Professional Documents
Culture Documents
Upper respiratory tract infection (URI) represents the most common acute
illness evaluated in the outpatient setting. URIs range from the common cold
typically a mild, self-limited, catarrhal syndrome of the nasopharynxto life-
threatening illnesses such as epiglottitis (see the image below).
Practice Essentials
Hypertension affects approximately 86 million adults (20 years) in the United
States; it is a major risk factor for stroke, myocardial infarction, vascular
disease, and chronic kidney disease. See the image below.
2.2 (this
number is
American Indian/Alaska Native 28.4 13.7 9.3
considered
unreliable)
Source: Summary health statistics: National Health Interview Survey, 2015. Available
at:https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2015_SHS_Table_A-1.pdf. Accessed:
November 14, 2016.
NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey.
Prognosis
Most individuals diagnosed with hypertension will have increasing blood
pressure (BP) as they age. Untreated hypertension is notorious for increasing
the risk of mortality and is often described as a silent killer. Mild to moderate
hypertension, if left untreated, may be associated with a risk of atherosclerotic
disease in 30% of people and organ damage in 50% of people within 8-10
years after onset.
Death from ischemic heart disease or stroke increases progressively as BP
increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in BP
above 115/75 mm Hg, the mortality rate for both ischemic heart disease and
stroke doubles. [2]
Hypertensive retinopathy was associated with an increased long-term risk of
stroke, even in patients with well-controlled BP, in a report of 2907 adults with
hypertension participating in the Atherosclerosis Risk in Communities (ARIC)
study.[39, 40] Increasing severity of hypertensive retinopathy was associated with
an increased risk of stroke; the stroke risk was 1.35 in the mild retinopathy
group and 2.37 in the moderate/severe group.
In a meta-analysis of pooled data from 19 prospective cohort studies involving
762,393 patients, Huang et al reported that, after adjustment for multiple
cardiovascular risk factors, prehypertension was associated with a 66%
increased risk for stroke, compared with an optimal blood pressure (<120/80
mm Hg). [41, 42]Patients in the high range of prehypertension (130-139/85-89
mm Hg) had a 95% increased risk of stroke, compared with a 44% increased
risk for those in the low range of prehypertension (120-129/80-84 mm
Hg). [41, 42]
The morbidity and mortality of hypertensive emergencies depend on the
extent of end-organ dysfunction on presentation and the degree to which BP
is controlled subsequently. With BP control and medication compliance, the
10-year survival rate of patients with hypertensive crises approaches 70%. [43]
In the Framingham Heart Study, the age-adjusted risk of congestive heart
failure was 2.3 times higher in men and 3 times higher in women when the
highest BP was compared to the lowest BP. [44] Multiple Risk Factor
Intervention Trial (MRFIT) data showed that the relative risk for coronary
artery disease mortality was 2.3 to 6.9 times higher for persons with mild to
severe hypertension than it was for persons with normal BP. [45] The relative
risk for stroke ranged from 3.6 to 19.2. The population-attributable risk
percentage for coronary artery disease varied from 2.3 to 25.6%, whereas the
population-attributable risk for stroke ranged from 6.8-40%.
The Framingham Heart Study found a 72% increase in the risk of all-cause
death and a 57% increase in the risk of any cardiovascular event in patients
with hypertension who were also diagnosed with diabetes mellitus. [46]
Nephrosclerosis is one of the possible complications of long-standing
hypertension. The risk of hypertension-induced end-stage renal disease is
higher in black patients, even when blood pressure is under good control.
Furthermore, patients with diabetic nephropathy who are hypertensive are
also at high risk for developing end-stage renal disease.
Comparative data from the NHANES I and III showed a decrease in mortality
over time in hypertensive adults, but the mortality gap between hypertensive
and normotensive adults remained high. [47]
Clinical trials have demonstrated the following benefits with antihypertensive
therapy [2] :
Average 35-40% reduction in stroke incidence
Average 20-25% reduction in myocardial infarction
Average >50% reduction in heart failure
Moreover, it is estimated that 1 death is prevented per 11 patients treated for
stage 1 hypertension and other cardiovascular risk factors when a sustained
reduction of 12 mm Hg in systolic BP over 10 years is achieved. [2] However,
for the same reduction is systolic BP reduction, it is estimated that 1 death is
prevented per 9 patients treated when cardiovascular disease or end-organ
damage is present. [2]
Patient Education
Hypertension is a lifelong disorder. For optimal control, a long-term
commitment to lifestyle modifications and pharmacologic therapy is required.
Therefore, repeated in-depth patient education and counseling not only
improve compliance with medical therapy but also reduce cardiovascular risk
factors.
Various strategies to decrease cardiovascular disease risk include the
following:
Prevention and treatment of obesity: an increase in body mass index
(BMI) and waist circumference is associated with an increased risk of
developing conditions with high cardiovascular risk, such as
hypertension, diabetes mellitus, impaired fasting glucose, and left
ventricular hypertrophy [LVH] [48]
Appropriate amounts of aerobic physical activity
Diets low in salt, total fat, and cholesterol
Adequate dietary intake of potassium, calcium, and magnesium
Limited alcohol consumption
Avoidance of cigarette smoking
Avoidance of the use of illicit drugs, such as cocaine
Clinicians may also wish to refer patients to the following short video, which
provides a simplified but clear and concise overview about what hypertension
is, as well as its different stages, causes, and types.
