Dobutamine

Class: Inotrope/Pressor
Mechanism: Beta 1-adrenergic receptors
Prep:  



6mg x wt(kg) in 100cc



1cc/hr = 1 mcg/kg/min
Dose: 1-20 mcg/kg/minThe Gift

Dopamine

Dopamine
Class: Inotrope/Pressor
Mechanism: Stimulates alpha and beta1 adrenergic and dopaminergic receptors
Prep:



6mg x wt(kg) in 100cc



1cc/hr = 1mcg/kg/min
Dose:  1-20 mcg/kg/min

Epinephrine Infusion

Class: Inotrope/Pressor, Anti-arrythmic
Mechanism: Stimulates alpha and beta adrenergic receptors
Prep: 



0.6 mg x wt(kg) in 100cc



1cc/hr = 0.1 mcg/kg/hr
Dose: 0.1-1.0 mcg/kg/min
Syringe pump: Mix 200mcg (0.2ml) in 50ml of D5W in 60cc syringe.

Prostaglandins

Prostaglandins
Standard Concentration = 3 mcg/ml
Dose range = 0.05 - 0.1 mcg/kg/min
Max = 0.4 mcg/kg/min
Prep = Add 0.6 ml Prostin VR Pediatric (alprostadil) to 99.4 cc IVF to total 300mcg per 100cc
Go to infusicalc for rates!

Furosemide (Lasix)

Class: Potent loop diuretic
Dose:



Neonates 1-2 mg/kg IV q 12-24h



Infants/Children 1-2 mg/kg IV q6-12h

Transpostion of the Great Vessels (d-TGA)

    Aorta arises from RV and pulmonary artery from LV creating parallel circulations.


1 - atrial septal defect or patent foramen ovale
2 - aorta connected to right ventricle
3 - patent ductus arteriosus
4 - pulmonary artery connected to left ventricle
With the presence of an atrial septal defect, two parallel blood flows exist, with one recirculating oxygenated blood and one recirculating de-oxygenated blood. As shown in this diagram, mixing occurs via the atrial septal defect.
Pathophysiology



Cyanotic defect resulting in delivery of  inadequately oxygenated blood. 



Parallel circulation exists as systemic venous blood enters the right heart normally but exits through the aorta back to the body.



Pulmonary venous blood (oxygenated blood) enters the left heart normally but exits through the PA to the lungs



Requires intracardiac mixing to survive. Degree of cyanosis/acidosis depends on number, location and size of intracardiac and extracardiac shunts- ASD, VSD, PDA.
Assessment



Depends on degree of shunting.



Cyanosis within 24 hours of birth most common and if septum is intact.



Hepatomegaly, tachycardia, tachypnea if with VSD.
Management



IV, O2, Monitor



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Stabilization on prostaglandins necessary if atrial communication not sufficient.



If large VSD present may need CHF management, consider Lasix

Truncus Arteriosus

    A single arterial trunk arises from the base of the heart giving rise to both pulmonary and systemic circulations.


Pathophysiology



Cyanotic defect resulting in delivery of  inadequately oxygenated blood. 



Single arterial trunk from the base of heart gives rise to the pulmonary artery, aorta, and coronary circulation.



Accompanied by unrestrictive VSD and single semilunar valve.



Type of truncus is differentiated by the existence and location of the main pulmonary artery and branch PA's.



Type I: Short MPA segment arises from trunk then branches into right and left PA.



Type II: PA's arises seperately from trunk but in close proximity. No MPA



Type III: PA's arises seperately from trunk but at some distance. No MPA
Assessment



Poor feeding, diaphoresis, tachypnea, and cyanosis.



Symptoms and signs of congestive heart failure are probably more common findings than cyanosis in patients presenting early in life.
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.

Tricuspid Atresia

   
    Tricuspid valve is missing, preventing blood from flowing from the right atrium into the right ventricle. Because the right ventricle has no blood to pump, it remains small and underdeveloped.


1 - atrial septal defect
2 - absent tricuspid valve
3 - ventricular septal defect
Blood is shunted through an atrial septal defect to the left atrium and through the ventricular septal defect to the pulmonary artery. The shaded arrows indicate mixing of the blood.
Pathophysiology



Cyanotic defect resulting in delivery of  inadequately oxygenated blood. 



Child's survival depends on the presence of an ASD and a VSD. The ASD allows the venous blood to flow from the right atrium into the left atrium. There, venous blood mixes with oxygen-rich blood from the lungs, flows to the left ventricle, into the aorta and out to the body. The rest of the mixture is pumped from the left ventricle through the VSD into the right ventricle, and on through the pulmonary artery back to the lungs.



Often associated with PDA
Assessment



History is dependent on amount of pulmonary blood flow (presence of a VSD, degree of PS/PA)



Cyanosis commom early on and expected by 1 month of age due to obligatory  atrial shunt.



CHF history may occur with VSD and no PS



Hypoxic spells occur in 16-45% of patients under 6 months of age.



Clubbing of digits common in patients over 3 months of age



JVD
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Initial stabalization of tricuspid atresia and pulmonary stenosis is a prostaglandin infusion until surgery.



CHF management for patients with nonrestrictive pulmonary flow, consider Lasix.

Ventricular Septal Defects (VSD)

Total Anomalous Venous Return

Total Anomalous Venous Return
Occurs when all four pulmonary veins drain anomalously into the right heart.


1 - superior vena cava
2 - atrial septal defect
3 - left innominate vein
4 - pulmonary veins
Oxygenated blood returning from the lungs is routed back into the superior vena cava, rather than the left atrium. The presence of an atrial septal defect is necessary to allow partially oxygenated blood to reach the left side of the heart.
Pathophsiology



Cyanotic defect resulting in delivery of  inadequately oxygenated blood. 



Pulmonary veins have no connection to the left atrium. Left atrium is often small and non-compliant.



An atrial septal defect is considered part of the complex and is mandatory for survival.



All venous blood (oxygenated from pulmonary veins and unoxygenated from SVC/IVC) enters the right heart and exits the pulmonary artery. This creates pulmonary overcirculation and pulmonary hypertension.



Pulmonary veins may be obstructed and blood cannot exit the lungs.This creates a critical situation of low cardiac output from LV volume underloading, severe pulmonary congestion from the obstruction, hypoxemia and acidosis.
Assessment



Obstructed veins have marked respiratory distress, cyanosis, dyspnea, tachycardia, and tachypnea.



Obstructed TAVR is difficult to differentiate from PPHN.
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Correct acidosis



Treat CHF as needed, consider Lasix and Inotropic support.



Prostaglandins may make the situation worse in cyanotic obstructed veins by increasing pulmonary overcirculation.

Fallot's Tetralogy

Tetralogy of Fallot
    TOF involves four defects within the heart. These are VSD, an overriding aorta (wrongly positioned overtop the ventricular septum), right ventricular hypertrophy, and a partial or complete obstruction of blood flow from the right ventricle (also termed RVOT-right ventricular outflow tract obstruction and most often results from pulmonary stenosis).


1 - pulmonary stenosis (a form of right
ventricular outflow tract obstruction)
2 - right ventricular hypertrophy
3 - overriding aorta
4 - ventricular septal defect
The degree of pulmonary stenosis controls the
flow patterns. The shaded blue arrows show blue
blood mixing with red blood. The broken white
arrows indicate diminished blood flow through
the pulmonary artery.
Pathophysiology



Cyanotic defect resulting in delivery of  inadequately oxygenated blood. 



Blood enters the right heart normally. RV outflow obstruction causes shunting across the VSD to the aorta thereby mixing systemic venous with oxygenated blood from LV causing cyanosis.



Severity of pulmonary stenosis determines the severity of cyanosis.



Classic hypoxic episodes: Marked increasing cyanosis, hyperpnea, and irritability progressing to unconciousness, seizures, or cardiac arrest.
Assessment



Dependent on severity of pulmonary stenosis. If severe they will be ductal dependent from neonatal period and require immediate surgery. If not severe symptoms may be mild: dyspnea on exertion, clubbing, squatting, and cyanosis



Systolic ejection murmur at left sternal border.



CXR- Boot shaped heart from absence of PA segment
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Prostaglandins in the neonate if needed.



Classic hypoxic spells are treated with sedation, volume (Hct 45% or greater), bicarb, O2, knee to chest positioning, and intubation/paralyzation if needed. Morphine is drug of choice to relieve agitation.



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.

Pulmonary artery stenosis

Pulmonary Artery Stenosis
Pulmonary valve is conical or dome shaped formed by the fusion of valve leaflets and may be bicuspid.


1 - narrowed pulmonary valve
Blood flow patterns are normal but blood flow through the
pulmonary artery is reduced as indicated by the broken white arrows.
Pathophysiology



Obstructive defect... Generally, severe stenoses in the neonatal period are associated with CHF symptoms and/or cyanosis depending on the location of the lesion.



Considered a right outflow tract obstruction.



In severe cases there may be tricuspid regurgitation and RA dilatation.
Assessment



In the neonatal period, patients may present with symptoms of right-sided heart failure or cyanosis.



The presence of cyanosis from right to left shunting indicates moderate pulmonary stenosis



Oxygen saturations usually normal



Severe pulmonary stenosis can be associated with decreased cardiac output, right ventricular hypertrophy, early congestive heart failure (CHF), and cyanosis.
Intervention



IV, O2, Monitor



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



If the patient has a known large left-to-right shunt, such as PDA or ventriculoseptal defect (VSD) and is in respiratory distress consider Lasix.

Patent ductus atriosus

Patent Ductus Arteriosus (PDA)
    Persistence of a normal fetal channel connecting the aorta and pulmonary artery. This normally closes 12-24 hours after birth by a rise in perivascular PO2. It may be re-opened however in response to a strong stimulus such as acidosis, hypoxemia, or prostaglandin.
 

