Fat Embolism: Diagnosis and Treatment

Transcription

1 of 5
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Kirsten Odegard, MD
Department of Anesthesiology
New York University Medical Center
Introduction
Fat embolism syndrome follows long bone fractures. Its classic presentation consists of an
asymptomatic interval followed by pulmonary and neurologic manifestations combined with
petechial hemorrhages. The syndrome follows a biphasic clinical course. The initial
symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat
globules that are too large to pass through the capillaries. Unlike other embolic events, the
vascular occlusion in fat embolism is often temporary or incomplete since fat globules do
not completely obstruct capillary blood flow because of their fluidity and deformability. The
late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty
acids which then migrate to other organs via the systemic circulation.
Etiology
Many aspects of the fat embolism syndrome remain poorly understood, and disagreement
about its etiology, pathophysiology, diagnosis and treatment persists. It is therefore difficult
to determine the incidence of this complication. It ranges from less than 2% to 22% in
different studies. Fat embolism has been associated with many nontraumatic disorders. It
is most common after skeletal injury, and is most likely to occur in patients with multiple
long bone and pelvic fractures. Patients with fractures involving the middle and proximal
parts of the femoral shaft are more likely to experience fat embolism. Age also seems to be
a factor in the development of FES: young men with fractures are at increased risk.
Fat embolism and FES are also more likely to occur after closed, rather than open,
fractures. Two events promote entrance of marrow contents into the circulation following a
fracture: movement of unstable bone fragments and reaming of the medullary cavity during
placement of an internal fixation device. Both of these cause distortion of and increased
pressure within the medullary cavity, permitting entry of marrow fat into torn venous
channels that remain open even in shock because they are attached to the surrounding
bone.
Multiple fractures release a greater amount of fat into the marrow vessels than do single
fractures, increasing the liklihood of FES.
Pathophysiology
There are two theories which have gained acceptance:
1
The mechanical theory: FES results from physical obstruction of the pulmonary and
systemic vasculature with embolized fat. Increased intramedullary pressure after injury
forces marrow into injured venous sinusoids, from which the fat travels to the lung and
occludes pulmonary capillaries. Fat emboli can cause cor pulmonale if adequate
compensatory pulmonary vasodilation does not occur.
1
The biochemical theory: Circulating free fatty acids are directly toxic to pneumocytes
and capillary endothelium in the lung, causing interstitial hemorrhage, edema and chemical
pneumonitis.
It is also possible that coexisting shock, hypovolemia and sepsis, all of which reduce liver
flow, facilitate the development of FES by exacerbating the toxic effects of free fatty acids.
Clinical Presentation
A thorough knowledge of the signs and symptoms of the syndrome and a high index of
suspicion are needed if the diagnosis is to be made.
An asymptomatic latent period of about 12-48 hours precedes the clinical manifestations.
The fulminant form presents as acute cor pulmonale, respiratory failure, and/or embolic
phenomena leading to death within a few hours of injury.
Clinical fat embolism syndrome presents with tachycardia, tachypnea, elevated
temperature, hypoxemia, hypocapnia, thrombocytopenia, and occasionally mild
neurological symptoms.
A petechial rash that appears on the upper anterior portion of the body, including the chest,
08/10/2007 11:03
2 of 5
neck, upper arm, axilla, shoulder, oral mucous membranes and conjunctivae is considered
to be a pathognomonic sign of FES, however, it appears late and often disappears within
hours. It results from occlusion of dermal capillaries by fat, and increased capillary fragility.
CNS signs, including a change in level of consciousness, are not uncommon. They are
usually nonspecific and have the features of diffuse encephalopathy: acute confusion,
stupor, coma, rigidity, or convulsions. Cerebral edema contributes to the neurologic
deterioration. Hypoxemia is present in nearly all patients with FES, often to a Pa02 of well
below 60 mmHg. Arterial hypoxemia in these patients has been attributed to
ventilation-perfusion inequality and intrapulmonary shunting. Acute cor pulmonale is
manifested by respiratory distress, hypoxemia, hypotension and elevated central venous
pressure.
The chest X-ray may show evenly distributed, fleck-like pulmonary shadows (Snow Storm
appearance), increased pulmonary markings and dilatation of the right side of the heart.
Laboratory Tests
Laboratory tests are mostly nonspecific:
2
Serum lipase level increases in bone trauma - often misleading.
3
Cytologic examination of urine, blood and sputum with Sudan or oil red O staining
may detect fat globules that are either free or in macrophages. This test is not sensitive,
however, and does not rule out fat embolism.
4
Blood lipid level is not helpful for diagnosis because circulating fat levels do not
correlate with the severity of the syndrome.
5
Decreased hematocrit occurs within 24-48 hours and is attributed to intra-alveolar
hemorrhage.
6
Alteration in coagulation and thrombocytopenia.
In summary, the diagnosis of FES may be difficult because, except for the petechiae, there
are are no pathognomonic signs.
Treatment
The most effective prophylactic measure is to reduce long bone fractures as soon as
possible after the injury.
Maintenance of intravascular volume is important because shock can exacerbate the lung
injury caused by FES. Albumin has been recommended for volume resuscitation in addition
to balanced electrolyte solution, because it not only restores blood volume but also binds
fatty acids, and may decrease the extent of lung injury.
Mechanical ventilation and PEEP may be required to maintain arterial oxygenation.
High dose corticosteroids have been effective in preventing development of FES in several
trials, but controversy on this issue still persists.
Conclusion
A high index of suspicion is needed to make the diagnosis of the often fatal fat embolism
syndrome.
References
Capan LM, Miller SM, Patel KP: Anesth Clin N Amer, 11:1 (Mar), 1993.
Gossling HR, Ellison LH, Degraff AC: Fat embolism: The role of respiratory failure and its
treatment. J Bone Joint Surg 56A: 1327, 1974.
Gossling HR, Pellegrini VD: Fat embolism syndrome: A review of the pathophysiology and
physiologic basis of treatment. Clin Orthop 165:68, 1982
Peltier LF: The diagnosis and treatment of fat embolism. J Trauma 11:661, 1971.
Weisz GM, Steiner E: The cause of death in fat embolism. Chest 59:511, 1971.
Fat Embolism Syndrome: Orthopaedic Review. 22:567-71, 1993 May.
"Pulmonary Embolism" in Stoelting RK, Dierdorf SF: Anesthesia and Co-Existing Disease,
Third Edition. New York. Churchill Livingstone. pp192 - 193.
08/10/2007 11:03
3 of 5
Gurd's Criteria for Diagnosis of FES
- Discussion:
- Dx of FES requires at least one sign from major criteria and at least
four signs from the minor criteria category;
- Gurd's Major Criteria:
- axillary or subconjuctival petechia
- occurs transiently (4-6 hours) in 50-60 % of the cases;
- hypoxemia (PaO sub 2, <60 mmHg; FiO sub 2, <= 0.4)
- central nervous system (CNS) depression disproportionate
to hypoxemia, and pulmonary edema;
- Gurd's Minor Criteria:
- tachycardia (more than 110 beats per minute)
- pyrexia (temperature higher than 38.5 degrees)
- emboli present in retina on funduscopic examination
- fat present in urine
- sudden unexplainable drop in hematocrit or platelet values
- increasing sed rate;
- fat globules present in sputum;
- Misc:
- occurs w/in 72 hours of skeletal trauma;
- shortness of breath;
- altered mental status;
- occasional long tract signs and posturing;
- urinary incontinence;
Fat Embolism Syndrome:
- Discussion:
- FES results when embolic marrow fat macroglobules damage small vessel
perfusion leading to endothelial damage in pulmonary capillary beds
leading to respiratory failure and ARDS like picture;
- risk factors for FES:
- long bone frx (esp femoral shaft);
- risk is higher w/ non-operative therapy but is also higher w/ over-zealous
reaming of femoral canal;
- multiple trauma w/ major visceral injuries and blood loss;
- incidence may be as high as 5-10%;
- controversies: Is the method of frx fixation relevant?
- as noted by EH Schemitsch et al in an experimental animal study, the amount of
of embolized fat measured at 24 hours after pressurization of the IM canal
was not affected by the method fixation;
08/10/2007 11:03
4 of 5
- frx fixation was not associated w/ evidence of acute accumulation, nor did it
have any effect on pulmonary artery pressure;
- concluded that pulmonary dysfunction from fat emboli depends on addtional
factors,
and the method of frx fixation was not a significant factor;
- Labs:
- hypoxia on ABG;
- fallen hemoglobin (3-5 g)
- early thrombocytopenia;
- fat demonstrated in blood clots
- CXR:
- nonspecific serial chest roentgenograms;
- Prevention:
- immediate frx fixation may lower incidence of FES (ref)
- consider prophylactic steroids for prevention of FES in patients w/ isolated long bone
trauma;
- references:
- Fat embolism prophylaxis with corticosteroids. A prospective study in
high-risk patients.
- Low-dose corticosteroid prophylaxis against fat embolism.
- Fat embolism and the fat embolism syndrome. A double-blind therapeutic
study.
- The use of methylprednisolone and hypertonic glucose in the prophylaxis of
fat embolism syndrome.
- pulse ox monitoring for subclinical hypoxemia may also be beneficial;
- Treatment:
- once FES occurs, it is mandatory that perfusion be maintained, especially in older
patients;
- all to often in this disorder, the orthopaedists defers the care of these patients
to the anesthesiologists who in many cases take a "crisis intervention stratedgy"
- this is guaranteed to fail in older patients;
- to adequately treat FES patients, the orthopaedist must take a "pro-active"
intervention
statedgy to ensure that perfusion is maintained as soon as FES is diagnosed;
- specific requirements include:
- SG monitoring (w/ continuous mixed VO2 monitoring);
- arterial line for monitorying blood pressure and ABG;
- metabolic acidosis or suboptimal mixed VO2 indicates sub-optimal perfusion;
- maintenance of perfusion by optimizing:
- cardiac output
- influenced by preload, afterload, and thru use of inotropic agents;
- hematocrit: must be aggressively be kept above 30% w/ pRBC;
08/10/2007 11:03
5 of 5
- most pts will require mechanical ventilation as they enter respiratory failure;
[ Close Window ]
08/10/2007 11:03
1 of 5
Kirsten Odegard, MD
Department of Anesthesiology
New York University Medical Center
Introduction
Fat embolism syndrome follows long bone fractures. Its classic presentation consists of an
asymptomatic interval followed by pulmonary and neurologic manifestations combined with
petechial hemorrhages. The syndrome follows a biphasic clinical course. The initial
symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat
globules that are too large to pass through the capillaries. Unlike other embolic events, the
vascular occlusion in fat embolism is often temporary or incomplete since fat globules do
not completely obstruct capillary blood flow because of their fluidity and deformability. The
late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty
acids which then migrate to other organs via the systemic circulation.
Etiology
Many aspects of the fat embolism syndrome remain poorly understood, and disagreement
about its etiology, pathophysiology, diagnosis and treatment persists. It is therefore difficult
to determine the incidence of this complication. It ranges from less than 2% to 22% in
different studies. Fat embolism has been associated with many nontraumatic disorders. It
is most common after skeletal injury, and is most likely to occur in patients with multiple
long bone and pelvic fractures. Patients with fractures involving the middle and proximal
parts of the femoral shaft are more likely to experience fat embolism. Age also seems to be
a factor in the development of FES: young men with fractures are at increased risk.
Fat embolism and FES are also more likely to occur after closed, rather than open,
fractures. Two events promote entrance of marrow contents into the circulation following a
fracture: movement of unstable bone fragments and reaming of the medullary cavity during
placement of an internal fixation device. Both of these cause distortion of and increased
pressure within the medullary cavity, permitting entry of marrow fat into torn venous
channels that remain open even in shock because they are attached to the surrounding
bone.
Multiple fractures release a greater amount of fat into the marrow vessels than do single
fractures, increasing the liklihood of FES.
Pathophysiology
There are two theories which have gained acceptance:
1
The mechanical theory: FES results from physical obstruction of the pulmonary and
systemic vasculature with embolized fat. Increased intramedullary pressure after injury
forces marrow into injured venous sinusoids, from which the fat travels to the lung and
occludes pulmonary capillaries. Fat emboli can cause cor pulmonale if adequate
compensatory pulmonary vasodilation does not occur.
1
The biochemical theory: Circulating free fatty acids are directly toxic to pneumocytes
and capillary endothelium in the lung, causing interstitial hemorrhage, edema and chemical
pneumonitis.
It is also possible that coexisting shock, hypovolemia and sepsis, all of which reduce liver
flow, facilitate the development of FES by exacerbating the toxic effects of free fatty acids.
Clinical Presentation
A thorough knowledge of the signs and symptoms of the syndrome and a high index of
suspicion are needed if the diagnosis is to be made.
An asymptomatic latent period of about 12-48 hours precedes the clinical manifestations.
The fulminant form presents as acute cor pulmonale, respiratory failure, and/or embolic
phenomena leading to death within a few hours of injury.
Clinical fat embolism syndrome presents with tachycardia, tachypnea, elevated
temperature, hypoxemia, hypocapnia, thrombocytopenia, and occasionally mild
neurological symptoms.
A petechial rash that appears on the upper anterior portion of the body, including the chest,
08/10/2007 11:04
2 of 5
neck, upper arm, axilla, shoulder, oral mucous membranes and conjunctivae is considered
to be a pathognomonic sign of FES, however, it appears late and often disappears within
hours. It results from occlusion of dermal capillaries by fat, and increased capillary fragility.
CNS signs, including a change in level of consciousness, are not uncommon. They are
usually nonspecific and have the features of diffuse encephalopathy: acute confusion,
stupor, coma, rigidity, or convulsions. Cerebral edema contributes to the neurologic
deterioration. Hypoxemia is present in nearly all patients with FES, often to a Pa02 of well
below 60 mmHg. Arterial hypoxemia in these patients has been attributed to
ventilation-perfusion inequality and intrapulmonary shunting. Acute cor pulmonale is
manifested by respiratory distress, hypoxemia, hypotension and elevated central venous
pressure.
The chest X-ray may show evenly distributed, fleck-like pulmonary shadows (Snow Storm
appearance), increased pulmonary markings and dilatation of the right side of the heart.
Laboratory Tests
Laboratory tests are mostly nonspecific:
2
Serum lipase level increases in bone trauma - often misleading.
3
Cytologic examination of urine, blood and sputum with Sudan or oil red O staining
may detect fat globules that are either free or in macrophages. This test is not sensitive,
however, and does not rule out fat embolism.
4
Blood lipid level is not helpful for diagnosis because circulating fat levels do not
correlate with the severity of the syndrome.
5
Decreased hematocrit occurs within 24-48 hours and is attributed to intra-alveolar
hemorrhage.
6
Alteration in coagulation and thrombocytopenia.
In summary, the diagnosis of FES may be difficult because, except for the petechiae, there
are are no pathognomonic signs.
Treatment
The most effective prophylactic measure is to reduce long bone fractures as soon as
possible after the injury.
Maintenance of intravascular volume is important because shock can exacerbate the lung
injury caused by FES. Albumin has been recommended for volume resuscitation in addition
to balanced electrolyte solution, because it not only restores blood volume but also binds
fatty acids, and may decrease the extent of lung injury.
Mechanical ventilation and PEEP may be required to maintain arterial oxygenation.
High dose corticosteroids have been effective in preventing development of FES in several
trials, but controversy on this issue still persists.
Conclusion
A high index of suspicion is needed to make the diagnosis of the often fatal fat embolism
syndrome.
References
Capan LM, Miller SM, Patel KP: Anesth Clin N Amer, 11:1 (Mar), 1993.
