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toxic doses of injectables
- AMINES hydrolyzed in the liver
- Lidocaine Xylocaine 0.5, 1.0, 2.0 Intermediate 300mg 500mg
- Mepivacaine Carbocaine 0.5, 1.0, 1.5, 2.0, 3.0 Intermediate 300mg not available
- Poiocaine 0.5, 1.0, 1.5, 2.0, 3.0 Intermediate 300mg not available
- BupivacaineMarcaine 0.25, 0.50, 0.75 high 175mg 225mg
- Sensorcaine 0.25, 0.50, 0.75 high 175mg 225mg
- Etidocaine Duranest 1.0, 1.5 high 300mg 400mg
- ESTER hydrolyzed in the blood(pseudocholinesterase)
- Benzocaine T O P I C A L O N LY
- Cocaine TAC T O P I C A L O N LY
- Procaine Novocaine 0.5, 1.0, 2.0 low 750mg 1000mg
- Chloroprocaine Nesacaine 1.0, 2.0, 3.0 low 800mg 1000mg
- Tetracaine Pontocaine 0.1, 0.25 high 75mg 100mg
- TABLE 3-12. MAXIMUM LOCAL ANESTHETIC DOSAGES.
- *Local anesthetic
- Lidocaine 300 500
- Bupivacaine 175 225
- *In order to calculate the proper volume of local anestheitc for injection, the following mass per volume proportions are helpful: there are 2.5 mg/ml in a 0.25% solution, 5 mg/ml in a 0.5% solution, 10 mg/ml in a 1 % solution, and 20 mg/mlin a 2% solution.
anatomy of triceps surae and posterior tibialis
- GASTROCNEMIUS MUSCLE
- Origin: medial and lateral condyles of the femur
- Insertion: middle one-third of the posterior aspect of the calcaneus
- Action: plantarflex ankie, flex knee
- Innervation: tibial nerve(S1, S2)
- Arterial Supply: sural artery(an end artery)
- SOLEUS MUSCLE
- Origin: posterior head and upper one-third of the fibula, and soleus line of the tibia
- Insertion: middle one-third of the posterior aspect of the calcaneus
- Action: plantarflex ankle
- Innervation: tibial nerve(S1, S2)
- Arterial Supply: posterior tibial artery
- PLANTARIS MUSCLE
- Origin: lateral condyles of the femur
- Insertion: medial one-third of the posterior calcaneus
- Action: plantarflex ankle, flex knee
- Innervation: tibial nerve(L5, S1, S2)
- Arterial Supply: sural artery
- NOTE: abscent in 7% of population
- TIBIALIS POSTERIOR MUSCLE
- Origin: posterior two thirds of the interosseous membrane and the adjacent tibia and fibula
- Insertion: plantarly on the navicular(major insertion site), medial and intermediate cuneiform, and base of the second, third, and fourth metatarsal
- Action: invert the foot, adduct foot, plantarflex ankle
- Innervation: tibial nerve(L4, L5)
- Arterial Supply: sural, peroneal, and posterior tibial arteries
nerves in the mayo block are:
medial dorsal cutaneous nerve, deep peroneal nerve, saphenous nerve, medial plantar nerve.
nerves in the mini mayo block, tailor's bunion :
4th common digital nerve (dorsal and plantar), lateral dorsal cutaneous nerve, superficial branch of the lateral plantar nerve
what are the 5 w's of a fever:
- POST-OP MANAGEMENT/ COMPLICATIONS
- Intraoperative-transfusion reaction-malignant hyperthermia-pre-existing sepsis
- Post-op 0-6 hours
- -pain-rebound from cold operating room-anesthesia reaction-endocrine cause(thyroid crisis, adrenal insufficiency)
- 24-48 hours-atelectasis-aspiration pneumonia(after general)-dehydration-constipation
- 72 hours or greater-infection(3-7 days)-DVT-thrombophlebitis from IV-UTI(especially if catheterized)-drug allergy
- Five "W"s (mnemonic for remembering cause of post-op fever)
- Wind-atelectasis, aspiration pneumonia, PE
- Wound-infection, thrombophlebitis(IV site), pain
- Water-UTI, dehydration, constipation
- Wonder drugs- virtually any drug can cause fever(pt appears less ill than fever suggests)
Describe Lisfrancs joint? Which ligaments are stronger?
