are stereoisomers differing in configuration
at only one asymmetric carbon. (g) An aldose is a sugar with an aldehyde carbonyl
group. (h) A ketose is a sugar with a ketone carbonyl group.
33. (a) See Fig. 7-7. (b) The number of chiral centers is 5; all the carbons except C-6. (c)
The number of possible stereoisomers for a compound with n chiral centers is 2n; in this

Page 11
 case, 25, or 32 possible isomers.
34. Epimeric pairs should have one carbon of altered stereochemistry compared to each
other, as long as that carbon is not the anomeric carbon. Remember that all of the
pyranoses shown readily interconvert to the linear version and to their opposite anomer.
Therefore, C and D are anomers of each other, but are both epimers of A. Likewise, E
and F are anomers of each other, but both are epimers of B.
35. (a) 2 pyranoses; (b) 1  4; (c) yes. There is a free anomeric carbon on one of the
monosaccharide units that can undergo oxidation upon ring-opening.
36. Free hemoglobin has more positively charged residues (both lysine side chains and free
amino ends) than glycated hemoglobin, where these amines have been converted to
uncharged Schiff bases (see Box 7-1). Therefore, free hemoglobin is more positively
charged than glycated hemoglobin and ion exchange chromatography could be used.
(Whether one uses anion or cation exchange chromatography depends on the pI of
hemoglobin (6.9) and the pH of the buffer; see Chapter 3.)
37. (a) A reducing sugar is one with a free carbonyl carbon (aldehyde) that can be oxidized
to the carboxylic acid by Cu2+ or Fe3+. (b) You should have converted the aldehyde
carbon of linear glucose to a carboxylic acid. (c) Fructose is a ketose, which cannot be
readily oxidized; that is, it does not act as a reducing agent in its unaltered form.
Fructose must first undergo an isomerization to glucose, a reaction that is readily
catalyzed by acidic or basic conditions. (d) The carbonyl carbons of sucrose are C-1 of
glucose and C-2 of fructose. When the carbonyl carbons are involved in glycosidic
linkages, they are no longer accessible to oxidizing agents. In sucrose (Glc(1 
2)Fru), both oxidizable carbons are involved in the glycosidic linkage.
38. g; b; c; d; f; e; h; a
39. Because virtually all peptides are linear (i.e., are formed with peptide bonds between the
-carboxyl and -amino groups), the variability of peptides is limited by the number of
different subunits. Polysaccharides can be linear or branched, can be - or -linked,
and can be joined 1  4, 1  3, 1  6, etc. The number of different ways to arrange
20 different sugars in a branched oligosaccharide is therefore much larger than the
number of different ways a peptide could be made with an equal number of residues.
40. The enzymes that act on these polymers to mobilize glucose for metabolism act only on
their nonreducing ends. With extensive branching, there are more such ends for
enzymatic attack than would be present in the same quantity of glucose stored in a linear
polymer. In effect, branched polymers increase the substrate concentration for these
enzymes.
41. The molecule is branched, with each branch ending in a nonreducing end. (See Fig.
7-13c.)
42. The polymers are essentially insoluble and contribute little to the osmolarity of the cell,
thereby avoiding the influx of water that would occur with the glucose in solution.
They also make the uptake of glucose energetically more feasible than it would be with
free glucose in the cell.
43. (a) For the structure of amylose, see Fig. 7-13a. The repeating unit is -D-glucose
linked to -D-glucose; the glycosidic bond is therefore (1  4). (b) Cellulose has the
same structure as amylose, except that the repeating units are -D-glucose and the
glycosidic bond is (1  4). (See Fig. 7-14.)
44. The ruminant animals have in their rumens microorganisms that produce the enzyme

Page 12
 cellulase, which splits the (1  4) linkages in cellulose, releasing glucose. Humans
do not produce an enzyme with this activity; the human digestive enzyme -amylase
can split only (1  4) linkages (such as those in glycogen and starch).
45. Uronic acids such as glucuronic acid, and sulfated hydroxyl groups, such as
GalNAc4SO3– and GlcNAc6SO3–. (See Fig. 7-22.)
46. A typical proteoglycan consists of a core protein with covalently attached
glycosaminoglycan polysaccharides, such as chondroitin sulfate and keratin sulfate.
The polysaccharides generally attach to a serine residue in the protein via a trisaccharide
(gal–gal–xyl). (See Fig. 7-24, p. 253.)
47. Both are made up of proteins and polysaccharides. In proteoglycans, the carbohydrate
moiety dominates, constituting 95% or more of the mass of the complex. In
glycoproteins, the protein constitutes a larger fraction, generally 50% or more of the
total mass.
48. A proteoglycan aggregate is a supramolecular assembly of proteoglycan monomers.
Each monomer consists of a core protein with multiple, covalently linked
polysaccharide chains. Hundreds of these monomers can bind noncovalently to a
single extended molecule of hyaluronic acid to form large structures.
49. Hydrophilic carbohydrates can alter the polarity and solubility of the proteins. Steric
and charge interactions may influence the conformation of regions of the polypeptide
and protect it from proteolysis. Carbohydrates attached to proteins can provide binding
sites for lectins.
50. Newly synthesized serum glycoproteins bear oligosaccharide chains that end in sialic
acid. With time, the sialic acid is removed. Glycoproteins that lack the terminal sialic
acid are recognized by asialoglycoprotein receptors in the liver, internalized, and
destroyed.
51. Lectins are proteins that bind to specific oligosaccharides. They interact with specific
cell-surface glycoproteins thus mediating cell-cell recognition and adhesion. Several
microbial toxins and viral capsid proteins, which interact with cell surface receptors, are
lectins.
