For the low groin approach 30gm acticin with visa acne 101e, after opening the sac and reducing its contents best acticin 30gm skin care products for rosacea, amputate it order acticin 30 gm otc skin care 11 year olds. It is not necessary to close Pitfalls and Danger Points the neck of the sac with sutures (Ferguson). It is important, however, to clear the femoral canal of any fat or areolar tis- Injuring or constricting femoral vein sue so the sutures can bring the inguinal ligament into direct Transecting an aberrant obturator artery contact with Cooper’s ligament and the pectineus fascia. This maneuver obliterates the femoral canal but leaves an opening of 6–8 mm adjacent to the femoral vein. Equally Operative Strategy good results can be obtained if the femoral canal is obliter- ated by inserting a plug of Marlex mesh. The technique Choose the operative approach (low groin, high inguinal, or avoids all tension on the suture line. A low groin To reduce an incarcerated femoral hernia, an incision approach under local anesthesia is an excellent choice for the may be made to divide the constricting neck of the hernial sac. If hem- orrhage is indeed encountered during this maneuver and the artery cannot be ligated from below, control the bleeding by finger pressure, and rapidly expose the inner aspect of the pelvis by the Henry approach, which involves a midline incision from the umbilicus to the pubis, after which the peritoneum is swept in a cephalad direction to expose the femoral canal from above. It should be empha- sized that this complication is so rare it does not constitute a significant disadvantage of the low approach to femoral herniorrhaphy. If the sutures drawing the inguinal ligament down to Cooper’s ligament must be tied under excessive tension, abandon this technique. Then insert a plug of nonabsorbable mesh to obliterate the femoral canal, as described below. Carry the incision down to the external oblique aponeurosis and the inferior aspect of the inguinal ligament. Identify the hernial sac as it emerges deep to the inguinal ligament in the space between the lacunar ligament and the common femoral vein (Fig. Often the peritoneum is covered by two or more layers of tissue, each of which may resemble a sac. When the bowel or the omentum remains incarcerated after opening the sac, incise the hernial ring on its medial aspect by inserting a scalpel between the sac and the lacunar ligament (Figs. After returning the bowel and the omentum to the abdominal cavity, amputate the sac at its neck. Although it is not necessary to ligate or suture the neck of the sac, this step may be performed if desired (Fig. Using a peanut sponge, push any remaining preperitoneal fat into the abdominal cavity, thereby clearing the femoral canal of all extraneous tissues. The needle is then passed through the inguinal ligament and through Cooper’s ligament in one simultaneous motion. Cooper’s liga- ment is indistinguishable from the periosteum overlying the cephalad aspect of the pubic ramus. An alternative method involves placing the stitch through the inguinal ligament and then positioning a narrow retractor in the femoral canal to take a bite of Cooper’s ligament and pectineus fascia. Identify the com- mon femoral vein where it emerges from underneath the inguinal ligament, and leave a gap of 4–6 mm between the femoral vein and the most lateral suture (Fig. If strangulated bowel requiring resection is encountered after opening the hernial sac, make a second incision in the midline between the umbilicus and the pubis. Elevate the peritoneum from the pel- vis by blunt dissection until the iliac vessels and the femoral hernial sac are identified. Incise the constricting neck of the femoral canal on its medial aspect and reduce the strangulated bowel. After resecting the bowel, irrigate the femoral region with a dilute antibiotic solution, and repair the femoral ring from below as already described. Monro, who strongly favored the low groin approach, emphasized that the sutures should be tied loosely so they form a lattice- work of monofilament nylon. The same end can be accomplished even more simply by inserting a rolled-up plug of Marlex mesh as advocated by Lichtenstein and Shore. After the hernial sac has been eliminated and all the fat has been cleared from the femoral canal, insert this Marlex plug into the femoral canal. The diameter of the plug may be adjusted by using a greater or lesser length of Marlex, as required. Insert the needle first through the inguinal ligament, then through the Marlex plug, and Anesthesia finally into the pectineal fascia or Cooper’s ligament. General or regional anesthesia with good muscle relaxation After the two sutures have been tied, the plug should fit is required. After irrigating the wound with a dilute antibiotic solution, check for complete hemostasis Incision and then close the skin incision without drainage. If the Start the skin incision at a point two fingerbreadths above the patient accumulates serum in the incision postoperatively, symphysis pubis (Fig. Carry the incision