The plantar ligaments are thicker, and dorsal displacement is most common.
the plantar ligaments are stronger than dorsal-dorsal dislocations are more common
- LISFRANC'S FRACTURE/DISLOCATION REPAIR-Most injuries occur in the dorsal direction-The Lisfranc's ligament is the strongest interosseous tarsometatarsal ligament and the integrity of the Lisfranc's joint depends upon this ligament.It's disruption can result in the lateral displacement of the rest of the tarsometatarsal joints.-There is no interosseous ligaments between the 1st and the 2nd metatarsals
- LISFRANC'S LIGAMENT-attaches the medial cuneiform to the second metatarsal-aka-the medial interosseous tarsometatarsal ligament-strongest interosseous tarsometatarsal ligament-this ligament plus the recessed 2nd metatarsal are responsible for most of the stability at the Lisfranc's joint-responsible for the avulsion type fracture of the base of the medial aspect of the 2nd metatarsal
- D I A G N O S I S-Stress abductory radiographs may be helpful-Look for avulsion fractures of the 2nd metatarsal-Though often not appreciated radiographically small fractures plantarly are usually present along the joint and a CT may help with the diagnosis-A dorsal or plantar deviation of the second metatarsal base from the medial cuneiform may be palpated or appreciated radiographically
- T R E A T M E N T
- Open or closed anatomic reduction with percutaneous pinning as close to the time of injury as possible is the treatment of choice Casting unstable joints without fixation or primary arthrodesis is rarely effective The second metatarsal is reduced first followed by the 1st then 3-5 Inadequate reduction results in long term arthrosis The long term sequela of this injury, when not adequately reduced, is arthrosis at which time arthrodesis is indicated
- Lisfranc Fracture Dislocation-this injury constitutes 1% of all reported fractures,however the diagnosis is missed in almost 20% of cases. Anatomical considerations include the "keystone" nature of the second metatarsal base in the intercuneiform recess,which provides a significant amount of stability to the midfoot complex. The tarsometatarsal joint (TMJ) is bound together by a series of transverse dorsal and plantar ligaments, as well as intermetatarsal ligaments. There is a distinct absence of an intermetatarsal ligament between the first and second metatarsals. The plantar ligaments are thicker, and dorsal displacement is most common. The ligament attaching the medial cuneiform to the first metatarsal is the largest ligament at this level. The most important ligament of the TMJ is Lisfranc's interosseous ligament, which attaches the base of the second metatarsal medially to the lateral aspect of first cuneiform. Lisfranc's ligament is often involved in avulsion fracture of the second metatarsal base. The Hardcastle classification (also know as Queno and Kuss) is the standard system for identifying TMJ fracture/dislocations(Fig. 10-17), and categorizes these injuries as depicted in Table 10-3.TABLE 10-3. THE HARDCASTLE CLASSIFICATION OF LlSFRANC FRACTURE DISLOCATIONS.
