SEPTIC ARTHRITIS   Pyogenic infection of a joint space. It is a particularly serious infection of in children, because of potential for complete damage to joint cartilage and long term sequalae Sites Septic arthritis affects the hip and the knee most commonly, although the elbow, ankle, and shoulder are often involved. Smaller distal joints are less likely to be affected by septic arthritis than are larger proximal ones. Age  Septic arthritis can occur in those of any age, but it predominantly affects young children. In children, septic arthritis most commonly occurs in those younger than 3 years. Septic arthritis is uncommon from age 3 years to adolescence. The incidence increases during adolescence with the appearance of gonococcal infections. Etiology §  Staphylococcus aureus-most common §  Streptococcus pneumoniae, group B streptococci, Gonococcus species §  Escherichia coli §  Haemophilus species especially in infants §  Klebsiella species §  Gonococcus §  Pseudomonas species §  Candida species Mechanisms of infection 1. Blood spread from a distant site-Most common 2.Direct invasion through §  Penetrating wound §  Intra-articular injection §  arthroscopy §  Direct spread from an adjacent bone abscess, osteomyelitis or cellulitis 2nd most common cause of septic arthritis is spread from adjacent osteomyelitis. In anatomic locations where the metaphysis of the bone is intraarticular, such as the hip and the shoulder, a metaphyseal focus of osteomyelitis may penetrate  Predisposing Conditions -Rheumatoid arthritis -IV drug abuse -Immunosuppression - Chronic debilitating disorders; Immunosuppressive drug therapy; AIDS -Presence of joint prosthesis -Arthroscopy  Pathophysiology The usual trigger is a haematogenous infection which settles in the synovial membrane. There is an acute inflammatory reaction - acute synovitis, with a serous then seropurulent exudate and an increase in synovial fluid and joint pressure. As pus appears in the joint, articular cartilage is eroded and destroyed partly by enzymes released from synovium, inflammatory cells and pus. Once the articular cartilage is lost, it cannot be replaced with further growth because it has little or no ability to heal or remodel. 2. Ultrasound Joint effusion evaluation and aspiration may be done. In children the joint 'space' may seem to be widened (because of the fluid in the joint) & there may be slight sublaxation of the joint. With E. coli infections there is sometimes gas in the joint. Narrowing or irregularity of the joint space are late feature 3.MRI Incase of complications with soft tissue involvement –menisci injury or spread to cause oseomyelitis. Evaluation of epipyseal necrosis in children Differential diagnosis 1.Acute osteomyelitis 2.Gout & pseudogout 3.Trauma - Traumatic synovitis or haemarthrosis 4.Haemophilic bleed 5.Acute Rheumatic fever - typically pain flits from joint to joint 6.Gaucher's disease - Presents as acute joint pain & fever without any organism being found ('pseudo-osteitis') 7.Bursitis and tenosynovitis 8.Sickle cell disease in crises MANAGEMENT To prevent irreparable damage to the articular cartilage, prompt diagnosis and treatment are mandatory. Principles of management 1.Immobilization of the joint to control pain 2.Administration of appropriate antimicrobial therapy 3. Adequate and timely drainage of the infected synovial fluid. Immobilization and supportive management a) NSAIDS -Analgesics for pain and reduce inflammation b) IV fluids for dehydration c) Rest the joint on a splint -hip infection, the joint should be abducted & 30° flexed, on traction; §  To reduce pain §  To prevent dislocation §  To keep the synovial cavity open to allow circulation §  In children;To prevent slipping of the upper femoral epiphysis and strengthen the perichondral ring d)Empirical antibiotic therapy After aspiration of joint for microscopy ,culture and sensitivity and drawing of blood for blood cultures then empirical antibiotics started: Less than 4years - Augmentin or 3rd generation cephalosporins-cover the bram negatives and staph, aureus Older children & Adults - Flucloxacillin & Fusidic acid IV for 2-7days & then orally for another 3wks In children, give cod-liver oil which reduces inflammation by supplying Omega 3 reducing the formation of arachidonic acid necessary for the formation of prostaglandins that mediate inflammation.