1 - open or patent ductus arteriosus
The shunt or abnormal flow is from aorta to
pulmonary artery as indicated by the shaded red arrow
Pathophysiology



Acyanotic defect...usually left to right shunt as blood is shunted from areas of high to low resistance. This causes pulmonary overcirculation and frequently CHF results.



When ductus fails to close normally, blood will shunt from the left to the right into the pulmonary artery and lungs resulting in pulmonary overcirculation leading to CHF.



A large PDA will result in a low diastolic pressure and may result in poor coronary perfusion.
Assessment



Presentation depends on the magnitude of the left to right shunt.



Pre-term infants may present in sever low cardiac output states.



Machinery like continuous murmur can be heard at the left upper sternal border.



Hx of poor feeding, irritability, tachycardia, and tachypnea.



Pulse pressure is wide.



Peripheral pulses may be bounding.



CXR shows enlarged cardiac silhouette. Pulmonary vascular markings may be accentuated in moderate to large shunts.
Intervention



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Medical therapy is control CHF, consider Lasix. 



Closure of the PDA with indomethican if kidney function and platelet levels are assured.



Surgical Ligation.

Hypoplastic left heart syndrome

Hypoplastic Left Heart Syndrome
Marked hypoplasia (underdevelopment) or even absence of the left ventricle and severe hypoplasia of the aorta. Often a coarctation of the aorta is also present. The main pulmonary artery is enlarged, and gives rise to a large ductus arteriosus. This allows blood to flow from the right ventricle into the aorta and out to the body. Other characteristics of HLHS often include a combination of aortic and mitral stenosis or aortic and mitral atresia.


1 - patent foramen ovale
2 - pinched aorta
3 - patent ductus arteriosus
4 - narrowed aorta
5 - hypoplastic left ventricle
6 - aortic atresia
The lack of a developed left ventricle, plus the aortic coarctation leads to reversed blood flow through the aorta. Partially oxygenated blood reaches the aorta after travelling through the patent foramen ovale, up the pulmonary trunk and through the patent ductus arteriosus. The major blood flow to the systemic circulation is through the PDA.
Pathophysiology



Obstructive defect... Generally, severe stenoses in the neonatal period are associated with CHF symptoms and/or cyanosis depending on the location of the lesion.



Often a coarctation of the aorta is also present.



The main pulmonary artery is enlarged, and gives rise to a large ductus arteriosus. This allows blood to flow from the right ventricle into the aorta and out to the body.



Other characteristics of HLHS often include a combination of aortic and mitral stenosis or aortic and mitral atresia.



Right sided structures, PA, coronary arteries, and lungs normal.



PDA and ASD are essential for survival and considered a part of the complex.



Systemic venous blood returns normally to RA and flows normally out RV through pulmonary artery. Flows across PDA to aorta and supplies systemic flow but with mixed blood. Pulmonary venous blood empties into LA and flows across ASD, this oxygenated blood mixes with normal venous return



Death occurs within 1 week if not treated.
Assessment



As the ductus arteriosus begins to close normally over the first 24-48 hours of life, symptoms of cyanosis, tachypnea, respiratory distress, pallor, lethargy, metabolic acidosis, and oliguria develop. Without intervention to reopen the ductus arteriosus, death rapidly ensues.



Symptoms of CHF become evident and if unrecognized will progress to vascular collapse.



The PaO2 is optimally between 30-45 mmHg, and the PaCO2 is ideally between 45-50 mm Hg.



Assessment of PaO2 and PaCO2 is important for respiratory management and manipulation of pulmonary vascular resistance by mechanical ventilation and the addition of supplemental inhaled nitrogen.
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Blood flow to the systemic circulation (coronary arteries, brain, liver, kidneys) is dependent on flow through the ductus arteriosus. If a diagnosis is suspected, start prostaglandin (PGE) infusion immediately to establish ductal patency and ensure adequate systemic perfusion



Avoid supplemental oxygen unless severe hypoxia is present (SaO2 < 60%)



Most infants should remain in room air with acceptable oxygen saturation (pulse oximeter) in the 60's.



Maintain balance between systemic and pulmonary blood flow by manipulating SVR and PVR.



If cyanotic with low pulmonary blood flow... hyperventilate, hyperoxygenate, relieve pulmonary congestion, maintain Hct over 45%.



Pulmonary overcirculation may result in hypotension and acidosis as systemic circulation is compromised.



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.



Factors that can affect PVR:

Intervention
Effect on PVR
Effect on systemic O2 delivery
Increasing Hct
Increases
Increases
Decreasing Ph
Increases
Increases
Increasing PCO2
Increases
Increases
Hyperventilation
Decreases
Decreases
PEEP
Increases
Increases
Inotropes (dopa or Epi)
None
Increases (by raising CO)

 

Pulmonary atresia

Pulmonary Atresia
    Complete obstruction of the pulmonary artery resulting in total diversion of blood from the right ventricle into the aorta.


1 - atrial septal defect
2 - patent ductus arteriosus
3 - absent pulmonary valve
4 - hypoplastic right ventricle
Abnormal blood flow (as indicated by the shaded blue arrow) is from the right atrium and right ventricle through an atrial septal defect to the left side of the heart. Blood can reach the pulmonary arteries only through a patent ductus arteriosus.
Pathophysiology



Survival depends on the ductus remaining open in the early days of life (in order for blood to reach the lungs), or on the presence of other connecting blood vessels between the Aorta and the Pulmonary Arteries in the lungs (Collaterals).
Assessment



Usually born at term, and cyanosis is apparent within hours.



Develop progressively worsening cyanosis and tachypnea associated with closure of the PDA.



Normal arterial pulses usually are present.
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Initial treatment consists of maintaining ductal patency with continuous IV prostaglandin infusion.



To correct metabolic acidosis in a sick neonate, replace fluids and administer sodium bicarbonate.



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.
Home
 
 

Double outlet ring ventricle

Double Outlet Right Ventricle (DORV)
    Both great arteries (pulmonary and aortic) arise from the right ventricle. Always associated with a VSD.


1 - overriding aorta
2 - ventricular septal defect
Pathophysiology



Cyanotic defect resulting in delivery of  inadequately oxygenated blood. 



De-oxygenated blood enters the aorta from the right ventricle and is returned to the body.



VSD location can be subaortic, subpulmonic or doubly committed large VSD.



Varying degrees of pulmonary stenosis may be present.
Assessment



Subaortic or subpulmonary VSD with pulmonary stenosis



These children present with histories similar to those of children with Tetralogy of Fallot.



If pulmonary oligemia is present, severe cyanosis is seen in the newborn period and the condition is recognized early.



Beyond the newborn period, cyanosis may be accompanied by hypercyanotic spells, polycythemia, and failure to thrive.



Subaortic VSD without pulmonary stenosis



These children present with histories similar to those of children with a large VSD and pulmonary hypertension.



Oxygenation is relatively normal, and patients usually present with CHF and failure to thrive.



Referral usually occurs later unless associated left heart lesions are present.



Subpulmonary VSD without pulmonary stenosis



These children present with histories similar to those of children with transposition of the great arteries.



Cyanosis varies, with oxygen saturations ranging from 40-80%.
Management



IV, O2, Monitor



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Management of CHF if present, consider Lasix.



Use oxygen only to relieve hypoxemia, since it is a pulmonary vasodilator and can exacerbate left-to-right shunt and CHF.



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.

Coarctation of aorta

Coarctation of the Aorta
Narrowing of aorta causing elevation of pressure proximally and decreased pressure distally.


1 - pinched or coarcted aorta
Flow patterns are normal but are reduced below
the coarctation. Blood pressure is increased in
vessels leaving the aorta above the coarctation.
The broken white arrow indicates diminished
blood flow through the aorta.
Pathophysiology



Obstructive defect... Generally, severe stenoses in the neonatal period are associated with CHF symptoms and/or cyanosis depending on the location of the lesion.



Constriction of aorta either discrete or significant in length.



Almost always at the junction of the ductus and aorta just distal to the left subclavian artery.



Most severe form of coarctation is the interrupted aortic arch which is a congenital absence of a portion of the aorta.
Assessment



Young patients may present in the first 3 weeks of life with poor feeding, tachypnea, and lethargy and progress to overt CHF and shock.



Keys to the diagnosis include blood pressure discrepancies between the upper and lower extremities as well as reduced or absent lower extremity pulses to palpation.



Differential cyanosis (pink upper extremities with cyanotic lower extremities) may occur when right-to-left flow across a PDA provides lower body flow. Although often not obvious to the eye, this may be documented by preductal and postductal pulse oximetry.
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Check pulse ox pre-ductal and post-ductal.



Severe CHF may benefit from intubation with positive pressure ventilation and Lasix



Prostaglandins to open Ductus



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.

Atrioventricular septal defect

Atrioventricular Septal Defect (AVSD)
    A defect in the atrial and ventricular wall and various degress of atrioventricular valve regurgitation due to deficiency of endocardial cushion tissue.


1 - atrial septal defect
2 - abnormal tricuspid valve
3 - abnormal mitral valve
4 - ventricular septal defect
The shunt or abnormal flow is from left atrium to
right atrium, left ventricle to right ventricle
(as indicated by the shaded red arrows). Tricuspid
and mitral valve regurgitation occurs as a result
of the abnormal tricuspid and mitral valves
Pathophysiology



Acyanotic defect...usually left to right shunts as blood is shunted from areas of high to low resistance. This causes pulmonary overcirculation and frequently CHF results.



Characterized by a large atrial and ventricular septal defects and a common atrioventricular valve.



Usually results in a net left to right shunt once PVR decreases and causes pulmonary overcirculation.