- TypeA (total, homolateraldislocation) The most common TMJ fracture/dislocation, it displays disruption of the entire TMJ in the sagittal or transverse plane. This injury usually involves lateral displacement of all of the metatarsal
- B (partial dislocation) 1. Medial displacement of the first metatarsal alone or with metatarsals 2, 3, 4, not 5 2. Lateral displacement of one or more of the lesser metatarsals (not the first metatarsal)
- C ( divergent) Displays the first metatarsal dislocated medially and the lesser metatarsals either partially or totally dislocated laterally in the sagittal and/or transverse planes
- Although the Hardcastle classification is most commonly used, Wilson also classifiedLisfranc joint fracture/dislocations, as depicted in Table 10-4.264 Management of Foot and Ankle Trauma Ch. 10Total Incongruity Partial IncongruityType ALateral dislocationType 82Figure 10.17TABLE 10-4. THE WILSON CLASSIFICATION OF LlSFRANC FRACTURE DISLOCATIONS.ClassPlantar-flexion-Stage Description of the fracturesupination-most common Dorsolateral dislocation of metatarsals 2-5II Dorsolateral dislocation of metatarsals 1-5Plantarflexion pronation Medial dislocation of first metatarsalII Medial dislocation of first metatarsal, dorsolateraldislocation of metatarsals 2-5Plantarflexion Dorsal dislocation of second metatarsal base and/orfracture dislocation base of first metatarsal
The mechanism of TMJ injury is usually a crushing force
applied to the forefoot with the ankle plantarflexed. The second metatarsal must be dislocated first
, either by transverse base fracture or medial avulsion by Lisfranc's ligament, in order to disrupt the TMJ. Clinical findings include localized signs and symptoms of fracture/dislocation, and it is critical to assess the neurovascular status to the forefoot. The foot may appear grossly shorter than the contralateral limb. Radiographs can be difficult to assess, and attention should be directed at the first metatarsocuneiform interfaces, as well as the base of the second metatarsal. One should also look for a compression fracture of the cuboid. Transverse and sagittal plane stress views can add information, and the CT scan has become a mainstay of diagnostic accuracy in regard to this injury. Treatment begins with attempted closed reduction and immobilization, if indicated. Distal traction can be achieved by suspending the foot above the table with Chinese finger traps until adequate soft tissue relaxation ensues. Counterweights strapped around the ankle can be used to enhance distraction. An external fixation frame can also be used to effect distraction and stabilization. Attention is directed at trying to relocate the second metatarsal base into the intercuneiform recess, then to reduction of the first metatarsal-medial cuneiform joint depending on the fracture/dislocation pattern. Percutaneous pin stabilization may be attempted after reduction, however this is notoriously difficult. If closed reduction fails, it may be due to tibialis anterior or peroneus longus interposition, or due to the avulsion fragment of the second metatarsal base. ORIF may be performed via 3 dorsal incisions:1) dorsomedial first met-cuneiform, 2) between second and third metatarsals and corresponding cuneiforms, and 3) between fourth and fifth metatarsals and the cuboid. The first metatarsal is generally fixed first, followed by the remaining metatarsals from medial to lateral. Pin stabilization is recommended as follows: Type A-1 wire stabilizing first metatarsal-cuneiform and a second stabilizing the fifth metatarsal-cuboid joints.Type B (medial type)-2 pins stabilizing the first metatarsal-cuneiform.Type C-2 pins medial and one lateral.A BK cast is then used for 8-12 weeks, the first 6-8 weeks being non-weight bearing.The pins are removed after 6-8 weeks.
LISFRANC'S FX/DISLOCATIONCLASSIFICATION(Hardcastle)Type Aftotal or homolateral)-disruption of the entire Lisfrancjt complexin a sagittal or transverse plane(almostalways lateral)-most common typeType Bfpartial)Type B1-medial incongruity with the 1st metatarsalforced medially-medially displacement involving the 1stmet alone or with met's 2, 3, 4, but not 5.Type B2-lateral incongruity with the lesser metatarsalsforced laterally I556CHAPTER 32POCKET PODIATRICS 3RD EDITIONTRAUMAType C(diverqent)Type C1-partial divergence with the 1st met mediallyand the 2nd met laterally displacedType C2-total divergence with the 1st met displacedmedially and the lesser met's displaced laterally
Describe the different medications for gout (acute vs chronic and reason behind them)
- lndomethacin(lndocin)-25-50mg tid [25, 50, supp 50, susp25mg/5ml] (Indocin SR)-75mg PO qd/bid-strong NSAID
- Allopurinol(Zyloprim, Purinol)-200-300mg PO qd/bid [100, 300]-inhibits xanthine oxidase(a major enzyme in uric acid synthesis)
- Colchicine-po 1mg initially, ,5mg q1-2h until nausea/vomiting or diarrhea occur to a maximum dose of 7-8mg[0.5, 0.6], IV 2mg initially,then ,5mg q6h to a maximum dose of 4mg-acts by interfering with WBCs ability to phagocytize urate crystals thus reducing inflammation-very effective for acute attacks, but side effects often outweigh the advantages-can be used as a diagnostic tool for acute gout, if symptoms are relieved, it was gout
- Probenecid(Benemid)-250mg PO bid x7 days, then 500 bid -inhibits the reabsorption of uric acid in the proximal tubules
- Sulfinpyrazone(Anyurane)-100-200mg PO bid [100, 200]
- A recurrent acute arthritis that affects peripheral joints, most notably the 1st MPJ. The arthritis stems from a build up of monosodium urate crystals in and around joints and tendons. Supersaturated hyperuricemic body fluids crystalize causing a severe red hot swollen joint. The arthritis may become chronic and deforming. Not all hyperuricemic persons develop gout. A build up of uric acid crystals in the joint may be from excessive breakdown or over production of purines. Gout classically begins in the evening or early morning and tends to occur in previously damaged joints.