laterally for a distance 105 Femoral Hernia Repair 937 of 8–10 cm, and expose the anterior rectus sheath and the to the inguinal canal (Fig. Elevate the caudal skin flap medially, and deepen the incision through the full thickness of sufficiently to expose the external inguinal ring. Mobilizing the Hernial Sac If the femoral hernia is incarcerated, it is possible to mobi- lize the entire pelvic peritoneum except for that portion incarcerated in the femoral canal (Fig. If the her- nia cannot be extracted by gentle blunt dissection around the femoral ring, incise the medial margin of the femoral ring, and extract the hernial sac by combining traction plus exter- nal pressure against the sac in the groin. Although the pres- ence of an aberrant obturator artery along the medial margin of the femoral ring is a rarity, there may be one or two small venous branches that require suture-ligation prior to incising the medial margin of the ring. If strangulation mandates bowel resection, enlarge the incision enough so adequate exposure for a careful intes- tinal anastomosis may be guaranteed. If bowel has been resected, change gloves and instruments before initiating the repair. Chassin Suturing the Hernial Ring several interrupted sutures of 2-0 Tevdek or Prolene The superficial margin of the femoral ring consists of the (Figs. These structures are just superficial margin of the femoral ring contains only the iliopu- deep to the inguinal ligament. The deep margin of the femoral bic tract or it also catches a bite of inguinal ligament is imma- ring is Cooper’s ligament, which represents the reinforced terial so long as the tension is not excessive when the knot is periosteum of the superior ramus of the pubis. If closing the ring by approximating strong tissues would the hernial defect, suture the strong tissue situated in the super- result in tension, it is preferable to suture a small “cigarette” of ficial margin of the femoral ring to Cooper’s ligament with Marlex into the femoral ring from the cephalad approach. Postoperative Care Early ambulation Perioperative antibiotics are employed in patients with intes- tinal obstruction or those who have had bowel resection for strangulation. Use nasogastric suction selectively in patients with intestinal obstruction or bowel resection. Complications Deep vein thrombosis has been reported secondary to constriction of the femoral vein by suturing. Iliopubic tract repair of inguinal and femoral hernia: the posterior (preperitoneal) approach. Chassin† The multitude of repair techniques available for ventral Indications (incisional) hernia repair attests to lack of satisfaction with any one method. At the time of this writing, more than ten Good-risk patients should undergo elective repair of a ventral kinds of prosthetic sheets (generically called “mesh,” although hernia with any defect of more than 1–2 cm. Early repair not all are strictly speaking mesh) and five kinds of biologic of the small hernia is a simple procedure.

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This consists of maintaining of muscles and joints in good working condition till the arrival of downgrowing axons order acticin 30 gm line acne jeans review. All affected joints are put through full passive movements daily to prevent contracture to develop purchase 30 gm acticin with amex acne ziana. Encouragement to the patient is of utmost necessity to restore function during the period of recovery purchase 30gm acticin fast delivery skin care 90210. Progress is always checked by taking records of the electrical reactions of the muscles and skin sensitivity. Failure to recover or regression after initial recovery, is an indication for exploration of the injured nerve. This is required to deal with the perineural scar or to remove intraneural fibroma. The majority of these nerve lesions remain in continuity and are non-degenerative in type. In these cases the treatment is directed to reduce the fracture or dislocation and a conservative treatment is given for the nerve problem, which consists of prevention of stretching of the muscles supplied by the nerve by proper splints and prevention of pressure sores. Of the other half of the cases, about 80-90% will gradually recover, that is the proximal nerve fibres will grow down the degenerated distal fragment. In these cases the quality of regeneration is quite satisfactory as there is no chance of maldistribution of nerve fibres. In only 10% of cases, there may not be any evidence of recovery at the expected time. So when recovery does not reach the first motor branch in the expected time, which is calculated by the recovery rate of approximately 25 mm (1 inch) in a month, exploration is indicated. Complete division will produce a terminal neuroma at the distal end of the proximal segment. In the proximal segment of the divided nerve there will be retrograde degeneration upto the first node of Ranvier. After an interval of 10 days to fortnight the distal ends of the axons in the proximal segment will start to grow downwards. But by this time the gap between