Techniques Femur Dislocation: Ortolani – determined if femur is already dislocated Barlow – determined if femur can be dislocated
PTB Classification
I – TB exposure and no signs of infection II – TB infection and no evidence of disease III – TB clinically active IV – TB clinically not active (treatment failure, relapse, treated) V – PTB suspect
Stage I – The carcinoma strictly confined to the cervix (extension to the corpus would be disregarded).
IA – The invasion carcinoma which can be diagnosed only by microscopy, with deepest invasion less than or equal to 5mm and the largest extension more than or equal to 7mm.
IA1 – measured stromal invasion of less than or equal to 3mm in depth and extension of more than or equal to 7 mm.
IA2 – measured stromal invasion of more than 3mm and not more than 5mm with an extension of not more than 7mm.
IB – Clinically visible lesions limited to the cervix uteri or pre-clinical cancers greater than stage AI
IB1 – clinically visible lesion less than or equal to 4cm in greatest dimension.
IB2 – clinically visible lesion more than 4cm in greates dimension.
Stage II – Cervical carcinoma invades beyond the uterus, but not the pelvic wall or to the lower third of the vagina.
IIA – without parametrial invasion
IIA1 – clinically visible lesions less than or equal to 4cm in greatest dimension.
IIA2 – clinically visible lesion more than 4cm in greatest dimension.
IIB – with obvious parametrial invasion
Stage III – The tumor extends to the pelvic wall and/or causes hydronephrosis or non-functioning kidney.
IIIA – tumor involves lower third of the vagina, with no extension to the pelvic wall
IIIB – extension to the pelvic wall and/or hydronephrosis or nonfunctioning kidney
Stage IV– The carcinoma has extended beyond the true pelvis or has involved (biopsy proven) the mucosa of the bladder or rectum. A bullous edema, as such, does not permit a case to be allotted to Stage IV
The abnormal protrusion of a peritoneal sac, often with abdominal contents, through the femoral canal.
The predisposing factor is the anatomy of the femoral canal with distinct unyielding boundaries of
medially the lacunar ligament
anteriorly the inguinal ligament
posteriorly the pectineal ligament and pubic bone
laterally the femoral vein
The canal only usually consists of loose connective tissue and lymph node (Cloquet’s node).
Risk Factors
females (have a wider angle between the inguinal ligament and pectineal part of the pubic bone and a wider femoral canal)
pregnancy
raised intraabdominal pressure (heavy lifting, cough or straining due to constipation or prostatism)
25 times less common than inguinal hernias female : male is 4 : 1
History
As femoral hernias are often small, they often go unnoticed until they become strangulated or obstructed, presenting as a surgical emergency (up to 80%) with symptoms of pain, abdominal distention, nausea, vomiting, absolute constipation. Also presents with lower abdominal discomfort, or lump or bulge in the groin region.
Physical Examination
Careful inspection will show a swelling in the groin below and lateral to the pubic tubercle (although if large, may tend to spread up and over the inguinal ligament). There is absence of a cough impulse over the inguinal ring. If incarcerated or strangulated, the hernia may be very tender. Signs of bowel obstruction (e.g. distension, high pitched bowel sounds). Other differentials include inguinal hernia, lymphadenopathy, hydrocele or lipoma of the spermatic cord, groin or psoas abscess, saphena varix or femoral aneurysm.
Pathology
The narrow margins of the femoral canal predispose to incarceration of the hernia contents that could consist of omentum, bowel, extraperitoneal fat or other organs such as ovary. The vascular supply becomes compromised and involved tissues become ischaemic and gangrenous if the hernia is not operated on promptly.
Ultrasound: if a different diagnosis is suspected, but should not delay surgery if an incarcerated hernia is suspected.
Management
Emergency: Resuscition is very important, with attention to rehydration and correction of electrolyte imbalances, placement of an NG tube if vomiting, antibiotics if signs of sepsis and surgical repair as definitive treatment.
Surgery: Principles involve dissection of the sac, observing and reducing the contents, excising the sac and repairing the defect, usually by approximation of the inguinal and pectineal ligaments using non-absorbable sutures. Three approaches:
Low (Lockwood) transverse incision over the hernia.
Transinguinal (Lotheissen) incision above and parallel to the inguinal ligament, through the external oblique, inguinal canal and transversalis fascia (may have a higher recurrence rate).
High (McEvedy) approach using an oblique, paramedial or unilateral Pfannenstielincision, opening the rectus sheath, retracting rectus medially and dividing transversalis to expose the femoral canal. This is used if strangulation is suspected. The sac is opened and contents inspected. If viable, they are reduced or if nonviable bowel is present, this is resected (may necessitate a lower midline incision if a high approach is not used).
Complications
Femoral hernias commonly strangulate, resulting in bowel obstruction, ischemia and gangrene, which may necessitate surgical resection.
Of surgery: The lacunar ligament can be incised, occasionally causing bleeding from an aberrant obturator artery running medially.
Prognosis
Outcome is generally good with prompt and appropriate surgery, recurrence after repair is uncommon (< 3%).
The abnormal protrusion of a peritoneal sac through a weakness of the abdominal wall in the inguinal region.