- SIGNS AND SYMPTOMS-asymmetrical monoarticular arthritis-sudden onset, red hot swollen joint-low grade fever is sometimes present-more common in men(20:1)-joint sparing(chronic gout may be joint destructive)-most commonly first attacks the 1st MPJ(called Podagra), followed by Lisfranc's and then the heel-crunchy tophi felt in ears, olecranon bursa, and Achilles tendon.NOTE: Formalin dissolves gouty tophi
- X-ray-rat bites-cloud sign-punched out lesions-Martel's sign-overhanging margins
- Aspiration-negatively birefringent yellow needle shaped crystals, when parallelto axis of the lens and blue when perpendicular.Blood work-Hyperuricemia(>7.5mg/dl ) not conclusively diagnostic for goutTREATMENTFor effective Tx determination must be made as to whether the pt. is anover producer of uric acid(metabolic gout) or an under excreter(renalgout).POCKET PODIATRICS 3RD EDITIONARTHROPATHIES197CHAPTER 9OVERPRODUCEROF URIC ACIDUNDER EXCRETEROF URIC ACIDName -metabolic gout -renal gout(more common)Diagnosis -uric acid level above600mg in a 24 hr urinesample-uric acid level below 600mgin a 24 hr urine sampleCause -genetic enzyme defect-tumor1 ° kidney problem2° kidney problem-lead poisoning-excessive acidsflacticacid, ASA)Treatment Allopurinol-xanthine oxidaseinhibitor-300mg QDProbenecid-competes with uric acid forreabsorption from kidneys-250mg BIDxIwk, thendouble the dose, thenincrease by 500mg/dayevery 4wks(not to exceed2g/day)-Avoid foods and medications that exacerbate gout-organ meat(liver sweetbread, kidney, heart, brains)-lard-anchovies and sardines-ETOH especially red wine-diuretics(increases osmolarity)PSEUDOGOUT(Chondrocalcinosis, Calcium pyrophosphate dihydrate, CPPD)DESCRIPTION-associated with acute or chronic inflammatory arthritis-caused by deposition of calcium pyrophosphate dihydrate(CPPD)crystals in the joint-symptoms are similar to those of gout but it tends to run a longercourse(reaches maximum severity at 1-3 days, and resolves in 1week or longer)-the knee is most often involved(50%) followed by the ankle, wrist,and shoulder-risk increases with age, trauma, patients hospitalized for othermedical conditions and those with metabolic dz(hypothyroidism,hyperthyroidism, gout, amyloidosis)-associated with high grade fever198 POCKET PODIATRICS 3RD EDITIONARTHROPATHIESDIAGNOSIS-microscopic examination of joint aspiration reveals rhomboid crystals-radiographically-calcifications of the articular cartilage or meniscusTREATMENT-immobilization, NSAID, analgesics
- Three factors that are commonly associated with the formation of thrombi
- 1. Stasis: Arrhvthmias. Ml, CHF, heart failure, Immobilization, obesity,varicose veins, dehydration)
- 2. Blood vessel injurv (trauma. Fx, IV)
- 3. Hvpercoagulability: Neoplasm. oral contraceptives, pregnancy, Sx,polycythemia
- Full dose(treatment for DVT)
- IV ADMINISTRATION-get baseline PTT-5,000-10,000u IV bolus, then 750-1,500u/hr IV-monitor PTT q8h (maintain PTT at 1.5-2 above control)
- SubQ ADMINISTRATION-get baseline PTT-5,000u IV bolus and 10,000-20,OOOu subQ, then 8,000-10,OOOusubQ q8h or 15,000-20,OOOu subQ BID-monitor PTT q8h(maintain PTT at 1.5-2 above control)