the divided nerve ends has been replaced by organic clots and fibrous tissue, which prevent further downgrowth of the axons. So suturing of the nerve is the only treatment available if restoration of function is to be achieved. In the distal segment of the divided nerve, Wallerian degeneration of the axons occurs, which is described in detail below. It is only noteworthy here that the schwann cells proliferate to form a small bulb-like projection from which these cells grow proximally towards the downgrowing axons by chemotaxis. In neurotmesis, the quality of regeneration is less perfect even after accurate nerve suturing. A motor nerve fibre may grow down a sheath previously occupied by a sensory fibre. Similarly, a sensory fibre may grow down the sheath of a motor fibre and cannot make connection with the motor end-plate. So the recovery of function will be worst in mixed motor and sensory nerves as axons of motor fibres may be well united with sensory fibres of the distal fragment. Thus recovery from the radial nerve injury at the elbow will be better than the ulnar nerve or median nerve injury at the wrist. Neurotmesis is seen in war and severe industrial injuries with extensive soft tissue damage. Such nerve repair can be of two types — primary nerve repair and secondary nerve repair. In clean tidy incised wounds when presented within 6 hours of injury immediate suturing of the divided nerve is the ideal treatment, which is known as primary nerve repair. In untidy contaminated wounds and in case of incised wounds when presented after 6 hours of occurrence, nerve suturing should be postponed until 3 or 4 weeks after injury. If a nerve is seen divided during the course of excision of a contaminated wound, the ends of the divided nerves are approximated by a stitch of fine silk, which prevents retraction during the waiting period. The idea of secondary nerve repair is that — (a) infection of the recent wound does not jeopardise the healing of the nerve suture, but that of late wound does; (b) the nerve sheath remains delicate and friable in an untidy wound which is not an ideal tissue for suturing as it is easily tom by slightest tension. After about 3 weeks epineural fibrosis makes the sheath thicker and tougher to facilitate suturing. The cells of the sheath of Schwann proliferate forming a slight bulb at the commencement of the distal end from which sprouts of Schwann cells grow proximally towards the downgrowing axons of the proximal segments by chemotaxis. The proximal portion of the divided nerve also shows similar Wallerian degeneration, but only upto the first node of Ranvier. After a short interval which varies from 10 days to fortnight the axons begin to regenerate and begin to subdivide to produce an excess of end bulbs alongwith proliferating Schwann cells to produce a swelling at the end, which is known as proximal neuroma or terminal neuroma. After incomplete division affecting only one side of the peripheral nerve, a lateral neuroma or a swelling at the place of incomplete division develops due to proliferating Schwann cells and axons. Similarly if only the central fibres of a nerve trunk are injured, a central neuroma may develop. In these successful cases, the axons regenerate crossing the gap in close application to the Schwann cells from the proximal to the distal cut end. The Schwann cells from the neurilemma that covers the myelin sheath proliferate actively. This proliferation occurs in the both proximal and distal ends which move towards each other. If the gap is a small one ultimately they meet each other and forms empty tubes for regeneration of the axons to occur. The activity of the Schwann cells increases rapidly after the 4th day after injury and reaches its pick at about the end of the 3rd week. Maldistribution of fibres is greatest in the case of mixed motor and sensory nerves, as the motor fibres may enter into the empty tubule of sensory nerves and motor nerve cannot have any action on the sensory end organ and thus wasted. Such maldistribution is also seen in motor nerves which supply a large number of small muscles. The result is best in case of a pure motor nerve which supplies a few groups of large muscles concerned in coarse movements e. The result is worse in case of mixed sensory and motor nerves supplying a large number of small muscles concerned in fine movements e. From the above discussion it is clear that while nerve suturing care must be taken to avoid axial rotation of either cut end to ensure full anatomical continuity. Following suture there is a period of week before sufficient axons arrive in the peripheral stump to cause any reflex response to pinching. After crossing the site of severence the axons grow down the peripheral nerve at the rate of 2 mm per day. Regeneration is not possible (unsuccessful cases) when (i) there is a big gap between the two cut ends and (ii) when there is considerable fibrosis between the two cut ends (probably due to infection). This can be done by — • The muscle most proximal to the nerve injury should be tested for muscle power.