52. A newly formed flu virus needs to get out of its host cell in order to infect new cells and
make more virus. As the new virus buds off the host cell, it initially binds (via lectins)
to cell surface receptors located in the membrane that are specific for sialic acid
residues. The release from these receptors is facilitated by a viral sialidase that cleaves
the sialic acid from the oligosaccharides displayed on the surface of the host cell. After
these sialic residues are removed the virus can depart and find a new host for
replication. Both Tamiflu and Relenza are inhibitors of the viral neuraminidase, thus
blocking the release of new flu viruses.
53. First, one synthesizes as many different oligosaccharides as possible and attaches them
to known specific locations on a glass slide in micro-droplets. One then takes a
potential lectin (fluorescently labeled) and passes it over the glass slide. After
performing some selectivity washes, one looks for fluorescently labeled spots that show
to which oligosaccharides the lectin has bound.

Page 13
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require the quantity which he makes in sixteen days. Nevertheless, it
may become harmful after undergoing transformation into
ammonium carbonate or other substances.
Among the most poisonous substances in the urine are the
extractive and coloring materials. Normal urine loses one-half of its
toxicity by decoloration; bile acts in the same way. Urea alone
represents about one-eighth of the total toxicity of urine. Ammonia is
toxic, but present in small amounts. The coloring matters of the urine
cause two-thirds of its toxicity, the remainder of which is to be
ascribed to its mineral salts, which it contains in the following
proportion: A liter of urine ordinarily contains 44 Gm. of solid matter,
of which 32 are organic, 12 mineral. Of the latter, potassium salts
constitute 3 Gm., sodium salts 7.5 Gm., and other earthy salts
constitute the remainder.
In these conditions physicians have relied largely upon purgatives,
hoping thereby to remove urea from the blood. But intestinal
elimination has no elective affinity for it, and removes it only in its
normal proportion with the balance of the blood. Purgatives,
however, help, first, by dehydrating the tissues—i. e., removing water
with toxic material in solution. But they should be followed by
restoring to the tissues pure water. By bleeding more extractives are
removed than by any other channel, except by the kidneys. A
bleeding of 32 Gm. removes from the body as much toxic matter as
would 280 Gm. of a liquid diarrhea or 100 liters of perspiration. This
much may be removed by two leeches. It is especially in the
subacute nephritis of scarlatina, etc., that bleeding finds its greatest
indication. If the kidneys are chronically diseased, the utility of
bleeding is doubtful. Between the arterial capillaries of the bowels,
however, and the liver is found a mass of blood accumulated in the
portal vessels. This may be regarded as a reserve which can be
thrown into the general circulation when needed, in order that
thereby arterial tension may be augmented and the function of the
kidney increased. Cold injections into the bowels will often
accomplish this, and serious anuria frequently disappears after their
use. It is advisable, also, to make use of urea by subcutaneous
administration, as the most powerful diuretic known, surface friction,
caffeine, digitalis, etc., being far behind it in efficiency. In the form of
intoxication noted in the eclampsia of puerperal patients inhalations
of chloroform are valuable. Potassium salts should, under these
circumstances, never be employed. An exposure of urine in
compressed air will diminish its toxicity, on account of contact with
the oxygen; the most toxic bacteria are those which grow without
oxygen. Consequently patients inhaling this gas may overcome this
kind of auto-intoxication.
The value of an active liver is not appreciated by most surgeons to
the full extent. The blood of the portal vein is so much more toxic
than that of the hepatic vein that it is evident that the function of the
liver is to purify and remove the toxic material from the blood that
comes from the intestines. This has been called by Flint and others
the depurative action of the liver. The activity of the liver also may be
proved by grinding up a freshly removed liver with alkaloids, whereby
the latter are chemically changed.
That the facts above stated, or others related thereto, have not
been lost sight of by surgeons is shown by such expressions as
septic enteritis, enterosepsis, etc., which are used by various writers.
In previous publications the writer has made a separate topic of so-
called intestinal toxemia, which he has preferred to introduce here as
one of the many possible auto-intoxications. It is a condition not
always permitting of exact definition, nor, still less, can the exact
toxic agency be indicated in a given case. Nevertheless, it has been
made plain that there is perhaps no condition which so predisposes
to sapremia, septicemia, or even pyemia as this vague condition of
intestinal toxemia, which, notwithstanding, is so often present. Many
surgical patients present forms of blood poisoning in which the
poison has not proceeded from the wound, for which the surgeon is
not responsible, except that he may have neglected to avail himself
of certain precautions.
The auto-intoxications, then, which have peculiar interest for the
surgeon may be conveniently classified as follows:
1. Those caused by failure in the function of particular organs;
e. g., myxedema, cretinism, and cachexia strumipriva from thyroidal
failure; pancreatic diabetes, where the islands of Langerhans are
invaded (interstitial pancreatitis, q. v.); Addison’s disease from
adrenal failure (this being at present the prevailing belief).
 2. Those caused by general disturbance of metabolism, where its
incomplete or abnormal products reach the general circulation, e. g.,
oxaluria, gout, diabetes. (See Diabetic Gangrene.)
3. Those caused by retention in particular organs or tissues of
disturbed metabolic products, e. g., the toxemias following serious
burns and many septic conditions.
4. Those due to excessive formation of more or less normal
products, e. g.:
(a) Hydrothionemia, i. e., the presence of hydrogen sulphide in the
blood. This results from one form of gastro-intestinal putrefaction and
causes violent symptoms with evidences of hydrogen sulphide
poisoning. It is seen in some cases of gastric dilatation, especially
those caused by pyloric obstruction (q. v.).