Often associated with Down's syndrome.
Assessment



Symptoms of CHF and pulmonary overcirculation usually occur early in infancy.



A normal oxygen saturation is usually present unless a V/Q mismatch from pulmonary changes from a large left to right shunt are present.



Systolic ejection murmur at left sternal border.



CXR shows an enlarged heart.
Intervention



IV, O2, Monitor



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Management of CHF, consider Lasix.



Pulmonary hypertensive crisis (rapid fall in BP and heart rate with concomitant rise in PAP to systemic levels or higher) is treated with hyperventilation, hyperoxygenation, pulmonary vasodilators, sedation, and paralysis.



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.

Atrial septal defect

Aortic stenosis

Narrowing in the LV outflow tract creates an increased workload on the heart.



1 - narrowed aortic valve
Flow patterns are normal but blood flow to the aorta
is reduced as indicated by the broken white arrows.

Pathophysiology



Obstructive defect...Generally, severe stenoses in the neonatal period are associated with CHF symptoms and/or cyanosis depending on the location of the lesion.



Malformation of the aortic valve that causes obstruction to ejection of blood from LV.



Produces LV hypertrophy, decreased LV function, and compromised flow to the myocardium.



Common to have associated lesions (PDA, VSD, Coarct).



Neonates may present with critical aortic stenosis
Assessment



Neonates who present with critical aortic stenosis and low cardiac output have reduced or absent pulses, poor perfusion, and CHF.



Tachycardic, Tachypnic



CXR demonstrates normal to minimal enlargement of heart size, rounding of the cardiac apex, left atrial enlargement if severe stenosis, and pulmonary congestion.
 
Management



IV, O2, Monitor.



3cc/kg/hr D10W  for infants under 1 year of age, D5W if over 1 year.



Check pulse ox pre-ductal and post-ductal.



Severe CHF may benefit from intubation with positive pressure ventilation and Lasix



Stabilization of the neonate with critical aortic stenosis requires prostaglandin therapy. Opening the ductus with PGE can restore systemic blood flow.



Inotropic drugs to increase cardiac output if needed.



Epinephrine, Dopamine, Dobutamine.



Foley catheter insertion to follow renal perfusion and urine output.



ABG to follow acidosis.

ENTAMOEBA HISTOLYTICA

 

 

 

Microbiology

Enteric protozoan
Cyst: 5-20 micrometer with one to four nuclei
Trophozoite (ameba): 12-60 micrometer with a single nucleus, a centrally located nucleolus with a uniformly distributed peripheral chromatin
Many strains, differentiated by isoenzyme analysis

Epidemiology

10% of the world is infected 
50,000-100,000 E. histolytica-associated deaths per year (third leading parasitic cause of death in the world)
Endemic in Mexico, India, West and South Africa and portions of Central and South America
Vast majority (90%) of patients remain asymptomatic
High risk factors for invasive diseases in North America: 
recent immigration, institutionalization and homosexuality
Transmission by fecal-oral route

Clinical syndromes

Intestinal:
Asymptomatic colonization
Acute amebic colitis
Fulminant colitis
Ameboma
Extraintestinal
Hepatic abscess
Pleuropulmonary
Peritonea
Pericardial
brain abscesses

Diagnosis

Serology (generally positive after 7 days)
Cyst and parasite in stool (rapid examination after special coloration: modify Kinouyn: as trophozoites die rapidly)

Comments on treatment

Surgical drainage if abscess
Asymptomatic cyst passer:
recommended: Paromomycin or Iodoquinol
alternative: diloxanide furoate
Diarrhea
recommended: Metronidazole and (Paromomycin or Iodoquinol)
alternative: (tinidazol or ornidazole) and (Paromomycin or Iodoquinol)
Extraintestinal infection: 
Metronidazole and Iodoquinol

HELICOBACTER PYLORI AND PEPTIC ULCER

 

 

 

Microbiology

Formerly Campylobacter pylori
Spiral-shaped gram-negative bacillus
Ability to survive the acidic pH of gastric fluids

Epidemiology

Implicated as a cause of duodenal and gastric ulcers
Infection increasing with age
Natural reservoir in humans
Transmission is fecal-oral

Clinical syndromes

Duodenal and gastric ulcers
Dyspepsia (non-ulcer)
Gastric carcinoma

Diagnosis

Urease test (breath test)
Culture
Gastric biopsy
Serology

Comments on treatment

Susceptible in vitro to a variety of antimicrobial agents: Tetracycline, Metronidazole, Amoxicillin and Clarithromycin
Resistance to these antibiotics has been described (associated with treatment failures)
Recommended: see Ulcer, Gastric & Duodenal for more details
Amoxicillin and Clarithromycin and (omeprazole or lansoprazole)
Alternative: 
bismuth and Tetracycline and Metronidazole and omeprazole

Hepatitis-B

 

 

 

Microbiology

Outmoded designation: serum hepatitis, due to its historically recognized route of percutaneous transmission (interesting to note that most of the patients with "serum hepatitis" were not actually infected with HBV)
Partially double-stranded DNA virus member of the hepadnavirus family (hepatotropic DNA viruses)
Reverse-transcriptase activity associated with the viral DNA
HBSag
product of the S gene of HBV
major surface protein
several subtypes
anti-HBs is the protective antibody
extremely large production during an infection (500µg/ml or 10 trillions particles per ml)
HBcAg
core antigen
product of the C gene
HBeAg
soluble nucleocapsid protein
reliable marker of replication and infectivity

Epidemiology

Virus found in every body fluid of infected individuals (saliva, tears, CSF, seminal fluid, ascites, breast milk, gastric fluid, synovial fluid, pleural fluid, urine and even (rarely) feces)
Low infectivity with oral ingestion of the agent
Sexual and perinatal transmission are important routes
Carrier state in human (more than 200 millions in the world) is the main reservoir
Prevalence is 0.1 and 0.5% in normal population but as high as 20% in some high risk groups
Higher risk groups: 
Down's syndrome
leprosy
leukemia
Hodgkin's
polyarteritis
IVDU 
hemodialysis patients
spouse of acutely infected persons
sexually promiscuous people
people who required repeated transfusions (low risk with present-day blood products with screening

Clinical syndromes

Subclinical
Fulminant acute hepatitis
Chronic persistent hepatitis
Chronic active hepatitis
Hepatocellular carcinoma

Diagnosis

Serology

Comments on treatment

Acute: no therapy recommended
Chronic
recommended: interferon-alfa (2a or 2b) (4-6 months of treatment. 33% will respond)
alternative: lamivudine (duration not established)
Prevention (after transplantation for HBV-induced cirrhosis

HIV-AIDS

 

 

 

Microbiology

One of the four known pathogenic human retroviruses and a member of the Lentiviruses
Two recognized subtypes of HIV:
HIV-1 causes AIDS worldwide
HIV-2 produces an AIDS-like illness but appears to be less pathologic
Each virion has 2 identical copies of a single-stranded viral RNA genome
Goes through reverse transcription (RNA into double-stranded DNA)
Contains three essential genes for viral replication: gag (Group-specific AntiGen), pol (polymerase) and env (envelop)

Epidemiology

HIV is now the leading cause of death of men aged 25-40, the sixth leading cause of death of adolescent males 15-24 years of age, and the fourth leading cause of death in women 25-44 years of age.
By the year 2000, the World Health Organization estimates that there will be 40 million HIV-infected individuals worldwide.
Male homosexuality continues to be the most common mode of transmission, but I.V. drug use and heterosexual transmission continues to rise
HIV in women continues to rise
Minorities account for a disproportionate amount of AIDS

Clinical syndromes

Category A:
Asymptomatic HIV infection
Persistent generalized lymphadenopathy (PGL)
Acute (primary) HIV illness
Category B
Symptomatic, not A or C conditions
Examples include but not limited to:
Bacillary angiomatosis
Candidiasis, vulvovaginal: persistent >1 month, poorly responsive to therapy
Candidiasis, oropharyngeal
Cervical dysplasia, severe, or carcinoma in situ
Constitutional symptoms (eg, fever >38.5°C or diarrhea >1 month)
NB: attributed to HIV infection or have a clinical course or management complicated by HIV
Category C
Candidiasis: esophageal, trachea, bronchi
Coccidioidomycosis, extrapulmonary
Cryptococcosis, extrapulmonary
Cervical cancer, invasive
Cryptosporidiosis, chronic intestinal (>1 month)
CMV retinitis, or other than liver, spleen, nodes
HIV encephalopathy
Herpes simplex with mucocutaneous ulcer >1 month, bronchitis, pneumonia
Histoplasmosis: disseminated, extrapulmonary
Isosporiasis, chronic (>1 month)
Kaposi's sarcoma
Lymphoma: Burkitt's, immunoblastic, primary in brain
M. avium or M. kansasii, extrapulmonary
M. tuberculosis: pulmonary or extrapulmonary
Mycobacterium, other species disseminated or extrapulmonary
Pneumocystis carinii pneumonia
Pneumonia: recurrent (>2 episodes in 1 year)
Progressive multifocal leukoencephalopathy
Salmonella bacteremia, recurrent
Toxoplasmosis, cerebral
Wasting syndrome due to HIV

Diagnosis

Serology (ELISA and Western Blot)
PCR
CD4 counts

Comments on treatment

For more info see: AIDS

 Primary: 
PI (protease inhibitors) + 2 NRTIs (nucleoside reverse-transcriptase inhibitors)

Indinavir + ZDV + 3TC
Nelfinavir + d4T + ddI
(Sequinavir ± ritonavir) + [(ZDV + DDC) or (d4T + 3TC)
Alternative : 
2 NRTIs (ZDV, ddI, DDC, d4T, 3TC) + NNRTI (delavirdine , nevirapine, efavirenz)
[(ZDV + 3TC) or (d4T + ddI) or (ZDV + DDC) or (d4T + 3TC)] +(efavirenz or delavirdine or nevirapine)