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These casts develop as an accumulation of the normal amount of tubular protein; they do not necessarily mean disease safe 30gm acticin acne under armpit. Red cell Glomerulonephritis Broad acticin 30 gm skin care oils, Chronic renal failure waxy Granular Also called “dirty” or “muddy”; are associated with acute tubular necrosis and represent accumulated epithelial cells White Pyelonephritis buy acticin mastercard skin care products, interstitial nephritis cell Table 8-1. The ratio of albumin to creatinine is a good estimate of the albumin that would have been collected in a 24 hour collection, and is much easier to do. Therefore, serum creatinine values should always be compared to a given patient’s baseline. Hence, if the creatinine goes from 1 to 3 over a period of 2 days in a patient with renal injury, this is consistent with nonfunctioning kidneys. For example, in rhabdomyolysis or contrast-induced renal failure, it may develop over several hours, while in aminoglycoside toxicity it may take 1-2 weeks. The distinction cannot be made by a single serum creatinine test, but requires serial determinations. The term azotemia literally means the buildup of azole groups or nitrogen in the blood. Volume-depleted patients present with signs of orthostatic or frank hypotension and tachycardia. This demonstrates a reduction of effective arterial volume a physiologic term for perfusion of organs, determined by intravascular volume, blood pressure, and cardiac output. Since the underlying physiology is systemic vasodilation, treatment with vasoconstrictors may be useful. This beneficial effect is most likely secondary to the decrease in intra-glomerular hypertension. This may come by obstruction of any part of the renal collection system (renal pelvises to urethra). Prostate: hyperplasia and cancer Neurologic disease: Neurogenic bladder: patients have a history of obstructive symptoms followed by sudden onset of oliguria or anuria. This may be due to multiple sclerosis, spinal cord lesions, or peripheral neuropathy. Clinical Presentation: Patients may experience a distended bladder in prostatism or neurologic disorders. Urine output may diminish or cease, proceeded by incomplete voiding in prostate or bladder diseases. The urinalysis is variable, from normal (neurogenic bladder) to hematuria (stones, bladder cancer, clots). Prostate or bladder outflow disease may be detected by finding large volumes of urine in the bladder after passing a Foley urinary catheter (a large post-void residual volume). After urinating (voiding), there should be no more than 50 mL of urine left in the bladder. If this post-void residual is markedly elevated, it implies an obstruction to the flow of urine out of the bladder. Treatment is based on quickly relieving the cause of the obstruction: For bladder/prostate disease, do Foley catheter insertion. For ureteral/pelvic obstruction, do nephrostomy tube insertion (percutaneous or transurethral). Clinical Recall Which of the following lab values is most likely in patients with prerenal azotemia? Causes include ischemia and hypoperfusion of the kidney (shock, sepsis, heart failure) and tubular toxins (aminoglycosides, contrast dyes, amphotericin, myoglobin [rhabdomyolysis], cisplatin). Next comes a reduction/cessation of urine flow (oligo- or anuria) as the tubules necrose and the glomerular ultrafiltrate back- leaks into the blood instead of forming urine. With severe or prolonged injury, the tubular cells will necrose and slough off into the urine and become visible as renal tubular epithelial cells or granular/muddy brown/pigmented casts. The rising serum creatinine (over days) is accompanied by reduced urine output or anuria. Treatment focuses on correcting the underlying cause (no therapy can reverse the renal failure). Volume repletion with normal saline is often given to make sure there is no prerenal component and may reduce contrast-induced renal failure, but it does not reverse it once it occurs. Dialysis may be needed if uremic symptoms occur, and is stopped once the tubules recover. Rhabdomyolysis can be caused either by (a) sudden/severe crush injury, seizures, or severe exertion, or (b) hypokalemia, hypophosphatemia, or medications (e. The toxicity is because the pigment is directly toxic to the tubular cells as well as from precipitation of the pigment in the tubules. The degree of toxicity is related to the duration of contact of the tubular cells with the hemoglobin or myoglobin, so is compounded by dehydration. Hyperuricemia due to release of purines from damaged muscles Treatment is normal saline to increase urine output and decrease toxin contact time. There is no test which can confirm a specific toxin as the etiology of the renal failure. Other causes of renal failure must first be excluded, and the toxin must be identified and promptly withdrawn. There is no specific therapy that can reverse the renal insufficiency of any direct-acting toxin. Aminoglycoside-related nephrotoxicity (10–20% of all drug-induced nephrotoxicity) is usually reversible. Unlike contrast dyes, aminoglycoside toxicity generally takes 5–10 days of administration to result in toxicity. Renal + failure due to aminoglycosides is frequently non-oliguric (so K levels are usually not elevated). Prevention is from limiting duration of use and by reducing trough levels by giving the antibiotic once a day. Once-a-day dosing allows high bactericidal levels with the same efficacy and very low trough levels. This antifungal agent is associated with renal insufficiency as well as distal renal tubular acidosis (non-anion gap metabolic acidosis with hypokalemia and high urine pH). Like aminoglycosides, it occurs only after several days or weeks of amphotericin use, and is usually reversible with prompt discontinuation of the drug. Unlike the antibiotics, radiocontrast used in radiology can result in renal failure in as little as 12–24 hours after the use of the agent. N-acetyl cysteine and sodium bicarbonate are often added but are of uncertain value. Uric acid toxicity occurs via intratubular crystallization, and usually occurs in the setting of tumor lysis syndrome after treatment of leukemias and lymphomas. Prevention is with vigorous hydration, sodium bicarbonate, and allopurinol prior to receiving chemotherapy. Allopurinol reduces the production of uric acid by inhibiting conversion of xanthine to hypoxanthine to uric acid. Uric acid stones precipitate in an acidic urine, unlike oxalate crystals, which precipitate in alkaline urine.