(b) Acetonuria and Acetonemia.—The former sometimes follows
chloroform anesthesia, and occurs especially in diabetes (particularly
after removal of the pancreas in experimental animals). Acetone per
se is nearly or quite harmless, but its congeners, diacetic and beta-
oxybutyric acids, are very toxic. The danger in so-called acetonuria
is from acid intoxication by these acids, which has been described as
“excessive acidosis,” and its co-existence with glycosuria makes
diabetes certain, while prognosis is grave in proportion to its
presence. Prominent among the symptoms produced by it are
delirium and coma.
When either or all of these three substances are present in the
blood its alkalinity is reduced and its ability to absorb carbon dioxide
impaired; hence, acetonemia is evidenced by carbon dioxide
poisoning. To the brain symptoms above noted is added a peculiar
odor in the breath—sweetish or ethereal. This has been noted in
pyemia. This condition may set in after various operations, but
whether due to disease, the traumatism itself, or to chloroform may
not always be determined.[3]
[3] See paper by Brewer, Annals of Surgery, 1902, vol. xxxvi, No. 4, p.
481.

(c) Cystinuria.
(d) Coma of cancerous cachexia (coma carcinomatosum).
 (e) Exophthalmic goitre, from excess of thyroidal activity
(thyroidism).
Besides the above there is auto-intoxication proceeding especially
from the gastro-intestinal and hepatic systems. Of the former, the
best surgical examples are seen in the tetany which occasionally
takes its rise from a dilated stomach, and which may be cured by a
pyloroplasty or a gastro-enterostomy; in the nephritis which follows
stercoremia of intestinal obstruction; and in oxaluria, with its painful,
serious, and often deforming or crippling joint affections. Of the latter
we have examples in the cholemia of acute atrophy or of biliary
obstruction, and in the uremia of hepatic origin which occasionally
terminates a surgical case.
In addition to the above there should also be mentioned the auto-
intoxications of pregnancy, with the consequent salivation, peripheral
neuritis, pigmentations of the skin, icterus, and pruritus, which are
mainly attributed to perverted action of the liver or kidneys.
The practice of preparing patients for operation by a course of
purgatives, emetics, etc., is based upon the recognition of certain
principles. The general symptoms included under the name
enterosepsis, stercoremia, copremia, are due to the activity of the
colon bacillus, which seems to be made more virulent by certain
conditions of diet or retained fecal excretions, and to such an extent
that it wanders widely from its normal habitat and may be found in
distant parts of the body. Enterosepsis may be mistaken for surgical
fever, and is to be distinguished from it, perhaps, only by the study of
the excretions of a case and establishing the fact that they are free,
and that consequently pyrexia, etc., cannot be due to diminished
elimination. Aside from the migrations of the colon bacillus, it is also
possible for auto-intoxication to occur. Thus that which is stercoremia
one day may later become a genuine septicemia, vital resistance
being so lowered as to permit of local infection. The various
conditions are so often merged that it is difficult to separate and
identify them. Nevertheless, enterosepsis differs from sapremia in
that in the one instance the putrefying material is contained within a
normal cavity, whereas in sapremia it is contained within an
abnormal cavity, in either case corresponding to a septic
suppository, varying, however, in the place of insertion, also in the
nature of the surrounding tissues, which in the latter case are more
capable of absorption and of becoming infected than in the former.
A determination of indol and indican is often of the greatest value,
both in determining the extent of infection and the presence of pus.
Indol is set free under the following circumstances: (a) Suppuration
in a closed cavity. (b) Continued suppuration in a cavity with an
outlet. (c) Ulceration or necrosis of tissue. The degree of indicanuria
will depend on the length of time pus has been present, the
possibility of absorption from the tissues surrounding it, and its
degree. When pus is fully formed in a serous sac the indican
reaction becomes intense according to the length of time pus has
been present. This is particularly true in the empyemas of childhood.
In continued suppuration with a free outlet the production of indol will
be great; but the amount finally eliminated will depend upon the
character of the surrounding tissue. When solid tissue, like bone,
becomes affected, the elimination of indol is intense. Rapid biogenic
degeneration of tissue causes an increased amount of indol to be
deposited in the liver, and it is possible at postmortem, by simple
extraction with absolute alcohol, to take from the liver this excess
deposit in the shape of its oxidation product, indigo blue. Lardaceous
degeneration is characterized by marked and persistent elimination
of indol, which seems to be a product of tyrosin. It occurs frequently
in the liver, in which indol is notably deposited. Its primary factor is
deposited by the blood, in which latter indol circulates and is
oxidized. Lardaceous material gives a red or blue color with oxidizing
agents, which latter yield with indol an indigo red or blue.