Practice Essentials
Type 2 diabetes mellitus consists of an array of dysfunctions characterized by
hyperglycemia and resulting from the combination of resistance to insulin
action, inadequate insulin secretion, and excessive or inappropriate glucagon
secretion. See the image below.
Background
According to the 2011 US Renal Data System (USRDS) data, in the year
2009, hypertensive nephrosclerosis (HN) accounted for 28% of patients
reaching end-stage renal disease (ESRD). The rate of ESRD attributed to
hypertension has grown 8.7% since the year 2000. [1] Hypertensive
nephrosclerosis is reportedly the second most common cause of ESRD in
white people (23%) and is the leading cause of ESRD in black people (46%).
The histologic effects of nephrosclerosis are demonstrated in the images
below.
Nephrosclerosis. The
glomerular tuft is shrunken, with wrinkling of the capillary walls (asterisk),
global glomerular sclerosis (arrow), and complete obliteration of the capillary
loops and glomerular ischemia (periodic acid-Schiff stain at 250X
magnification).
Nephrosclerosis. Glomerulus
with wrinkling of glomerular basement membranes accompanied by reduction
of capillary lumen diameter (silver stain at 400X magnification).
Nephrosclerosis. Fibrointimal
proliferation of the arcuate artery (periodic acid-Schiff stain at 150X
magnification).
The lack of firm criteria on which to base a histologic diagnosis and the lack of
a clear demonstration that hypertension initiates the development of renal
failure likely indicate that the true prevalence of hypertensive nephrosclerosis
has been overestimated. The paradoxical results of increasing incidence of
renal failure despite wider antihypertensive drug therapy and reduction in
hypertensive target events, such as stroke and cardiovascular disease, raises
questions about the causal role of hypertension in this disorder.
Unlike morbidity and mortality of stroke and coronary disease, incident cases
of ESRD attributed to hypertension continue to increase. Some authors
suggest that many of these cases are more likely related to other factors,
including small vessel injury related to aging, diabetes, or obesity -related
kidney injury.
A couple of important points have been made in different studies. First, among
an unselected sample of community-based participants in the Framingham
Heart Study, the combination of hypertension and a mild reduction in the
glomerular filtration rate (GFR) was found to be an important risk factor for the
development of new-onset kidney disease. Other factors noted were diabetes,
obesity, smoking, and a low high-density lipoprotein cholesterol level. Second,
systolic blood pressure (BP) is a strong, independent predictor of a decline in
kidney function among older persons with isolated systolic hypertension. This
is a significant finding because most cases of uncontrolled hypertension in the
United States are due to systolic hypertension among older adults.
Most patients reaching ESRD from any cause are hypertensive, with
nephrosclerosis being the classic finding in end-stage kidneys. Regardless of
the etiology, once hypertension develops, a cycle of renal injury,
nephrosclerosis, worsening of hypertension, and further renal injury is
established. As a result, in a patient presenting with ESRD, determining
whether nephrosclerosis is the cause or the consequence of chronic renal
injury may be difficult.
Pathophysiology
Furthermore, Tracy and Ishii (2000) postulate that nephrosclerosis may not be
a single disease entity in the sense of responding to a single etiology, such as
hypertension or aging. [4] Rather, nephrosclerosis appears to be multifactorial.
It may be, in part, a consequence of fibroplasias in microscopic arteries
causing ischemic damage to some nephrons; however, it also may be the end
product of a mixture of converging separate pathologic conditions, ie, "second
hits," of which only some are known.
Genetically mediated animal models of hypertension, including the Dahl rat
and the spontaneous hypertensive rat (SHR), have been used to investigate
the role of hypertension in the development of nephrosclerosis. Fundamental
differences exist among the strains and between rat and human hypertension.
The SHR most closely resembles human essential hypertension. The SHR
becomes hypertensive without exposure to salt. Micropuncture studies in
hypertensive rats demonstrate an increased preglomerular vasoconstriction
that is effective in preventing the development of intraglomerular
hypertension. In fact, the SHR develops little renal damage, unless
uninephrectomized. In these animals, rigorous BP control does not prevent
the development of proteinuria and the pathologic changes of hypertensive
nephrosclerosis. The Dahl salt-sensitive rat develops proteinuria before
hypertension and before a high-sodium diet is administered.
Genetics
A genetic link for hypertension and related renal failure is supported by studies
demonstrating familial clustering of hypertensive nephrosclerosis in black
people and, to some extent, in white people.
This genetic predisposition may be the reason why tighter control of BP in this
black population does not slow the progression of kidney disease. Some
authors argue that hypertension in this setting is secondary to underlying renal
injury. [13]
Epidemiology
Frequency
United States
International
Mortality/Morbidity
According to the 2011 USRDS, the annual mortality rate for patients on
hemodialysis in the United States is 23.3%. Hypertensive nephrosclerosis
accounts for more than one third of patients on hemodialysis.
Race
In persons of all age groups, ESRD is more common in black people; the rate
of developing ESRD is 3.5 times higher than the rate found among whites.
The increased susceptibility of black patients with hypertension to develop
progressive renal failure cannot be explained solely by the higher prevalence
of hypertension, severity of hypertension, or socioeconomic factors because
the rate of new ESRD cases has remained stable in African Americans,
whereas it has grown 7.2% among white, and, in addition, the rates of stroke
and cardiovascular mortality have decreased equally in both white and African
American populations.
Results from the MRFIT trial indicated that effective BP control was
associated with stable renal function in white people but not in black people.