Gossling HR, Ellison LH, Degraff AC: Fat embolism: The role of respiratory failure and its
treatment. J Bone Joint Surg 56A: 1327, 1974.
Gossling HR, Pellegrini VD: Fat embolism syndrome: A review of the pathophysiology and
physiologic basis of treatment. Clin Orthop 165:68, 1982
Peltier LF: The diagnosis and treatment of fat embolism. J Trauma 11:661, 1971.
Weisz GM, Steiner E: The cause of death in fat embolism. Chest 59:511, 1971.
Fat Embolism Syndrome: Orthopaedic Review. 22:567-71, 1993 May.
"Pulmonary Embolism" in Stoelting RK, Dierdorf SF: Anesthesia and Co-Existing Disease,
Third Edition. New York. Churchill Livingstone. pp192 - 193.
08/10/2007 11:04
3 of 5
Gurd's Criteria for Diagnosis of FES
- Discussion:
- Dx of FES requires at least one sign from major criteria and at least
four signs from the minor criteria category;
- Gurd's Major Criteria:
- axillary or subconjuctival petechia
- occurs transiently (4-6 hours) in 50-60 % of the cases;
- hypoxemia (PaO sub 2, <60 mmHg; FiO sub 2, <= 0.4)
- central nervous system (CNS) depression disproportionate
to hypoxemia, and pulmonary edema;
- Gurd's Minor Criteria:
- tachycardia (more than 110 beats per minute)
- pyrexia (temperature higher than 38.5 degrees)
- emboli present in retina on funduscopic examination
- fat present in urine
- sudden unexplainable drop in hematocrit or platelet values
- increasing sed rate;
- fat globules present in sputum;
- Misc:
- occurs w/in 72 hours of skeletal trauma;
- shortness of breath;
- altered mental status;
- occasional long tract signs and posturing;
- urinary incontinence;
Fat Embolism Syndrome:
- Discussion:
- FES results when embolic marrow fat macroglobules damage small vessel
perfusion leading to endothelial damage in pulmonary capillary beds
leading to respiratory failure and ARDS like picture;
- risk factors for FES:
- long bone frx (esp femoral shaft);
- risk is higher w/ non-operative therapy but is also higher w/ over-zealous
reaming of femoral canal;
- multiple trauma w/ major visceral injuries and blood loss;
- incidence may be as high as 5-10%;
- controversies: Is the method of frx fixation relevant?
- as noted by EH Schemitsch et al in an experimental animal study, the amount of
of embolized fat measured at 24 hours after pressurization of the IM canal
was not affected by the method fixation;
08/10/2007 11:04
4 of 5
- frx fixation was not associated w/ evidence of acute accumulation, nor did it
have any effect on pulmonary artery pressure;
- concluded that pulmonary dysfunction from fat emboli depends on addtional
factors,
and the method of frx fixation was not a significant factor;
- Labs:
- hypoxia on ABG;
- fallen hemoglobin (3-5 g)
- early thrombocytopenia;
- fat demonstrated in blood clots
- CXR:
- nonspecific serial chest roentgenograms;
- Prevention:
- immediate frx fixation may lower incidence of FES (ref)
- consider prophylactic steroids for prevention of FES in patients w/ isolated long bone
trauma;
- references:
- Fat embolism prophylaxis with corticosteroids. A prospective study in
high-risk patients.
- Low-dose corticosteroid prophylaxis against fat embolism.
- Fat embolism and the fat embolism syndrome. A double-blind therapeutic
study.
- The use of methylprednisolone and hypertonic glucose in the prophylaxis of
fat embolism syndrome.
- pulse ox monitoring for subclinical hypoxemia may also be beneficial;
- Treatment:
- once FES occurs, it is mandatory that perfusion be maintained, especially in older
patients;
- all to often in this disorder, the orthopaedists defers the care of these patients
to the anesthesiologists who in many cases take a "crisis intervention stratedgy"
- this is guaranteed to fail in older patients;
- to adequately treat FES patients, the orthopaedist must take a "pro-active"
intervention
statedgy to ensure that perfusion is maintained as soon as FES is diagnosed;
- specific requirements include:
- SG monitoring (w/ continuous mixed VO2 monitoring);
- arterial line for monitorying blood pressure and ABG;
- metabolic acidosis or suboptimal mixed VO2 indicates sub-optimal perfusion;
- maintenance of perfusion by optimizing:
- cardiac output
- influenced by preload, afterload, and thru use of inotropic agents;
- hematocrit: must be aggressively be kept above 30% w/ pRBC;
08/10/2007 11:04
5 of 5
- most pts will require mechanical ventilation as they enter respiratory failure;
[ Close Window ]
08/10/2007 11:04
Fracture Healing
1 of 7
Fracture Healing
Inflammation
Remodelling
Repair
Factors
inluencing
bone healing
Electricity and
bone healing
08/10/2007 11:04
Fracture Healing
2 of 7
Bone Healing & Repair [Back To Top]
Bone response is a continual process beginning with Inflammation then Repair (soft then
hard callus) , then Remodelling . This process is influenced by biological & mechanical
factors, local & systemic:
Factors influencing bone healing [Back To Top]
Systemic
Local
Age / Co-morbidity
Degree of local trauma / soft tissue
Hormones
Degree of bone loss
Functional activity
Vascular injury
Nerve function
Type of bone fractured
Nutrition
Degree of immobilisation / stability
Drugs (NSAID)
Sterility / Infection
Growth Factors
Local pathological condition
Cigarette Smoke
Energy of Injury
Anatomic location
Inflammatory response
[Back To Top]
- Time of injury to 24-72 hours
Haematoma " bleeding from # site & soft tissue -> haematoma & fibrin clot ->
source of haemopoietic cells which can secrete GF.
Injured tissues and platelets release vasoactive mediators, growth factors and other
cytokines.
These cytokines influence cell migration, proliferation, differentiation and matrix
synthesis.
Growth factors recruit fibroblasts, mesenchymal cells & osteoprogenitor cells to the
fracture site.
Macrophages, PMNs & mast cells (48hr) arrive at the fracture site to begin the
process of removing the tissue debris.
Granulation tissue forms around # ends
Osteoblasts, fibroblasts proliferate
08/10/2007 11:04
Fracture Healing
3 of 7
Reparative response
[Back To Top]
- 2 days to 2 weeks
Vasoactive substances (Nitric Oxide & Endothelial Stimulating Angiogenesis Factor)
cause neovascularisation & local vasodilation
Undifferentiated mesenchymal cells migrate to the fracture site and have the ability
to form cells which in turn form cartilage, bone or fibrous tissue.
The fracture haematoma is organised and fibroblasts and chondroblasts appear
between the bone ends and cartilage is formed (Type II collagen).
The amount of callus formed is inversely proportional to the amount of
immobilisation of the fracture. If bone ends not in continuity " bridging soft callus
occurs, this is later replaced via endochondral ossification by woven bone " hard
callus
Medullary callus supplements bridging callus but takes much longer.
Thus " healing varies with type of treatment:
In fractures that are fixed with rigid compression plates there can be primary bone
healing with little or no visible callus formation. Get cutting cone-type remodelling.
Cast closed treatment " Periosteal bridging callus with endochondral ossification.
IM Nailing " early periosteal bridging callus, late medullary callus via endochondral
ossification
Ex-Fix: less rigid " periosteal bridging callus, more rigid primary cortical healing.
Inadequate treatment / healing: Hypertrophic non-union with failed endochondral
ossification and Type II collagen predominating.
Types of callus :
External (bridging) callus
From the fracture haematoma
Ossifies by endochondral ossification to form woven bone
Internal (medullary) callus
Forms more slowly and occurs later
Periosteal callus
Forms directly from the inner periosteal cell layer.
Ossifies by intramembranous ossification to form woven
bone
Remodelling:
[Back To Top]
- Middle of repair phase up to 7 years. Woven bone replaced by lamellar bone.
Remodelling of the woven bone is dependent on the mechanical forces applied to it
(Wolff's Law - 'form follows function') allowing bone to assume its normal
configuration and shape based on the stresses it is exposed to.
Fracture healing is complete when there is repopulation of the medullary canal
Cortical bone
Remodelling occurs by invasion of an osteoclast "cutting cone" which is then
followed by osteoblasts which lay down new lamellar bone (osteon)
Cancellous bone
Remodelling occurs on the surface of the trabeculae which causes the
trabeculae to become thicker
Biomechanical Steps of Fracture Healing [Back To Top]
Four steps described:
Step
Collagen Type
Mesenchymal
I,II (III, V)
08/10/2007 11:04
Fracture Healing
4 of 7
Chondroid
II, IX
Chondroid-osteoid
I, II, X
Osteogenic
I
Important cytokines / Growth factors in bone healing: [Back To Top]
BMP
Osteoinductive, induces metaplasia of mesenchymal cells into osteoblasts
Target cell for BMP is the undifferentiated perivascular mesenchymal cell.
BMP stimulates bone formation.
TGF-b
Induces mesenchymal cells to produce type II collagen and proteoglycans
Induces osteoblasts to produce collagen. Found in # haematoma, regulates
cartilage and bone formation in callus. Coating porous implants with it
enhances bone ingrowth.
PDGF
Attracts inflammatory cells to the fracture site
FGF
Stimulates fibroblast proliferation
IGF-II
Stimulates type I collagen production, cartilage matrix synthesis and cellular
proliferation
IL-1
IL-6
Hormonal influences on bone healing [Back To Top]
Hormone
Effect
Mechanism
Cortisone
Decr.
Decreased callus production
Calcitonin
Incr.
Unknown
TH/PTH
Incr.
Bone remodelling
GH
Incr.
Increased callus volume
Androgens
Incr.
Increased callus volume
Electricity and fracture healing
[Back To Top]
Stress generated potentials - Serve as signals that modulate cellular activity
Piezoelectric effect and streaming potentials are examples of stress generated
potentials
Piezoelectric effect: charges in tissues are changed secondary to mechanical
forces
Streaming potentials: occur when electrically charged fluid is forced over a tissue
(cell membrane) with a fixed charge
Transmembrane potentials: generated by cellular metabolism
Fracture Healing " electrical prop of cart & bone depend on their charged
molecules.
Devices intend to stimulate # repair by altering a variety of cellular activities.
Direct current stimulates an inflammatory like response
Alternating current affects cyclic AMP, collagen synthesis and calcification
during the repair phase
Pulsed electromagnetic fields initiate calcification of fibrocartilage
Ultrasound
[Back To Top]
Can decrease the time to clinical healing and radiological union
Clin. studies show: Low-intensity pulsed u/s accelerates # healing and incr.
mechanical strength callus.
08/10/2007 11:04
Fracture Healing
5 of 7
Theory " cells respond to mechanical energy of u/s signal
Radiation on Bone
[Back To Top]
Long term bone injury after high dose due to damage to haversian system and
decrease in cellularity.
Immediate postop irradiation has adverse effect on incorporation of ant. spinal
interbody strut grafts " this effect is eliminated by delaying it 3 weeks.
High dose irradiation " 90kGy " dose needed for viral inactivation of allograft signif.
Reduces its structural integrity.
Bone Grafting
[Back To Top]
4 prop of bone graft:
1.
2.
3.
4.
Osteoconductive matrix: scaffold into which bone growth occurs
Osteoconductive factors: GF " BMP, TGF-B promote bone formation
Osteogenic cells: primitive mesechymal cells, osteoblasts, osteocytes
Structural integrity
Autografts or allografts commonly used
Cancellous bone used for grafting non-union or cavitary defect as is quickly
remodelled and incorporated by creeping substitution.
Cortical bone - slower turnover, used for structural defect
Osteoarticular (osteochondral) allograft used increasingly for tumour surgery.
Immunogenic (cartilage vulnerable to immune response " cytotoxic inj from
antibodies and lymphocytes)
Articular cartilage is preserved with glycerol treatment
Cryogenic preserved graft leave few viable chondrocytes
Tissue matched fresh graft produce minimal immunogenic effect and
incorporate well
Vascularised Bone Graft " tech difficult, more rapid union with preserve most cells.
Best used for irradiated tissues or large tissue defects. Nb. Donor site morbid
Non-vasc bone graft " more common than vasc.
Allograft can be
Fresh " incr antigenicity
Fresh frozen " less immunogenic than fresh, preserves BMP
Freeze-dried (lyophilized) loses structural integrity, depletes BMP, least
immunogenic, lowest likelihood viral transmission, purely osteoconductive.
AKA " 'croutons.'
Bone matrix gelatine " digested source of BMP
Demineralised bone matrix (Grafton) " is osteoconductive and osteoinductive
Bone marrow cells of allograft incite the greatest immunogenic response compared with
other constituents.
Five stages of Graft Healing (Urist)
1.
2.
3.
4.
5.
Inflammation " chemotaxis stim. by necrotic debris
Osteoblast differentiation " from precursors
Osteoinduction " osteoblast and osteoclast function
Osteoconduction - new bone forming over scaffold
Remodelling " continues for years
Specific Bone Grafts:
Cortical " incorporate through slow remodelling of existing haversian systems via resorption
(weakens graft) followed by deposition of new bone (restore strength).
Cancellous " revasc. more quickly, osteoblast lay down new bone on old trabeculae, later
remodelled via creeping substitution.
Synthetic " calcium, silicon or aluminium based
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Fracture Healing
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Silicate based (silicate dioxide) " bioactive glasses, glass-ionomer cement
Calcium phosphate based " capable of osseoinduction and conduction, biodegrade
at very slow rate- prepared as ceramics (apatite crystals)
Tricalcium phosphate
Hydroxyapitate
Calcium sulphate " osteoconductive
Calcium carbonate osteoconductive
Coralline hydroxyapetite
Aluminia "aluminium oxide bonds to bone in resonse to stress/strain between
implant and bone
Hard tissue " replacement polymer
Distraction Osteogenisis - use of distraction to stimulate formation of bone
- use in limb lengthening, hypertrophic non-union, deformity correction, segmental bone
loss
- in optimal stable condition " bone formed by intramembranous ossification
- in unstable environment bone forms via endochondral ossification
- if extremely unstable pseudoarthrosis
- Histology phases: latency 5-7 days, distraction at 1mm/day, consolidation twice as long
as distraction.
- Optimal conditions for bone formation in distraction osteogenesis:
Low energy osteotomy
Minimal soft tissue strip
Stable ex-fix eliminate shear, torsion, bend
Latency period, distraction at 1mm/day, consolidation phase
Functional use of limb ie wt bearing.
Heterotopic Bone Formation (HO)
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Ectopic bone in soft tissue
Commonly due to injury / surgical dissection
Myositis Ossificans MO - a form of HO in muscle
Traumatic brain injury specifically prone to HO " recurrence after resection likely if
neurologic compromise
If resecting after THR wait 6 mths
Radiation is adjuvant for recurrence " 700 rad doses prevent prolif and differentiation
of primordial mesenchymal cells into osteoprogenitor cells that can form
osteoblastic tissue.
Oral diphosponates inhibit mineralization but not prevent formation of osteoid matrix
HO incidence after THA in Pagets patients is high " 50%.
Bone Healing Abnormalities
[Back To Top]
Delayed Union - # allowing free movement of bone ends at 3 to 4 mths Nonunion " no
radiographic evidence of union with clinical motion and pain at 6mths
Each # has its own time to union (#NOF non-union = 12 months)
Factors: Excessive or too little motion at #site, too much space, soft tissue
interposition, inadequate fix, infection, avascularity
Classified (Weber & Chech):
I Hypervascular a) Elephants foot b) Horses foot c) Oligotrophic
II Avascular a) Dystrophic(torsion wedge) b) Necrotic (communited) c) defect (gap)
d) Atrophic
Management " correct cause of non-union " infection, soft tissue interposn, bone
graft # gaps
Bone graft at time of internal fixation for communition involving more than 1/3 diam
bone.