The practical outcome of such a chapter as this is, then, to insist
as strongly as possible on the preparation of patients, whenever this
is feasible, for an ordeal which comprises the combined effect of
anesthesia and consequent disturbance of secretion and elimination,
with loss of blood and of strength, and subsequent confinement in
bed, with, moreover, all that this entails in further impairment of
activities of important organs. It is not always possible, practically
rarely so in emergency cases, to adopt these precautions; in which
cases they must be atoned for, as far as possible, by extra attention
in the same directions after the emergency is passed or has been
met. In the former case, however, the functions of the skin, the
kidneys, and the abdominal viscera should be regulated, the first by
hot-air baths; the second by this same measure in conjunction with
copious draughts of pure water, the correction of hyperacidity of the
urine, and the administration of whatever drugs may be of benefit as
diuretics, etc.; and the third by a course, perhaps covering several
days, of gentle or active purgation, by which the alimentary canal will
be entirely emptied of all that may serve to act as a source of
poisoning. In addition to this, in certain cases careful massage will
dislodge from the muscles and other tissues material which they
ought not to retain, and which will be washed away, as it were, by
the extra amount of fluid which this preparation, necessitates. Again,
the activity of the heart should be stimulated, perhaps by digitalis,
but preferably by that best of all tonics, strychnine, which is to be
administered hypodermically in average doses of a thirtieth or
twenty-fifth of a grain, morning and night. When these precautions
are taken, patients will successfully pass through trying ordeals
without anything which may give rise to alarm. When they are not
possible, the risk of operating, even in a small way, is materially
enhanced. So, too, after operations when these precautions have
not been taken, it is necessary to give careful attention to atoning for
their lack by such active purgation as a now reduced patient may
bear—by hot-air baths, if feasible, and by the administration of such
intestinal antiseptics as charcoal, naphthalin, corrosive sublimate,
bismuth salicylate, salol, etc., for the purpose of reducing to the
lowest possible minimum the opportunity for formation of poisons
which will disturb the proper repair of injury.
 CHAPTER VII.
THE SURGICAL FEVERS AND SEPTIC
INFECTIONS.

SURGICAL FEVER, KNOWN ALSO AS TRAUMATIC FEVER, OR

ASEPTIC WOUND FEVER.
Formerly the surgical fevers were all grouped together, and a
certain amount of febrile disturbance was looked for after any injury.
But with the introduction of antiseptic methods and the healing of
wounds by primary union, with absence of all septic phenomena,
and the use of the clinical thermometer, it is noted that there is a
certain rise of temperature more or less quickly after an operation or
reception of a wound, with fever of mild grade, persisting for several
hours or two or three days, and with other accompaniments. This
phenomenon has been carefully studied, and so separated from the
septic fevers as to deserve a distinct recognition under the names
above given, of which the most common in this country is surgical
fever.
As long as this fever is free from indications of septic character it is
without significance and needs only symptomatic treatment. It begins
usually within the first twenty-four or thirty-six hours, after which the
temperature may rise, progressively or with a morning remission, to
a height of 102° or possibly 103°. In children we are more likely to
get extremes in this regard than in healthy adults. It will be followed
by some disturbance of alimentary function, glazing or drying of the
tongue, deficiency in urinary secretion, and subside generally
spontaneously—invariably so if cathartics, diuretics, cool sponge
baths, etc., are used. It is usually due to the retention of blood clot,
ligatures, etc., or tissues which have been ligated and whose stumps
remain; in all instances there is some foreign material to be
removed. This means unusual phagocytic activity, perhaps
temporary leukocytosis, with active metamorphosis of clot and other
material, of all of which the elevated temperature is an
accompaniment and expression. It is not unlikely that the antiseptic
materials used may sometimes occasion this pyrexia.
Iodoform and carbolic acid are among the drugs in common use
which are known to be irritating and capable of producing toxic
symptoms. Often after the use of the latter the urine will be
discolored and will furnish the clue to the fever. In young children
particularly, and not infrequently in adults, mental disturbance, even
active delirium, may characterize the case. This is not always to be
explained by cerebral anemia due to loss of blood during the
operation or accident, but is probably due to drug toxemia or to
intoxication from materials furnished by the altered tissues.
Surgical fever of strict type may merge into a more or less
continuous fever as the result of intestinal toxemia permitted by
failure to evacuate the bowels, and this intestinal toxemia may be a
predisposing cause of genuine septic infection. Consequently a
surgical fever which does not disappear within two days is to be
viewed with suspicion, especially if it does not subside after the
administration of cathartics.
Some surgical fevers are accompanied by eruptions, a number of
which may be due to drugs and some to intrinsic poisons. Thus
carbolic acid and iodoform give rise occasionally to erythematous
eruptions, and the concomitant administration of drugs like
potassium iodide, quinine, antipyrine, and copaiba may produce
urticarial or other manifestations. Again, it is known that certain
toxins—produced, e. g., by the bacillus pyocyaneus—are capable of
causing dilatation of the superficial vessels and various flushes or
eruptions. To one of these, which dilates the capillaries, Bouchard
has given the name of ectasine. Consequently it by no means
follows that every eruption or rash following operations or injuries is
of a specific character. On the other hand it seems to be established
by numerous observers—among whom Paget is perhaps the most
prominent—that surgical patients, particularly the young, are
particularly liable to infection by scarlatina; and in the experience of
Thomas Smith, of forty-three children whom he cut for stone, ten had
scarlet fever. Therefore, in spite of the fact that a certain number of
cases of eruption may have been mistaken for scarlet fever, it is
undoubtedly true that in surgical and puerperal cases patients are
more than usually liable to this invasion. The use of antitoxins or
serums is also occasionally followed by intense urticaria.
The subject of surgical fever may then be epitomized as consisting
of elevation of temperature with certain accompanying disturbances,
which appear to be essentially due to the results of tissue
metabolism, including also metabolism of blood clot, ligatures, etc. It
is not a necessary nor conspicuous accompaniment of all surgical
cases, and in some individuals, even after grave operations, it will
scarcely be noted. It is more likely to be extreme in children than in
adults. As a result of excessive loss of blood it may be postponed. It
may be complicated and prolonged by any one of the auto-
infections, particularly that already mentioned in the preceding
chapter as intestinal toxemia, as a result of which septic infection
may ensue, and that which was at first a legitimate surgical fever
may thus become merged into a septic condition. In the absence of
auto-infection, and with appropriate treatment, surgical fever should
quickly subside until it becomes indistinguishable about the second
or third day.