In the AASK trial, which specifically evaluated black populations, intensive
control of BP in nonproteinuric patients did not decrease progression of kidney
disease.
Several renal, hormonal, physiologic, and genetic factors have been proposed
as explanations for the increased rate of hypertension and progression of
chronic kidney disease in African Americans. These include increased BP
sensitivity to high-salt diet, increased renal vascular resistance, decreased
renal blood flow, increased tortuosity and occlusion in the interlobular and
arcuate arteries based on renal angiograms in African Americans, and
decreased nephron mass secondary to low birth weight (more common in
African Americans). Lastly, the increased variant in APOL1 gene has been
proposed as the cause of the increased rate of ESRD in African Americans.
Age
Background
Patient education
Pathophysiology
Epidemiology
International occurrence
Data from Los Angeles and New York show that musculoskeletal tuberculosis
affects primarily African Americans, Hispanic Americans, Asian Americans,
and foreign-born individuals.
Although some series have found that Pott disease does not have a sexual
predilection, the disease is more common in males (male-to-female ratio of
1.5-2:1).
In the United States and other developed countries, Pott disease occurs
primarily in adults. In countries with higher rates of Pott disease, involvement
in young adults and older children predominates. [10, 11]
Prognosis
Current treatment modalities are highly effective against Pott disease if the
disorder is not complicated by severe deformity or established neurologic
deficit.
Deformity and motor deficit are the most serious consequences of Pott
disease and continue to be a serious problem when diagnosis is delayed or
presentation of the patient is in advanced stages of the disease. [12]
Morbidity
Pott disease most commonly involves the thoracic and lumbosacral spine.
However, published series have shown some variation. [14, 15, 16, 17] The lower
thoracic vertebrae make up the most common area of involvement (40-50%),
followed closely by the lumbar spine (35-45%). In other series, proportions are
similar but favor lumbar spine involvement. [18] Approximately 10% of Pott
disease cases involve the cervical spine.
During a surgical procedure to set a fracture, the bone fragments are first repositioned (reduced) into their normal
alignment. They are held together with special implants, such as plates, screws, nails and wires.
Internal fixation allows shorter hospital stays, enables patients to return to function earlier, and reduces the incidence
of nonunion (improper healing) and malunion (healing in improper position) of broken bones.
The implants used for internal fixation are made from stainless steel and titanium, which are durable and strong. If a
joint is to be replaced, rather than fixed, these implants can also be made of cobalt and chrome. Implants are
compatible with the body and rarely cause an allergic reaction.
Plates
Plates are like internal splints that hold the broken pieces of bone together. They are attached to the bone with
screws. Plates may be left in place after healing is complete, or they may be removed (in select cases).
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Screws
Screws are used for internal fixation more often than any other type of implant. Although the screw is a simple device,
there are different designs based on the type of fracture and how the screw will be used. Screws come in different
sizes for use with bones of different sizes. Screws can be used alone to hold a fracture, as well as with plates, rods,
or nails. After the bone heals, screws may be either left in place or removed.
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Nails or Rods
In some fractures of the long bones the best way to hold the bone pieces together is by inserting a rod or nail through
the hollow center of the bone that normally contains some marrow. Screws at each end of the rod are used to keep
the fracture from shortening or rotating, and also hold the rod in place until the fracture has healed. Rods and screws
may be left in the bone after healing is complete. This is the method used to treat the majority of fractures in the
femur (thighbone) and tibia (shinbone).
(Left) This x-ray shows a healed thighbone fracture treated with intramedullary nailing. (Right) In this x-ray, the thighbone
fracture has been treated with plates and screws.
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Wires/Pins
Wires are often used to pin the bones back together. They are often used to hold together pieces of bone that are too
small to be fixed with screws. In many cases, they are used in conjunction with other forms of internal fixation, but
they can be used alone to treat fractures of small bones, such as those found in the hand or foot. Wires are usually
removed after a certain amount of time, but may be left in permanently for some fractures.
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External Fixators
An external fixator acts as a stabilizing frame to hold the broken bones in proper position. In an external fixator, metal
pins or screws are placed into the bone through small incisions into the skin and muscle. The pins and screws are
attached to a bar outside the skin. Because pins are inserted into bone, external fixators differ from casts and splints
which rely solely on external support.
In many cases, external fixation is used as a temporary treatment for fractures. Because they are easily applied,
external fixators are often put on when a patient has multiple injuries and is not yet ready for a longer surgery to fix
the fracture. An external fixator provides good, temporary stability until the patient is healthy enough for the final
surgery.
Other times, an external fixator can be used as the device to stabilize the bone until healing is complete.
There may be some inflammation or, less commonly, infection associated with the use of external fixators. This is
typically managed with wound care and/or oral antibiotics.
External fixation is often used to hold the bones together temporarily when the skin and muscles have been injured.
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Other Considerations
Sterile conditions and advances in surgical techniques reduce, but do not remove, the risk of infection when internal
fixation is used. The severity of the fracture, its location, and the medical status of the patient must all be considered.
In addition, no technique is foolproof. The fracture may not heal properly or the plate or rod may break or deform.
Although some media attention has focused on the possibility that cancer could develop near a long-term implant,
there is little evidence documenting an actual cancer risk and much evidence against that possibility. Orthopaedic
surgeons are continuing their research to develop improved methods for treating fractures.
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External Fixation
External Fixation of Lower Leg
External fixationof the lower leg is a surgical procedure to externally immobilise and fix a
bone following a fracture allowing the bone to heal effectively. Physiotherapy after external
fixation surgery is essential to mobilise and return function in the lower leg.