Malunion " bony healing in unacceptable position in any plane. Treat by correcting anatomic
abnormality
Avascular Necrosis " due to disruption of blood supply can lead to non-union, OA, collapse
" more common with intra-articular # esp. of femoral head/neck, femoral condyles, prox.
scaphoid, prox. humerus and talar neck.
Links:
Mechanics of Fracture Healing
Implants for Fracture Fixation
08/10/2007 11:04
Fracture Healing
7 of 7
Sponsored Links
www.ebimedical.com
www.biometeurope.com
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08/10/2007 11:04
Head Injuries
1 of 2
Head Injuries
GLASCOW COMA SCALE
Eye Opening:
Motor:
Verbal:
6-obey commands
5-orientated
4-spontaneous
5-localizes pain
3-to voice
4-withdraws
2-to pain
3-decorticate
1-nil.
2-deceribrate
4-confused
3-inappropriate
2-incomprehensible
1-nil.
1-nil.
Indications for SXR:
1. LOC
2. amnesia
3. neurological signs
4. external injury
5. penetrating injury
6. CSF otorrhea/ rhinorrhea
7. difficult to assess
8. child <5yrs w/ ?NAI or tense fontanelle
9. headache/ vomiting (>2)
10. return visit
Indications for Admission:
1. Depressed consciousness
2. Post-traumatic seizure
3. focal neurological deficit
4. skull #
5. Persistant headache or vomiting
6. on anticoagulants or haemophilic
7. alcohol/drug abuse
8. no responsible attendant
9. unknown MOI
10. child w/ Hx of unconsciousness
Indications for CT Scan:
1. Confusion (GCS<14) after initial resuscitation
2. Unstable state
3. Dx uncertain
4. Skull #
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Head Injuries
2 of 2
Referral to Neurosurgeons:
1. skull fracture with confusion or fit or neuro deficit
2. compound depressed skull fracture
3. base of skull #
4. penetrating injury
5. coma despite resus
6. Deterioration of GCS >2 points.
Note: No # & orientated = 1:6000 chance of ICH, # & confused = 1:4 chance of ICH.
Head Injury Powerpoint Presentation by J.A. Alonso
[ Close Window ]
08/10/2007 11:04
Hypovolaemic shock
1 of 3
Hypovolaemic shock
Grades of hypovolaemic shock
Grade 1
15% blood volume (~750 ml)
Mild resting tachycardia
Alert
Cross-match 2U
Grade 2
15 - 30% blood volume (750 - 1500 ml)
Moderate tachycardia, fall in pulse pressure, delayed capillary return
Anxious / aggressive
Cross-match 2U
Grade 3
30 - 40% blood volume (1500 - 2000 ml)
Hypotension, tachycardia, low urine output
Drowsy / aggressive
4U Type-specific blood
Grade 4
> 40% blood volume (2000 -2500 ml)
As above but with profound hypotension
Drowsy / unconscious
2U universal blood + 4U type-specific + 6U cross-matched
Fluid resuscitation
Early volume intravascular volume replacement in trauma patients is essential
The ideal resuscitation fluid is uncertain
Timing and end-points of resuscitation unclear
Normal Blood volume = 80ml/Kg
Resuscitation for Infants and Children:
LR bolus 20 ml/kg x 2-3 as required
then pRBC 10 ml/kg x 1 - continue fluid administration until CVP > 5mmHg;
Daily Fluid Requirements:
minimum requirements for fluid balance can be estimated from the sum of the urine
output necessary to excrete the daily solute load (500 ml/ day) plus insensible
(evaporative) water losses from the skin and resp tract (500-1000 ml/day) minus the
amount of water produced from endogenous metabolism (300 ml/day)
the kidney must excrete about 600 mOsm of solute/day (primarily Na, K, and urea)
in the normal adult
since the maximum urinary concentrating ability is 1200 mOsm/kg, the minimum
urine output required to excrete the osmotic load is 500 ml/day
it is customary to administer 2000-3000 ml of water daily to produce about
1000-1500 ml/day urine output, since there is no advantage gained by minimizing
urine output
Total Body Water: = 43
litres(61%)
Intracellular water- 31
litres(44%)
Extracellular water- 12
litres(17%)
Blood Volume- 5
litres(7%)
(80ml/Kg)
Plasma3.2
litres(4.5%)
Extravascular- 7
litres(8-11%)
Normal Fluid Balance:
Output (litres/day): lungs
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Hypovolaemic shock
2 of 3
0.7, skin 0.7, faeces 0.1,
kidney 1.5.
Intake: 'metabolic water'
0.3, food 1.0, oral fluids
1.7.
Paediatric Crystalloid Fluid
therapy (maintenance):
1st 10kg- 4ml/kg/hr
2nd 10kg- 2ml/kg/hr
Subsequent kg- 1ml/kg/hr
Resuscitation: Bolus of
20ml/kg & monitor
response.
Nutritional Requirements:
Water 30-50ml/kg/day
calories 30-50kcal/kg/day
Nitrogen 0.2-0.35g/kg/day
(1g N2 = 6.5g protein)
Sodium 1mmol/kg/day
Potassium 1mmol/kg/day
Weight Gain should be
0.3kg/day
Packed red blood cells
Provide best volume expansion and oxygen carrying capacity
Needs cross-matching and not immediately available
Dilutional coagulopathy occurs with massive transfusion
Crystalloid versus colloid resuscitation
More than 40 randomised controlled trials of crystalloid vs. colloid resuscitation
published
None has shown either type of fluid to be associated with a reduction in mortality
No single type of colloid has been shown to be superior
Albumin solution may be associated with slight increase in mortality
Colloids can more rapidly correct hypovolaemia
Also maintain intravascular oncotic pressure
Crystalloids require large volume but are equally effective
Cheaper and have fewer adverse side effects
Hypertonic solutions
Subjected to recent intensive investigation
Can resuscitate patient rapidly with a reduced volume of fluid
May reduce cerebral oedema in patients with severe head injuries
Oxygen therapeutic agents
Currently being extensively investigated in clinical trials
Not widely used at present outside of clinical trials
Potential advantages over blood include:
Free potential viral contamination
Longer shelf life
Universal ABO compatibility
Similar oxygen carrying capacity to blood
Agents being studied include:
Perflurocarbons
Human haemoglobin solutions
Polymerised bovine haemoglobin
Intraosseous infusion
Venous access can be difficult in the hypovolaemic child
If difficulty experienced then intraosseous route can be used as an alternative
Medullary canal in a child has a good blood supply
Drugs and fluids are absorbed into venous sinusoids of red marrow
Red marrow replaced by yellow marrow after 5 years of age
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Hypovolaemic shock
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Less effective in older children
Systemic drug levels are similar to those achieved via the intravenous route
Technique is generally safe with few complications
Indications
Major trauma
Extensive burns
Cardiopulmonary arrest
Septic shock
Contraindications
Ipsilateral lower limb fracture
Vascular injury
Technique
Intraosseous access achieved with specially designed needles
Short shaft allows accurate placement within the medullary canal
Handle allows controlled pressure during introduction
Usually inserted into antero-medial border of tibia, 3 cm below tibial tubercle
Correct placement checked by aspiration of bone marrow
Both fluids and drugs can be administered
Fluid often needs to be administered under pressure
Once venous access achieved intraosseous needle can be removed
Complications
Complications are rare
Needles are incorrectly placed or displaced in about 10% patients
Complications include:
Tibial fracture
Compartment syndrome
Fat embolism
Skin necrosis
Osteomyelitis
[ Close Window ]
08/10/2007 11:05
Metabolic response to trauma
1 of 5
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content.
Definition of Trauma
Initiating Factors
Hormonal Mediators
Effects of Various Mediators
The Anabolic Phase
Clinical and Theraputic Relevance
SUMMARY
Phase
Duration
Role
Physiological
Hormones
<24hrs
maintenance of blood volume;
catecholamines
decr. BMR, decr. Temp, decr. O 2 consumption;
vasoconstriction; incr. CO, incr. HR; acute phase proteins
Catecholamines, Cortisol, Aldosterone
Catabolic
3-10 days
maintenance of energy
incr. BMR, incr. Temp., incr. O 2 consumption, negative
nitrogen balance
Incr. glucagon, insulin, cortisol,
catecholamines - but insulin resistance
Anabolic
10-60 days replacement of lost tissue
positive nitrogen balance
Growth hormone, IGF
Ebb
Flow
1. Definition of Trauma
Bodily injury is accompanied by systemic as well as local effects. Any stress, which includes injury, surgery, anaesthesia, burns, vascular occlusion, dehydration,
starvation, sepsis, acute medical illness, or even severe psychological stress will initiate the metabolic response to trauma.
Following trauma, the body responds locally by inflammation and by a general response which is protective, and which conserves fluid and provides energy for repair.
Proper resuscitation may attenuate the response, but will not abolish it.
The response is characterised by an acute catabolic reaction, which precedes the metabolic process of recovery and repair. This metabolic response to trauma was
divided into an ebb and flow phase by Cuthbertson .
The ebb phase corresponds to the period of severe shock characterised by depression of enzymatic activity and oxygen consumption. Cardiac output is below normal,
core temperature may be subnormal, and a lactic acidosis is present.
The flow phase can be divided into
a catabolic phase with fat and protein mobilisation associated with increased urinary nitrogen excretion and weight loss, and
an anabolic phase with restoration of fat and protein stores, and weight gain.
In the flow phase, the body is hypermetabolic, cardiac output and oxygen consumption are increased, and there is increased glucose production. Lactic acid may be
normal.
2. Initiating Factors
Hypovolaemia
Afferent Impulses
Wound Factors
Toxins/Sepsis
Oxygen Free Radicals
The magnitude of the metabolic response depends on the degree of trauma and the concomitant contributory factors such as drugs, sepsis and underlying systematic
disease. The response will also depend on the age and sex of the patient, the underlying nutritional state, the timing of treatment and its type and effectiveness. In
general, the more severe the injury, (i.e. the greater the degree of tissue damage), the greater the metabolic response.
The metabolic response seems to be less aggressive in children and the elderly and in the premenopausal female. Starvation and nutritional depletion also modify the
response. Patients with poor nutritional status have a reduced metabolic response to trauma compared to well-nourished patients.
Burns cause a relatively greater response than other injuries of comparable extent probably because of the propensity for greater continued volume depletion and heat
loss.
Wherever possible, it is critical to try to prevent, or reduce the magnitude of the initial insult, since by doing so it may be possible to reduce the nature of the response,
which while generally protective, may be harmful. Thus aggressive resuscitation, control of pain and temperature, and adequate fluid and nutritional provision are critical.
The precipitating factors can broadly be divided into
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2.1 Hypovolaemia
Decrease in circulating volume of blood
Increase in alimentary loss of fluid
Loss of interstitial volume
Extracellular fluid shift
2.2 Afferent Impulses
Somatic
Autonomic
2.3 Wound Factors : Inflammatory and cellular
Eicosanoids
Prostanoids
Leucotrienes
Macrophages
Interleukin-1 (IL-1)
Proteolysis Inducing Factor (PIF)
Platelet Activating factor
2.4 Toxins / Sepsis
Endotoxins
Exotoxins
2.5 Oxygen Free Radicals
The above will be discussed in detail:
2.1 Hypovolaemia
It is said that hypovolaemia, specifically involving tissue hypoperfusion is the most potent precipitator of the metabolic response. Hypovolaemia can also be due to
external losses, internal shifts of extracellular fluids, and changes in plasma osmolality. However, the most common cause is blood loss secondary to surgery or traumatic
injury.
Class of Shock
% Blood Loss
Volume
Class I
15%
< 750 ml.
Class II
30%
750 - 1500 ml.
Class III
40%
2000 ml.
Class IV
>40%
> 2000 ml
Class III or Class IV shock is severe, and unless treated as a matter of urgency, will make the situation much worse.
The hypovolaemia will stimulate catecholamines which in turn trigger the neuroendocrine response. This plays an important role in volume and electrolyte conservation
and protein, fat and carbohydrate catabolism. Early fluid and electrolyte replacement, and parenteral or enteral surgical nutrition administering amino acids to injured
patients losing nitrogen at an accelerated rate; and fat and carbohydrates to counter caloric deficits may modify the response significantly. However, the availability of the
methods should not distract the surgeon from his primary responsibility of adequate resuscitation.
2.2 Afferent impulses
Hormonal responses are initiated by pain and anxiety. The metabolic response may be modified by administration of adequate analgesia, which may be parenteral,
enteral, regional or local. Somatic blockade may need to be accompanied by autonomic blockade, in order to minimise, or abolish the metabolic response.
2.3 Wound factors
Endogenous factors prolong or even exacerbate the surgical insult, despite the fact that the primary cause can be treated well. Tissue injury activates a specific response,
along two pathways:
Inflammatory (humoral) pathway
Cellular pathway
Uncontrolled activation of endogenous inflammatory mediators and cells may contribute to this syndrome.
Both humoral and cell derived activation products play a role in the pathophysiology of organ dysfunction. It is important, therefore, to monitor post-traumatic biochemical
and immunological abnormalities wherever possible.
2.3.1 Immune Response - Inflammatory pathway
The inflammatory mediators of injury have been implicated in the induction of membrane dysfunction.
Eicosanoids
These compounds, derived from eicosapolyenoic fatty acids, comprise the prostanoids and leucotrienes (LT). Eicosanoids are synthesised from arachidonic acid which
has been synthesised from phospholipids of damaged cell walls, white blood cells and platelets, by the action of phospholipase A2. The leucotrienes and prostanoids
derived from the arachidonic acid cascade play an important role.
Prostanoids
Cyclo-oxygenase converts arachidonic acid to prostanoids, the precursors of prostaglandin (PG), prostacyclins (PGI) and thromboxanes (TX). The term prostaglandins is
used loosely to include all prostanoids.
The prostanoids (prostaglandins of the E and F series, prostacyclin (PGI 2 ) and thromboxane synthesised from arachidonic acid by cyclo-oxygenase (in TXA 2 ),
endothelial cells, white cells, and platelets, not only cause vasoconstriction (TXA 2 and PGF 1 ), but also vasodilatation (PGI 2 , PGE 1 and PGE 2 ). TXA 2 activates and
aggregates platelets and white cells, and PGI 2 and PGE 1 inhibits white cells and platelets.
Leucotrienes
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Lipoxygenase, derived from white cells and macrophages, converts arachidonic acid to leucotrienes (LTB4, LTC4 and LTD4). The leucotrienes (LTB4, LTC4, and LTD4)
cause vasoconstriction, increased capillary permeability and bronchoconstriction.
2.3.2 Immune Response - Cellular pathway
There are a number of phagocytic cells, (neutrophils, eosinophils, and macrophages), but the most important of these are the polymorphonuclear leucocyte, and the
macrophages. Normal phagocytosis commences with chemotaxis, which is the primary activation of the metabolic response, via the activation of complement.
The classical pathway of complement activation involves an interaction between the initial antibody and the initial trimer of complement components C 1 , C 4 , and C 2 . In
the classical pathway, this interaction then cleaves the complement products C 3 and C 5 , via proteolysis to produce the very powerful chemotactic factors C 3a and C 5a
(anaphylotoxins).