Proceeding then in the order of pathological complexities, the first
of the surgical infectious fevers to be considered is sapremia.

SAPREMIA.
The term sapremia will be used here as indicating a condition
which is often likened to an intoxication produced by a supposititious
septic suppository. The term was first used by Duncan, and was
largely confined to puerperal cases. Some of the most ideal cases of
sapremia are those of puerperal origin.
In each of the three conditions comprised under the general term
of septic infection it is not now a question of particular organisms, but
of intoxication by products which are more or less common to at
least several of them. In a general way, they are mainly due to the
activity of the organisms already grouped as pyogenic. Those which
produce pus are capable of causing septic infection. In addition to
these, it is probable that certain of the saprophytes or ordinary
putrefactive organisms may produce the same effect.
Symptoms.
—In sapremia the symptoms begin promptly, depend for their
intensity upon the dosage of poison, and recede quickly as soon as
the source of poisoning is removed or its activity subdued. An
instance of the possible causes of sapremia will perhaps best
illustrate its pathology. Take, for example, the act of delivery of the
full-term fetus. At the completion of this operation there is left a fresh,
bleeding wound of large area which is more or less exposed to
putrefactive agencies. This is reduced with the contraction of the
uterine walls to a comparatively small cavity containing more or less
freshly coagulated blood. As long as this clot does not putrefy it is
disintegrated inoffensively, to be discharged in large part with the
lochia. If germs of putrefaction enter, either during the act of labor or
afterward, and linger, putrefactive processes are set up in the clot
with the prompt production of certain toxins and ptomains. There is
here then a septic suppository with conditions favorable for
absorption by the containing tissues. How quickly the poisoning may
show itself, and how soon it may subside after removal of the
putrefying clot, daily experience may tell.
Sapremia then is intoxication produced by absorption of the results
of putrefaction of a contained material within a more or less closed
cavity, whose walls are capable of absorption of noxious products as
they form. As long as putrefaction is essentially limited to the
contained mass, and does not spread to and involve the containing
or surrounding tissues the case is one of sapremia. As soon as the
process spreads from the containing tissues the case merges from
one of sapremia into one of septicemia. That this may occur in any
case without prompt intervention will be readily understood.
Sometimes patients may die of sapremia, though rarely, and in such
case ordinarily as the result of gross neglect. Once the septicemic
process is begun, however, its spread cannot always be checked,
and the case which one day is sapremic and redeemable may later
become septicemic and practically lost.
The symptoms of sapremia are not essentially different from those
common to septic infection, save that ordinarily they are, at least at
first, milder. There are flushing of the face, dry tongue, mental
disturbance, pyrexia, while usually all the symptoms are ushered in
by a chill, which may have been preceded only by slight malaise.
These are followed by nausea and vomiting, with headache, and
often, later, by diarrhea or active purging. Later delirium may occur,
possibly even fatal coma. On postmortem examination there are few
changes revealed; alterations in the blood, a failure to coagulate,
and some softening of the spleen and liver would probably be the
only ones.
Treatment.—The treatment should be prompt and the cause
removed. In puerperal sapremia the uterus should be
emptied, antiseptic douches given, irrigating as often as necessary
to prevent offensive odor to the discharge, and combating general
signs of poisoning by plainly indicated measures. Heart depression
should be overcome by diffusible stimulants and hypodermic
injections of strychnine in doses of ¹⁄₂₅ grain or more. The bowels
should be unloaded by a mercurial followed by a saline cathartic;
suppression of urine treated by venesection and hot-air baths or
sweats; diuretics should also be prescribed, and fluids administered
copiously. If the patient is restless, an opiate should be given; if
delirious, necessary restraint should be resorted to.
Essentially the same measures should be pursued in a surgical
wound or in a case of compound fracture, or any injury where
retained material may be undergoing changes already alluded to.
General measures should be the same. Purgatives are advisable in
these cases.
Chronic Sapremia.—Chronic sapremia is a better name for what
used to be known as hectic fever. It is
characterized by rapid, feeble pulse, a temperature but little elevated
in the morning and rising to 102° or 103° in the latter part of the day,
with profuse perspiration, or sometimes colliquative sweats that
leave patients exhausted. There is usually a distinctive flushing of
the cheeks. Emaciation is a marked feature in most instances. Hectic
means simply habitual fever. It is met with particularly in tuberculous
cases, whether of lungs or bones or joints, in empyema, psoas
abscess, and most all chronic pyogenic infections. It is frequently
followed by or associated with amyloid or waxy degeneration of the
liver, kidneys, and spleen. This process commences in the walls of
the bloodvessels and by its spread to the surrounding connective
tissue leads to notable enlargement of these organs, with
albuminuria, edema, ascites, and the usual associated phenomena.
Treatment.—Treatment, in addition to that already indicated above,
should be addressed to removal of the cause. In all instances it
should comprise attention to elimination, digestion, nutrition, and
fresh air. By such measures even distinct amyloid changes may be
arrested, or possibly improved.
Cryptogenetic or Spontaneous Septicemia.—Cryptogenetic or
spontaneous
septicemia is a term applied to those cases in which the port of entry
of the germs is no longer visible—e. g., a hypodermic puncture—or
cannot be positively determined. On careful study this may be found
to consist of a small focus where pus is forming within narrow
confines and under great pressure. Under these circumstances, as
Kocher has shown, toxic virulence is rapidly augmented. This is
doubtless one reason why the septic features of many cases of
osteomyelitis and appendicitis are so pronounced.