The bones in the lower leg include the tibia (shin bone) and the fibula (smaller long bone). A
fracture of the lower leg can affect the shaft of one or both of the bones in the lower leg.
Fractures of the tibia / fibula are mainly caused by either a direct blow to the lower leg or by
a twisting force when the foot is fixed. There are many different types and severity of
fractures. The various severities of fractures to the lower leg include:
Closed fractures (where the skin is not broken by the fracture fragments)
Open fractures (where the fracture fragments have broken through the skin)
The skin and tissues that cover the front of the tibia and fibula are very thin and as a result
of this, a significant number of fractures to the lower leg are displaced, open fractures.
The main symptoms that follow a fracture to the lower leg include severe pain and reduced
mobility as the leg will be extremely painful and difficult to move. With fractures of the lower
leg there will be deformity at the site of the fracture, especially with open fractures. As a
result of the large amount of tissue damage and loss of blood at the fracture site, there will
also be a considerable amount of swelling and discolouration.
Treatment of lower leg fractures can vary depending on the severity of the fracture. If the
bone is still in its correct alignment (non-displaced) then immobilisation with use of a splint
or cast followed by physiotherapy is recommended. If the fracture is out of position
(displaced) but the skin is still intact (closed fracture) then ORIF of the lower leg (open
reduction internal fixation) is required.
In severe cases, external fixation surgery is necessary. External fixation surgery is a method
of holding together the fragments of a fractured bone by using transfixing metal pins through
the fragments and a compression device attached to the pins outside the skin surface. The
main indications for the use of external fixation surgery are in cases where there has been a
displaced, open fracture (the bone is out of position and has broken through the skin). Also
external fixation is indicated when there is high risk of infection, considerable bone loss at
the fracture site, and when other methods such as ORIF of the lower leg are inappropriate.
Common types of external fixation used in the treatment of a lower leg fracture include X-
Fix and Llizarov.
External fixation is a procedure that sets and immobilises the fractured bone in its correct
alignment so as to enable and facilitate adequate healing of the lower leg. The method
provides rigid fixation of the bones outside the body (external) in cases where other forms of
immobilizationare inappropriate. External fixation is performed in an operating room,
normally under general anaesthesia. During external fixation small holes are drilled into
uninjured areas of bones around the fracture and special bolts or wires are screwed into the
holes. Outside the body, a rod or a curved piece of metal with special ball-and-socket joints
joins the bolts to make a rigid support. The fracture can be set in the proper anatomical
configuration by adjusting the ball-and-socket joints. After the rods are fixed, regular
cleaning where the pins have been insertedmust be performed to prevent infection at the
site of surgery.In most cases it may be necessary for the external fixator to be in place for
many weeks or even months. Most fractures of the lower leg heal from between 6 and 12
weeks. After this time the external fixators are removed using specialised wrenches and can
be removed without any anaesthesia.
Once the external fixator has been removed, it is imperative to undergo a comprehensive
and prolonged course of physiotherapy to maximise the success of the procedure and to
help ensure the return of full or near to full function in the lower leg post fracture.
During the months you have external fixators inserted into your lower leg you will be given
elbow crutches to provide protection, support and independence. You will experience pain in
the area of insertion along with abnormal sensations. You will be given medication to control
for pain, reduce swelling and prevent infection. The pin sites can be a source of infection
therefore you will be shown by hospital staff how to carry out effective wound care and you
may have to return to the hospital for regular check ups during s period.
After you have had the external fixators removed, you will experience pain, swelling and
stiffness in and around the fracture site. You will have decreased range of movement,
strength and muscle control in your lower leg as a result of the surgery and prolonged
immobilisation. You will be non-weight bearing initially with progression to full weight bearing
being encouraged as soon as possible. A comprehensive physiotherapy programme with
Physio.co.uk should be initiated as soon as possible after the external fixators have been
removed to regain mobility as well as full or near to full function in your lower leg. You will
not be able to drive until you have full and painless function in your affected leg.
Physiotherapy after External Fixation of the Lower Leg
Physiotherapy can begin immediately after you have had external fixation of your lower leg
to help reduce pain, swelling and stiffness. It is encouraged to begin physiotherapy as soon
as possible as this will help you regain mobility and improve range of movement and
strength in your affected leg. Physio.co.uk offers a comprehensive physiotherapy course
that will maximise the success of the surgery, prevent any problems occurring and ensure
the return of full or near to full function in your lower leg. Rehabilitation can take up to 6
months after you have had ORIF surgery to your lower leg. The main goals of your
rehabilitation with Physio.co.uk include:
To re-establish independence
0-4 weeks
The main goals of your physiotherapy programme in the first month after undergoing
external fixation will be to reduce pain and swelling in your lower leg. Your physiotherapy
programme with Physio.co.uk will aim to gradually introduce you back to gentle activity.