Direct: Protrusion of the hernial sac occurring directly through the transversalis fascia and posterior wall of the inguinal canal, medial to the inferior epigastric vessels.
Indirect: Protrusion of the hernia sac, through a deep inguinal ring with coverings of the spermatic cord, following the path of the inguinal canal.
Etiology
Congenital: Abdominal contents enter the inguinal canal through a persistent processus vaginalis.
Acquired: Increase intraabdominal pressure together with muscle and transversalis fascia weakness.
Congenital indirect inguinal hernias in 4% of male births.
In adults peak age is 55–85 years.
History
Asymptomatic or patient often notices a lump or swelling in the groin. May present due to discomfort or pain, irreducibility, increase in size or symptoms of complications.
Physical Examination
Groin lump that may extend to the scrotum or labia in women. Distinguished from femoral hernias by emerging above and medial to the pubic tubercle.
Examine the patient standing; the hernia is associated with a cough impulse. Indirect hernias may be controlled by pressure over the deep inguinal ring. Auscultation may reveal bowel sounds from within the hernia. The hernia may be irreducible if incarcerated, very tender if strangulated, and may be associated with signs of complications, e.g. bowel obstruction and systemic upset, pyrexia and tachycardia.
Pathology
Classification:
Indirect (60%)
right side is more common than left due to right testis descending later
Direct (35%)
emerge through Hesselbach’s triangle (medially the lateral border of the rectus, laterally the inferior epigastric vessels and inferiorly the inguinal ligament).
combination ‘pantaloon’ hernia (5%).
Hernias can be described as reducible, irreducible (incarcerated) or strangulated.
Laboratory Request
If acute with painful irreducible hernia:
Bloods: CBC, U&Es, CRP clotting and G&S if operative intervention likely. ABGs may be useful for indicating the presence of bowel ischemia within the hernia (metabolic acidosis, elevated lactate).
Imaging: Upright Chest X-ray and Abdominal X-ray. Ultrasound may be useful in excluding other causes of groin lumps (e.g. hydrocoele).
Management
Surgical: Elective repair for uncomplicated hernias. Can be carried out under local, epidural, spinal or general anaesthesia. There are several types of surgical repair (herniorrhaphy).
[1] Mesh (Lichtenstein) repair: Oblique incisionabove the inguinal ligament, with opening of the external oblique aponeurosis and the spermatic cord gently freed. An indirect sac is dissected from the cord, opened (herniotomy) and the contents reduced. The sac is excised and the defect repaired, using a mesh to reinforce the defect in transversalis fascia. This is the most common procedure. Other open techniques include the Shouldice repair, which uses nonabsorbable sutures to reinforce the defect, and the Stoppa repair.
[2] Laparoscopic mesh repairs: Now common with transabdominal preperitoneal and totally extraperitoneal approaches used. In general, laparoscopic repair results in earlier recovery and return to normal activities.
Emergency: Necessary in obstructed or strangulated hernia. Laparotomy with bowel resection may be indicated if gangrenous bowel is present within the hernia. Insertion of mesh may not be suitable in this case.
Complications
incarceration
strangulation
bowel obstruction
Maydl’s hernia (strangulated W-shaped small bowel loop)
Richter’s hernia (strangulation of only part of the bowel wall circumference)
From surgery:
pain
wound infection
hematoma
penile or scrotaledema
nerve damage or neuroma formation
osteitis pubis
mesh infection
testicular ischemia
recurrence
Prognosis
Tend to slowly enlarge if left alone. Annual risk of strangulation 0.3–3%. Surgical mesh repair usually has a good outcome with recurrence in < 5% of cases.
Chronic inflammation of the pancreas with permanent structural changes leading to impaired endocrine and exocrinefunction and recurrent abdominal pain.
Recurrent severeepigastric pain, radiating to back
relieved by sitting forward
exacerbated by eating or after an episode of binge drinking
May be associated with bloating and pale offensive stools (steatorrhea).
Diarrhea
Weight loss
Thirst
Polyuria
Physical Examination
Epigastric tenderness.
Epigastric fullness (due to pseudocyst).
Signs of weight loss, malnutrition and alcohol abuse.
Pathologic Feature
Disruption of normal glandular architecture due to chronic inflammation and fibrosis, calcification, ductal dilatation, cyst and stone formation.
Laboratory Request
Blood:
glucose (elevation may indicate endocrine dysfunction)
glucose tolerance test
amylase and lipase (usually normal)
Liver function panel (elevated if common bile duct obstruction)
Ultrasound: Percutaneous or endoscopic.
ERCP or MRCP: Early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternating dilatation (‘chain of lakes’ appearance).
Abdominal X-ray: Pancreatic calcification may be visible.
CT scan: Pancreatic cysts, calcification.
Tests of pancreatic exocrine function: Fecal elastase.
Management
General: Dietary advice and alcohol abstinence.
Acute: Analgesics for exacerbations of pain.
Chronic: Pain management may need specialist pain clinic, treatment of diabetes (e.g. insulin). Pancreatic enzyme replacements (e.g. Creon, Pancrease). Endoscopic stenting of strictures may be possible.