SEPTICEMIA.
According to the views thus enunciated, the difference between
sapremia and septicemia is not one of character as much as of
location. In septicemia the putrefactive action is no longer confined
to material enclosed by (yet not of) the tissues themselves, but has
spread from this to the surrounding living cells, which are being
attacked by bacterial enemies; in other words, we deal with infection
of living tissues rather than with mere intoxication. This is a
progressive invasion of tissues by continuity, with a constantly
proceeding systemic intoxication by poisons produced in larger
quantities. So rapid may this action be—as may be seen in
malignant diphtheria—that the individual speedily succumbs before
evidences of abscess or local gangrene appear. On the other hand,
providing that the toxic action is less pronounced or the patient’s
vitality more enduring,—i. e., his tissues more resistant—abscess,
phlegmon, or local gangrene may result in the destruction of tissue
being limited to the environs of the parts first involved. Bacteria are
also found in the blood.
 While septicemia then may be a direct continuance of an original
sapremia, it is not intended to intimate that it may not originate de
novo; that is, many cases may begin as a pronounced septicemia
from a local infection. This is the case, for instance, with the majority
of dissecting wounds, etc.
Symptoms.—In septicemia there is a period of incubation, usually
two or three days, often longer. If this follows an
operation, the mild fever which would indicate the slumbering fire is
usually regarded as surgical fever. But when this rises and is
followed by prostration, with alimentary disturbance, loss of appetite,
headache, etc., followed by typhoidal symptoms, the alarm is
sounded and should be quickly heeded. Usually, but not always,
there is a preliminary or premonitory chill, after which prostration will
be more marked than before. The severity of the symptoms cannot
be foretold from the size, location, or character of the wound. The
character of the fever is essentially continued, usually with morning
remissions. Gussenbauer has called attention to a class of cases in
which subnormal temperature is caused by the absorption of
ammonia compounds. To these he has given the name
ammoniemia. This condition may be seen in connection with
gangrenous hernia, and has even been mistaken for shock (Warren).
(See also acetonemia, in previous chapter.)
In septicemia from infection of a visible portion of the body there
are usually seen evidences of lymphangitis and perilymphangitis of
septic character. These will be evidenced by tender and purplish
lines, extending subcutaneously along the course of the known
lymphatics or in connection with the more prominent subcutaneous
veins. The lymph nodes, into which these visible vessels as well as
the deeper ones empty, become enlarged and tender; the whole
lymphatic system participates; the spleen in aggravated cases
becomes notably enlarged, and even the bone-marrow more or less
involved. Diarrhea is commonly an early but controllable symptom. A
hematogenous icterus of mild degree is another frequent
accompaniment. The conjunctiva becomes discolored and the skin
slightly so. Should the blood be examined marked leukocytosis will
be noted, and should cultures be made from it, in many instances at
least, the organisms at fault can be detected and recovered from it.
The vigor of the heart muscle is seriously impaired; the pulse
becomes rapid and weak. In scarcely any form of septic infection is
this more prominent than in diphtheria; and microscopic examination
shows the rapid disintegration of the cells of the heart muscle, as
well as those of other parts of the body, even to the almost complete
molecular disintegration of the nuclei. Erythematoid, pustular, and
even hemorrhagic eruptions are met with upon the skin, some of
which are probably to be explained by thrombosis of the dermal
capillaries. Certain complications are not infrequent, among which
inflammations of the pericardium and endocardium—e. g., ulcerative
endocarditis—are frequent. As the case becomes aggravated the
temperature rises irregularly; the hot, dry skin becomes cold and
clammy; prostration and indifference more marked; diarrhea more
colliquative; icterus more pronounced; urine more reduced in
quantity or suppressed; and these symptoms are succeeded by
indifference, mental apathy, stupor or delirium, and finally death, the
patients being comatose and collapsed.
While these are the general indications of septicemia, the wound
or site of injury has undergone changes which are also
characteristic. They comprise the edema and redness of wound
margins, which may be seen even in sapremia, followed by
increasing tumefaction, escape of foul-smelling discharge, and finally
by sloughing and gangrene of the parts involved. On microscopic
examination the capillaries are filled with infective thrombi and vessel
walls infiltrated with microörganisms, which abound also in the lymph
spaces. Bacterial infection can be traced in microscopic sections
from the infected area, from the point in the neighborhood of the
wound where microbes infest the tissues to points remote from it,
where they are sparsely found, if at all. The same evidences of
infection may be traced along the lymphatic vessels, and often the
veins.
Postmortem Evidences.—The postmortem evidences of
septicemia are indicative on first sight:
the blood is of the consistency of tar and does not coagulate;
evidences of putrefaction are plain to sight and smell; the serous
membranes, particularly the pia mater, are often extravasated; the
muscles are discolored and of a darker hue than natural, edema of
the lung is frequent; the intestines reveal a gastro-intestinal catarrh,
the duodenum and rectum showing punctate hemorrhages; the
spleen is darkened, enlarged, and softened; the liver shows similar
signs, less marked, and at times an emphysematous condition due
to putrefactive gases. Cultures can be made from the fluids and
tissues of organs thus affected. It is also of importance to emphasize
that such material is powerfully and often fatally infectious; some of
the worst forms of dissecting wounds and instances of fatal infection
have come from carelessness in making these postmortem
examinations.