Physio.co.uk will focus on maintaining the range of movement and strength in your affected
and unaffected leg. Additionally, your physiotherapy will include activities that aim to
progress your ability to weight bear as soon as possible. Your rehabilitation will include:
Crutch training
Passive (assisted) range of movement exercises for affected leg (knee, ankle etc)
5-8 weeks
During the second month of your rehabilitation with Physio.co.uk your physiotherapy will
focus on the continuation and progression of activities from previous weeks. Your
physiotherapy programme with Physio.co.uk will continue to focus on controlling pain and
swelling. Physio.co.uk will also continue to focus on improving range of movement nd
flexibility along with increasing muscle strength and control. Your physiotherapy will include:
Strengthening exercises for muscles of affected leg (calf, hamstring, quadriceps etc)
Stretching exercises for muscles of affected leg (calf, hamstring, quadricep etc)
Static bicycle
9-12 weeks
Pain control
Flexibility exercises
Strengthening exercises for muscles in affected and unaffected leg (calf, hamstring,
quadriceps, tibialis anterior etc)
Hydrotherapy
Static bicycle
3-6 months
Following three months of successful rehabilitation with Physio.co.uk you will have seen
marked improvements in the function of your lower leg and you will be experiencing minimal
if no pain and swelling. After 12 weeks, the external pins will have been surgically removed
and you will now be fully weight bearing. The main goals of your physiotherapy will continue
to focus on the progression of exercises from previous weeks. Your physiotherapy will
concentrate on activities that help improve the strength in the muscles of your lower leg by
consistently building up resistance in the strengthening exercises. You should have full
range of movement and your physiotherapy will aim to maintain and improve flexibility of
both your lower limbs. Your rehabilitation will continue with proprioception and gait training.
Cardiovascular activities such as hydrotherapy, cycling and gentle jogging can be included
in your programme. Functional activities that focus on specific tasks related to your lifestyle,
hobbies or job will also be included in your physiotherapy programme.
The success of your recovery after external fixation surgery will highly depend on you
commitment to your physiotherapy programme as well as the condition of your leg prior to
the surgery. Recovery will take up to 6 months.
Summary
External fixation of the lower leg is a surgical procedure that uses rods or plates to
immobilise and fix a bone following a fracture to allow the bone to heal in its correct
position. Fractures in the lower leg can occur along the shaft of the tibia (shin bone), along
the shaft of the fibula (smaller long bone) or both. Treatment of a fracture to lower leg can
vary depending on the severity of the injury. In severe cases where the bone is displaced
and the fracture fragments have broken the skin (open fracture) external fixation is the most
commonly utilised procedure. External fixation is required to enable correct alignment as
well as facilitating adequate healing of the lower leg. External fixation allows the return of
function as well as preventing future complications and deformation of the lower leg.
Physiotherapy with Physio.co.uk after external fixation is crucial to ensure the success of
the surgery, prevent the likelihood of any future problems and to help you achieve the return
of full or near to full function within your lower leg. Commitment to a personal physiotherapy
programme with Physio.co.uk will allow a more rapid return to everyday activities, work,
hobbies, and sport. Call Physio.co.uk now on 0330 088 7800 for more
information or to book an appointment please contact us.
Add:
External fixation is a useful tool in the management of fractures and certain difficult orthopedic
problems such as limb length discrepancy. External fixation a useful tool in fracture management and
in the case of pelvic fracture it may be a primary life saving device
With external fixation, pins and/or wires are percutaneously inserted into the bone and held in place
by an external frame.
External fixation is most successful in superficial bones like tibia than deeper bones like femur or
humerus here the chance of pin tract sepsis is greater.
External fixators consist of modular components which are assembled to form a stable construct
between bone fragments and an adjustable beam system. The beam system is joined to the bone by
means of a number of pins screwed into the bone.
Arthrodesis
o Maintains stability
o Eases dressing
Ligamentotaxis
Infected fractures
Burns
Provides rigid fixation when other forms of immobilization are not feasible. For example,
severe open fractures cannot be managed by plaster casts or internal fixation due to risk
involved.
Allows other treatments like dressing changes, skin grafting, bone grafting, and irrigation, is
possible without disturbing the fracture alignment or fixation.
Allows immediate motion of the proximal and distal joints This aids in reduction of edema and
nutrition of articular surfaces and retards capsular fibrosis, joint stiffening, muscle atrophy,
and osteoporosis.
External fixators cause less disruption of the soft tissues, osseus blood supply, and
periosteum. This makes externa fixation excellent choice in
o In chronic trauma where the extremity is covered in thin skin grafts and muscle flaps,
o Patients with poor skin healing
Ability to fix the bone avoid fixation at the site of fracture or lesion, and still obtained
the rigid fixation
Pins inserted in the bones are exposed to internal environment and risk of pin tract infection is
always there
Fracture may occur through pin tracts after frame removal. Extended protection may be
required.
Assembly of the fixator lies outside the limb, is cumbersome and needs meticulous care. High
degree of compliance and motivation is required
In fixators with pins near the joint or fixators that span joint, joint stiffness can occur.
In strictest sense there are two types of fixators unilateral and circular. A combination of two is
called hybrid fixators.
They are called so because they are generally are distinguished from circular frames in that they are
positioned on one side of the limb. Unilateral frames allow the limb to remain functional, avoid
complications, and provide bony stability
Monobody designs
The monobody frames have considerable intrinsic stability owing to their heavy and rigid design.
Pin-to-bar fixators.
These are kind of fixators use combination of schanz screws, rods and clamps which are assembled to
form a construct.
Circular Fixators
Ilizarov External Fixation Device in Tibia. Note the circular rings and thin wires
Image Credit: Wikipedia
These kind of external fixators use construct formed by circular rings, wires, connecting rods, and
struts. This is quite versatile type of external fixator. A partial ring is commonly used around
the proximal and around the shoulder and proximalfemur where a full ring would not fit comfortably.