Paget's Disease of Bone

Definition

Condition characterised by high rates of bone resorption and disorganised immature new bone formation ® abnormal remodelling of bone

First described by Sir James Paget in 1876 and evidence of the disease found in Neanderthal man


Incidence

Affects more than 3% of population over 40 years of age around 2% of the population at age 40 to around 10% in the elderly (more than 80 years)

Relatively common in Anglo-Saxons, Britain, Germany and Australia

Britain has the highest recorded prevalence

In Australia the prevalence among British born immigrants is intermediate between the British rate and the native born Australians

Rare in Scandinavia, Russia, Italy, Asia, Africa and the Middle East

Affects American whites and blacks equally ® suggest environmental factor contributing to aetiology

Male : Female 7:6

Probably equal overall incidence but in younger individuals males slightly more frequent

Only occasionally presents in people under 50 years

There is evidence of a decline in incidence of the disease in Britain and USA


Aetiology

The primary abnormality is thought to lie in the osteoclasts but the precise cause remains unknown

Viral aetiology

suggested by the isolation of viral intra-nuclear inclusion bodies in osteoclasts on EM which resemble those of measles (Rebel 1976, Mills 1976)

Antigen to measles virus, simian virus 5 and human parainfluenza virus type 3 detected in abnormal osteoclasts (Basle 1985)

Measles virus not detected (Gordon 1991)

Canine distemper virus (CDV) in 41% of Pagetic osteoclasts, osteocytes and osteoblasts (Gordon 1991)

Slow virus type aetiology consistent with familial incidence

Ralston, 1994 investigated Pagets and normal bone with reverse-transcriptase and polymerase chain reaction

no difference in IL-1, IL-6, TNF-?, TNF-?, b-FGF, TGF-?, IGF-1

possibility that Pagets bone turnover is due to local elaboration of other osteotropic factors

Birch (Ralston) 1994 unable with PCR to detect measles and CDV aetiology for Pagets disease

Relationship to pets has been postulated but not substantiated

Genetic, as family history found in 15 - 20% of cases, and the site and extent of disease similar in family members (dominant inheritance with low penetrance (Sofaer 1983)

Extraordinary geographic variations in prevalence (see data on incidence)

Probably, Pagets disease is caused by infection with a common and widespread virus superimposed on genetic variation for susceptibility and perhaps severity of disease (Sofaer, 1983)

Interaction between hereditary and environmental factors

Geographical variations in the prevalence of Paget's disease remain unexplained and the viral hypothesis remains unproven

Also postulated

a disorder of hormonal secretion

vascular aetiology

autoimmune disease

monoclonal IgM


Clinically

Variable picture with the majority being discovered incidentally following X-Ray or elevated alkaline phosphatase

Only a minority of patients become symptomatic (5%)

Monostotic in 17% and polyostotic in 83% (pelvis 70%, Lumbar spine 50%, femur 50%, skull 45%, tibia 30%, humerus 30%, clavicle ® visible deformity in 13%, hand and foot 3 - 5%)

The disease may for many years be localised to part or the whole of one bone

Affected bones may remain asymptomatic or ® pain (dull constant ache) and become bent

Pain is worse at night, but rarely severe unless sarcoma or fracture supervene

Lesions detected on bone scan are usually painful whereas many lesions seen on X-Ray are not

Bone looks bent, feels warm (may be 5o warmer than unaffected side)and thick (osteitis deformans)

If generalised may ® headache, deafness (with impairment of hearing in 30 - 50% of cases), deformities, stiffness, limb pain and sometimes fracture and heart failure, occasionally pressure on the optic nerve may ® blindness

Facial and trigeminal nerves may also be affected

Spinal stenosis may occur ® root or cord problems infrequently or a vascular steal syndrome may ® spinal claudication

Features suggestive of pain of Pagetic origin in the back are non-specific low back pain without radiculopathy, normal or minimal findings on examination, vertebral sclerosis in radiographs, isolated vertebral involvement in bone scan and enlarged vertebra and neural arch, normal facet joints and no bony impingement

Canal stenosis occurs gradually as the expanding vertebral body reduces the canal diameter, may be kyphosis, and back ache and root pain is common

Cardiac failure associated with arterial calcification and calcification of heart valves and myocardium as well as being a high output state

About 20% of Pagets patients have fractures which may be complete or incomplete and as many as 40% ® delayed or non-union

Tinnitus and vertigo are common complaints

Coxa vara is also a feature with considerable antero-lateral bowing of the legs

When involves a joint may ® painful erosive arthritis due to altered stresses secondary to deformity and abnormal subchondral bone ® collapse or loss of resilience

X-Rays

Early ® osteoporosis circumscripta

Disease involvement usually seen at one end of the bone (generally proximal)

The bone as a whole is thick and bent

Density in the vascular stage is decreased and it is increased in the sclerotic stage

Trabeculae are coarse and widely separated

In vascular stage areas of porosis shape

Bone Grafts

Indications

To provide stability (cortical bone best)
To provide linkage, ie replace missing bone
To stimulate osteogenesis

Bone grafts may be

Osteo-conduction
The graft provides a scaffold for bone deposition

Osteo-induction
Graft derived factors actually stimulate the recipient to invade the structure with osteogenic activity.


Physiology of remodelling and bone grafts

1. Activation
Local and systemic factors involved

2. Resorption
Appearance of osteoclasts from ? haematopoietic stem cell precursors or macrophage lineage. (pre osteoclasts may be endothelial cells, circulating monocytes, reticuloendothelial cells and fibroblasts)

3. New Bone Formation
Osteoblasts also from the marrow ® deposit osteoid ® mineralisation of the matrix.

Graft incorporation

Haematoma forms around implanted bone and only surface cells remain viable by diffusion.
Necrosis of graft follows ® inflammatory response and formation of a fibro vascular stroma.
Blood vessels and osteogenic precursors infiltrate the graft.
A neo vascular response results in increased porosity and decreased mass of the graft.
New bone formation follows and finally remodelling.

Cortical bone grafts are approximately 40-60% weaker than normal bone from 6 weeks to 6 months after transplantation. Returns to normal 1-2 years after transplant.

Factors adversely affecting incorporation
Vascularity
Infection
Foreign Material
Malnutrition
Drugs eg
(indocid, diphosphonates)

Types

Autografts

From the patient themselves, but most still dies
Vascularized autografts ® no resorption and either end of the transplanted segment heals in a way analogous to fracture healing.

Allografts

Transferred from one individual living or dead to another of the same species. Antigenicity altered by freezing / radiation. Radiation ® alters collagen ® depress graft incorporation. Osteochondral graft survival enhanced by immersion in glycerol.
Fresh grafts ® immunological response and less reliable incorporation
The sequence of events of incorporation is qualitatively similar to that for autografts, but it is delayed and less extensive (allografts are biologically inferior to autografts).

Xenografts

Bone taken from a different species, similar to allograft bone after freezing and irradiation.

Collection and distribution of donor bone in South Australia

Age limit for donation 16-60 years

Femoral Heads

Written consent required from the donor to use the bone and perform blood tests (HIV, HepB, VDRL)
Swabs taken of acetabulum and femoral head ® MCS
Biopsy of femoral head ® Histopathology
Head placed in 2 sterile bags, sterile container & un-sterile bag
Stored in -70oC ultra cold freezer
If sever osteoporosis identified bone is X-Rayed and decision made about keeping the bone

Exclusions
Hepatitis
Infection
Tumour
Rheumatoid
Alcohol / Drug abuse
Steroid treatment
Pre-senile dementia
Transfusion in last 6/12

All bone for re implantation receives 2.5 mrad of g irradiation and the bone marked ready for use.

Long bones

Consent form relatives
Tissue obtained under sterile conditions
Blood tests taken as for femoral heads
Dimensions of each bone recorded and computerised for later matching

Exclusions
Fresh bone must be 16 - 30 years old
Frozen bone can be up to 12 hours post death
Fresh bone need beating heart or in first few hours
Exclusion if in ICU > 72 hours (infection)

Allograft infection rate 10-12% and more than 80% of infected allografts are associated with clinical failure

Synthetic Grafts

Hydroxyapatite
Not biodegradable and is brittle but acts as an osteo-conductive medium

Tricalcium Phosphate
Biodegradable and is replaced by new bone but unpredictable rate of resorption and lengthy incorporation

These grafts can be used alone or mixed with autograft. Useful to fill defects where the intrinsic mechanical strength of the graft is unimportant.

Many drugs (chemotherapeutic agents, NSAIDs etc) negatively influence new bone formation in the intact skeleton and to some degree the repair associated with fractures.
Similar findings result from irradiation


Papineau Technique

Wound excision, open cancellous grafting which irradicates infection, encourages healing of the skin by granulation and results in solid bony union.

Swab for culture ® appropriate antibiotic pre-operatively
Tomograms or CT etc to define extent of sequestrum
Excision of infected tissue down to bleeding living tissue
Splint the bone if inadequate or deficient
Defect in bone must be saucerised
Development of granulation tissue ® base for subsequent graft
Secondary excision of areas not covered by granulation tissue
Within 2/52 operation for application of cancellous graft
Change dressings at 5/7 ® washing and daily dressing
Continue dressings 3/52 ( ® 3 colour changes)
By the end of the third month entire graft incorporated into granulation tissue
SSG applied if required
FWB allowed at 7/12 for osteomyelitis, 9/12 where some continuity has been preserved and 12/12 if part of the shaft was completely resected.

Traction

Introduction

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.