Pain control: As the majority of sensory nerves to the pancreas transverse the celiac ganglia and splanchnic nerves, both celiac plexus block and transthoracic splanchnicectomy offer variable degrees of pain relief.
Surgical: Indicated if medical management has failed. Options include proximal resection (pancreaticoduodenectomy) or lateral pancreaticojejunal drainage (Puestow procedure).
Complications
Local:
pseudocysts
biliary duct stricture
duodenal obstruction
pancreatic ascites
pancreatic carcinoma
Systemic:
diabetes mellitus
steatorrhea
hyperglycaemic coma
chronic pain syndromes (dependence on strong analgesics)
Prognosis
Surgery improves symptoms in 60–70% but results are often not sustained. Life expectancy is reduced by 10–20 years.
sudden onset of severe epigastric or abdominal pain
radiating to back
relieved by sitting forward
aggravated by movement
anorexia, nausea and vomiting
history of gallstones
alcohol intake
Physical examination will elicit
epigastric tenderness
fever
shock
tachycardia
tachypnea
jaundice (may be present)
hypoactive bowel sounds (secondary to ileus)
If severely hemorrhagic:
Turner sign (flank bruising)
Cullen sign (periumbilical bruising)
Prognosis
Insult results in activation of proenzymes within the duct/acini resulting in tissue damage and inflammation.
Varies in severity from mild glandular and interstitialedema to frank parenchymal necrosis and hemorrhage with release of inflammatory mediators into the systemic circulation.
Saponification (foaming) may be seen due to action of lipases and proteases on pancreatic tissue.
Laboratory Requests:
Amylase (usually > 3x normal)
Serum lipase
CBC (increase WBC, increase hematocrit)
U&Es
increase glucose
increase CRP > 100 at 48 hours (severe prognosis)
decrease Calcium
LFT (deranged if due to gallstone pancreatitis or alcohol)
ABG (for hypoxia or metabolic acidosis)
Ultrasound is useful to reveal gallstones or biliary dilatation. Pancreas often difficult to visualise due to overlying bowel gas. Upright Chest X-ray: Mainly to exclude other causes of an acute abdomen. There may be pleural effusion. Abdominal X-ray: To exclude other causes of acute abdomen. Psoas shadow may be lost. CT scanning for severe cases.
Note:Amylase level does not correlate with severity.
Management
(1) Intensive supportive care:
Fluid and electrolyte resuscitation and close monitoring. NPO. Urinary catheter and NG tube. Analgesia. Later, nutritional support may be necessary. Prophylactic antibiotics have not been shown to reduce mortality but are often given. If it is gallstone pancreatitis, stone removal by ERCP can be considered in severe cases or with cholestatic jaundice.
(2) Earlydetectionandtreatmentofcomplications:
Monitor respiratory function, renal function and clotting. Management in ICU may be necessary for severe cases.
(3) Surgical:
For necrotising pancreatitis. Drainage and debridement of all necrotic tissues should be performed.
Complications
pancreatic necrosis
pseudocyst
abscess
pancreatic ascites
chronic pancreatitis (with diabetes and malabsorption)
Severe Systemic Complications
multiorgan dysfunction
sepsis
renal failure
ARDS
Prognosis
20% follow severe fulminating course with high mortality (pancreatic necrosis associated with 70% mortality)
Opacification of the lens of the eye. Majority of cases are idiopathic age-related (‘senile cataracts’). Numerous secondary causes including:
Local:
previous eye trauma
uveitis
intraocular tumors
Systemic:
diabetesmellitus
metabolic disorders
galactosemia
hypocalcemia
Wilson disease
skin disease
atopic dermatitis
scleroderma
drugs (steroids)
X-ray and UV radiation
myotonic dystrophy
genetic syndromes (Down syndrome)
Congenital: congenitalrubellasyndrome.
Major cause of treatable blindness worldwide.
History
Gradual onset painless loss of vision.
Glare from bright light, vision may worsen in bright light (especially with central lens opacity).
Some may experience monocular diplopia and see haloes around lights.
Some may notice that they can read without glasses (nuclear sclerotic cataract may increase lens-converging power).
In infants, there may be amblyopia or nystagmus.
Physical Examination
1. Loss of red reflex and hazy lens appearance. 2. Reduced visual acuity.
Pathologic process
(Seen with slit-lamp microscope) In the early stages, there is compression of lens fibre in the central portion of the lens (nuclear sclerosis), with gradual change of the crystalline lens nucleus from translucent to brown or gray. There may be areas of granular opacities (e.g. in posterior subcapsular subtype).
Management
Congenital cataracts must be treated urgently to avoid amblyopia. The decision for surgery depends on the effect of the cataracts on the patient’s vision and life. Surgical: Phacoemulsification (using ultrasound probe) followed by aspiration of lens material and insertion of intraocular lens implant is curative. Specific complications:
posterior capsule opacification
vitreous humour loss
endophthalmitis
Usually done as day surgery. Post-op care should include steroid drops (for inflammation), antibiotic drops (infection prophylaxis), avoidance of strenuous exercise and ocular trauma.
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