Schanz Screws
Connecting rods
Clamps
Each of the components can come in different dimensions to suit the scale of the bone to which they
are to be applied and to permit variation in the shape and configuration of the final bone-external
fixator construct.
Schanz screws
Schanz screws are partially threaded pins. These are available in different diameters and lengths of
shaft and threaded part and with different tips.
Standard screws have trocar-shaped tips. They require predrilling. Self-drilling and self-cutting screws
are available.
Schanz screws are available in steel and titanium. Shanz pins with hydroxyapatite coating are aso
available. This makes bone purchase better and allows easier osseointegration, preventing loosening.
Pins with hydroxyapatite coating may be preferred for long-term application of external fixators, eg,
bone transport or deformity correction.
Rods/tubes
The AO fixators consist of systems in four sizes, depending on the size of the rod:
Mini: 2 mm system for fingers. Includes multipin clamps for K-wires and 2 mm longitudinal
rods.
Currently the 4.7mm short threaded Schanz screw is used in cortical bone and the 5.0mm long
threaded screw in cancellous bone. For hand and wrist application smaller sizes are used.
Connecting rods are made of stainless steel of carbon fibre. The latter are very strong and are also
radiolucent which is helpful when assessing bone alignment on x-ray.
Clamps
The clamps provide the connection between the tubes or rods and the pins. Likewise, rods or tubes
can be connected to each other using the appropriate clamps (tube-to-tube). If one clamp allows the
connection of both tubes and rods, they are called combination clamps.
Clamps are available in three sizes with identical clamp design and application technique.
A larger tube to tube clamp permits two fracture components to be held together in relatively stable
alignment irrespective of the position the Schanz pins take up in the bone.
The bending stiffness of unilateral fixators is dependent on the plane of the half pins and the plane of
loading with anteriorly mounted frames providing greater bending stiffness. When these frames were
loaded out of plane, with varusvalgus and torsional forces, they had poor control of the bone
fragments with significant motion at the fracture site.
Farther the last Schanz screw placed on the fragment on each side of fracture, stiffer the
construct
Closer the he longitudinal connecting tube/bar to the bone. Stiffer the construct
Circular Fixator
Ilizarov fixator is a typical circular fixator. Circular fixators consist of series of rings or arches which are
connected to each other by connecting rods and rings are fixed to the bones by means of tensioned
wires.
Many modifications can be added and accordingly the implant used in particular fracture is used
according to the indication for use and goals of the surgery.
Ilizarov fixtor is very versatile fixator and most people know it because it is used for lengthening the
bones.
In circular external fixators, frame stability is greatly impacted by ring properties. Smaller diameter
rings are more stable than larger rings of the same thickness but a ring should not put pressure on
the tissues and the final size is dictated by limb girth.
Different diameter rings may be used in the same frame to adjust to contours of the limb. Centralizing
the bone is preferred but eccentric positioning has been found to have no adverse effect.
Increasing the span of the rings across the bone controlling both near and far ends of each
segment
3. Drilling a pilot hole to remove bone debris and to reduce frictional resistance and so heat
production during pin insertion.
4. Achieving a firm pin fit with radial distribution of forces the pin is 0.2mm larger than the
pilot hole and this induces compression on the bone termed radial pre-load.
Complications may arise in the fixator itself or most commonly at the bone pin interface. As with any
fracture especially in severe injury complications may occur at the fracture as a direct result of the
injury.
This this may be the most common complication, occurring in about 30% of patients. The infection
varies from minor skin inflammation to osteomyelitis requiring sequestrectomy.
Neurovascular Injury
The radial nerve in the distal half of the arm and proximal half of the forearm, thedorsal sensory radial
nerve just above the wrist, and the anterior tibial artery and deep peroneal nerve at the junction of
the third and fourth quarters of the leg are the structures most often involved.
The pins are known to penetrate vessels, cause thrombosis when they are adjoining the vessel, cause
late erosion of the vessel, arteriovenous fistulas, and the formation of aneurysms.
Pins inserted through tendons may restrain normal excursion and can lead to tendon rupture, or
muscle fibrosis
Fracture Complications
Non union and delayed union can be seen with any mode of fixation and can occur with external
fixator also.
Refracture can occur after fixator removal and the fracture needs protection for extended period after
fixator is removed.
Kirschner wires
Intramedullary nails
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Open Reduction Internal Fixation (ORIF) involves the implementation of implants to guide the
healing process of a bone, as well as the open reduction, or setting, of the
bone. Open reduction refers to open surgery to set bones, as is necessary for
some fractures. Internal fixation refers to fixation of screws and/or plates, intramedullary bone nails
(femur, tibia, humerus) to enable or facilitate healing. Rigid fixation prevents micro-motion across
lines of fracture to enable healing and prevent infection, which happens when implants such as
plates (e.g. dynamic compression plate) are used. Open Reduction Internal Fixation techniques
often are used in cases involving serious fractures such as comminuted or displaced fractures or, in
cases where the bone otherwise would not heal correctly with casting or splinting alone.
Risks and complications may include bacterial colonization of the bone, infection, stiffness and loss
of range of motion, non-union, mal-union, damage to the muscles, nerve damage and
palsy, arthritis, tendonitis, chronic pain associated with plates, screws, and pins, compartment
syndrome, deformity, audible popping and snapping, and possible future surgeries to remove the
hardware.