The so-called alternative pathway seems to be the main route following trauma. It is activated by properdin, and proteins D or B, to activate C 3 convertase, which
generates the anaphylotoxins C 3a and C 5a . Its activation appears to be the earliest trigger for activating the cellular system, and is responsible for aggregation of
neutrophils and activation of basophils, mast cells and platelets to secrete histamine and serotonin which alter vascular permeability and are vasoactive. In trauma patients,
the serum C 3 level is inversely correlated with the Injury Severity Score (ISS). Measurement of C 3a is superior because the other products are more rapidly cleared from
the circulation. The C 3a /C 3 ratio has been shown to correlate positively with outcome in patients after septic shock.
The short-lived fragments of the complement cascade, C 3a and C 5a , stimulate macrophages to secrete interleukin-l (IL-1) and its active circulating cleavage product
proteolysis inducing factor (PIF). These cause proteolysis and lipolysis with fever. IL-1 activates T 4 helper cells to produce IL-2 which enhances cell-mediated immunity.
IL-1 and PIF are potent mediators stimulating cells of the liver, bone marrow, spleen and lymph nodes to produce acute-phase proteins which include complement,
fibrinogen, a2-macroglobulin, and other proteins required for defence mechanisms.
Monocytes can produce plasminogen activator, which can adsorb to fibrin to produce plasmin. Thrombin generation is important due to its stimulatory properties on
endothelial cells.
Activation of factor XII (Hageman Factor A) stimulates kallikrein to produce bradikinin from bradykininogen, which also affects capillary permeability and vaso-activity. A
combination of these reactions causes the inflammatory response.
2.4 Toxins
Endotoxin is a lipopolysaccaride component of bacterial cell walls. Endotoxin causes vascular margination and sequestration of leucocytes, particularly in the capillary
bed. At high doses, granulocyte destruction is seen. A major effect of endotoxin, particularly at the level of the hepatocyte my be to liberate Tumour Necrosis Factor
(TNF) in the macrophages.
Toxins derived from necrotic tissue or bacteria, either directly or via activation of complement system, stimulate platelets, mast cells and basophils to secrete histamine
serotonin.
2.5 Oxygen Free Radicals
Oxygen radical formation by white cells is a normal host defence mechanism. Changes after injury may lead to excessive production of oxygen free radicals, with
deleterious effects on organ function.
3. Hormonal Mediators
Pituitary
Adrenal
Pancreatic
Renal
Other
During trauma, several hormones are altered. Adrenaline, noradrenaline, cortisol, and glucagon are increased, while certain others are decreased. The
sympathetic-adrenal axis is probably the major system by which the body's response to injury is activated. Many of the changes are due to adrenergic and catecholamine
effects, and catecholamines are increased after injury.
3.1 Pituitary
The hypothalamus is the highest level of integration of the stress response. The major efferent pathways of the hypothalamus are endocrine via the pituitary and the
efferent sympathetic and parasympathetic systems.
The pituitary gland responds to trauma with two secretory patterns. Adrenocorticotrophic hormone (ACTH), prolactin, and growth hormone levels increase. The
remainder are relatively unchanged.
Pain receptors, osmoreceptors, baroreceptors and chemoreceptors stimulate or inhibit ganglia in the hypothalamus to induce sympathetic nerve activity. The neural
endplates and adrenal medulla secrete catecholamines . Pain stimuli via the pain receptors also stimulate secretion of endogenous opiates, b -endorphin and
pro-opiomelanocortin (precursor of the ACTH molecule) which modifies the response to pain and reinforces the catecholamine effects. The b -endorphin has little effect,
but serves as a marker for anterior pituitary secretion.
Hypotension, hypovolaemia in the form of a decrease in left ventricular pressure, and hyponatraemia stimulate secretion of vasopressin, antidiuretic hormone (ADH)
from the supra-optic nuclei in the anterior hypothalamus, aldosterone from the adrenal cortex, and renin from the juxtaglomerular apparatus of the kidney.
As osmolality increases, the secretion of ADH increases, and more water is reabsorbed, thereby decreasing the osmolality - (negative feedback control system). Volume
receptors are located in the atria and pulmonary arteries, and osmoreceptors are located near ADH neurones in the supra-optic nuclei of the hypohalamus. ADH acts
mainly on the connecting tubules of the kidney but also on the distal tubules to promote reabsorption of water.
Hypovolaemia stimulates receptors in right atrium and hypotension stimulates receptors in the carotid artery. This results in activation of paraventricular hypothalamic
nuclei which secrete releasing hormone from the median eminence into capillary blood which stimulates the anterior pituitary to secrete adrenocorticotrophin (ACTH).
ACTH stimulates the adrenal cortex to secrete cortisol, and aldosterone. The control of ACTH secretion is uncertain, but AVP may have a role. Changes in glucose
concentration influence the release of insulin from the b cells of the pancreas, and high amino-acid levels, the release of glucagon from the pancreatic a cells.
Plasma levels of growth hormone are increased. However, the effects are transitory, and have little long term effect. Growth hormone reverses catabolism following injury.
3.2 Adrenal Hormones
Plasma cortisol and glucagon levels rise following trauma. The degree is related to the severity of injury. The function of glucocorticoid secretion in the initial metabolic
response is uncertain, since the hormones have little direct action, and they seem primarily to augment the effects of other hormones such as the catecholamines.
With passage into the later phases after injury, a number of metabolic effects take place. Glucocorticoids exert catabolic effects such as gluconeogenesis, lipolysis, and
amino acid breakdown from muscle. Catecholamines also participate in these effects by mediating insulin and glucose release and the mobilisation of fat.
There is an increase in aldosterone secretion, and this results in a conservation of sodium, and thereby, water.
Catecholamines are released in copious quantities following injury, primarily stimulated by pain, fear, and baroreceptor stimulation.
3.3 Pancreatic Hormones
There is a rise in the blood sugar following trauma. The insulin response to glucose in normal individuals is reduced substantially with alpha adrenergic stimulation, and
enhanced with beta adrenergic stimulation.
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3.4 Renal Hormones
Aldosterone secretion is increased by several mechanisms. The renin-angiotensin mechanism is the most important. When the glomerular arteriolar inflow pressure falls,
the juxtaglomerular apparatus of the kidney secretes renin, which acts with angiotensinogen to form angiotensin I. This is converted to angiotensin II, a substance which
stimulates production of aldosterone by the adrenal cortex. Reduction in sodium concentration stimulates the macula densa, a specialised area in the tubular epithelium
adjacent to the juxtaglomerular apparatus, to activate renin release. An increase in plasma potassium concentration also stimulates aldosterone release. Volume decrease
and a fall in arterial pressure stimulates release of ACTH via receptors in the right atrium and the carotid artery.
3.5 Other hormones
Atrial natriuretic factor (ANF) or atriopeptin is a hormone produced by the atria, predominantly the right atrium of the heart, in response to an increase in vascular
volume. ANF produces an increase in glomerular filtration and pronounced natriuresis and diuresis. It also produces inhibition of aldosterone secretion which minimises
kaliuresis and causes suppression of ADH release.
ANF has highlighted the heart's function as an endocrine organ. ANF has great therapeutic potential in the treatment of intensive-care patients who are undergoing
parenteral therapy.
4 Effects of the Various Mediators
4.1 Hyperdynamic state
Following illness or injury, the systemic inflammatory response occurs, in which there is an increase in activity of the cardiovascular system, reflected as tachycardia ,
widened pulse pressure , and a greater cardiac output .
There is an increase in the metabolic rate, with an increase in oxygen consumption , increased protein catabolism , and hyperglycaemia .
The cardiac index may exceed 4.5 litres / minute / m 2 after severe trauma or infection in those patients who are able to respond adequately. Decreases in vascular
resistance accompany this increased cardiac output. This hyperdynamic state elevates the resting energy expenditure to more than 20% above normal. In an inadequate
response, with a cardiac index of less than 2.5 litres / minute / m 2 , oxygen consumption may fall to values of less than 100 ml. / minute / m 2 (Normal = 120 - 160 ml /
minute / m 2 ). Endotoxins and anoxia may injure cells and limit their ability to utilise oxygen for oxidative phosphorylation.
The amount of ATP synthesised by an adult is considerable. However, there is no reservoir of ATP or creatinine phosphate, and therefore cellular injury and lack of
oxygen results in rapid deterioration of processes requiring energy. and lactate is produced. Because of anaerobic glycolysis only 2 ATP equivalents instead of 34 are
produced from one mole of glucose in the Krebs cycle.
Lactate is formed from pyruvate, which is the end product of glycolysis. It is normally reconverted to glucose in the Cori cycle in the liver. However, In shock, the oxidation
reduction (redox) potential declines and conversion of pyruvate to acetyl co-enzyme A for entry into the Krebs cycle is inhibited. Lactate therefore accumulates because
of impaired hepatic gluconeogenesis, causing a severe metabolic acidosis .
A persistent lactic acidosis in the first three days after injury not only correlates well with Injury Severity Score (ISS), but also confirms the predictive value of lactic
acidosis towards subsequent Adult Respiratory Distress syndrome.
Accompanying the above changes is an increase in oxygen delivery to the microcirculation. Total body oxygen consumption (VO 2 ) is increased. These reactions
produce heat, which is also a reflection of the hyperdynamic state.
4.2 Water and salt retention
The oliguria which follows injury is a consequence of the release of antidiuretic hormone (ADH) and aldosterone.
Secretion of ADH from the supra-optic nuclei in the anterior hypothalamus is stimulated by volume reduction and increased osmolality. The latter is mainly due to an
increased sodium content of the extracellular fluid. Volume receptors are located in the atria and pulmonary arteries, and osmoreceptors are located near ADH neurones
in the hypothalamus. ADH acts mainly on the connecting tubules of the kidney but also on the distal tubules to promote reabsorption of water.
Aldosterone acts mainly on the distal renal tubules to promote reabsorption of sodium and bicarbonate and increased excretion of potassium and hydrogen ions.
Aldosterone also modifies the effects of catecholamines on cells, thus affecting the exchange of sodium and potassium across all cell membranes. The release of large
quantities of intracellular potassium into the extracellular fluid may cause a significant rise in serum potassium especially if renal function is impaired. Retention of sodium
and bicarbonate may produce metabolic alkalosis with impairment of the delivery of oxygen to the tissues. After injury urinary sodium excretion may fall to 10-25
mmol/24 hours and potassium excretion may rise to 100-200 mmol/24 hours.
4.3 Effects on Substrate metabolism.
Carbohydrates
Fat
Amino Acids
4.3.1 Carbohydrates
Critically ill patients develop a glucose intolerance which resembles that found in pregnancy and in diabetic patients. This is as a result of both increased mobilisation,
and decreased uptake of glucose by the tissues. The turnover of glucose is increased, and the serum glucose is higher than normal.
Glucose is mobilised from stored glycogen in the liver by catecholamines, glucocorticoids and glucagon. Glycogen reserves are limited, and glucose can be derived from
glycogen for 12 to 18 hours only. Early on, the insulin blood levels are suppressed (usually lower 8 units/ml) by the effect of adrenergic activity of shock on degranulation
of the b cells of the pancreas. Thereafter gluconeogenesis is stimulated by corticosteroids and glucagon. The suppressed insulin favours the release of amino acids from
muscle which are then available for gluconeogenesis. Growth hormone inhibits the effect of insulin on glucose metabolism.
Thyroxine also accelerates gluconeogenesis, but T 3 and T 4 levels are usually low or normal in severely injured patients.
As blood glucose rises during the phase of hepatic gluconeogenesis, blood insulin concentration rises, sometimes to very high levels. Provided that the liver circulation is
maintained, gluconeogenesis will not be suppressed by hyperinsulinaemia or hyperglycaemia, because the accelerated rate of glucose production in the liver is required
for clearance of lactate and amino acids which are not used for protein synthesis. This period of breakdown of muscle protein for gluconeogenesis and the resultant
hyperglycaemia characterises the catabolic phase of the metabolic response to trauma.
The glucose level following trauma should be carefully monitored. A hyperglycaemia may exacerbate ventilatory insufficiency, and may provoke an osmotic
diuresis, and hyperosmolality . The optimum blood glucose level is between 4 and 10 mmol/ L. Control of the blood glucose is best achieved by titration with
intravenous insulin, based on a sliding scale. However, because of the degree of insulin resistance associated with trauma, the quantities required may be considerably
higher than normal.
Parenteral nutrition may be required, and this may exacerbate the problem. However, glucose remains the best energy substrate following major trauma. 60 - 75% of
the caloric requirements should be supplied by glucose, with the remainder being supplied using a fat emulsion.
4.3.2 Fat
The principal source of energy following trauma is adipose tissue . Lipids stored as triglycerides in adipose tissue are mobilised when insulin falls below 25
units/mI. Because of the suppression of insulin release by the catecholamine response after trauma, as much as 200-500 g of fat may be broken down daily after severe
trauma. Tumour necrosis factor (TNF) and possibly IL-1 play a role in the mobilisation of fat stores.
Catecholamines and glucagon activate adenyl-cyclase in the fat cells to produce cyclic adenosine monophosphate (cyclic AMP). This activates lipase which promptly
08/10/2007 11:06
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hydrolyses triglycerides to release glycerol and fatty acids. Growth hormone and cortisol play a minor role in this process as well. Glycerol provides substrate for
gluconeogenesis in the liver which derives energy by b -oxidation of fatty acids, a process inhibited by hyperinsulinaemia.
Ketones are released into the circulation and are oxidised by all tissue except the blood cells and the central nervous system . Ketones are water soluble and will
pass the blood brain barrier freely permitting rapid central nervous system adaptation to ketone oxidation.
Free fatty acids provide energy for all tissues and for hepatic gluconeogenesis. Canitine, synthesised in the liver, is required for the transport of fatty acids into the cells.
There is a limit to the ability of traumatised patients to metabolise glucose, but a high glucose load make management of the patient much more difficult. For this reason,
nutritional support of traumatised patients requires a mixture of fat and carbohydrate.
4.3.3 Amino acids
The intake of protein by a healthy adult is between 80 and 120 g of protein - 1 to 2 gm protein / Kg / day. This is equivalent to 13-20 g of nitrogen per day. In the absence
of an exogenous source of protein, amino acids are principally derived from the breakdown of skeletal muscle protein. Following trauma or sepsis the release rate of
amino acids increases by three to four times. This process appears to be induced by proteolysis inducing factor (PIF) which has been shown to increase by as much
as eight times in these patients. The process manifests of marked muscle wasting.
Cortisol, glucagon and catacholamines also play a role in this reaction. The mobilised amino acids are utilised for gluconeogenesis or oxidation in the liver and other
tissues, but also for synthesis of acute-phase proteins required for immuno-competence, clotting, wound healing and maintenance of cellular function .
Certain amino acids like glutamic acid, asparagine and aspartate can be oxidised to pyruvate, producing alanine or to a -ketogluterate, producing glutamine. The others
must first be deaminated before they can be utilised. In the muscle, deamination is accomplished by transamination from branched chain amino acids. In the liver amino
acids are deaminated by urea production which is excreted in the urine. After severe trauma or sepsis as much as 20 g/day of urea nitrogen is excreted in the
urine . Since 1g urea nitrogen is derived from 6,25 g degraded amino acids, this protein wastage to 125 g/day.
One gram of muscle protein represents 5 g wet muscle mass. Such a patient would be losing 625 g of muscle mass per day. A loss of 40% of body protein is usually
fatal, because failing immunocompetence leads to overwhelming infection . Cuthbertson 1 showed that nitrogen excretion and hypermetabolism peaked several
days after injury, returning to normal after several weeks. This is a characteristic feature of the metabolic response to illness. The most profound alterations in metabolic
rate, and nitrogen loss occur after burns.