Traction by Gravity

Really only applies to fractures of the upper limb (hanging cast)


Definitions

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

In weight traction it is the tension in the apparatus which remains constant and the length depends on the amount of tearing of the intermuscular septum and fibrous tissue of the limb

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 10o as that with that on a normal mattress at 30 - 40o 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

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.

Tibia Fractures

Proximal Tibial Fractures

Mechanism

young pt - high energy trauma
old pt minor fall

Classification AO

extrarticular
intraarticular, unicondylar
intraarticular, bicondylar

60% are lat plateau
15% are med plateau
25% involve both

Evaluation

assess assoc injuries, neurovasc examination
XRay: plain films, biplanar tomography, CT

Treatment

Extraarticular

CR if necessary, AKPOP or cast brace

Intraarticular

Undisplaced
AKPOP/ cast brace

Displaced
ORIF / BG/ cast brace for split depression
simple depression fracture may be amenable to elevation without plating using an arthroscopic assisted technique
type C fracture- often very comminuted, difficult to reconstruc, thus CR/cast bracing often preferable

Note association with meniscal lesions in ~20%
collateral or cruciate lig injuries in ~20%

Complications

nonunion
rare

malunion
more common with nonop treatment
Bicondylar fracture
knee instability due to either malunion or ligament injury

infection
more common in bicondylar fracture - increased op time, exposure, hardware

Prognosis

ref: Anglen and Healy "tibial plateau fractures" Orthopaedics 11:1527-1534, 1988
Undisplaced fracture 85% satisfactory with nonop treatment
Displaced fracture 78% satisfactory with ORIF, 54% with nonop treatment
Lachiewicz and Funcik "factors influencing the results of ORIF of tibial plateau fractures"
CORR 259: 210-215, 1990
44 fractures, 2.7 yr FU, 91% good or excellent, implant removal needed in 1/3 pts

Tibial Spine Fractures

Mechanism

hyper extension or hyperflexion® avulsion

Classification

Meyers and McKeever "Fractures of the intercondylar eminence of the tibia"
JBJS 52A: 1677-1684, 1970

Type 1: undisplaced
Type 2: displaced hinging posteriorly
Type 3: displaced with complete separation

Treatment

Type 1 + 2 CR with knee in extension likely to be successful- if not ORIF
Type 3 ORIF

Prognosis

good , low incidence of late instability
if malunion may get impingement in extension

Avulsion of the Tibial Tubercle

ref: Ogden etal "fractures of the tibial tuberosity in adolescents" JBJS 62A:205-215, 1980

Mechanism

usually in vigorous sports- violent contraction of quads in sudden acceleration or deceleration

Classification

Type 1 fracture
across the secondary ossification centre level with the post border of the inserting patellar tendon

Type 2 fracture
at the junction of the primary and secondary ossification centres
of the prox tibial epiphysis

Type 3
fracture propagates across the primary ossification centre= SH type 3

Treatment

ORIF , protect in extension , ROM exs

Prognosis

excellent

Tibial Shaft Fractures

Classification AO

Type A simple

a single circumferential disruption of the diaphysis - may be:

Spiral
Oblique ( angle more than 30 deg)
Transverse (angle less than 30 deg)

Type B multifragmentary: wedge

a fracture with one or more intermediate fragments in which after reduction, there is some contact bw the main fragments- may be:

Spiral wedge
Bending wedge
Fragmented wedge

Type C Multifragmentary: complex

a fracture with one or more intermediate fragments in which after reduction , there is no contact bw the main prox and distal fragments- may be:

Spiral
Segmental
Irregular

Treatment - closed injury

Nonoperative

best for fracture without significant comminution, shortening or displacement at the time of fracture. ie low energy fracture
AKPOP for 6/52, then convert to cast brace or PTB
union in approx 16 wks for simple fracture, longer for more complex injury (av 18 wks)
ref: Sarmiento etal "Tibial shaft fractures treated with functional braces: experience with 780 fractures" JBJS 71B: 602-609, 1989
90% healed with 1cm or less shortening
nonunion rate 2.5%

Operative

indicated in:
pt requires early return to work
displaced ie higher energy fracture
Failure of closed treatment
IM nailing:
ref: Hooper etal "Conservative management or closed nailing for tibial shaft fractures : a randomised prospective trial " JBJS 73B: 83-85, 1991
infection rate ~ 1-2%
angulatory deformities rare
shorter hospital stay, less OPD visits
earlier return to work

Treatment - Open Fractures

Wound management as for any compound fracture
IM Nailing
Court-Brown etal "Infection after intramedullary nailing of the tibia" JBJS 74B: 770-774, 1992
Tornetta etal " treatment of grade 3B open tibial fractures- a prospective randomised comparison of external fixation and nonreamed nailing" JBJS 76A:13-19, 1994

Grade 1
IM nailing - same figures as for closed fracture

Grade 2
infection 3.8%

Grade 3
A: infection 5.6%
B: infection 12.5%

External fixation:
Use for grade 3B and 3C
rates of infection same as nailing for grade 3B with added problem of pin tract infection, delayed union also a feature of ex fixation.
sometimes need to convert from ex fix to IM nail- risk of infection in the face of recent pin tract infection is ~ 20%, However if the ex fix is removed within 3 wks of application + wait another 2 wks,can nail with infection rate of ~ 5%
Ref: Johansen etal " Objective criteria accurately predict amputation following lower extremity trauma " J Trauma 30: 568-573, 1990

The MESS

1. Skeletal/ soft tissue injury

a. Low energy
eg simple fracture, civilian gunshot
1
b. Medium energy
eg open or multiple fractures, dislocation
2
c. High energy
eg close range shotgun, military gunshot, crush
3
d.

Spine Fractures

Cervical Spine Fractures

Anatomy

spinal cord occupies ~ 35% of canal at the level of the Atlas and ~ 50% of the canal in the lower cervical region (C2-7) and the thoracolumbar spine

History

nature of incident
any neurological symptoms, any change in neurol status
LOC
head/ pectoral girdle injury

Examination


observe

head control
head injuries, pectoral girdle injuries: contusion
voluntary movement of all 4 limbs
Priapism
any limitation of movement of the pts head to either side

Palpate

tenderness over head + back off neck
step in spines
local haematoma

Neurological exam


Sensory

C2
back of head
C3
front of neck
C4
lat and inf over clavicles down to 2nd interspace
C5 - T1
upper limb
T2
below nipple
T10
unbilicus
L1
groin
L2- S2
lower limb
S3- S5 + coccygeal roots
perianal/ saddle


-once the sensory level is determined, examine distally for any evidence of sparing.
Sacral sparing indicates preservation of the lateral columns and recovery of lost muscle function is quite likely

Motor

after the sensory exam the diagnosis of a root lesion or cord lesion can be made and the completeness determined
Examine sequential nerve roots

C4
pt breaths diapragmatically
C5/6
biceps
C5
deltoid
C6
ECRL/ECRB
C7/8
triceps
C7
EDC
C8
FDP/FDP
T1
intrinsics
L1/2
adductors
L3/4
knee extension
L5/1
knee flexion
L4
tib ant
L5
EHL/ peronei
S1/2
ankle plantar flexion


Rectal inability of the pt to feel the finger in the rectum confirms a complete sensory lesion

If sphincter doesn't contract voluntarily about the finger + there are no other signs of voluntary motor power,complete motor paralysis is confirmed

Bulbocavernosus reflex: a squeeze on the glans, a tap on the mons or a tug on the catheter stimulating the trigone of the bladder causes reflex contraction of the anal sphincter about the gloved finger

If spinal shock is present a complete lesion cannot be diagnosed with certainty- if the bulbocavernosus has not returned in 24 hrs its absence is due to complete lesion as spinal shock resolves within 24 hrs

Spinal Cord Lesions

Spinal Shock

Wrt spinal cord injury = a spinal cord nervous tissue dysfunction based on physiologic dysfunction rather than structural disruption.
Spinal shock has resolved when the reflex arcs below the level of the injury begin to function again

Root injuries

are essentially peripheral nerve injuries , partial recovery is expected
root avulsion is rare except in plexus injury

Incomplete spinal cord lesions

any sparing distal to the injury = incomplete lesion= possible recovery
the greater the sparing the greater the prognosis

Brown- Sequard

an injury to either side of the cord (hemisection)
ipsilateral: muscle paralysis and jt position/ vibration loss
contralateral: pain and temperature loss
- good prognosis, 90% regain bladder / bowel function + walk

Central cord syndrome

most common incomplete cord injury, assoc with extension injury to Cx spine in middle aged pt

Impact direct to the central grey matter®severe flaccid LMN paralysis of the upper limbs

Damage to the central portion of the corticospinal and spinothalamic long tracts in the white matter®UMN spastic paralysis of the lower limbs and trunk
The sacral tracts are peripheral and are usually spared and the pt has sacral sparing

Prognosis
50-60% have progressive return of motor and sensory function to lower limbs- but poor recovery of hand function due to irreversible damage to the central grey matter

Anterior cord syndrome

complete motor and sensory loss apart from dorsal column sparing with deep pressure/ proprioception/ vibration as only remaining modality

prognosis
good if recovery progressive within 24 hrs
after 24 hrs prognosis poor
10-15% have recovery

Posterior cord syndrome

loss of deep pressure/ proprioception/ vibration only

Complete Cord Injuries

Frankel classification of Neurological Deficits in pts with Cord injuries

ref: Frankel etal "The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia: Part 1."
Paraplegia 7: 179-192, 1969
Types

absent motor and sensory function
sensation present, motor function absent
sensation present, motor function present but not useful (gd 2-3/5)
sensation present motor function active and useful ( gd 4-5/5)
normal motor and sensory function