In infants, the entire epiphysis, which is still largely cartilaginous, may be severely damaged; in older children, vascular occlusion may lead to necrosis of the epiphyseal bone. The continued swelling of the joint may cause it to dislocate. Dislocation is particularly common at the hip in infants. In children, necrosis of the epiphysis may also include necrosis of the reserve zone of the physis, with cessation of growth In adults, the effects are usually confined to the articular cartilage, but in the late cases, there may be extensive erosion due to synovial proliferation & growth. If the infection goes untreated, it will spread to the underlying bone or burst out of the joint to form abscesses & sinuses. In adults untreated septic arthritis may cause: 1.Partial loss of articular cartilage & fibrosis of the joint with pain and stiffness. 2.Loss of articular cartilage & bony ankylosis 3.Bone destruction & permanent deformity of the joint 4. Extend into the underlying bone, leading to osteomyelitis. 5. Extracapsular infectious complications such as myositis and abscess formation in adjacent soft tissues. Clinical presentation 1.Acute painful joint 2.Diffuse swelling of the joint 3.The overlying skin looks red 4.Local warmth & marked tenderness 5.Swinging fever 6.Rapid pulse 7.Reluctance to move the limb ('pseudoparesis') - All movements are restricted, & often completely abolished, by pain & spasm Investigations Gold standard   Joint aspiration m/c/s - Leukocyte counts >50,000/ml Normal synovial fluid leukocyte count - <300/ml Non-infective inflammatory disorders - >10,000/ml Laboratory 1.FHG - ↑WBC –neutrophilia 2.ESR and C-reactive proteins elevated 3.Blood culture - May be positive Imaging 1.Plain X-ray Early disease show soft tissue swelling around the joint and a widened joint space from joint effusion. Displacement of adjacent fat pads may be present, especially in infants and children. With progression of the disease, plain films reveal joint-space narrowing as articular cartilage is destroyed. Loss of visualization of the white cortical line over large areas of the joint surface soon ensues as bone destruction begins to develop. Plain film findings of superimposed osteomyelitis may develop (periosteal reaction, bone destruction, sequestrum formation). Surgical intervention-Arthrotomy If there is frank pus in the joint or if the hip joint of a child is involved with septic arthritis, immediate surgery is indicated. The joint must be surgically decompressed. Pus and fibrinous debris must be removed. In these instances, septic arthritis is a true orthopedic emergency Under general anaesthesia the joint is opened through a small incision, drained & washed out with physiological saline. A small catheter is left in place & the wound is closed; suction-irrigation is continued for another 2-3days. Surgery -In very young infants -When the hip is involved (Joint is opened from behind) -If the aspirated pus is very thick For knee, arthroscopic debridement from the lateral aspect & copious irrigation may be equally effective Older children with early septic arthritis (symptoms for <3days) involving any joint except the hip - Repeated closed aspiration of the joint; however, if there is no improvement within 48hrs, open drainage will be necessary. Post-op; -Intact articular cartilage - Physiotherapy -Destroyed articular cartilage - The joint is splinted in the optimum position awaiting ankylosis (stiffness or fixation of a joint by disease or surgery

PEPTIC ULCER DISEASE Definition -Peptic ulcer disease (PUD) refers to a discrete mucosal defect in the portions of the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion. -The mucosal break, 3 mm or greater in size with depth, Pathophysiology: -Results from imbalances between the mucosa protective factors and those that tend to cause injury to mucosa. Injurious factors include the following: 1)       H pylori leading cause of PUD and is associated with virtually all ulcers not induced by NSAIDs 2)       NSAIDs 3)       Acid and pepsin. 4)       Cigarette Smoking 5)       Ethanol 6)       Bile acids 7)       Steroids 8)       Psychological stress. Important protective or defensive factors are -Mucus -Bicarbonate -Mucosal blood flow -Prostaglandins -Alkaline tide -Hydrophobic layer -Restitution -Epithelial renewal. Clinical presentation History: 1-Epigastric pain (the most common symptom) ü  Gnawing or burning ü  Occurs 1-3 hours after meals ü  Relieved by food or antacids ü  Might occur at night ü  Might radiate to back (consider penetration) 2-Nausea 3-Vomiting, which might be related to partial or complete gastric outlet obstruction 4-Dyspepsia, including belching, bloating, distention, fatty food intolerance 5-Heartburn 6-Chest discomfort 7-Anorexia, weight loss 8-Hematemesis or melena resulting from gastrointestinal bleeding -Dyspeptic symptoms