Fever and pyuria with negative urine culture or polymicrobial urine culture are suggestive order genuine acticin acne face mask. Antibiotics for gram-negative rods Third-generation cephalosporins purchase acticin 30 gm on line skin care guide, antipseudomonal penicillin discount acticin 30gm with visa acne 30 years old, or ticarcillin/clavulanate, often in combination with an aminoglycoside, for example Antibiotics alone are unlikely to be successful. Over the last 4 days, he developed an ulcer over the proximal portion of his tibia just below the knee. He has a sinus tract in the center of the red, inflamed ulcer that is draining purulent material. Osteomyelitis is an infection of any portion of the bone including marrow, cortex, and periosteum. Acute hematogenous occurs mostly in children in the long bones of the lower extremities and is secondary to a single organism 95% of the time. The most commonly involved bones are the tibia and femur, and the location is usually metaphyseal due to the anatomy of the blood vessels and endothelial lining at the metaphysis. In adults, hematogenous osteomyelitis accounts for about 20% of all cases and the most common site is the vertebral bodies (lumbar vertebrae are most frequently involved). Secondary to contiguous infection can occur in anyone with recent trauma to an area or placement of a prosthetic joint. Although this is secondary to a single organism most of the time, a higher percentage is polymicrobial in origin. Vascular insufficiency is mostly seen age >50, with diabetes or peripheral vascular disease, resulting in repeated minor trauma that is not noticed because of neuropathy and decreased sensation. With vascular insufficiency, there is often an obvious overlying or nearby ulceration or wound. Plain x-ray: Usually the initial test because it is more easily obtained, easily read, and inexpensive. The disadvantage is that 50–75% of bone calcification must be lost before the bone itself appears abnormal, which usually takes at least 2 weeks to develop. Bone biopsy and culture: This is the best diagnostic test but also the most invasive. Acute hematogenous osteomyelitis in children can usually be treated with antibiotics alone; however, osteomyelitis in adults requires a combination of surgical (wound drainage and debridement, removal of infected hardware) and antibiotic therapy. Antibiotic therapy depends on the specific isolate obtained, which must be as precise as possible because empiric treatment for 6–12 weeks would be undesirable. Chronic osteomyelitis must be treated for as long as 12 weeks of antibiotic therapy, and in some cases, even longer periods of antibiotics may be required. The most common etiology is bacterial; specifically, Neisseria gonorrhoeae, staphylococci or streptococci, but Rickettsia, viruses, spirochetes, etc. Generally, bacterial arthritis is divided into gonococcal and nongonococcal types. Sexual activity is the only significant risk factor for gonococcal septic arthritis. A total of 1–5% of people with gonorrhea will develop disseminated disease, and 25% will have a history of recent symptomatic gonorrhea. Additional routes may include bites (animal or human), direct inoculation of bacteria into the joint through surgery or trauma, or spread of infection from surrounding structures such as bone. Any cause of bacteremia can seed the joint because the synovium does not have a basement membrane. Culture of joint aspirate fluid is positive in 90–95% and Gram stain is positive in 40–70%. Only 50% of joint aspirates have positive synovial fluid culture; <10% of blood cultures are positive. In the aggregate, culture of the other sites has a greater yield than culturing the joint itself. Bacterial arthritis is usually treated by a combination of joint aspiration and antimicrobial therapy. In the absence of a specific organism seen on a stain or obtained from culture, good empiric coverage is nafcillin or oxacillin (or vancomycin) combined with an aminoglycoside or a third-generation cephalosporin. It is largely caused by the spread of infection from wounds contaminated by Clostridium perfringens (the toxins produced by clostridia play a significant role in tissue