Assessment of Cx cord injuries

Plain XR

direct XR evidence of instability

Increased angulation bw spinous processes more than 11 deg than in adjacent segments
Ant or post translation of the vertebral bodies more than 3.5 mm
segmental disc space widening on lat XR
facet jt widening
malalignment of spinous processes of ant view
Rotation of the facets on lat XR
at tilt of vertebral body on ant XR

XR findings suggestive of unstable injuries

Increased retro pharyngeal space - ant to C3 normal not more than 3 mm
C4 + below- normal varies 8-10 mm
minimal compression fracture of ant vertebral bodies
Avulsion fracture at or near insertion of spinal ligs
nondisplaced fracture lines

Tomography

good for posterior elements, dens fracture

CT

assess bony encroachment on canal , best method for accurate bone definition

MRI

evaluate neural elements
disc disruption
ligamentous disruption

Stress XR's

flexion/ extension contraindicated in altered state of consciousness

Scapular and Clavicle Fractures

Sternoclavicular Joint

Anatomy

Diarthrodial jt, both jt surfaces covered by fibrocartilage
Artic surface of clavicle larger than that of the sternum, jt surfaces not congruent

Ligaments

intraarticular disc- fibrocartilage, divides jt into 2 cavities, rarely perforated
- runs from synchondral junction of 1st rib + sternum to sup + post aspect of med clavicle. Ant and post it blends with the capsule.
- acts to prevent med displacement of the med clavicle
Costoclavicular lig ( = rhomboid lig) - form the upper surface of the 1st rib and synchondral junction with the sternum to the rhomboid tubercle on the inf surface of the clavicle. Has 2 laminae - run in same pattern as the int and ext oblique muscles.
- ant fibres act to prevent upward motion of the clavicle
- post fibres act to prevent downward motion of the clavicle
Interclavicular lig - connects the superomed ends of each clavicle with the capsule and the upper sternum
- acts to prevent upward motion of the med clavicle
Capsule - thickened ant and post with the post being strongest
- prevents upward displacement of the med clavicle

Ossification

the clavicle is the 1st long bone of the body to ossify ( 5th intrauterine wk)
the med epiphysis is the last to appear (~ 18 ) and last to close ( ~ 25)
The capsule attaches to the epiphysis and the costoclavicular lig attaches to the metaphysis.
Thus in a SH 1 injury the costoclavicular lig is detached from the metaphysis or torn while the capsule and epiphysis remain intact.
In a SH 2 injury the costoclavicular lig remains attached to the distal fragment comprising the epiphysis and a piece of metaphysis

Classification

Anterior - most common, caused by lat compression with the shoulder rolling backward
Posterior - uncommon, caused by lat compression with the shoulder rolling forward
Injuries to the jt can be

sprain
acute dislocation
recurrent dislocation
unreduced dislocation

Symptoms and signs

severe pain increased by any movement of the arm ( post more painful than ant )
the affected shoulder appears shortened and thrust forward cf the normal side

Anterior

the med clavicle can be observed and palpated ant to the sternum
med clavicle may be fixed or mobile

Posterior

the med prominence of the normal clavicle is absent
the med clavicle is not palpable
may be venous congestion
breathing or swallowing difficulties
pneumothorax
shock due to damage to great vessels

XRay

AP view difficult to interpret
Hobbs view - pt seated, leans over table with arms up and head resting in hands, cassette on table ~ under pts neck, XR beam directed vertically down
Serendipity view : pt supine, 40 deg cephalic tilt view
Tomography
CT - gold standard

Treatment

Sprain: Rest, sling, gradual return to activity

Dislocation, anterior

most ant dislocations are unstable - notwithstanding -

CR - GA, pt supine, sandbag under centre of back
assistant pushes shoulders back
surgeon pushes clavicle back into place
in most cases this will not remain reduced - pt counselled that the risks of ORIF outweigh the cosmetic benefits of reduction
postreduction - if stable - clavicular rings to maintain position
if unstable - sling, gradual return to activity
NB cosmetic and functional deficit minimal if unreduced


Dislocation, posterior

once reduced are usually stable
may need to involve thoracic surgeon if mediastinal structures compromised

CR - GA, pt supine, sandbag under centre of back
gentle traction in line of clavicle, countertraction by assistant - this alone may reduce the dislocation
if not reduced, add manipulation with a towel clip - will reduce with clunk
rarely CR fails therefore ® OR
same position, free drape arm
involve thoracic surgeon
incision parallel to med 7-10 cm clavicle
reduction -
if stable treat as for CR
if unstable - excise the med 1- 1.5 cm clavicle and secure the remaining clavicle to the 1st rib with dacron tape
post op - clavicular rings 6 wks

Unreduced dislocation

Anterior
functional and cosmetic deficit minimal if any - no treatment indicated

Posterior
due to risk to mediastinal structures - OR indicated ( as above)


Clavicular Fractures

Classification

Type 1

middle 1/3 fractures ~ 80%

Type 2

distal 1/3 fractures ~ 15%

minimal displacement bw conoid and trapezoid ligs
ie both ligs intact
(a). fracture med to coracoclavicular ligs - displaced
(b). fracture bw conoid and trapezoid lig - displaced - ie conoid lig ruptured, trapezoid lig intact
intraartic fracture of AC jt - no lig disruption or displacement
Paediatric: ligaments intact attached to periosteum while prox frag displaces up through the disrupted periosteal sleeve
Comminuted with ligaments not attached prox or dist, but an inferior, comminuted fragment

Type 3 prox 1/3 fractures ~ 5%

minimal displacement
signif displacement ie ligs ruptured
intraarticular
epiphyseal separation - children and young adults
comminuted

Assoc injuries

Skeletal AC and SC dislocations
head and neck injuries
fracture 1st rib
Scapulothoracic dissociation
Lung and pleura PTX or haemothorax
tears of trachea or main bronchi
Brachial Plexus ulnar n most often involved in direct trauma
Vascular unusual - vessels protected by subclavius and deep cervical fascia

Mechanisms of injury

birth trauma clavicle compressed against maternal symphysis in a cephalic presentation or direct traction in a breech deli

Pelvic and Acetabular Fractures

General

Classification (Tile)

Type A: Stable

A1
Fracture not involving the ring
avulsion fracture of ASIS,AIIS or ischium
fracture of iliac wing

A2
Stable minimally displaced ring fractures

Type B:

Rotationally unstable / Vertically stable

B1
Open book

B2
Lateral compression (ipsilateral post and ant fractures)
Stage
separation of the symphysis less than 2.5 cm
-implies no post lesion
separation of symphysis more than 2.5 cm, unilat
more than 2.5 cm, bilat
-implies disruption of sacrospinous + ant sacroiliac ligs

B3
Lateral compression (contra-lateral post and ant fractures= bucket handle)
- the rotation of the bucket handle can cause gross pelvic deformity or significant LLD
External fixation ® definitive treatment, to aid or maintain reduction

Type C:

Rotationally and vertically unstable
C1: Unilateral
C2: Bilateral
C3: Associated with acetabular fractures
External fixation ® partial stability ® reduce bleeding, relieve pain and aid in nursing the patient
Posterior stabilisation may also be required
ref : Tile " pelvic ring fractures :should they be fixed" JBJS 70B:1-12, 1988

Classification (Apley)

1. Avulsions:

Due to violent muscle action
Sartorius from ASIS
Rectus femoris from AIIS
Adductor longus from pubis
Hamstrings form ischial tuberosity
Treatment ® rest and reassurance

2. Ring fractures:

Stable fractures ® symptomatic treatment
Disruption of posterior structures ® 4 - 6 weeks RIB
Unstable fractures;

Four poster
Open book
Malgaine type

Direct fractures of the iliac wing ® bed rest
Stress fractures of the pubis / pubic rami are not uncommon in osteoporotic patients

3. Acetabular fractures:

Anterior pillar (not WB part of joint)
Posterior pillar (often associated with dislocation of hip and involves WB part of joint ® ORIF)
Transverse
Comminuted both column type (difficult to reduce and degenerative changes common)

4. Sacral / coccygeal fractures

Investigations:

Clinical examination

® associated injuries (bladder, urethra, spine, femurs etc)
signs hip ROM
obvious instability on compression/ springing
Destots sign- blood above inguinal lig or in scrotum
Roux's sign- decrease distance from gt troch to pubic tubercle
Earle's sign- tender swelling on PR

X-Rays

® standard AP
inlet view (tilt X-Ray beam 40o caudad) -shows post displacement
outlet view- ( 40o cranial beam)-shows superior migration or rotation
2 Judet views
CT scan and reconstructions ® plan surgical approach
Angiography and embolisation of bleeding vessels may be life saving

Treatment:

Resuscitation

fluid replacement
antishock garment
embolisation
direct surgical intervention
application of Ex Fix can reduce venous and bony bleeding signif

Provisional stabilisation

for fractures that increase pelvic volume ie open book (B1) or vertical shear (C3)
apply ex fix or pelvic clamp percutaneously in emerg room
Ex fix- 2 pins placed percut in Ileum- 1 at ASIS, 1 at iliac tubercle, at ~ 45 deg to each other- complate frame as anterior rectangle

By Type

A
symptomatic, mobilisation

B1
Stage 1 no stabilisation
2+3 stabilise with Ex fix or ant plate

B2+3
most need no stabilisation

B3 - displaced bucket handle
if LLD less than 1.5 cm- accept
if LLD more than 1.5 cm or pelvic deformity excessive- reduction by ER of hemipelvis with pins in the iliac crest, maintained with anterior frame