To measure the rates of transfer and utilisation of amino acids mobilised from muscle or infused into the circulation, the measurement of central plasma clearance rate of
amino acids (CPCR-AA) has been developed. Using this method a large increase in peripheral production and central uptake of amino acids into the liver has been
demonstrated in injured patients, especially if sepsis is also present. The protein-depleted patient can be improved dramatically by parenteral or enteral alimentation
provided adequate liver function is present. Amino acid infusions in patients who ultimately die, cause plasma amino acid concentration to rise to high levels with only a
modest increase in CPCR-AA. This may be due to hepatic dysfunction caused by anoxia or toxins liberated by bacteria responsible for sepsis. Possibly. inhibitors, which
limit responses to IL-l and PIF, may be another explanation.
4.4 The Gut
The intestinal mucosa has a rapid synthesis of amino acids. Depletion of amino acids results in atrophy of the mucosa causing failure of the mucosal antibacterial barrier.
This may lead to bacterial translocation from the gut to the portal system and is probably one of the causes of liver injury, overwhelming infection and multisystem failure
after severe trauma. The extent of bacterial translocation in trauma has not been defined. The presence of food in the gut lumen is a major stimulus for mucosal cell
growth. Food intake is invariably interrupted after major trauma. The supply of glutamine may be insufficient for mucosal cell growth, and there may be an increase in
endotoxin release, bacterial translocation, and hypermetabolism. Early nutrition (within 24 - 48 hours), and early enteral rather than parenteral feeding may prevent or
reduce these events.
5. The Anabolic Phase
During this phase the patient is in positive nitrogen balance , regains his weight and restores his fat deposits. The hormones which contribute to anabolism are growth
hormones, androgens and 1 7-ketosteroids. The utility of growth hormone , and also more recently, of insulin-like growth factor (IGF-1) in reversing catabolism
following injury, is critically dependent on adequate caloric intake.
6. Clinical and Therapeutic Relevance
Survival after injury depends on a balance between the extent of cellular damage, the efficacy of the metabolic response and the effectiveness of treatment.
Hypovolaemia due to both external losses and internal shifts of extracellular fluid seems to be the major initiating trigger for the metabolic sequence. Fear and pain, tissue
injury, hypoxia and toxins from invasive infection add to the initiating factor of hypovolaemia. The degree to which the body is able to compensate for injury is astonishing,
although sometimes the compensatory mechanisms may work to the patient's disadvantage. Adequate resuscitation to shut off the hypovolaemic stimulus is important.
Once hormonal changes have been initiated, the effects of the hormones will not cease merely because hormonal secretion has been turned off by replacement of blood
volume.
Thus once the metabolic effects of injury have begun, therapeutic or endogenous restitution of blood volume may lessen the severity of the metabolic consequences but
cannot prevent them.
Mobilisation and storage of the energy fuel substrates, carbohydrate, fats and protein is regulated by insulin, balanced against catecholamines, cortisol and glucagon.
However, infusion of hormones have failed to cause more than a modest response.
Rapid resuscitation, maintenance of oxygen delivery to the tissues, removal of devitalised tissue or pus, and control of infection, are the cornerstones. The best metabolic
therapy is excellent surgical care.
Therapy should be aimed at removal of the factors triggering the response . Thorough resuscitation, elimination of pain, surgical debridement and where necessary
drainage of abscesses and appropriate antibiotic administration, coupled with respiratory and nutritional support to aid defence mechanisms are of fundamental
importance.
Adapted from K. D. Boffard, Trauma Unit, University of the Witwatersrand, South Africa
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08/10/2007 11:06
Multiple Trauma / ATLS
1 of 4
See Powerpoint presentation
outline
reception
primary survey
secondary survey
radiology
procedures
limb injuries
spinal injuries
reception
Prehospital Information
Nature of Incident
Number, age & sex of casualties
ABCD
Management & Effect
ETA
Airway & Cervical Spine control
Assess: Ask name, facial/neck injuries, vomit
Clear Airway: with sucker or Magill forceps
Chin Lift - one hand on chin, thumb in mouth, pull forward.
Jaw Thrust
Orotracheal intubation with in-line neck stabilisation: absent gag & poor ventilation, head
injury..
100% oxygen at flow rate 15 l/min.
Full cervical spine immobilisation - hard collar & lateral supports with straps across
forehead & chin.
Breathing
Inspect neck & thorax - NB trachea, neck veins
Respiratory Rate
Auscultate
Life Threatening thoracic conditions: (Trauma Clinicians Often Miss Fractures )
Tension pneumothorax
Cardiac tamponade
Open chest wound
Massive haemothorax
Flail chest
circulation
Shock assessment: skin colour, capillary refill, mental state, pulse, blood pressure
control haemorrhage
2 large(14g) cannulas peripherally.
Withdraw 20ml blood for FBC, U&E, Gluc., X-match.
warmed crystalloids
Blood:
full x-match
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type specific
O Neg.
dysfunction
pupils - size, equal, response to light.
conscious level:
A lert
V erbal stimuli
P ain stimuli
U nresponsive
exposure
clothing - remove all
cold - be aware of Hypothermia, keep warm (warmed blankets)
secondary survey
head-to-toe
log-roll
PR (& PV)
tubes - 2 large peripheral IV; urinary catheter, NGT, (chest drain, DPL, central line,
arterial line)
analgesia, anti-tetanus, antibiotics
X-Rays: (done after Primary Survey)
lateral cervical spine (followed by AP & peg view in X-Ray dept. when patient
stable- do not remove collar until all 3 films cleared)
chest
pelvis
ATLS-C-spine, pelvis, chest AP
A- adequacy & alignment
B- bones - margins & architecture - follow bone margins & comment on general density
& architecture.
C- cartilage/joints - joint spaces, surfaces.
S- soft tissues - swelling, air in tissues (open wound/ open fracture)
history (AMPLE)
Allergies
Medications
Past medical history
Last meal
Events of injury
cricothyroidotomy
last resort for airway control.
Y connector with O2 at 15 l/min.
Intermittent jet insufflation- sedate & paralyze, only for 30-45min., caution for FB
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intercostal drain
4th or 5th intercostal space, mid-axillary line
local anaesthetic down to pleura
'above the rib below'
blunt dissection. finger exploration
pass large drain on forceps superior & posterior.
underwater drain
pursestring suture
pericardiocentesis
Beck's Triad- shock,distended neck veins, muffled heart souns
ECG monitor
wide bore long sheathed needle
enter 2cm below left xiphochondral junction, aiming 45 degrees posterior towards
tip of left scapula.
positive -> urgent thoracotomy
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Limb injuries
Primary survey
Secondary survey
Immobilisation & reduction
Pain control
Wound Care:
Antibiotic prophylaxis
Tetanus cover
Photograph
Betadine dressing
Culture swab
Debridement (generous)
Irrigation
Fracture stabilisation
LEAVE WOUND OPEN
spinal injuries
primary suvey:
A:cervical spine control, intubation(blind tracheal, fibre-optic laryngoscope,
naso-tracheal), nasogastric tube (ileus)
B:intercostal paralysis
immobilisation - scoop, spinal board
secondary survey:
Log Roll -swelling, tenderness, steps, gaps
Neurological exam. - NB. bulbocavernosus reflex
Neurogenic shock: - hypotension, bradycardia [be aware of Pt.s on B-blockers], warm
periphery
Spinal Shock: flaccid limbs, reduced reflexes, reduced sensation, Urinary retention,
paralytic ileus. [return of bulbocavernosus reflex indicates end of Spinal Shock]
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08/10/2007 11:06
Open (Compound) fractures
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Goals
Prevention of infection
Healing of the fracture
Restoration of function
Classification - Gustilo and Anderson
Type 1
Wound less than 1cm long
Moderately clean puncture, where spike of bone has pierced
the skin
Little soft tissue damage
No crushing
Fracture usually simple transverse or oblique with little
comminution
Type
11
Laceration more than 1cm long
No extensive soft tissue damage, flap or contusion
Slight to moderate crushing injury
Moderate comminution
Moderate contamination
Extensive damage to soft tissues
Type
111
High degree of contamination
111A
Fracture caused by high velocity trauma
Includes any segmental or severely comminuted closed or open
fractures, regardless of the size of the wound
111B
Soft tissue coverage of the bone is adequate.
Extensive injury to or loss of soft tissue, with periosteal
stripping and exposure of bone,
Massive contamination
Severe comminution of fracture
111C
After debridement a segment of bone is exposed and a local or
free flap is required to cover it
Any fracture with an arterial injury which requires repair,
regardless of the degree of soft tissue injury
Steps in management
ABC
30% of patients with an open fracture have other life threatening injuries
Assess neurovascular status of the limb
Swab wound
Photograph & Cover wound
Tetanus prophylaxis
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Give IV antibiotics
Cephalosporin (Cefuroxime 1.5g stat)
If type 11 or 111 add an aminoglycoside (Gentamycin ). This combination
covers gram positive and gram negative bacteria
Penicillin added if a farmyard injury to cover Clostridium Perfringens
Give IV antibiotics for 48-72 hours post injury and again for 48-72 hours each
time a further procedure is performed. Prolonged antibiotics for more than 3
days does not further prevent infection . Restricting the antibiotics should
minimise the emergence of resistant bacteria
70% of open fractures are contaminated with bacteria at the time of injury
Most common initial contaminants are skin flora (Staph Epidermidis,
proprionobacterium acnes, Corynebacterium species, Micrococcus)
Despite this, many infections are caused by Staph aureus and pseudomonas
aeruginosa suggesting hospital acquired infection
Operative debridement and copious irrigation
Small wounds should be extended and excised to allow adequate exposure
Unattached bone should be discarded
For type 11 and 111 fractures irrigate with 5-10 litres of saline
Repeat debridement at 48 hourly intervals
Stabilisation of the fracture
Reduces rates of infection
Promotes soft tissue healing
Facilitates wound care
Allows mobilisation of the limb , particularly important in multiply injured
patients
Preferably performed at the time of initial debridement
Coverage and closure of the wound
Aim for soft tissue coverage of the wound as early as possible to avoid
infection, optimise the milieu for bone healing
Timing of coverage- 1990 aiming for coverage by 5-7 days was reasonable
Now 'fix and flap' treatment advocated by some ( Gopal et al. JBJS. [Br]
2000;82-B:959-66. )
Options in stabilisation of an open fracture
No one method is optimum for stabilisation of all open fractures
External fixation
Advantages
Versatile
Disadvantages
Risk of pinsite infection
Ease of application with minimal
operative trauma
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Maintenance of access to wound
Intramedullary nailin g
Plate and screws
Useful in displaced intraarticular fracture fixation
Splints casts and traction
Can be used in stable type 1 fractures
Beware compartment syndrome
Options in coverage and closure of the wound
Primary delayed closure
Suturing skin directly
Split skin graft
Flaps
Choice depends on
Age and needs of patient
Location size and condition of the defect
The likelihood that further reconstruction will be needed
The associated zone of surrounding soft tissue injury
The tissues available for the flap
Types of flap
Fasciocutaneous
Transposed muscle pedicle
Free microvascular muscle flap
Compartment syndrome
Can occur in open fractures beware!!!!!!
Amputation indications
Absolute indications
Type 111C injury accompanied by damage to the posterior tibial nerve
Type 111 C injury with massive loss of bone
See MESS score
Fix and flap: the radical orthopaedic and plastic treatment of severe open fractures of
the tibia
S. Gopal, S. Majumder, A. G. B. Batchelor, S. L. Knight, P. De Boer, R. M. Smith
From St James's University Hospital, Leeds and York District Hospital, York, England
J Bone Joint Surg [Br] 2000;82-B:959-66.
We performed a retrospective review of the case notes of 84 consecutive patients who
had suffered a severe (Gustilo IIIb or IIIc) open fracture of the tibia after blunt trauma
between 1990 and 1998. All had been treated by a radical protocol which included
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early soft-tissue cover with a muscle flap by a combined orthopaedic and plastic
surgery service. Our ideal management is a radical debridement of the wound outside
the zone of injury, skeletal stabilisation and early soft-tissue cover with a vascularised
muscle flap. All patients were followed clinically and radiologically to union or for one
year.
After exclusion of four patients (one unrelated death and three patients lost to
follow-up), we reviewed 80 patients with 84 fractures. There were 67 men and 13
women with a mean age of 37 years (3 to 89). Five injuries were grade IIIc and 79 grade
IIIb; 12 were site 41, 43 were site 42 and 29 were site 43. Debridement and stabilisation
of the fracture were invariably performed immediately. In 33 cases the soft-tissue
reconstruction was also completed in a single stage, while in a further 30 it was
achieved within 72 hours. In the remaining 21 there was a delay beyond 72 hours,
often for critical reasons unrelated to the limb injury. All grade-IIIc injuries underwent
immediate vascular reconstruction, with an immediate cover by a flap in two. All were
salvaged. There were four amputations, one early, one mid-term and two late, giving a
final rate of limb salvage of 95%. Overall, nine pedicled and 75 free muscle flaps were
used; the rate of flap failure was 3.5%. Stabilisation of the fracture was achieved with
19 external and 65 internal fixation devices (nails or plates). Three patients had
significant segmental defects and required bone-transport procedures to achieve
bony union. Of the rest, 51 fractures (66%) progressed to primary bony union while 26
(34%) required a bone-stimulating procedure to achieve this outcome. Overall, there
was a rate of superficial infection of the skin graft of 6%, of deep infection at the site of
the fracture of 9.5%, and of serious pin-track infection of 37% in the external fixator
group. At final review all patients were walking freely on united fractures with no
evidence of infection.
The treatment of these very severe injuries by an aggressive combined orthopaedic
and plastic surgical approach provides good results; immediate internal fixation and
healthy soft-tissue cover with a muscle flap is safe. Indeed, delay in cover (>72 hours)
was associated with most of the problems. External fixation was associated with
practical difficulties for the plastic surgeons, a number of chronic pin-track infections
and our only cases of malunion. We prefer to use internal fixation. We recommend
primary referral to a specialist centre whenever possible. If local factors prevent this
we suggest that after discussion with the relevant centre, initial debridement and
bridging external fixation, followed by transfer, is the safest procedure.
Sponsored Links
www.ebimedical.com
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08/10/2007 11:06
Physeal Fractures
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the
site policies for rules on diseminating site content.
Physeal Fractures
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08/10/2007 11:06
Physeal Fractures
Aetiology of premature partial growth plate arrest
1. Trauma: 80%
Salter-Harris Type 1: 5%
Salter Harris Type 2: 5%
Salter Harris Type 5: 0% ?
2. Infection: 10%
3. Tumour: 5%
4. Iatrogenic (pins, stapes): 2%
5. Irradiation: 2%
6. Burns: 1%
Location of physeal arrest
1.
2.
3.
4.
5.
6.
7.
8.
9.
Distal Femur: 39%
Proximal Tibia: 18%
Distal Tibia: 30%
Distal Radius: 5%
Distal Ulna: 3%
Distal Fibula: 1%
Proximal Humerus: 1%
Proximal Phalanx Great Toe: 1%
Pelvis (tri-radiate): 1%
Types of Bridge formation
1. Peripheral
Involves the zone of Ranvier, important in latitudinal growth of the physis.
May -> severe angular deformity -> surgical approach from the periphery excising the overlying
periosteum.
2. Linear
Osseous bridge extends as a linear structure across the physis. Most common site is the medial
malleolus. May also lead to significant angular deformity -> may remove making a tunnel through the
bone.