So far as concerns the character of the wound, which is most likely
to be followed by septicemia, there is but little to be said. Wounds
made by infected tools, the butcher’s knife, the anatomist’s scalpel,
etc., are the most dangerous. All forms of phlegmonous erysipelas,
many cases of gangrene following frostbite, nearly all instances of
traumatic gangrene, most cases of carbuncle, and, in fact, all similar
lesions, are likely to be followed by septicemia. The so-called
spontaneous cases have an equally infectious origin, though one
which is concealed. In unrecognized instances of appendicitis, for
instance, and in many other conditions, although the path of infection
may not be easily traced, it is, nevertheless, always present, and can
be found if diligent search is made. The nasal cavity, the tonsils, the
teeth, the middle ear, the deep urethra, and the rectum are often
overlooked as offering possibilities for septic infection which may
follow this general type.
Treatment.—This should be both local and general. Local
treatment should consist in complete and absolute
removal of the active cause. This comprises the reopening of
wounds, evacuation of clot, cutting or scraping away of sloughs and
gangrenous tissue, with cauterization of the exposed living tissue, in
order that absorption may be prevented, and will often include
amputation or extirpation of a part. For tissues which are not too
completely riddled by disease, and lost beyond possibility of
redemption, continuous immersion in hot water offers the best
possible prospect. By it putrefaction seems checked, the separation
of dead from living tissues is accelerated, relief of pain or discomfort
is afforded, and disinfection of material which is foul and infectious is
guaranteed. An excellent local application is the mixture of resorcin 5
parts, ichthyol 10 parts, ung. hydrarg. 40 parts, and lanolin 45 parts,
already mentioned in Chapter IV, or the application of brewers’
yeast. (See chapter on Ulcers.) Of great value also will be found the
silver ointment of Credé (Unguentum Credé). This permits of
absorption of silver through the unbroken skin (as in the case of ung.
hydrarg.), and the dissemination throughout the system of the
antiseptic virtues of the silver itself. To ensure its greatest efficiency
this ointment should be thoroughly rubbed in, especially over parts
which are not too tender. Many cases of septic infection promptly
yield under the influence of the argentine preparations which Credé
has lately introduced.
In suitable cases also the subcutaneous injections of
antistreptococcic serum will be followed by beneficial effects. The
earlier the injection is given the better the prospect of benefit.
Evidence is strongly in favor of this serum as a prophylactic
measure, especially before operations, when septic pneumonia or
other septic accidents are feared.
Another measure of great utility in selected cases is the
intravenous infusion of a solution of Credé’s soluble silver, made with
1 gram of silver in 1000 Cc. of sterilized water at a temperature of
105° to 110°. In cases of profound toxemia a small amount of blood
may be withdrawn (50 to 400 Cc.), for reasons stated in Chapter VI.
No hesitation need be felt in introducing 500 Cc. or even 1000 Cc. of
this solution. It is the ideal way of bringing a powerful non-toxic
antiseptic into immediate contact with pathogenic microbes.
There have been recent suggestions as to the intravenous
injection of very dilute formalin solution, in order to take advantage of
its remarkable germicidal activity; it has been employed in a few
cases, especially of puerperal sepsis, with success, 1 Cc. of
standard formalin solution is mixed with 800 Cc. of sterilized salt
solution. It has been shown that if 50 Cc. of this is thrown into the
veins of an average adult it will form with the 5000 Cc. of blood a
mixture of 1 to 200,000, in which strength it may be expected to
prove an efficient bactericidal agent. Indeed, a smaller amount or a
weaker preparation would probably suffice. Barrows has reported
success following two infusions, two days apart, of first 500 Cc., then
750 Cc. of a 1 to 5000 formalin solution. Still, these injections may
be followed by cramps in the arms, cardiac discomfort or distress,
and blood (or blood cells) in the urine. It would probably be well to
limit this use of formalin to those cases at least in which the
presence of cocci in the blood can be demonstrated by culture or
other method.
An excellent method in the local treatment of parts which admit of
it (hands and feet) is their exposure to dry hot air in the Kelly heater
or some similar apparatus. Hot air will be borne at a temperature of
210° to 220°, which may be destructive to germs while still tolerable
for a short time by the tissues. Clinton, of Buffalo, with whom this
method is original, reports that the temperature within the tissues
thus treated is raised to about 107°, which is above the thermal
death point of the ordinary pyogenic organisms, and that this method
gives better results than any other of treatment of septic infection of
those parts which can be subjected to it.
The general treatment of septicemia is, in the main, stimulant and
tonic. Fever is not to be treated with arterial sedatives nor often with
antipyretics. It is a symptom of poisoning, and its too prompt
suppression prevents both the recognition of the intoxication and the
measure of its degree. Pyrexia then is best combated with cool
sponge baths and stimulant measures of a general character. The
principal reliance must be upon nutrition and stimulants. Assimilation
may be impaired when gastro-intestinal catarrh is as prominent a
feature as it is in many of these cases. Consequently the simplest
and most assimilable food, often that which is predigested, should be
administered. Milk, eggs, beef peptonoids, and fruits are among the
most appropriate. The best stimulants and tonics are alcohol and
strychnine. Strychnine is preferably administered hypodermically in
doses of ¹⁄₂₅ grain from two to four times a day. Heart depression is
best combated by this measure, or by quinine in large doses, while
digitalis and atropine may be added. For internal use alcohol is, par
excellence, the remedy. This is administered in doses only to be
measured by their effect. In fact, the administration of alcohol in
these cases is a matter of effect, and not of dosage. Aside from
these measures the intestinal antiseptics should be administered,
among these being corrosive sublimate, ¹⁄₁₀₀ grain, every three or
four hours, salol in large doses, bismuth salicylate, or naphthalin—
any or all of these in connection with powdered charcoal. Intestinal
pain and frequency of stool can be more or less controlled by opium,
while disinfection of the alimentary canal is only to be accomplished
by the above remedies, in connection with flushing of the colon with
saturated boric acid solution or something of that kind. Pain is to be
controlled by morphine administered subcutaneously.