that might suggest PUD are not specific because only 20-25% of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer. Physical: In uncomplicated PUD, clinical findings are few and nonspecific. -Epigastric tenderness -Parlor-mild-moderate -Succussion splash resulting from partial or complete gastric outlet obstruction Lab Studies: -In most patients with uncomplicated PUD, routine laboratory tests are usually unhelpful. -Documentation of PUD depends on radiographic and endoscopic confirmation. -If the diagnosis of PUD is unclear or complicated and PUD is suspected, obtaining CBC, liver function tests (LFTs), amylase, and lipase might be useful. Imaging Studies: Upper gastrointestinal series a)Double-contrast radiography However, it has been replaced largely by diagnostic endoscopy, when available. -It is not as sensitive as endoscopy for the diagnosis of small ulcers (<0.5 cm). -It does not allow for obtaining a biopsy to rule out malignancy in the setting of a gastric ulcer or to assess for H pylori infection in the setting of a gastroduodenal ulcer. b)Upper GI endoscopy -Preferred diagnostic test in the evaluation of patients with suspected PUD -Highly sensitive for the diagnosis of gastric and duodenal ulcers -Allows for biopsies and cytologic brushings in the setting of a gastric ulcer in order to differentiate a benign ulcer from a malignant lesion -Allows for detection of H pylori infection with antral biopsies for a rapid urease test and/or histopathology in patients with PUD §  Rapid urease tests are considered the endoscopic diagnostic test of choice. One or more gastric biopsy specimens are placed in the rapid urease test kit. If H pylori are present, bacterial urease converts urea to ammonia, which changes pH and produces a color change. §  Histopathology, the criterion standard for the diagnosis of H pylori §  Culture primarily is used in research studies Non endoscopic or noninvasive tests §  Carbon breath tests detect active H pylori infection by testing for the enzymatic activity of bacterial urease. In the presence of urease produced by H pylori, labeled carbon dioxide (heavy isotope, carbon-13, or radioactive isotope, carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled. §  Fecal antigen testing identifies active H pylori infection by detecting the presence of H pylori antigens in stools. This test is more accurate than antibody testing and less expensive than urea breath tests. §  Serology-Antibodies (immunoglobulin G [IgG]) to H pylori can be measured in serum by ELISA  SURGICAL ASPECTS OF PUD BLEEDING When should operation be performed? What operation should be done? Clinical predictors of continued/recurrent bleeding 1)       Shock (SBP < 100 mmHg) 2)       Anemia (hemoglobin <7, <10) 3)       High transfusion requirement (2000 cc/24, 5 units total) 4)       Age > 60 (comorbidities) 5)       Bleeding rate of > 600cc/hour as measured hematemesis -Clinical and endoscopic features can predict rebleeding and mortality -Early operation an appropriate consideration, ideally after stabilization, if rebleeding risk is high -Availability of endoscopic hemostatic techniques can greatly diminish need for urgent surgery in many, but not all cases Value of endoscopic treatment and re-treatment -80-100% initial hemostasis rates -75% success with endoscopic retreatment -Slight increased risk of perforation with thermal re-rx Choice of operation--gastric ulcers -Generally higher rebleeding rate with gastric lesions compared to duodenal -Location and setting influence choice of operation Gastric ulcer typology (Modified Johnson Classification) Type I:  incisura, lesser curve Type II:  associated duodenal ulcer disease Type III:  antral/prepyloric Type IV:  high lesser curve/gastroesophageal junction Type V:  associated with NSAID use Choice of operation--type I, II, III -Distal gastrectomy incorporating ulcer and Billroth I reconstruction -No vagotomy necessary in pure type I setting -Add vagotomy if type II, ongoing ulcerogenic stimulus (alcohol, steroids, NSAID’s), type III within 3 cm of pylorus -Consider vagotomy and pyloroplasty with oversew or wedge excision if unacceptable risk for gastrectomy, accept 15% higher risk of rebleeding  Billroth I (gastroduodenostomy) Billroth II (gastrojejunostomy) Choice of operation--type IV -Pauchet procedure (distal gastectomy with lesser curve tongue-extension to incorporate higher ulcer and Billroth I reconstruction) -Csendes operation (gastrectomy incorporating portion of GE junction on lesser curve side and esophagogastrojejunostomy) -Kelling-Madlener procedure (antrectomy with oversew/bx of ulcer left in situ)  PEPTIC PERFORATION Nonoperative treatment Operative treatment –risk status –definitive surgery vs. simple closure –? laparoscopy Nonoperative treatment-Indications 1.Water soluble contrast study documenting sealed perforation 2.Age<70 3.NG tube, antibiotics, acid suppression, IVF 4.Improving exam and clinical signs within 12 hours -70% success rate in avoiding surgery, 35% longer hospital stay Operative treatment--risk assessment -Age>70 -perforation>24 hours -SBP<100 -poorly controlled comorbid conditions define high risk patient Graham patch Benefits of definitive operation -High risk of recurrent ulcer disease (48-60%) if simple closure done, though this can be lowered by longterm acid suppression -PCV lowers above to 3-7%, can be combined with patch closure