damage). It is strongly associated with traumatic injury (50%), shrapnel in war, and motor vehicles in peacetime. The trauma may be as minor as an intramuscular injection; however, the wound must be deep, necrotic, and without exit to the surface. Symptoms usually begin <1–4 days of incubation after the wound; they include pain, swelling, and edema at the site of the wound. Crepitation over the site and renal failure are late developments, usually prior to death. Direct visualization (usually at surgery) of pale, dead muscle with a brownish, sweet-smelling discharge is ultimately diagnostic. High-dose penicillin (24 million/day) or clindamycin (if penicillin allergic) is necessary, but surgical debridement or amputation is the absolute center of treatment. Clinical Recall What is the most appropriate treatment strategy in the management of gas gangrene? On physical examination, there is a systolic murmur at the lower left sternal border. Infective endocarditis is colonization of heart valves with microbial organisms causing friable infected vegetations and valve injury. Bacterial endocarditis produces large vegetations and may affect any value in the heart, although left- sided lesions of the aortic and mitral valves are more common. Relative Risk of Predisposing Conditions for Infective Endocarditis Organism Incidence,% Native valves Streptococcus viridans 50–60 Enterococci 5–15 Other streptococci: 15–20 Staphylococcus aureus 20–30 Staphylococcus epidermidis 1–3 Gram-negative bacilli <5 Fungi (Candida, Aspergillus, Histoplasma) <3 Culture negative <5 In narcotic addicts Staphylococcus aureus 60–95 Staphylococcus epidermidis 5–10 Streptococci 10–20 Enterococci 8–10 Gram-negative bacilli 4–8 Fungi 4–5 Diphtheroids 1–2 Prosthetic valves Acutely: first 2 months after surgery Staphylococcus epidermidis 40–50 acutely; 10–20 later Streptococcus viridans 5–20 acutely; 40–60 later Staphylococcus aureus 15–20 acutely; 20–30 later Enterococci 5–10 Other streptococci 1–5 Culture negative <5 Table 7-5. Microorganisms Responsible for Infective Endocarditis Acute infective endocarditis is caused by bacteremia. Seed previously abnormal valves Produce smaller vegetations composed of fibrin, platelets, debris, and bacteria Risk factors include ventricular septal defect with shunt; stenosis of any valve; prosthetic valve; indwelling catheter; bicuspid aortic valve; mitral valve prolapse; and Marfan syndrome Clinical course has slow onset with vague symptoms, leading to malaise, low- grade fever, weight loss, and flu-like symptoms. Less fatal than acute endocarditis: 5-year survival 80–90% with treatment Clinical manifestations Symptoms, % Signs, % Chills, 41 Heart murmur or changing murmur, 80–90 Weakness, 38 Fever, 90 Dyspnea, 36 Embolic events, 50 Sweats, 24 Skin manifestations, 50 Anorexia, weight loss, 24 Splenomegaly, 28 Malaise, 24 Septic complications, 19 Cough, 24 Mycotic aneurysms, 18 Skin lesions, 21 Glomerulonephritis, 10 Stroke, 18 Digital clubbing, 12 Nausea, vomiting, 17 Retinal lesions, 5 Chest pain, 16 Table 7-6. To diagnose endocarditis, 2 major criteria are required: positive blood cultures and abnormal echocardiogram. If 1 of the major criteria is absent, 1 major plus 3 minor criteria will constitute a diagnosis. Treatment decisions for infective endocarditis should be based on the identification of the organism found in blood culture and its specific antimicrobial sensitivities. Prior to the results of blood cultures, therapy can be started if the patient is very ill or there is very clear evidence of endocarditis such as fever, a clearly new or changing murmur, and embolic phenomena. Acceptable empiric therapy would be a combination of an antistaphylococcal drug such as nafcillin (or oxacillin), a streptococcal drug such as penicillin (or ampicillin), and gentamicin. Vancomycin and gentamicin are the standard empiric treatment for infective endocarditis. Therapy of Specific Microorganisms Causing Endocarditis Note the criteria for surgery in infective endocarditis. Prophylactics are indicated when there is both a serious underlying cardiac defect and a procedure causing bacteremia.

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