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It is over thirty years since Arbuthnot Lane published his Operative Treatment of Fractures; but we still cannot compare conservative and operative principles from the viewpoint of basic science because the fundamental nature of fracture repair still eludes us. The best we can do is to compare the results of clinical practice; but there are so many variables (comminution, sepsis, mechanical details of the operation, blood supply, level of fracture, different observers, etc.) that a series of one or two hundred cases, which is a large series for any one operator, is soon reduced to statistical insignificance. Attempts to control the conditions of the fracture by using experimental animals have yielded nothing of importance compared with what we have learned ‘the hard way’ by developing operative techniques on the human subject.
The followers of Lane and Sherman believed that the failures of internal fixation would ultimately be eliminated by improved technique. We now know that internal splints are exposed to truly enormous forces and are subject to the phenomenon of failure by fatigue. Improvements in the design of plates and screws have reduced, but not eliminated, the mechanical failures which were common when techniques derived from the woodworker were used. The change to using electrolytically inert metals has only slightly diminished our problems, though there is no excuse for returning to the brass screws and reactive steel plates with which Lane himself achieved sufficient success to establish the method.
The precision with which it is possible to reduce a Pott's fracture by manipulation becomes a source of pleasure once the surgeon understands the mechanics of this reduction. My own satisfaction is increased when I recall the uncertainty of my own early attempts to reduce this fracture-dislocation and how I was once dependent on the X-ray as on a ‘lucky dip.’
The problem in treating a Pott's fracture is not so much how to reduce the fracture but how to make sure that it will stay reduced. I shall endeavour to indicate when I think it is dangerous to persist with closed reduction and when operative aid should be invoked.
Operative treatment of the Pott's fracture is not a procedure to be encouraged as a routine, because there are special complications of operative treatment quite as serious as the defects of closed treatment. In the ordinary Pott's fracture the functional and anatomical results of a skilful closed reduction should be perfect. Even if a small posterior marginal fragment remains displaced, the ankle possesses a latitude for recovery of function which is often astonishing. The open reduction of this fracture-dislocation can be a matter of considerable technical difficulty; to secure adequate exposure in the cramped space available may impair the blood supply of a detached fragment. If for any reason open reduction should be attempted, nothing less than a ‘hair-line’ restoration should be regarded as justifying it; incomplete reduction after open operation must be regarded as an error of judgment. If open reduction is considered imperative, then the minimum of metallic ‘hardware’ should be used.
The reduction of a supracondylar fracture of the humerus can become a comparatively simple feat if it is undertaken without delay and if the surgeon who has the first opportunity of treating it has a clear mental picture of its mechanism. The first reduction is the one most likely to succeed; after subsequent attempts the elbow becomes so indurated that the swelling may obstruct even the most expert manipulator.
ANATOMY OF THE FRACTURE
In the supracondylar fracture of the humerus the fracture line passes more or less transversely through the metaphysis at a variable distance from the epiphyseal line. When the fracture line is extremely close to the epiphyseal line it sometimes appears in the X-ray almost as an epiphyseal separation, but in every case a thin shell of the diaphysis is adherent to the distal fragment.
There are three elements in the displacement of the distal fragment of the supracondylar fracture: (i) posterior displacement, (2) lateral (or medial) displacement, and (3) rotary displacement.
In the manipulative reduction to be described, the rotary deformity will more or less correct itself under the influence of the tense fascial structures in the course of the preliminary phase of reduction by traction. An error of 10 degrees of rotation will not affect the functional or cosmetic result, though it will give rise to interesting appearances in the radiograph which need special comment (see below).
Opinions vary considerably on the frequency of late symptoms following unsatisfactory reductions of a Bennett's fracture. Casualty officers do not usually find it an easy fracture to reduce, and because it is also quite a common injury, one can presume that numerous cases must be treated inexpertly every year; but even so, the number of cases presenting themselves with symptoms of traumatic arthritis is remarkably few. However, this is no reason why a high standard of manipulative reduction should not be expected. The reduction of this fracture presents no great mechanical difficulty but it demands from the surgeon a fine sense of touch, and for this reason the injury could well be used as a ‘passing-out’ test for the student of closed reduction.
ANATOMY OF THE FRACTURE
As its alternative name implies, the ‘stave’ fracture is often sustained in a bout of fisticuffs. An ill-delivered blow transmits force in the line of the thumb while in flexion, thereby shearing off the anterior part of the base of the metacarpal, and so allowing the bone to escape from the joint in a dorsal direction. The volar ligament of the carpo-metacarpal joint remains intact and this is responsible for holding the wedge-shaped fragment of the metacarpal in its normal relation with the articular surface of the trapezium. The essential deformity of this injury is one of angulation with the concave aspect on the volar side; the intact soft tissues which are to act as the ‘hinge’ for the reduction are thus to be found on the volar aspect of the base of the metacarpal.
Perfect anatomical restoration and perfect freedom of joint movement can be obtained simultaneously only by internal fixation. It is possible to argue that most of the difficulties of closed fracture treatment can be traced to the prevention of joint stiffness. Closed methods can offer anatomical restoration only if the start of joint movement is delayed. It is the significance of delay in starting joint movement which is the crucial point in understanding closed methods.
The ultimate recovery of full joint function after a fracture depends on many factors and not only on early exercise. This is suggested by the fact that the end results of conservative treatment, after a slow start, can often be surprisingly good, while those of operative methods, after a very promising start, can sometimes be disappointing. It is therefore obvious that we must review the factors which govern the recovery of joint movement following a fracture, so far as we know them.