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08/10/2007 11:06
Physeal Fractures
3. Central
The most severe type of injury and the most difficult to rectify surgically. Bridge is completely
surrounded by normal cartilage. Affects longitudinal growth predominantly. Needs to be approached
from the metaphysis. Do not replace bone excised from the bridge in filling the metaphyseal defect.
Harris lines appear after restoration of growth following a physeal injury, the line being due to slowing of
growth for a variable period following injury. If these lines are parallel to the physis then damage to growth is
unlikely
Excision of an osseous bridge that constitutes 50% or more of the entire area of the physis usually gives a
poor result.
Substances used to fill defect
Fat
Autogenous, no need to remove
May need second incision to get graft
May float out with release of tourniquet
Shown to enlarge as growth occurs
Silastic
Inert, mouldable to cavity and easily removed
Need special authorisation for use
Must be sterilised, infections reported
Fractures at site of insertion reported
PMMA
Light, inert, non-conductive, transparent (no barium)
Mouldable to defect, good haemostasis,
No fractures reported
No need to remove later but may be difficult if necessary
Packed sterile, no infections reported
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08/10/2007 11:06
Physical Abuse of Children / Non-Accidental Injuries
1 of 2
Statistics show that more than half the victims of child abuse have fractures. The orthopedic
surgeon will often be the first person to identify a potentially abused child.
The safest pathway for the child and clinician is to make a child abuse report in all
suspicious cases.
Risk Factors for Child Abuse
single parent household, particularly father-only households
Household income does not relate to increase risk
Medical History
(1) Who witnessed the event?
Child abuse is unusual in a group setting. If, by history, multiple adults
witnessed the event, it is more likely to be accidental, and it is easy to verify
the history.
If possible, the adult witnesses should be interviewed separately.
(2) Was there a delay in seeking medical care?
Child abusers tend to delay seeking care for their injured children.
(3) Is the history plausible?
(4) What is the mechanism of injury?
Does the parent's story fits that mechanism
(5) Does the history change over time?
Parents who have abused their children may modify the medical history over
time.
(6) History of failure to thrive
(7) previous unusual injury (eg, fractured femur in a child 6 months of age)
(8) A history of a serious high-risk injury or unexplained death in a sibling
(9) Missed immunizations
(10) Lack of medical records
Physical Examination
The child should be weighed and measured, since abused and neglected children
are often small for their age.
Every child should be undressed and examined for cutaneous injury, including a
careful inspection of the genitalia and anus, since many children who are victims of
physical abuse may also be sexually abused.
Palpation over the long bones and joints and assessment of joint motion
Any tender area suggesting a fracture should be radiographed even in an older child
where the skeletal survey is less valuable.
In young children with signs of head injury, such as altered states of consciousness,
seizure, apnea, or abnormal head growth, a detailed fundoscopic examination
should be done to assess for retinal hemorrhages.
Bruises to the external ears and face are commonly seen in children with closed
head injury.
The mouth should be examined for evidence of a torn frenulum of the upper lip or
other dental or mucous membrane trauma.
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The external ear canal and tympanic membranes may reveal evidence of "hidden"
injury such as hemotympanum.
Abdominal bruises or abdominal distension and vomiting may be clues to a
ruptured viscus.
Radiographic Evaluation
A skeletal survey should be obtained in any child less than 2 years of age where
there is a suspicion of physical child abuse.
If the skeletal survey is negative and there is a strong suspicion of fracture, an
isotope bone scan may identify fractures not seen on skeletal survey
Laboratory
Because children with certain genetic syndromes can bruise more easily, if the
physical examination suggests a syndrome (eg, laxity of skin and hypermobile joints
seen in Ehlers-Danlos syndrome), a genetic evaluation is indicated.
In a child with bruising, parents often suggest that the child bruises easily. A
prothrombin time, partial thromboplastin time, and platelet count are always
indicated. In a situation where easy bruising persists in a protected environment or
history or physical examination suggests coagulopathy, further more sophisticated
coagulation evaluation is suggested. .
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08/10/2007 11:07
Plaster of Paris
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Plaster of Paris
Plaster of Paris
K Sampathkumar, 2005
Plaster of Paris is a derivative of Gypsum
Gypsum is a very soft mineral composed of Calcium sulphate
dihydrate
Chemical formula for Gypsum CaSO 4 · 2H 2 O.
Because the gypsum from the quarries of the Montmartre district of
Paris has long furnished burnt gypsum used for various purposes, this
material has been called plaster of Paris.
How is Plaster of Paris formed?
Heating gypsum above approximately 150 °C partially dehydrates the
mineral by driving off exactly 75% of the water contained in its chemical
structure.
CaSO 4 ·2H 2 O + heat Ãƒ ¢ ' CaSO 4 · ½H 2 O + 1 ½H 2 O (steam)
The partially dehydrated mineral is called calcium sulfate hemihydrate or
commonly known as plaster of Paris (CaSO 4 · ½H 2 O).
·
The dehydration (specifically known as calcination ) begins at
approximately 80 °C (176 °F) and the heat energy delivered to the gypsum at
this time tends to go into driving off water (as water vapor) rather than
increasing the temperature of the mineral, which rises slowly until the water is
gone, then increases more rapidly.
·
This is an endothermic reaction.
·
calcium sulfate hemihydrate has an unusual property: when mixed
with water at normal (ambient) temperatures, it quickly reverts chemically to
the preferred dihydrate form, while physically "setting" to form a rigid and
relatively strong gypsum crystal lattice:
CaSO 4 · ½H 2 O + 1 ½H 2 O Ãƒ ¢ ' CaSO 4 ·2H 2 O This reaction is
exothermic .
·
This phenomenon is responsible for the ease with which gypsum can
be cast into various shapes including sheets (for drywall), sticks (for
blackboard chalk), and molds (to immobilize broken bones, or for metal
casting).
(CaSO 4 , 2 H 2 O) + heat = (CaSO 4 , ½ H 2 O) + 1.5 H 2 O
Plaster of Paris is a calcium sulfate hemi-hydrate : (CaSO 4 , ½ H 2 O)
derived from gypsum, a calcium sulfate dihydrate (CaSO 4 , 2 H 2 O), by
firing this mineral at relatively low temperature and then reducing it to powder.
Calcination of the gypsum at higher temperatures produces different types of
anhydrites (CaSO 4 ), as shown on the table below
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08/10/2007 11:07
Post-fracture infection
1 of 1
Post-fracture infection
Post-Fracture
Pathology & Diagnosis
Prevention & Treatment
Diagnosis
- Soft tissues/discharge
- X-rays
- Blood cultures
- ESR/CRP/WBC
- Further imaging
Gavin Bowyer
Anatomic Classification
Infection
Cierny & Mader; Orthop Rev
1987
Assessing the Problem
Post-Fracture Infection
Staging
- Cierny & Mader
- Anatomy and Physiology
- Stability
- Soft tissues
- Bacteriology
Physiological Class of Host
- A - Normal
- B - Compromised
- B1 - locally
- B2 - systemically (inc.
smoker!)
- B3 - local and systemic
- C - Treatment worse than
disease
Skeletal stability
- Stable, quality soft tissue
envelope
- Eradication of infection
Return to Function
Sponsored Links
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08/10/2007 11:08
Robert Danis
1 of 2
Robert Danis
By A. Danis
The work of Robert Danis on rigid internal
fixation and early functional rehabilitation
served as a stimulus to the founding of AO in
1958.
A graduate of the Free University of Brussels
in 1904, Robert Danis enjoyed a long and
brilliant career. Interested in thoracic surgery,
he conceived and constructed a positive
pressure anaesthetic apparatus that
prevented lung collapse with open
thoracotomy (1909), followed in 1912 with a
more simplified second model. He then
became interested in the surgery of the blood
vessels. He experimented with vascular
anastomoses and investigated the uses of
blood clotting after anastomosis. He invented
an automatic citration syringe for direct
transfusion from donor to recipient, as well as
an instrument for porto-caval anastomosis
without interruption of the circulation. His
works provide the material for his thesis on
"Vascular Anastomosis and Ligatures"
(1912).
He then undertook work on regional anesthesia, particularly of the trunk and the sacral
roots, for which he was awarded the Seutin prize in 1914.
Attached to the Hospice de Bruxelles during the period 1913 to 1920, he became familiar
with the surgery of hernias, amputation, of the breast and thyroidectomy, performed under
local or regional anesthesia on ambulant patients who, in the evening after surgery, were
taken home by cab. Danis then followed them up on a domiciliary basis.
In 192 1 he occupied the Chair of Theory and Practice of Operative Surgery and was
entrusted with the Directorship of the Gynaecological Clinic. Together with his mentor
Antoine Depage he developed a radical technique for mastectomy for breast cancer, with a
51 % five year survival.
A new area then started to absorb him, namely the operative treat-treatment of fractures.
On a new table of his own invention, the fracture was immobilized by traction and the
fragments then sutured with stainless steel wire, either using a transcortical technique, or
by cerdage. His book "Technique of Osteosynthesis" summarized his early results (1932).
Exasperated by the slowness of manufacturers, he installed in his cellar a fully equipped
mechanical workshop where he fashioned screws of various types and the necessary
associated instrumentation. He even manufactured a reciprocating saw driven by a cable
motor.
Constantly seeking perfection of his instrumentation he finally produced an axial
compression plate. By axially compressing the main bone fragments, it produced such
stability that early functional rehabilitation, without external splintage, became possible. The
sum of he and his collaborators' vast experience, almost 2000 cases in 20 years was
published in 1949 as " The Theory and Practice of Osteosynthesis ". This major work
earned him an international reputation and his election to the Presidency of the
International Society of Surgery. Without affecting his natural modesty he accepted
numerous honourable distinctions, including Doctor Honoris Causa of the Universities of
Strasbourg, Dublin and Paris, Honorary Fellowship of the Royal College of Surgeons of
England, of the American College of Surgeons, and the Association of Surgeons of Great
Britain and Northern Ireland, as well as Member of Honour of the Societies of Lyon,
Marseilles, of Greece and of Switzerland. He became Vice President of the Royal Academy
of Medicine of Belgium.
His teaching sessions enriched by blackboard
drawings, executed with both hands at the same
time, and also by cinÃƒ© film in the operating
theatre, led to a diagnostic and therapeutic style far
from dogmatic theory. He was a great patron and a
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Robert Danis
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teacher of rare authority, respected by his pupils.
adored by his patients.
As a student he was an accomplished swordsman
and shot. As a young doctor he hunted game in
Sudan in the company of Arnold Solvay. His trophies
of antelopes, buffalo and lion illustrated a synergetic
passion, which lasted his whole life. During the
German occupation of Belgium his guns were
replaced by a fishing rod.
In 1919, judging the car to be beyond his finances,
he conceived of a vehicle made of metal tubing with
a motor in the centre and the radiators on the sides.
Unfortunately, the weakness of the brakes caused
him to give up the project alter a year.
As a youngster it became evident that he was an accomplished artist in drawing water
colour, copper engraving and oil painting. His life never ceased to he enriched by his
pictures, sketches and caricatures. To his own self portraits he added those of his family,
the family pets and the countryside.
Finally setting aside the scalpel, his passion for music took over. Brought up among
musicians he had received his first piano lessons from his mother. He studied musical
theory and was able to learn by heart many entire musical scores. He played the guitar to
keep his fingers supple and then the saxophone, which he rapidly abandoned for the
harmonium, before returning to the piano.
In his last years he improvised numerous musical pieces, which he recorded as written
scores. On one of his trips he discovered the novel sounds of the electronic organ; thus
equipped, he played and recorded ceaseless dozens of compositions born of his musical
personality. Those gathered at his table, discovered with surprise that he also had great
talents in the kitchen.
His robust health shielded him from illness and without infirmity and in full possession of
his faculties he ignored the ageing process. His end was brief and without suffering.
[ Close Window ]
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Traction
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content.
Traction
Introduction
Introduction
Definitions
Specific Types of Traction
Knots
[Back To Top]
Traction produces a reduction through the surrounding soft parts which align the fragments by their tension.
When the shaft of a long bone is fractured the elastic retraction of muscles surrounding the bone tends to produce over-riding of the fragments. This tendency is greater when the muscles are
powerful and long bellied as in the thigh, when the fracture is imperfectly immobilised so that there is pain and therefore muscle spam and when the fracture is mechanically unstable because the
fragments are not in apposition or because the fracture line is oblique.
Continuous traction generated by weights and pulleys in addition to causing reduction of a deformity will also produce a relative fixation of the fragments by the rigidity conferred by the
surrounding soft tissue structures when under tension. It also enables maintenance of alignment while at the same time it is possible to devise apparatus which permit joint movement.
Traction may be applied through traction tapes attached to skin by adhesives or by direct pull by transfixing pins through or onto the skeleton.
Traction must always be apposed by counter traction or the pull exerted against a fixed object, otherwise it mealy pulls the patient down or off the bed.
Traction requires constant care and vigilance and is costly in terms of the length of hospital stay and all the hazards of prolonged bed rest - thromboembolism, decubiti, pneumonia and atelectasis
must be considered when traction is used
Excessive traction which leads to distraction of the fracture is undesirable. Once the fracture is reduced a decreasing amount of weight is required to maintain a reduction once the muscle stretch
reflex has been overcome and the fracture immobilised. For a femoral fracture no more than 10lbs should be used and for fractures of the tibia and upper limb less weight is required.
Skin Traction
Traction is applied to the skeleton through its attached soft tissued and in the adult should be used only as a temporary measure.
Skin is designed to bear compression forces and not shear. If much more than 8lbs is applied for any length of time it results in superficial layers of skin pulled off. Other difficulties such as
migration of the bandage may occur with lower weights.
Skeletal Traction
First achieved by the use of tongs.
The application of traction applied by a pin transfixing bone was introduced by Fritz Steinmann. Now a threaded Denham pin is preferred to prevent early loosening of the device.
The threaded portion of the Denham pin is offset, closer to the end of the pin held in the drill chuck and should engage only the proximal cortex of the recipient long bone.
Max. 18kg(40lb) can be used
Steinmann pin - 3mm diameter
Denham pin - 3mm & central threaded portion (resists lateral motion & thus infection)
Bohler Stirrup, Simonis Swivels(allow joint motion)
Braun Frame- can attach calcaneal/tibial/femoral
Pearson Attachment- for Thomas splint, allows knee flexion, with tibial skeletal traction, hinge centred on adductor tubercle of femur (axis knee rotation)
Traction by Gravity Really only applies to fractures of the upper limb (hanging cast)
Definitions
[Back To Top]
Traction on a limb demands either a fixed point from which the traction may be exerted (fixed traction) or an equal counter-traction in the opposite direction
(balanced traction)
Fixed Traction
The length of the limb remains constant and there is continuous diminution of traction force as the tone in the muscles diminishes and no further stimuli
results in activation of the muscle stretch reflex.
Pull is exerted against a fixed point for example tapes are tied to the cross piece of a Thomas splint and the leg pulled down until the root of the limb abuts
against the ring of the splint.
Pins in plaster is a form of fixed traction
Balanced Traction
The pull is exerted against an opposing force provided by the weight of the body when the foot of the bed is raised.
Combined Traction
May be used in conjunction with fixed traction where the weight takes up any slack in the tapes or cords while the splint maintains a reduction.
This combination facilitates less frequent checks and adjustment of the apparatus
Sliding Traction
First introduced by Pugh by applying traction tapes to the limb and fastening them to the raised foot of the bed which was then inclined head down.
He utilised this traction in the treatment of conditions such as Perthes where only one limb was fastened to the end of the bed enabling the pelvis on the
opposite side to slide down the bed more thus creating traction and abduction.