Closed Reduction Internal Fixation (CRIF) is reduction without any open surgery, followed by
internal fixation. It appears to be an acceptable alternative in unstable distressed or hyperfalotated
[need reference, no results on the web for "falotated"] lateral condylar fractures of the humerus in
children, but if fracture displacement after closed reduction exceeds 2 mm, open reduction and
internal fixation is recommended.[3] Various techniques of minimally invasive surgery for internal
fixation of bones have been reported. The treatment of fractures of the distal third of the tibia has
evolved with the development of improved imaging and surgical techniques. [4]
Background
Rabies is a viral disease that affects the central nervous system (CNS). The
genusLyssavirus contains more than 80 viruses. Classic rabies, the focus of
this article, is the prototypical human Lyssavirus pathogen. (See Etiology.)
There are 10 viruses in the rabies serogroup, most of which only rarely cause
human disease. The genus Lyssavirus, rabies serogroup, includes the classic
rabies virus, Mokola virus, Duvenhage virus, Obodhiang virus, Kotonkan virus,
Rochambeau virus, European bat Lyssavirus types 1 and 2, and Australian
batLyssavirus. (See Etiology.) Five antigenic variants of rabies strains are
recognized in the United States (see the image below).
Distribution of the 5 strains of
rabies virus and the associated wildlife in the United States.
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The rabies virus is a bullet-shaped virion with a single-stranded ribonucleic
acid (RNA) nucleocapsid core and lipoprotein envelope. Its nucleocapsid
material consists of Negri bodies, which are observed in the cytoplasm of
infected neurons (see the image below). The virus is transmitted in saliva or in
aerosolized secretions from infected animals, typically via a bite. The virus is
not hardy and is quickly inactivated by drying, ultraviolet rays, x-rays, trypsin,
detergents, and ether. (See Etiology.)
Hematoxylin and eosin stain
of Negri body in a rabies-infected neuron. Courtesy of the US Centers for
Disease Control and Prevention.
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The fatal madness of rabies has been described throughout recorded history,
and its association with rabid canines is well known. For centuries, dog bites
were treated prophylactically with cautery, with predictable and unfortunate
results. In the 19th century, Pasteur developed a vaccine that successfully
prevented rabies after inoculation and launched a new era of hope in the
management of this uniformly fatal disease. (See Treatment and Medications.)
Etiology
Rabies is a highly neurotropic virus that evades immune surveillance by its
sequestration in the nervous system. Upon inoculation, it enters the peripheral
nerves. A prolonged incubation follows, the length of which depends on the
size of the inoculum and its proximity to the CNS. Amplification occurs until
bare nucleocapsids spill into the myoneural junction and enter motor and
sensory axons. At this point, prophylactic therapy becomes futile, and rabies
can be expected to follow its fatal course, with a mortality rate of 100%.
The rabies virus travels along these axons at a rate of 12-24 mm/d to enter
the spinal ganglion. Its multiplication in the ganglion is heralded by the onset
of pain or paresthesia at the site of the inoculum, which is the first clinical
symptom and a hallmark finding. From here, the rabies virus spreads quickly,
at a rate of 200-400 mm/d, into the CNS, and spread is marked by rapidly
progressive encephalitis. Thereafter, the virus spreads to the periphery and
salivary glands.
From the standpoint of diagnosis and therapeutic opportunities, it is important
to understand that rabies does not cause cytotoxicity. Neuronal morphology
and lifespan is normal throughout the course of the disease. Death occurs
from global neurologic and organ dysfunction. The virion acts in the synaptic
space, where homology in amino acid sequences between neurotransmitter
receptors for acetylcholine, GABA, and glycine may afford a mechanism for
viral binding of these receptors. Thus, its action is neurotoxic, rather than
direct damage.
Further, as disease progresses, virus may no longer be viable or replicating in
tissue, although Negri bodies are present. If the virus could be contained or
the binding action reversed, a cure might indeed be possible.
Epidemiology
United States
Rabies is recognized as global zoonosis yet remains remarkably neglected,
despite unmatched lethality. It remains a threat underappreciated by
healthcare practitioners in many endemic areas, often owing to lack of rapid
diagnostic tools, postmortem evaluation, and public health reporting. Further,
few resources have been devoted to its mechanisms of disease and potential
therapeutic targets; the therapeutic approach remains a crude guess at best,
based on anecdotal experiences shared across the globe. Most attention has
focused on preventive strategies, which are fortunately highly effective where
implemented.
The prevalence of rabies varies by location depending on animal-control
effectiveness and immunization programs. The largest number of human
deaths annually was recorded during the first half of the 20th century, with an
average of 50 documented cases per year. Most were related to rabid-dog
exposure. After 1940, when canine rabies vaccination programs began, the
average number of documented cases declined to 2 per year. From 2001-
2005, 15 cases of human rabies were reported in the United States.
Human rabies reflects the prevalence of animal infection and the extent of
contact this population has with humans. Less than 5% of cases in developed
nations occur in domesticated dogs; however, unvaccinated dogs serve as the
main reservoir worldwide. Undomesticated canines, such as coyotes, wolves,
jackals, and foxes, are most prone to rabies and serve as reservoirs. These
reservoirs allow rabies to remain an indefinite public health concern, and
ongoing public health measures are critical to its control.Animal-control and
vaccination strategies currently supersede postexposure prophylaxis in
preventing the spread of rabies. Through such programs, rabies has been
eliminated in some parts of the United States, as well as several nations.