Causes: 1.H pylori infection -Most common cause of PUD -Associated with up to 70-80% of duodenal ulcers: however, rate is decreasing, suggesting an increasing number of H pylori–negative ulcers -Prevalence in complicated ulcers (ie, bleeding, perforation) significantly lower than that found in uncomplicated ulcer disease Found in: -90% patients with duodenal ulceration -70% patients with gastric ulceration -60% patients with gastric cancer 2.NSAIDS -Second most common cause of PUD -Addition of steroids potentiates risk -Accounts for many H pylori–negative ulcers 3.Severe physiologic stress ü  -Burns ü  -CNS trauma ü  -Surgery ü  -Severe medical illness 4.Hypersecretory states (uncommon) ü  -Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia (MEN-I) ü  -Antral G cell hyperplasia ü  -Systemic mastocytosis ü  -Basophilic leukemias 5.Systemic diseases with an increased risk of PUD ü  Cirrhosis ü  Chronic pulmonary disease ü  Renal failure and renal transplantation. 6.Additional rare, miscellaneous causes include ü  Radiation-induced or chemotherapy-induced ulcers ü  vascular insufficiency (crack cocaine), ü  Duodenal obstruction. DDX -Biliary Colic -Cholecystitis -Cholelithiasis -Gastritis, Acute -Gastritis, Chronic -Gastroesophageal Reflux Disease -Mesenteric Artery Ischemia -Myocardial Ischemia -Pancreatic Cancer  or Pancreatitis, Acute Chronic  Special studies -Obtaining a serum gastrin is useful in patients with recurrent, refractory, or complicated PUD and is useful in patients with a family history of PUD to screen for Zollinger-Ellison syndrome -A secretin stimulation test can be performed to distinguish Zollinger-Ellison syndrome from other conditions with a high serum gastrin, such as achlorhydria and antisecretory therapy with a proton pump inhibitor. Medical treatment Tripple therapy -Initial treatment typically requires a triple therapy with 2 antibacterial agents and an acid inhibitor, typically a proton-pump inhibitor (PPI). -Drug regimens most often include 2 weeks of antibacterial therapy concomitant with 4 weeks of acid suppression -In adults, standard Maastricht triple therapy is a combination of a PPI, amoxicillin, and clarithromycin. - In the event eradication fails, a quadruple therapy with PPI, bismuth, metronidazole, and tetracycline has been suggested. Less favorable options H2 Antagonists -65% healing at one month -85% healing at two months -If stop treatment - 90% recurrence at 2 years -If maintenance therapy - 20% recurrence at 5 years Surgical Care: -With the success of medical therapy, surgery has a very limited role in the management of PUD. -Potential indications for surgery include refractory disease, and complications of PUD include the following: §  Perforation usually is managed emergently with surgical repair. §  Obstruction -may persist or recur despite endoscopic balloon dilation. §  Massive hemorrhage and hemodynamic instability, recurrent bleeding on medical therapy, and failure of therapeutic endoscopy to control bleeding. The appropriate surgical procedure depends on the location and nature of the ulcer. §  Additional surgical options for refractory or complicated PUD include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly selective vagotomy. Operation for bleeding duodenal ulcer -Truncal vagotomy and pyloroplasty with oversew most attested and efficient operation in less stable patient -Antrectomy a useful alternative in stable patient with large ulcers (>2 cm) -Increased bleeding and rebleeding with giant ulcers -Nissen closure technique can be a helpful adjunct with large posterior ulcers into pancreas or adjacent structures What about H. pylori? •Clear data available showing lower rebleeding rates with H. pylori eradication GASTRIC OUTLET OBSTRUCTION -Acute vs. chronic, natural history -Nonsurgical options -Surgical options Natural history--peptic gastric outlet obstruction -68% of acute obstructions and 98% chronic obstructions ultimately require surgery -Nonoperative strategies for peptic GOO Balloon dilation -76% immediate improvement, but only 38% objective improvement at 3 mos. Issues -Parietal cell vs. truncal vagotomy -Dilation vs. drainage -Type of drainage procedure §  Pyloroplasty/duodenoplasty (Heineke-Mikulicz, Finney) §  Gastroduodenostomy (Jaboulay) §  Gastrojejunostomy §  Antrectomy/anastomosis