C
Options
Ant frame+ skeletal traction (supracondylar femoral pin)
-safe
-indicated if - adequate reduction of post sacroiliac complex
when post injury a iliac fracture rather than an S-I dislocation or a sacral fracture
-disadvantages traction for 8-12 wks
ORIF
- risks: bleeding - loss of tamponade, coagulopathy
infection
wound necrosis esp in post wounds
nerve damage
-indication: inadequate reduction of post injury(esp SI disloc)
open post wound
in assoc with acetabular fracture

Indications for Ex Fix

Type

B1
definitive treatment of stage 2+3

B2+3
to aid and maintain reduction

C
to produce partial stability to decrease bleeding, decrease pain, aid nursing
If ORIF to be performed should be delayed until patient stable, all investigations completed and operation planned but should not exceed 7 days

Complications:

Non-union / malunion ® high incidence of nerve, bladder etc complications at revision surgery (high incidence in Malgaine type 90%, and usually symptomatic)
ORIF delayed more than 3/52 ® callus formation which would limit reduction accuracy
Infection increased incidence associated with open bowel injury ® drain wounds
6% incidence and increased with ilio-inguinal approach ® avoid operations in febrile patients ® use prophylactic antibiotics
Nerve palsy (usually peroneal component) of sciatic nerve in 11.2% (17.4% of posterior fractures)
Ectopic bone formation in ~ 20% ® indomethicin useful ? carcinogenic effect of radiation in young people
Thrombo-embolic problems in ® anticoagulate for 6 - 8 weeks after open operation
RAH 3500 units heparin tds starting at 72 hours post injury or surgery and adjusted according to APTT (aim for APTT 31-36) ® warfarinise after one week post injury or operation ® therapeutic range (INR 2 - 2.5)
About 1/3 of unstable fractures (13% overall) have an associated urethral injury ® retrograde urethrogram prior to IDC ® cystogram ® IVP if indicated
Bladder rupture usually extra-peritoneal and may ® vesico colic, vesical fistulas
Impotence evident in ~ 40%
Post traumatic ost

Hand Fractures

Scaphoid Fractures

ref: Gelberman etal "Fractures and nonunions of the carpal Scaphoid"
JBJS 71A:1560-1565, 1989

Blood supply:

From the radial artery both the dorsal and palmar branches but only two direct vascular leashes are observed entering the scaphoid
The most important of these are the scaphoid branches of the dorsal carpal branch of the radial artery entering the bone though the foramina along its dorsal ridge supplying 70 - 80% of the bone including the entire proximal pole
A second vessel or group of vessels from the palmar and superficial palmar branches enter the scaphoid in the region of its tuberosity to perfuse the distal 20 - 30% of the bone
The dorsal approach to the scaphoid places these vessels entering the dorsal ridge at highest risk

Pathology:

Approximately 30% of fractures of the middle third and nearly 100% of those of the proximal fifth are associated with osteonecrosis of the proximal pole

Treatment:

ref: Gellman etal "Comparison of Short and Long Thumb Spica casts for nondisplaced fractures of the carpal Scaphoid" JBJS 71A: 354-357, 1989
A prospective randomised clinical trial demonstrated a statistically significant advantage for treatment with a long thumb spica cast
Should be splinted in slight flexion and ulna deviation
Unstable (displaced fractures) should be internally fixed

Prognosis:

Undisplaced fractures united in 8 - 12 weeks when treated in a long thumb spica cast
Fractures of the distal 1/3 can be expected to unite in 6 - 8 weeks
middle 1/3 in 8 - 12 weeks
proximal 1/3 in 12 - 23 weeks

Complications:

Scaphoid non union ® OA develops in the adjacent carpal joints in more than 90% of cases within 5 yrs
This will be associated with discomfort in the majority of cases
Non-union ® carpal instability ® degenerative arthritis
Treatment:

Russe BG - 92% union rate ( iliac crest BG placed from volar side) (Matti = graft from dorsum- not done as risk to blood supply)
BG with fixation either K-wires or Herbert Screw

Late OA - difficult to treat- options include

Autograft eg costochondral
Allograft
Implant: silicone not used due to synovitis, hence titanium
scaphoid excision combined with intercarpal fusion
total wrist fusion

Scaphoid Malunion
can get markedly flexed scaphoid with a humpback deformity
osteotomy has been described to correct this - potential risks are of AVN of prox fragment

Dislocation of the MCP Joint of the Thumb:

Blocks to reduction include

Collateral ligament
Volar plate displaced into the joint
FPB or FPL tendons
Osteochondral fractures
Head button-holed through anterior capsule
Proximal phalanx button-holed through the extensor tendon

Forearm Fractures

classification

Types

undisplaced
displaced
avulsion
transverse + oblique
comminuted
fracture / dislocations

Treatment

If undisplaced ® immobilise elbow for 3 - 4 weeks in a sling
If displaced (disruption or extensor mechanism) ® TBW
TBW with double twist ® strongest method of internal fixation for these fractures however a dorsal plate (positioned in tension) is also effective

Complications

reduced ROM - up to 50% have some loss of ROM - only ~ 3% have functional loss from this
post traumatic OA- rare as is a non wght bearing jt
Nonunion - ~5%
If high demand pt - ORIF/ BG
If low demand pt - may not need to do anything. Can excise the olecranon fragment with very good results ( as long as the coronoid and ant soft tissues are intact to provide stability)

Radial Head Fractures

Usually due to a fall onto the outstretched hand and may be associated with dislocation of the elbow
Over half of radial head fractures are associated with other injuries about the elbow

Classification: (Mason)

ref: Mason, M.L. "Some observations on fractures of the head of the Radius With a Review of 100 cases" Br J Surg 42: 123-132, 1954
Types

Undisplaced
Marginal fracture with displacement
Comminuted fracture with whole head involvement
Fracture of the radial head associated with dislocation of the elbow
NB: Type IV not described by Mason

Note that Essex- Lopresti (ALRUD) lesions can coexist

XRays

AP/ lat views of the elbow usually sufficient
fat pad sign
if no fracture seen but fat pad sign present - Radiocapitellar views with the forearm in neutral rotation and the XRay tube angled 45 deg cephalad

Treatment

Children

Acceptable angulation of 30o in young children as ® remodels with growth (15o in older children ie more than 10) and can expect 10o correction
If greater angulation than 30o ® either;
Manipulation under GA
Open reduction if more than 45o and irreducible
Never ® radial head excision in the young as ® ulna overgrowth

Adults

Type

nonoperative - early motion as soon as comfortable
without Essex- Lopresti
without mechanical block as for type 1
with mechanical block excise or ORIF
with Essex- Lopresti ORIF if at all possible ie retain head
May need to pin radius + ulna
without Essex- Lopresti or dislocation excise
with Essex- Lopresti aim to retain the head if at all possible
may need to transfix the radius and ulna to prevent translation
if the ant band of the MCL is disrupted need to repair primarily
aim to retain the radial head if at all possible

Summary

if head is salvageable do so
if Essex- Lopresti - save head, or if excise pin radius and ulna for 4-6/52
if elbow unstable ie MCL torn - save head, repair ligament if excise or not
In adults operation indicated if
Angulation more than 30o Depression of articular surface of more than 3mm
Greater than 1/3 of radial head involved

Complications


Reduced motion
Radial head overgrowth
Premature physeal closure
Non union
Avascular necrosis of the radial head
Alteration in the carrying angle
Neuromuscular problems (ie ® valgus with ulna nerve problems)
Radio/ulna synostosis
Myositis ossificans

Prognosis

The results of initial conservative management of Mason II and III fractures are no different to early excision
Also the results of delayed excision of the radial head are satisfactory giving some justification for the initial closed treatment of these fractures with delayed excision of the radial head to be considered at a later date if needed as symptoms develop

Fractures of Radius and Ulna

Galleazi fracture

fracture of distal 1/3 of radius with dislocation of the distal radioulnar jt ( Galleazi - 1934)

Treatment

ORIF in adults
CR/POP in children
aim to reduce accurately to ensure DRUJ reduction

Monteggia fracture

fracture of proximal ulna with dislocation of the prox radius ( Monteggia - Milan, 1814 )

Classification

( Bado)
Type

ant dislocation of radial head
post or posterolat dislocation of the radial head
lat or anterolat dislocation of the radial head
ant dislocation of the radial head with fracture of both radius and ulna at the diaphysis

Treatment

ORIF in adults
CR/POP in children
aim to reduce ulna - this reduces the prox jt

Nightstick Fracture

fracture ulnar diaphysis alone from a direct blow

Treatment

undisplaced
AEPOP or functional brace stopping supination/ pronation

displaced
ORIF

Prognosis

union in ~ 10 wks
nonunion - rare

Fracture of Shaft of Radius Alone

rare

Treatment

undisplaced
AEPOP or functional brace stopping supination/ pronation

displaced
ORIF

Fracture of Both Bones of Forearm

Classification based on the location in the forearm (proximal, middle or distal 1/3)

Treatment

Children

CR/POP - note the deforming forces of muscles at different levels of fracture
ORIF if unable to obtain or maintain reduction
Can accept 1cm overriding as long as the bones are correctly aligned and rotated
Can accept up to 20o angulation at the fracture in the skeletally immature (ie less than 10 years) ® no significant loss of pronation or supination providing the rotation of the individual bones is correct
Correction of angulation has been reported up to 18o (Larsen, 1988) mainly due to change in the orientation of the epiphyseal plate and appositional bone formation and resorption If close to cessation of growth require an anatomical reduction

Foot and Ankle Fractures

Ankle

Eponymous Types

Maisonneuve
either a med malleolus fracture or deltoid lig tear with a high fibular fracture

Le Fort - Wagstaffe
avulsion fracture of anterior margin of distal fibula at insertion of anterior tibio-fibular lig

Tillaux-Chaput
avulsion fracture of anterior tibial margin by the anterior tibio- fibular lig

Volkmanns triangle
the postero lat malleolar fracture

Classification: (Weber/ AO)