Terrestrial rabies in the United States is most common in raccoons on the
eastern coast and in skunks, foxes, coyotes, and dogs on the Texas-Mexico
border. Canine rabies, and to a lesser extent, bat rabies are significant
problems in Mexico and around the world. (Opossums are rarely infected and
are not considered a likely risk for exposure.)
The only rodent in the United States that can carry rabies long enough to
transmit it to humans is the groundhog. Other small rodents (eg, squirrels,
chipmunks, rats, mice) and lagomorphs (eg, rabbits, hares) usually die before
being able to transmit rabies virus to humans, and human disease has not
been documented from these mammals.
Domestic animals usually succumb to the virus strain predominant in their
geographic region. Other cases have been associated with dog or animal
bites in travelers returning from abroad, especially in countries where wild
canine rabies is endemic. In other countries, canines are the most common
source of rabies. Other animals, such as mongooses, jackals, ferrets, and
domestic farm animals, may be common sources. Human-to-human
transmission has only occurred with corneal and other organ
transplants. [1, 2] Transmission of virus in saliva through mucous membranes,
open wounds, or scratches is possible but rarely documented.
Rabies continues to adapt to new hosts and evolve transmissibility in
previously dead-end hosts. In Arizona 2001, a mutated bat strain was
confirmed to have developed both pathogenicity and transmissibility in both
foxes and skunks, which previously were not seriously affected or contagious
upon infection. Human encroachments into natural areas, as in suburban
development, have been associated with the spread of rabies strains in the
past. [3]
In addition, changes in epidemiology are expected to follow global climate
change and are most likely to be detected in areas of climate extremes. This
is being illustrated in Alaska, as increased viral transmission shifts from red
fox to arctic fox populations following warming trends. Increased surveillance
is needed to improve predictive models of epidemiology and human risk. [4]
Bats
Bat (avian) rabies appears to be widespread in the 49 continental states, and
since 1980, most endemic rabies cases in humans in the United States have
been associated with bat strains. [5]
Bat bites, if noticed by the patient, are generally thought to be trivial injuries
because of the small size of most temperate-zone species (eg, silver-haired
bats, eastern pipistrelles). In addition, bat bites can go completely
unrecognized by the patient; consequently, appropriate postexposure
prophylaxis is not administered.
One third of rabies cases occur in children, and most have no known
exposure to a rabid animal. Because children may not be able to recall
contact with a bat, if a bat is found in a room where a child has been sleeping,
the bat should be captured and submitted for examination to the county or
state health authorities. In 60% of cases, testing of the bat can avoid the need
for rabies immunization. [6]
At least 30 of the more than 39 species of bats in the United States have been
reported as rabid at some time.
Raccoons
Raccoons have been recognized a reservoir for rabies in the southeastern
United States since the 1950s. [7] Currently, the risk of raccoon transmission
exists in all of the eastern coastal states and Alabama, Pennsylvania,
Vermont, West Virginia, and Ohio.
Skunks
Three areas are associated with skunk-borne rabies: the north-central United
States, the south-central United States, and California. As recently as 2001, a
new skunk-borne variant arose from a bat strain and has since been quickly
spreading.
Dogs and cats
Cats are the most common domestic animals reported by US health
departments as being rabid, owing to the high number of unvaccinated strays
with possible contacts with bats and other mammals. [8, 9]
Dogs and cats along the Mexican border
Limited resources and minimal public health infrastructure in the bordering
communities have hindered efforts to maintain animal control through dog-
vaccination programs. Viral studies of human cases reported from US border
states implicate an urban canine rabies strain and a link to coyote rabies in
southern Texas. [10]
Lower-risk animal species in the United States
Any mammal is potentially at risk for rabies, some more than others. Lower-
risk animal species in the United States include dogs, cats, and ferrets in
areas not near a border. No person in the United States has ever contracted
rabies from a dog, cat, or ferret held in quarantine for 10 days. American
opossums are especially at low risk, because the species low body
temperature hinders replication.
Animal rabies vaccine
The vaccinia-rabies glycoprotein virus used in rabies vaccineladen baits for
wild animals is a self-replicating agent. This oral animal vaccine may cause
adverse effects in some humans exposed to it through animal bits, particularly
in hosts with altered immunocompetence and persons in whom smallpox
vaccination is contraindicated (eg, pregnant women, patients with an
exfoliative skin condition). [11]
Transplantation patients
The innate state of immunosuppression in this population often provides a
favorable environment for viral replication. Recipients of neurally derived
tissues are at highest risk; however, any tissue poses a risk. In 2004, kidneys
and liver were inadvertently transplanted from a donor from Texas with rabies
that had gone undiagnosed; the recipients developed clinical rabies within 30
days, resulting in 100% mortality. [12]
International
Rabies is more prevalent in the developing world than in industrialized
countries. The World Health Organization (WHO) estimates that rabies is
responsible for 35,000-50,000 deaths annually worldwide and that gross
underreporting is likely. An estimated 10 million people receive postexposure
prophylaxis each year after being exposed to animals with suspected rabies.
Unvaccinated dogs are the major reservoir for rabies.
Global reservoirs of rabies virus are as follows [13, 14] :
Europe - Foxes, bats
Middle East - Wolves, dogs
Asia - Dogs
Africa - Dogs, mongooses, antelopes
North America - Foxes, skunks, raccoons, insectivorous bats
South America - Dogs, vampire bats
Sex-related demographics
Encounters with rabid animal vectors may be increased in males, who may
have greater contact in certain geographic areas. Evidence to support this is
found in data on dog bites, which are observed more frequently in males than
in females.