The extent to which the patient slides down the bed is limited by the friction of the body against the mattress.
The traction was subsequently modified by Hendry using a mattress on a sliding frame which resulted in the same amount of traction with an inclination of 10
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Traction
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o
o
as that with that on a normal mattress at 30 - 40 inclination.
This is also really a form of balance traction where the amount of weight is determined by the inclination of the bed.
Specific Types of Traction
[Back To Top]
Thomas Splint Traction
Hugh Owen Thomas introduced his splint which he called "The Knee Appliance" in 1875.
The method of Hugh Owen Thomas uses fixed traction with the counter traction being applied against the perineum by the ring of the splint. This is in
contrast to other methods using weight traction which is countered by the weight of the body.
Backward angulation of the distal fragment can never be corrected by traction in the axis of the femur which only results in elongation with persistence
of the deformity.
A Thomas splint and fixed traction is only capable of maintaining a reduction previously achieved by manipulation. The use of supports enables
correction of angulation caused by muscle tension.
Placement of a large pad behind the lower fragment acts as a fulcrum over which backward angulation is then corrected by the traction force. The
pad should be ~ 6" in width, 9" long and 2" thick applied transversely across the splint under the distal fragment and popliteal fossa
It is the splint which controls alignment and not the traction.
The tension in the apparatus should only be that sufficient to balance resting muscle tone.
Suspension of the splint using an overhead beam in such a way to enable the splint to move easily with the patient when they move in bed.
Its use in combination with a Pearson Knee-flexion piece enables mobilisation of the knee while maintaining traction, alignment and splintage of the
fracture.
Thomas splint traction with Pearson knee flexion piece
Hamilton Russell Traction
Robert Hamilton Russell wrote "Fracture of the femur: A clinical study" in which he described his traction in 1924.
Sling under the distal 1/3 of the thigh providing upward lift as well as longitudinal traction in the line of the tibia.
The sling under the distal fragment controls posterior angulation and the lifting force is related to the main traction force through the medium of pullies.
No rigid splintage is used in this method
Combines a means of suspending the lower extremity and a means of applying traction in the axis of the femur.
Many other varieties of both skeletal and skin traction result in a similar effect.
Summary- 2 vectors, sling under knee, single cord + 3 pulleys or 2 traction cords (modified HR) (Need Balkan beams)
Buck Traction
Buck introduced simple horizontal traction in 1861.
Traction is analogous to Pugh's traction only the inclination of the bed is replaced by the application of weights over a pulley.
Bryant's traction
Vertical extension traction was described by Bryant in 1873 and applied to the management of femoral fractures.
The development of ischaemia of the lower leg through reduced perfusion resulted in limitation of its application to the short term management of a
fractured femur.
A modification of his traction has been shown to reduce the risk of limb ischaemia and may be applicable where prolonged traction is required in an
infant.
Braun Frame
This is mearly a cradle for the limb but a disadvantage is that the position of the pulleys cannot be altered and the size of the splint often does not fit
the limb as might be wished.
Lateral bowing is common as the splint and the distal fragment are fixed to the frame while the patient and the proximal fragment can move sideways
leaving the frame behind.
Perkins Traction
Here no splintage is used at all, the posterior angulation of the thigh is controlled by a pillow and the alignment and fixation depend entirely on the
action of continuous traction
Fisk Traction
o
Hinged version of a Thomas splint is arranged to allow 90 of knee movement. It is particularly attractive as it allows active extension of the knee
joint. Fixation and alignment is dependent entirely on the weight traction and the splint merely applies the motive power for assisted knee movement.
90 - 90 Traction
The thigh is suspended in the vertical plane by weight traction pulling vertically upwards. The ill effect of gravity as the cause of backward angulation
of the fragments is thus eliminated.
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Traction
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Charnley
Strongly recommends the use of a BK POP incorporating the Steinmann or Denham pin in the upper end in order to reduce pressure on the soft structures
around the knee.
Benefits of POP/Traction unit: (Charnley)
Foot supported at right angles to the tibia
Common peroneal nerve and calf muscles protected from pressure against the slings of the splint and the splint itself. The tibia is suspended from the
skeletal pin inside the POP so that an air space develops under the tibia as the calf muscles loose their bulk.
External rotation of the foot and distal fragments is controlled.
The tendo achilles is protected from pressure sores
Comfort; The patient is unaware of the traction when applied through the medium of a nail
Upper Limb A number of skin traction methods have been described and a number more utilised without documentation in the literature.
Dunlop's sidearm skin traction
for humeral supracondylar #
shoulder abducted 45deg, elbow flexed 45deg, weighted sling over distal humerus 0.5kg + weighted skin traction to forearm 1kg -> resultant force in
line of humerus.
Graham's extension skin traction
Ingerbrightsen's overhead skin traction
Skeletal pin traction can also be utilised:
Overhead
Overhead with secondary distal forearm traction directed cephalad
side arm pin traction
Spine
Halter- cervical spine spondylosis, 1.4-2.3kg
Cotrels- intermittent, for scoliosis, legs + halter
Useful Knots
[Back To Top]
Overhand
loop
Slip knot
Reef knot
Clove hitch
passes around an object in only one direction, thus puts very little strain on the rope fibers.
Tying it over an object that is open at one end is done by dropping one overhand loop over
the post and drawing them together. The other method of tying it is used most commonly if
the object is closed at both ends or is too high to toss loops over. The latter is used in
starting and finishing most lashings.
Barrel hitch
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Traction
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Definitions
[Back To Top]
Traction on a limb demands either a fixed point from which the traction may be exerted (fixed traction) or an equal counter-traction in the opposite direction (balanced traction)
Fixed Traction
The length of the limb remains constant and there is continuous diminution of traction force as the tone in the muscles diminishes and no further stimuli results in activation of the muscle
stretch reflex.
Pull is exerted against a fixed point for example tapes are tied to the cross piece of a Thomas splint and the leg pulled down until the root of the limb abuts against the ring of the splint.
Pins in plaster is a form of fixed traction
Balanced Traction
The pull is exerted against an opposing force provided by the weight of the body when the foot of the bed is raised.
Combined Traction
May be used in conjunction with fixed traction where the weight takes up any slack in the tapes or cords while the splint maintains a reduction.
This combination facilitates less frequent checks and adjustment of the apparatus
Sliding Traction
First introduced by Pugh by applying traction tapes to the limb and fastening them to the raised foot of the bed which was then inclined head down.
He utilised this traction in the treatment of conditions such as Perthes where only one limb was fastened to the end of the bed enabling the pelvis on the opposite side to slide down the bed
more thus creating traction and abduction.
The extent to which the patient slides down the bed is limited by the friction of the body against the mattress.
The traction was subsequently modified by Hendry using a mattress on a sliding frame which resulted in the same amount of traction with an inclination of 10 o as that with that on a normal
mattress at 30 - 40 o inclination.
This is also really a form of balance traction where the amount of weight is determined by the inclination of the bed.
Specific Types of Traction [Back To Top]
Thomas Splint Traction
Hugh Owen Thomas introduced his splint which he called "The Knee Appliance" in 1875.
The method of Hugh Owen Thomas uses fixed traction with the counter traction being applied against the perineum by the ring of the splint. This is in contrast to other methods using
weight traction which is countered by the weight of the body.
Backward angulation of the distal fragment can never be corrected by traction in the axis of the femur which only results in elongation with persistence of the deformity.
A Thomas splint and fixed traction is only capable of maintaining a reduction previously achieved by manipulation. The use of supports enables correction of angulation caused by
muscle tension.
Placement of a large pad behind the lower fragment acts as a fulcrum over which backward angulation is then corrected by the traction force. The pad should be ~ 6" in width, 9"
long and 2" thick applied transversely across the splint under the distal fragment and popliteal fossa
It is the splint which controls alignment and not the traction.
The tension in the apparatus should only be that sufficient to balance resting muscle tone.
Suspension of the splint using an overhead beam in such a way to enable the splint to move easily with the patient when they move in bed.
Its use in combination with a Pearson Knee-flexion piece enables mobilisation of the knee while maintaining traction, alignment and splintage of the fracture.
Thomas splint traction with Pearson knee flexion piece
Hamilton Russell Traction
Robert Hamilton Russell wrote "Fracture of the femur: A clinical study" in which he described his traction in 1924.
Sling under the distal 1/3 of the thigh providing upward lift as well as longitudinal traction in the line of the tibia.
The sling under the distal fragment controls posterior angulation and the lifting force is related to the main traction force through the medium of pullies. No rigid splintage is used in
this method
Combines a means of suspending the lower extremity and a means of applying traction in the axis of the femur.
Many other varieties of both skeletal and skin traction result in a similar effect.
Summary- 2 vectors, sling under knee, single cord + 3 pulleys or 2 traction cords (modified HR) (Need Balkan beams)
Buck Traction
Buck introduced simple horizontal traction in 1861.
Traction is analogous to Pugh's traction only the inclination of the bed is replaced by the application of weights over a pulley.
Bryant's traction
Vertical extension traction was described by Bryant in 1873 and applied to the management of femoral fractures.
The development of ischaemia of the lower leg through reduced perfusion resulted in limitation of its application to the short term management of a fractured femur.
A modification of his traction has been shown to reduce the risk of limb ischaemia and may be applicable where prolonged traction is required in an infant.
Braun Frame
This is mearly a cradle for the limb but a disadvantage is that the position of the pulleys cannot be altered and the size of the splint often does not fit the limb as might be wished.
Lateral bowing is common as the splint and the distal fragment are fixed to the frame while the patient and the proximal fragment can move sideways leaving the frame behind.
Perkins Traction
Here no splintage is used at all, the posterior angulation of the thigh is controlled by a pillow and the alignment and fixation depend entirely on the action of continuous traction
Fisk Traction
Hinged version of a Thomas splint is arranged to allow 90 o of knee movement. It is particularly attractive as it allows active extension of the knee joint. Fixation and alignment is
dependent entirely on the weight traction and the splint merely applies the motive power for assisted knee movement.
90 - 90 Traction
The thigh is suspended in the vertical plane by weight traction pulling vertically upwards. The ill effect of gravity as the cause of backward angulation of the fragments is thus
eliminated.
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Traction
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Charnley
Strongly recommends the use of a BK POP incorporating the Steinmann or Denham pin in the upper end in order to reduce pressure on the soft structures around the knee.
Benefits of POP/Traction unit: (Charnley)
Foot supported at right angles to the tibia
Common peroneal nerve and calf muscles protected from pressure against the slings of the splint and the splint itself. The tibia is suspended from the skeletal pin inside the POP so
that an air space develops under the tibia as the calf muscles loose their bulk.
External rotation of the foot and distal fragments is controlled.
The tendo achilles is protected from pressure sores
Comfort; The patient is unaware of the traction when applied through the medium of a nail
Upper Limb A number of skin traction methods have been described and a number more utilised without documentation in the literature.
Dunlop's sidearm skin traction
for humeral supracondylar #
shoulder abducted 45deg, elbow flexed 45deg, weighted sling over distal humerus 0.5kg + weighted skin traction to forearm 1kg -> resultant force in line of humerus.
Graham's extension skin traction
Ingerbrightsen's overhead skin traction
Skeletal pin traction can also be utilised:
Overhead
Overhead with secondary distal forearm traction directed cephalad
side arm pin traction
Spine
Halter- cervical spine spondylosis, 1.4-2.3kg
Cotrels- intermittent, for scoliosis, legs + halter
Useful Knots
[Back To Top]
Overhand
loop
Slip knot
Reef knot
Clove hitch
passes around an object in only one direction, thus puts very little strain on the rope fibers.
Tying it over an object that is open at one end is done by dropping one overhand loop over
the post and drawing them together. The other method of tying it is used most commonly if
the object is closed at both ends or is too high to toss loops over. The latter is used in
starting and finishing most lashings.
Barrel hitch
[ Close Window ]
08/10/2007 11:09
Traumatology and Orthopedic surgery in Europe
1 of 3
Adapted from U. Heim's historical review previously published in EFORT Bulletin
Accidental injury can be traced back throughout the history of mankind. Its treatment is
surgical and first concerned with saving life, and only then limbs or organs.
Emergency surgery is a dramatic art, the progress of which has been intimately linked to
warfare. Two remarkable military surgeons were J.F. Percy (1754-1825) and D. Larrey
(1768-1842) (Fig.1). Against military orders, they went with teams and equipment (the flying
ambulance) on to the Napoleonic battlefields to render immediate aid to the wounded. Their
example was long forgotten. It is only very recently that the surgeon himself has again been
able to be present at the site of modern traffic carnage.
Orthopedic surgery has its roots in antiquity. There was knowledge of the malformations
and deformities of growth, but no means of remedying them. "Cripples were left to survive
only by begging. Their plight was finally addressed (J. Rousseau: Discourse on the origins
and foundations of the inequality among men: Academy of Dijon, 1754) with a new concept
to take care of them: to correct their lesions, to educate them and, if possible, to return
them to society. By clearing them from the streets and into closed establishments the
esthetic sensibilities of the bourgeoisie were protected!
The first person to propose constructive therapeutic ideas was Andry (1658-1742), the
irascible Professor of Medicine in Paris and enemy of surgeons, who wrote in 1741
Orthopaedics or The art of preventing and correcting body deformities in children, published
in English in 1743 and in German in 1744. He had launched a movement.
In 1780 J.A.Venel(1740-179l), who qualified in Monipellier, founded the first Orthopedic
Institute at Orbe, in the Bernese countryside of the Vaud. This served as a model for many
similar Europe-wide establishments that were to open in the first decades of the 19th
century.
Early on, orthopedics became an independent discipline in which long-term treatment was
dominated by the goal of the improvement of the patients' "quality of life" (using current
terminology) but not an unattainable cure. Surgery played only occasionally a role. Children
were in-patients for months or years. These institutions were equipped for mechanical
therapy and gymnastics, each manufacturing prostheses, apparatus, machines and
instruments, and each with a school. Light, fresh air, sun and hydrotherapy were part of
their treatment, tire results of which were sometimes quite remarkable.
J.M. Delpech (1777-1832), Professor of Surgery at the University of Montpellier, was
typical. In 1828, he constructed his own Orthopedic Institute, equipped with vast therapeutic
installations. Delpech also first described subcutaneous tenotomy of tendo Achilhis for
clubfoot (1816). The young Stroniever (1804-1876) from Hannover learned of this
technique and began to practise it himself, but with gradual postoperative correction. A
young English surgeon, W. Little (1810-1894), himself a sufferer of clubfoot, went to
Hannover to have his deformity corrected by Stromeyer. Little had done research work on
the anatomy of clubfoot under Professor J. Muller (1801-1858) of Berlin, one of the leading
anatomists of his time. Delighted by Stromeyer's surgery, Little traveled back to Berlin to
08/10/2007 11:09
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demonstrate the cure to Professor Muller. Working with Muller at that time was
Dieffenbach, who was so amazed by the transformation that he immediately adopted
subcutaneous Achilles tenotomy for clubfoot, although he believed in immediate,
single-stage correction.
The Success of Little's treatment was such that, shortly afterwards in London, he founded
his own Institute for the Treatment of Club Foot, which in 1840 became the "Royal
Orthopedic Hospital'. This is an example of the transfer of knowledge within a Europe
where journeys were long and uncomfortable and where a variety of languages were
spoken.
Everything then changed with the introduction of the plaster cast in 1851 by Mathijsen
(1805-1878) and of anesthesia. Surgery became painless and the limbs could reliably and
individually be immobilized. But it was not before J. Lister (1827- 1912) described
antisepsis in 1867 that bony operations were safer. Expanded orthopedic surgery did not
eclipse the need for long-term cures of chronic illnesses such as rickets and tuberculosis,
which were treated in large country hospitals, such as Berck-Plage.