Type A
Transverse avulsion fracture of the fibula at the level of the ankle joint or below
Medial malleolus may be intact or sheared, and may be an associated compression fracture of the tibial edge
The tibio-fibular ligament complex is always intact
A1 isolated fibular fracture
A2 with fracture of med malleolus
A3 with a posteromedial fracture

Type B
Spiral fracture of the distal fibula beginning at the level of the syndesmosis
Part of the tibio-fibular syndesmotic ligament may be involved but the ankle mortise is stable following reduction of the fracture
B1 isolated fibular fracture
B2 with a med lesion ( malleolus or ligament)
B3 with a med lesion and fracture of posterolat tibia

Type C
Fracture of the fibula anywhere between the syndesmosis and the head of the fibula
The tibio-fibular ligament complex is always disrupted and diastasis screws should be inserted if it remains unstable after fixation of the fracture (ankle in neutral position when inserted)
C1 diaphyseal fracture of fibula- simple
C2 diaphyseal fracture of fibula- complex
C3 proximal fracture of fibula

Investigation

XRay
AP/lat/mortise views
stress views

Tomograms

CT
If X-Rays show a displaced malleolar fracture there must be a ligament injury somewhere around the mortice
Ramsey and Hamilton (1976) showed that lateral displacement of the talus in the mortice of 1mm an average 42% loss of articular contact and congruency

Treatment

Nonoperative

Indications
for undisplaced or stable fractures
for displaced fractures when anatomical reduction can be obtained and maintained without repeated manipulation
when pt general condition does not permit
when operative treatment delayed
obtained by reversing the mechanism of injury
maintained by AKPOP for rotationally unstable injuries, 3- point molding, ankle at 90
Undisplaced or stable fractures can be managed in BKPOP, WB PRN

Operative

Indications
failure of CR
when CR requires forced, abnormal positioning of the foot
for displaced or unstable fractures that result in displacement of the talus or
widening of the mortise of more than 1-2 mm

Aims
restore fibular length
anatomical jt surface reconstruction
close mortise: anatomic reconstruction of the fibula usually restores the mortise and restores stability to the syndesmosis
Syndesmotic fixation if: tibiofibular diastasis +/- high fibular fracture
instability post ORIF of fibula
Diastasis screws should be tri-cortical and not lagged
remove prior to WB
posterior malleolus- fix if more than 25% of artic surface and displaced more than 2mm most reduce with the fibular reduction

No significant benefit has been identified in the generally accepted regime of delayed application of plaster until after a reasonable range of movement has been achieved.

A paper from Nottingham suggests that females over 50 have higher incidence of complications of operative treatment- however this is a retrospective review and their overall figures are not very impressive ( Beauchamp etal "displaced ankle fractures in patients over 50 yrs of age" JBJS 65B: 329-332, 1983).
Their recommendation must be viewed with a degree of caution . A prospective trial from Chicago suggests that ORIF gives a better result in pts who are more than 50 yo ( Phillips etal JBJS 67A: 67, 1985)

Complications

Bone

nonunion
most of the med malleolus treated with CR- due to interposed tissue
treat if symptomatic with ORIF + BG

malunion

Wound

skin necrosis marginal necrosis in ~ 3%
care in handling tissue etc- treat with dressings

Infection

less than 2%, treat infection, leave fixation until fracture healed

Arthritis

incidence with severity of injury
degen changes in 10% of anatomically fixed , 85% if not adequately reduced - changes apparent within 18 mths
ref: Klossner "Late results of operative and nonoperative treatment of severe ankle fractures" Acta Chir Scand Suppl. 293: 1-93, 1962

Prognosis

There is a reduction in the incidence of arthrosis in patients where an anatomical reduction has been achieved
ref: Phillips etal JBJS 67A: 67-78, 1985 Prospective trial shows higher total ankle scores in those that are operatively treated- especially so in those pts more than 50 yrs old

Tillaux Fractures

Avulsion fracture of the anterolat distal tibia at site of attachment of the anterior tibio-fibular lig
= SH3 fracture

Triplane Fractures


Combine a Tillaux fracture with a type 2 S-H fracture
May be two or three part and fixation may cross the physis in these injuries as they occur when closure of the physis is imminent
Growth arrest occurs in 14% of all ankle fractures in the skeletally immature and appearance may be delayed for up to six months therefore need to check growth at one year

Treatment

ORIF

Prognosis

Residual dis

Femur Fractures

Intracapsular Fractures of the Proximal Femur

Blood supply to the head of the femur

ref: Crock " An atlas of the arterial supply of the head and neck of the femur in man"
CORR 152: 1727, 1980
Chung JBJS 58A: 961970, 1976

4 groups 1. Extracapsular arterial ring

= trochanteric anastomosis
major contributions posteriorly from the horizontal br of the med circumflex femoral , and, anteriorly from ascending br of the lat femoral circumflex artery

2. Ascending cervical branches

( = retinacular br's) arise from 1.
pass up beneath the synovial and capsular reflections in their passage they give branches to the metaphysis of the femoral neck
there is a free intramedullary anastomosis bw branches of the superior nuttrient artery system,br's of the extracapsular ring, br's of the ascending cervical branches, and the subsynovial ring
4 groups sup, inf, med, lat the lateral supplies most of the blood to femoral head
at the margin of the artic cartilage these vessels form a second ring the

3. Subsynovial intracapsular ring ( Chung)

( = circulus articuli vasculosis Hunter, 1743). This ring may be complete or incomplete (complete more often in males). From this ring epiphyseal branches arise that enter the femoral head

4. Artery of the lig teres

from the lat br of the obturator artery supplies small area about the fovea in the vast majority

Epidemiology

increased freq with
age
dementia
malignancy
chronic illness

decreased freq with
long term physical activity
supplemental Vit D3 and Cain elderly women
HRT

Classification

Garden R.S. " Reduction and Fixation of subcapital fracturesof the femur"
OCNA 5: 683712, 1984
Types

an incomplete or impacted fracture
a complete but undisplaced fracture
a complete partially displaced fracture
a completely displaced fracture

Eliasson etal "Displacement in femoral neck fractures"
Acta Orth Scand 59:359371, 1988
Displaced ( = Garden 1+2)
Undisplaced (= Garden 3+4)

Treatment

based on pt age and grade of fracture

Pt less than 65
and do not have a chronic illness, poor life expectancy ® ORIF

Pt bw 65 and 75
those with high functional demand ® ORIF
those with low demand , chronic illness® arthroplasty

Pt more than 75
arthroplasty

pts of any age with less than 1 yr life expectancy® hemiarthroplasty
pts less than 75 with a limited life expectancy of more than 1yr®bipolar

Internal fixation

Timing of treatment
reduction of a displaced fracture of the femoral neck improves blood supply to the femoral head reduction within 8 12 hrs minimises risk of AVN if reduce within 8 hrs risk of AVN in a displaced fracture is ~ 20%.
2448 hrs risk is ~ 40%
ref: Swiontkowski etal JBJS 66A: 837846, 1984

Closed Reduction
Leadbetter ( ref : JBJS 20:108113, 1938)
affected hip flexed to 90 deg in slight adduction, traction then applied, then the thigh is internally rotated , then while maintaining IR the thigh is abducted and brought down to level in extension
Open Reduction
indicated if CR fails
anterolat approach bw TFL + G medius, open capsule, disimpact and reduce
Method of fixation
3 cannulated screws
CHS not recommended as is too large an implant and if placed incorrectly can jeopardise blood supply
If CHS used use a derotation screw to control rotation

Arthroplasty

AMP for pts more than 70
THR for pts less than 70

Complications

AVN

undisplaced fracture ~ 10%
displaced fracture up to ~ 80% either partial or complete (variable reporting)

late segmental collapse occurs in
~ 10% undisplaced fracture
~ 30% displaced fracture

Failure of fixation

Nonunion
rare in undisplaced fracture
~ 30% in displaced fracture
treat with either a valgus osteotomy or an arthroplasty

DVT/PE
DVT ~ 40%
low dose warfarin in pts who justify risk of anticoagulation

Prognosis

ref: LuYao etal " Outcomes after displaced fractures of the femoral neck"
JBJS 76A: 1525, 1994
Metaanalysis of 116 papers

At 2 yrs after primary ORIF
nonunion in 33%
AVN in 16%
reoperation rate 2036% ( ie 2.5 times that for hemiarthroplasty)

At 2 yrs from hemiarthroplasty
dislocation 2%
reoperation rate 618%

At 2 yrs from THR
dislocation 11%


Intertrochanteric Fractures

classification

AO

proximal femur type
A1 pertrochanteric simple
A2 pertrochanteric multifragmentary
A3 intertrochanteric

Kyle, Gustilo and Premer JBJS 61A: 216221, 1979

type 1: stable undisplaced , no comminution
type 2: stable displaced , min comminuted. Reduction ®stable construct
type 3: unstable , large posteromed comminuted area
type 4: also have a subtrochanteric component

Treatment

Type 1,2,3: ORIF with CHS
Type 4: CHS if pyriformis fossa not intact, supplemental BG

2nd generation nail if pyriformis fossa intact
no advantage to use osteotomies if using a sliding screw device
ref : Hopkins , Nugent and Dimon "Medial displacement Osteotomy for unstable intertrochanteric fractures" CORR 245: 169172, 1989

Complications/ Prognosis

Mortality
~ 30% at 1 yr , after this the expected normal curve is followed

Infection
~1%

Nonunion
rare

Mechanical / technical failures
nail cutting out
pin penetration
fracture below implant seen esp in gamma nail


Subtrochanteric fractures

Classification

Type 1
High: fracture line extends into the lesser trochanter

Type 2
Low: lesser trochanter remain