No special attention need be given to the so-called septicopyemia.
It represents a mixed condition of septic intoxication, local infection,
and destruction, with metastatic abscess, and is a term appropriately
applied to cases which combine the significant features of each type.

PYEMIA.
The derivation of the term pyemia, which came into general use in
1828, is misleading. Although septic fever always accompanies
suppuration, it is not certain that pus as such circulates in the blood,
as the term pyemia implies, the error having arisen originally from
mistaking the contents of breaking-down thrombi for pus from
ordinary sources. While a recognition of the etiology of the disease is
new, the disease itself has been recognized for many centuries.
Pyemia is only met with in connection with suppuration, as far as
known, never without it. In those cases which appear to be free from
suppuration pus will be found. Pyemia may be described as
septicemia plus thrombotic and embolic accidents, which lead to
distribution of infectious material to all parts of the body. This
distribution is made by the bloodvessels, although to some extent
the lymphatics undoubtedly participate. When pyogenic organisms
reach bloodvessel walls they tend to set up a mycotic phlebitis,
which, by virtue of the coagulating blood, becomes soon what is
known as thrombophlebitis. Infection proceeding through the vessel
walls, the endothelial lining is loosened, while to these rotting spots
leukocytes adhere and coalesce into a more or less homogeneous
mass. This so-called white thrombus becomes also infected with
bacteria; portions of it, loosened and dislodged, are carried by the
returning blood stream to the right side of the heart, whence they are
distributed through the lungs. Dislodgement may be made by mere
force of the blood stream, or may be assisted by movements of the
part or handling of the same. These particles of thrombi are loaded
with the infectious organisms which began the disease, and
wherever one settles a reproduction of the original thrombophlebitis
is rapidly produced. In this way numerous infected thrombi are
formed within the vessels of the lungs, which, again, loosen, and are
now swept into the left side of the heart, whence they are distributed
with arterial blood in all directions. While it is true that they are
equably distributed, it is also positive that certain tissues seem more
capable of lodging and being attacked by the contained organisms
than are others. When it is once appreciated that each particle of
infected clot is capable of setting up, either in the lungs or in the
other tissues, upon the second distribution, other abscess formations
analogous in etiology to that from which came the first disturbance,
then the fundamental idea of metastatic abscess is fully impressed.
The term metastasis may be regarded as synonymous with
transportation, and metastatic abscesses are those produced by
transportation of infected particles from one part of the body to
another. Wherever they lodge similar trouble will result. Contiguous
minute metastatic abscesses quickly coalesce, and in this way large
collections of pus are formed. The blood also contains organisms not
attached to thrombi, and from the blood of the pyemic patient
cultures can at almost any time be made. Until this is done it will be
virtually impossible to incriminate any particular organism as the one
at fault. Thrombo-arteritis is the equivalent in the arteries of
thrombophlebitis in the veins, and is accompanied by the same
detachment of endothelium, adhesion of leukocytes, etc. Whenever
such a lesion occurs in artery or vein, coagulation necrosis takes
place and suppuration occurs around it. The metastatic abscess is
thus the result of breaking down of this affected tissue, and is often
called miliary abscess. Particles of infective thrombi cling also to the
valves of the heart and a septic endocarditis may result.
The possibility of so-called spontaneous or idiopathic pyemia is
occasionally discussed. This means a pyemia whose cause is
concealed. The explanation will be found sometimes in an acute
infectious osteomyelitis, sometimes in ulcerative endocarditis, or
inflamed appendix or other portion of the peritoneal cavity. Again, it
may proceed from middle-ear disease, in which there is so little
discharge as scarcely to attract attention. Thus causes which
predispose to suppuration (see Chapter III) come into play here, and
the influence of exposure, fatigue, starvation, etc., is not to be
ignored in furnishing an explanation for the so-called idiopathic
cases.
In the majority of instances, however, pyemia follows surgical
operations and injuries, among which are compound fractures, deep
injuries with small superficial evidence thereof, compound injuries of
the skull, and injuries by which veins are exposed. Inasmuch as the
typical pyemic manifestations require a certain length of time for their
development, the onset of this disease is more delayed than in the
case of septicemia. While the case may be manifestly one of septic
infection of unrecognizable type, the characteristic indications of
pyemia seldom appear in less than ten days, and frequently not for
several days longer.
Symptoms.—The symptoms of pyemia do not essentially differ
from those of other septic infections. The principal
difference is in the frequency of chill and range of temperature. Chills
are more common at the inception of the condition, and more
frequent throughout its continuance than in other septic conditions.
The chill may be slight or assume the proportions of a rigor, and
each chill is followed by colliquative sweat and exhaustion. In other
words, chills which are infrequent in septicemia are common in
pyemia. There is reason to believe that with each fresh distribution of
emboli we have one or more chills as the objective evidence thereof.
Distinctive also of pyemia is the temperature curve, which much
resembles that of intermittent fever, without the regularity of change
characteristic of malarial fevers. It is without regular remissions, and
has been referred to as irregularly intermittent. The first rise is abrupt
and usually excessive, while with each fresh chill or series of chills
similar abrupt alterations will be noted. These occur so frequently
and fluctuate so irregularly that in order to note them accurately the
temperature should be taken at least every two hours. The
temperature seldom drops to normal.