In the large towns of Germany, adult handicap was treated in a semi-ambulatory way in
those orthopaedic polyclinics (Leipzig 1875 was the first) which were associated with
universities. It was thus that German orthopedics developed a structure the Society was
founded in 1901) and became an independent branch of surgery before 1914.
In the UK, the hospital service was based entirely on a private system. Orthopedic hospitals
existed, but there were no truly specialised surgeons. The protagonists of change were H.
Thomas (1834-1891), known for Iris Thomas's splint, and his nephew, R. Jones
(1858-1933), who became the first president of SICOT. For them and their American
friends, limb traumatology was always part of orthopedics. It was, nevertheless, not until
1946 with the advent of the National Health Service, that each British hospital had its own
orthopedic and traumatology service.
In Italy, two orthopedic hospitals must be mentioned: The first, in an old monastery above
the city of Bologna and named after its donor, the surgeon F. Rizzoli (1809-80), and the
second in Milan, the Instituto Ortopedico. Galeazzi (1866-1852), whose founder described
in 1934 the forearm injury that bears his name.
In Bologna two directors were famous: A. Codivilla (1861-1912) (Fig.2), who published and
conversed fluently in four languages. He described in 1903 transcalcaneal limb traction. his
successor V. Putti (1880-1940), also a multilingual scholar, described in 1916 a
compression hand for the stable fixation of oblique shaft fractures and, in 1938 a
compression screw for fractures of the neck of the femur. At the meeting of the
International Society of Orthopedic Surgery in 1936 in Bologna he was then President. He
successfully proposed adding to the title "et de tramatologie". SICOT was born.
In France, orthopedics was firmly attached to pediatric surgery (the Chair of Kirmisson
(1848-1927) in 1901, then of OmbrÃ©danne). It was not until 1934 that P. Mathieu
(1877-1971) became a Professor of Adult Orthopedics. The turning point for French and
British orthopedics was the presence of all surgeons in the military front hospitals of the
First World War. This was their immersion in trauma. It was therefore not merely by chance
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that their two societies were formed in 1918 arid 1919.
In Belgium, he work of Robert Danis on rigid internal fixation and early functional
rehabilitation served as a stimulus to the founding of AO in 1958.
The German orthopaedic surgeons worked in large military hospitals, practically excluded
from experience at the battle front. The general surgeons preserved their interest in
traumatology, which became progressively independent after 1960. Now, each large
German hospital has a practically independent traumatology service which treats all
accidents and has but rare contact with orthopedics. The large, insurance companies
hospitals (BGU), founded since 1890 in the large industrial centres, have an intermediate
organisation. German traumatology (as in Austria and Hungarv, concentrating on
emergencies. is well developed. There is little contact between orthopedic traumatologists
in other European countries.
We must encourage future generations to learn not only the science and art of surgery but
also to learn languages, and to break down those barriers which remain.
[ Close Window ]
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1 of 2
Injury severity score
Background:
The Injury Severity Score was developed in 1974 by Baker et. al. from
Abbreviated Injury Scale to evaluate motor vehicle victims with multiple injuries.
The Injury Severity Score (ISS) was used to compare the severity of injuries
with an original study group of 2,128 victims, it was observed that the
mortality increased with the AIS grade of the most severe injury.
The mortality increased with regular increments when plotted against the
square of the AIS grade (a quadratic relationship).
When the victims with identical AIS grades for their most severe injury were
compared, injuries in the second and third body regions tended to increase
the risk of death. The Injury Severity Score was therefore defined as " the
sum of the squares of the highest AIS grade in each of the three most
severely injured areas ".
Bull (1975) found an age-dependent relationship and determined that LD50 (Lethal
dose for 50% patients) was an ISS of 40 for ages 15-44, 29 for ages 45-64 and 20
for ages 65 and older.
Bergvist et al (1983) while reviewing thirty years' cases of blunt abdominal trauma
found that in vehicular accident cases, ISS increased successively through the
periods indicating more severe trauma. Although not significant, the frequency of
severe trauma cases (ISS more than 50) increased and the frequency of mild
trauma decreased (ISS less than 25).
Simplified Trauma Chart made by Lorne Greenspan, Barry A. McLellan and Helen
Greig (1985) and used at Toronto General Hospital, Canada includes all the
necessary information for scoring found in 36 page AIS dictionary. This chart not
only facilities the scoring but also increases reliability by preventing errors in
searching through the AIS dictionary. The incorporation of the LD50 reference table
allows for the rapid evaluation of victim's age specific index severity.
Scores:
When ISS is below 25, the mortality risk is minimal and above 25, it is an almost
linear increase.
When ISS is 50, the mortality is 50%
When above 70, it is close to 100%.
If an injury is assigned an AIS of 6 (unsurvivable injury), the ISS score is
automatically assigned to 75.
Highest ISS score obtainable is 75.
For trauma patients of vehicular accidents, the scoring system is important for
assessing the effectiveness of medical care in reducing morbidity and mortality.
Advantages:
virtually the only anatomical scoring system in use
correlates linearly with
1. mortality
2. morbidity
3. hospital stay
4. other measures of severity.
Weaknesses:
Any error in AIS scoring increases the ISS error
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Many different injury patterns can yield the same ISS score
Injuries to different body regions are not weighted
Not a useful triage tool, as a full description of patient injuries is not known prior to
full investigation & operation
ISS Calculator: (From Trauma.org )
Injury AIS Score
1
Minor
2
Moderate
3
Serious
4
Severe
5
Critical
6
Unsurvivable
ISS Calculator
Abbreviated Injury Scale:
Head
Face
Chest
Abdomen
Extremity
External
Calculate
ISS:
Baker SP et al, "The Injury Severity Score: a method for describing patients with multiple
injuries and evaluating emergency care", J Trauma 14:187-196;1974
Copes WS, Sacco WJ, Champion HR, Bain LW, "Progress in Characterising Anatomic
Injury", In Proceedings of the 33rd Annual Meeting of the Association for the Advancement
of Automotive Medicine, Baltimore, MA, USA 205-218
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Mangled Extremity Severity Score (MESS)
1 of 2
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site
policies for rules on diseminating site content.
Johansen et al. 1990
Skeletal / soft-tissue injury
Low energy (stab; simple fracture; pistol gunshot wound)
1
Medium energy (open or multiple fractures, dislocation)
2
High energy (high speed RTA or rifle GSW)
3
Very high energy (high speed trauma + gross contamination)
4
Limb ischaemia
Pulse reduced or absent but perfusion normal
1*
Pulseless, paraesthesias, diminished capillary refill
2*
Cool, paralysed, insensate, numb
3*
Shock
Systolic BP always > 90 mm
0
Hypotensive transiently
1
Persistent hypotension
2
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Age (years)
< 30
0
30-50
1
> 50
2
* Score doubled for ischaemia > 6 hours
Limb salvage vs. amputation. Preliminary results of the Mangled Extremity Severity Score
In both the prospective and retrospective studies, a MESS score of greater than or equal to 7 had a 100% predictable
value for amputation
Objective criteria accurately predict amputation following lower extremity trauma.
Johansen K, Daines M, Howey T, Helfet D, Hansen ST Jr
Department of Surgery, Harborview Medical Center, University of Washington School of Medicine, Seattle 98104.
J Trauma 1990 May;30(5):568-72; discussion 572-3
MESS (Mangled Extremity Severity Score) is a simple rating scale for lower extremity trauma, based on
skeletal/soft-tissue damage, limb ischemia, shock, and age. Retrospective analysis of severe lower extremity injuries
in 25 trauma victims demonstrated a significant difference between MESS values for 17 limbs ultimately salvaged
(mean, 4.88 +/- 0.27) and nine requiring amputation (mean, 9.11 +/- 0.51) (p less than 0.01). A prospective trial of
MESS in lower extremity injuries managed at two trauma centers again demonstrated a significant difference
between MESS values of 14 salvaged (mean, 4.00 +/- 0.28) and 12 doomed (mean, 8.83 +/- 0.53) limbs (p less than
0.01). In both the retrospective survey and the prospective trial, a MESS value greater than or equal to 7 predicted
amputation with 100% accuracy. MESS may be useful in selecting trauma victims whose irretrievably injured lower
extremities warrant primary amputation.
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Revised Trauma Score
The Revised Trauma Score is a physiological scoring system, with high inter-rater reliability
and demonstrated accurracy in predictng death. It is scored from the first set of data
obtained on the patient, and consists of Glasgow Coma Scale, Systolic Blood Pressure
and Respiratory Rate.
Glasgow Coma Scale Systolic Blood Pressure Respiratory Rate Coded Value
(GCS)
(SBP)
(RR)
13-15
>89
10-29
4
9-12
76-89
>29
3
6-8
50-75
6-9
2
4-5
1-49
1-5
1
3
0
0
0
RTS = 0.9368 GCS + 0.7326 SBP + 0.2908 RR
Values for the RTS are in the range 0 to 7.8408. The RTS is heavily weighted towards the
Glasgow Coma Scale to compensate for major head injury without multisystem injury or
major physiological changes. A threshold of RTS < 4 has been proposed to identify those
patients who should be treated in a trauma centre, although this value may be somewhat
low.
The RTS correlates well with the probability of survival :
RTS Calculator: (From Trauma.org)
Systolic BP:
Resp. Rate:
Coma Score:
Calculate
RTS:
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Glascow Coma Scale:
The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of
three parameters : Best Eye Response, Best Verbal Response, Best Motor Response, as
given below :
Best Eye Response. (4)
1. No eye opening.
2. Eye opening to pain.
3. Eye opening to verbal command.
4. Eyes open spontaneously.
Best Verbal Response. (5)
1. No verbal response
2. Incomprehensible sounds.
3. Inappropriate words.
4. Confused
5. Orientated
Best Motor Response. (6)
1.
2.
3.
4.
5.
6.
No motor response.
Extension to pain.
Flexion to pain.
Withdrawal from pain.
Localising pain.
Obeys Commands.
Note that the phrase 'GCS of 11' is essentially meaningless, and it is important to break
the figure down into its components, such as E3V3M5 = GCS 11.
A Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate
injury and 8 or less a severe brain injury.
Teasdale G., Jennett B., LANCET (ii) 81-83, 1974.
Champion HR et al, "A Revision of the Trauma Score", J Trauma 29:623-629,1989
Champion HR et al, "Trauma Score", Crit Care Med 9:672-676,1981
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08/10/2007 11:10
Bibliography, Links & Recommended Reading
1 of 4
The following Websites & Books were used in compiling the Orthoteer
Summaries: ( Bold = Essential)
Books:
Review of Orthopaedics - Mark Miller
Campbells Operative Orthopedics - Terry Canale
Principles of Orthopaedic Practice - Dee & Hurst
Apley
Orthopaedic Knowledge Updates
Websites:
South Australian Orthopaedic Registrars' Notebook
Entrez-PubMed
University of Washington Radiology Webserver
Journals:
Current Orthopaedics
The Journal of Bone and Joint Surgery
BASIC SCIENCE
Sciences Basic to Orthopaedics - Sean Hughes & Ian
McCarthy; WB Saunders, 1998.
08/10/2007 11:11
2 of 4
The Developing Human - Moore & Persuad
duPont PedOrtho Education Modules
Resident Education Home Page, ALFRED I. DUPONT
INSTITUTE
British Society for Children's Orthopaedic Surgery
McGloughlin & Mann.Surgery of the Foot and Ankle.
1999. Mosby.
Barton. The Upper Limb & Hand. 1999.
Electronic Textbook of Hand Surgery
eRadius - International Distal Radius Fracture Study
Group
Copeland. Operative Shoulder Surgery. 1995.
Churchill Livingstone.
Websites:
Entrez-PubMed
Journals:
BASIC SCIENCE
The Developing Human - Moore &
Persuad
08/10/2007 11:11
3 of 4
Resident Education Home Page, ALFRED I.
DUPONT INSTITUTE
British Society for Children's Orthopaedic
Surgery
McGloughlin & Mann.Surgery of the Foot and Ankle. 1999.
Mosby.
eRadius - International Distal Radius Fracture
Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill
Livingstone.
Websites:
Entrez-PubMed
Journals:
BASIC SCIENCE
The Developing Human - Moore &
Persuad
Resident Education Home Page, ALFRED I.
DUPONT INSTITUTE
British Society for Children's Orthopaedic
Surgery
McGloughlin & Mann.Surgery of the Foot and Ankle. 1999.
Mosby.
08/10/2007 11:11
4 of 4
eRadius - International Distal Radius Fracture
Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill
Livingstone.
Apley
Websites:
Entrez-PubMed
Journals:
BASIC SCIENCE
Sciences Basic to Orthopaedics - Sean Hughes & Ian McCarthy; WB
Saunders, 1998.
The Developing Human - Moore & Persuad
Resident Education Home Page, ALFRED I. DUPONT
INSTITUTE
British Society for Children's Orthopaedic Surgery
McGloughlin & Mann.Surgery of the Foot and Ankle. 1999. Mosby.
eRadius - International Distal Radius Fracture Study Group
Copeland. Operative Shoulder Surgery. 1995. Churchill Livingstone.
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08/10/2007 11:11
Clinical governance
1 of 1
Clinical governance
CMO 's Update 22 - a communication to all doctors from the Chief Medical Officer
Clinical governance: quality in the new NHS was issued to the National Health Service
(NI-IS) on 16 March 1999. It provides the detailed guidance promised in A first class
service2, and builds on the responses to that consultation exercises.
The guidance provides a vision for the next five years, identifying the key features that all
NHS organisations will be expected to demonstrate. It takes a developmental approach,
focusing on the fundamental shift required to enable good clinical quality. The vision
emphasises the need for a move to a culture of learning - an open and participative culture
in which education, research and sharing of good practice thrive. It focuses in on the need
for a commitment to quality - across the organisation -supported by clearly identified local
resources. It reinforces the importance of multidisciplinary team-working, and the need for
clear accountability to and by the NHS Trust Board. It also makes the important link to the
need to work with users, carers and the public.
The guidance also makes the important links to other policies designed to modernise the
NHS, in particular the need for integrated planning, having the right workforce n place,
access to good information ~nd good research to support clinical lecisions.
The document recognises the need to deal with poor performance; tackling it early, and
learning from experience. Clinical governance is about improving quality - not just about
managing poor performance. The guidance focuses on the need to improve the quality of
services of the majority, by fostering a culture that enables learning and improvement, so
that quality infuses all aspects of the organisation's work.
There is however a need to identify the first steps to achieving the vision. The guidance
highlights the expectations of the NHS in the coming year. These focus on establishing
leadership, accountability and working arrangements, the conducting of a baseline
assessment, the formulation of a development plan and finally, the reporting arrangements
underpinning these steps.
Further information from: Mr Julian Brookes, Room 606 Richmond House, 79 Whitehall,
London SWIA 2NS.
Copies of the guidance can be obtained from Department of Health, PG Box 410,
Wetherby, LS23 7LN. Fax orders on 0990 210 266.
1.Department of Health. Clinical governance: quality in the new NHS.
London:
2.
Department of Health, 1999 (Health Circular: HSC 1999/065).
Department of Health. A first class service: quo/itt in the new NHS. London:
Department of Health, 1998 (Health Circular HSC 1998/113).
3.
Department of Health. A first class service: quality in the new NHS. Feedback
on Consultations. London. Department of Health, 1999 (Health Circular HSC 1999/033).
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08/10/2007 11:11

Fat Embolism: Diagnosis and Treatment

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