In studying the stiffness of a joint following a fracture of an associated bone the greatest danger to the furtherance of knowledge is the too facile acceptance of simple mechanistic explanations. It is probable that the processes concerned with the recovery of joint function are of great biological complexity. Too often there is a tendency to think of stiff joints in terms of stiff engine-bearings or of rusty door-hinges and, with this childlike concept, to devise apparatus to loosen the stiffness by repeated mechanical movements.
The development of HCV subgenomic replicons that produce high levels of one or more HCV polypeptides (Lohmann et al., 1999; Blight et al., 2000), in contrast to the very low and inconsistent levels of wild-type virus produced in tissue culture cells infected with HCV (Table 11.1 and Ch. 11), suggests that there are properties of wild-type HCV that normally attenuate virus gene expression and replication, and that when these constraints are removed, much higher levels of expression could be achieved. One of these constraints may be the complex secondary structural features within the 5' and 3' UTRs of the virus. Many laboratories are developing additional self-replicating replicons that are capable of persisting, and some at high copy number, within transfected or infected cells. These include replicons made from alphavirus (Garoff & Li, 1998; Ying et al., 1999), pestivirus (Moser et al., 1999), other flavivirus (Varnavski & Khromykh, 1999), and coronavirus (Thiel, Siddell & Herold, 1998) vectors. Whether the entire HCV polyprotein could be expressed from such constructs remains to be seen. In addition, since the HCV would be produced from artificial templates, it is not clear whether the sensitivity of virus gene expression and replication to putative antiviral agents would be the same or different to that of virus made from native HCV templates in an infected cell.
The human coronavirus 229E replicase gene encodes a
protein, p66HEL, that contains a putative
zinc finger structure linked to a putative superfamily
(SF) 1 helicase. A histidine-tagged form of this protein,
HEL, was expressed using baculovirus vectors in insect
cells. The purified recombinant protein had in vitro ATPase
activity that was strongly stimulated by poly(U), poly(dT),
poly(C), and poly(dA), but not by poly(G). The recombinant
protein also had both RNA and DNA duplex-unwinding activities
with 5′-to-3′ polarity. The DNA helicase activity
of the enzyme preferentially unwound 5′-oligopyrimidine-tailed,
partial-duplex substrates and required a tail length of
at least 10 nucleotides for effective unwinding. The combined
data suggest that the coronaviral SF1 helicase functionally
differs from the previously characterized RNA virus SF2
helicases.
From 1985 to 1988, a total of 2496 swine sera from 60 farms in the Tohoku District of the
Honshu Island of Japan were examined for antibodies to swine haemagglutinating
encephalomyelitis virus (HEV), human coronavirus (HCV) and bovine coronavirus (BCV) by
haemagglutination-inhibition (HI) test. Antibodies to HEV 67N strain and HCV OC43 strain
were highly prevalent with positivity rates of 82·1 and 91·4%, respectively, while seropositivity
rate to BCV Kakegawa strain was 44·2%. No clinical signs of HEV infection were noticed in
any farms including farms with relatively high seropositivity. The results suggested that HCV
or antigenitically related virus(es) as well as HEV might be perpetuated in swine in the Tohoku
District.
Background. It is not known whether psychological stress suppresses host resistance to infection. To investigate this issue, we prospectively studied the relation between psychological stress and the frequency of documented clinical colds among subjects intentionally exposed to respiratory viruses.
Methods. After completing questionnaires assessing degrees of psychological stress, 394 healthy subjects were given nasal drops containing one of five respiratory viruses (rhinovirus type 2, 9, or 14, respiratory syncytial virus, or coronavirus type 229E), and an additional 26 were given saline nasal drops. The subjects were then quarantined and monitored for the development of evidence of infection and symptoms. Clinical colds were defined as clinical symptoms in the presence of an infection verified by the isolation of virus or by an increase in the virus-specific antibody titer.
Results. The rates of both respiratory infection (P< 0.005) and clinical colds (P < 0.02) increased in a dose-response manner with increases in the degree of psychological stress. Infection rates ranged from approximately 74 percent to approximately 90 percent, according to levels of psychological stress, and the incidence of clinical colds ranged from approximately 27 percent to 47 percent. These effects were not altered when we controlled for age, sex, education, allergic status, weight, the season, the number of subjects housed together, the infectious status of subjects sharing the same housing, and virus-specific antibody status at base line (before challenge). Moreover, the associations observed were similar for all five challenge viruses. Several potential stress-illness mediators, including smoking, alcohol consumption, exercise, diet, quality of sleep, white-cell counts, and total immunoglobulin levels, did not explain the association between stress and illness. Similarly, controls for personality variables (self-esteem, personal control, and introversion-extraversion) failed to alter our findings.
Conclusions. Psychological stress was associated in a dose-response manner with an increased risk of acute infectious respiratory illness, and this risk was attributable to increased rates of infection rather than to an increased frequency of symptoms after infection. (N Engl J Med 1991; 325:606-12.)
Stressful life events are commonly believed to suppress host resistance to infection. When demands imposed by events exceed a person's ability to cope, a psychological stress response composed of negative cognitive and emotional states is elicited. Psychological stress, in turn, is thought to influence immune function through autonomic nerves innervating lymphoid tissue or hormone-mediated alteration of immune cells.