- Mini dose(prophylaxis for DVT)-5,OOOu subQ bid-surgical patients-give 1 hour pre-op followed by bid dose until ambulatory
- Warfarin(Coumadin, Panwarfin)loading dose 10mg PO qd x2-4 daysmaintenance dose 2-7.5mg PO qdmaintain PT about 2-2.5 times normaltreat 1st DVT episode for 3 months-Coumadin requires 16-48hrs to cause a measurable change in the PT,therefore begin Tx 2 days before discontinuing Heparin
- DEEP VENOUS THROMBOSIS(DVT)
- DESCRIPTION Partial or complete occlusion of a vein by thrombus with secondary inflammatory reaction in the wall of the vein. Arises approximately 80% of the time in the deep veins of the calf. Contributing factors include those of Virchow's Triad such as: CHF, MI, stroke,malignancy, Sx, trauma, immobilization, previous thromboembolic dz, obesity, pregnancy, oral contraceptives, and advanced age. The typical patient is a woman over 30 yrs old, on BCP's who smokes. There is a danger of pulmonary embolism in these patients. DVT usually results in destruction of the venous valves resulting in veins that are incompetent resulting in postphlebitic syndrome(venous insufficiency).
- SIGNS/SYMPTOMS-Symptoms arise over a period of hours to 1-2 days.-Self limiting and lasts 1-2 weeks-Distention of superficial venous collaterals, and slight fever and tachycardia may develop.-Physical exam is normal in 50% of pts-Painful swollen leg with dilated superficial veins and a palpable cord-(+) Homan's sign-dorsiflexion of foot causes deep pain in calf-Pulses are usually present
- DIAGNOSIS-Difficult to diagnose by Hx and PE-Venography remains the gold standard
- TREATMENT-Leg should be elevated -15-20°, trunk should be kept horizontal-Bedrest until local tenderness and swelling disappears-Heparin(bolus of 5,000-10,000 units IV followed by a continuous IV infusion of 500 units/kg every 24hrs).-PTT should be checked 4-6hrs after initial therapy and then at least every 24hrs. PTT levels should be maintained at 2-3 times the control value-Monitor ABGs-Pt should later be started on long term anticoags(Coumadin) loading dose of 10mg is given each day until PT increases.Then a smaller dose (5-7.5mg) is given to maintain PT ~1.3-1.5 above the control value. Pts should be Tx for 3 months for the 1st episode.
Antiembolism stockings 16-18mmHg DVT prophylaxis
72 hours or greater-infection(3-7 days)-DVT-thrombophlebitis from IV-UTI(especially if catheterized)-drug allergy
Five "W"s(mnemonic for remembering cause of post-op fever)Wind-atelectasis. aspiration pneumonia, PEWound-infection. thrombophlebitis(IV site), painWater-UTI. dehydration, constipationWalking-DVT
Wonder drugs- virtually any drug can cause fever(pt appears less illthan fever suggests)
DVTSurgical patients have additional risk factors for DVT's-bed rest-tourniquet-surgical trauma-infection-dehydration(due to NPO status)-change in medication(ie d/cASA)
Lower extremity deep vein thrombophlebitis (DVT, also known as venous thromboembolism,or VTE) presents with deep, aching pain and tightness in the calf or thigh. Pain upon active dorsiflexion of the ankle, or resistance to ankle dorsiflexion is known as Homan's sign, andis a nonspecific and unreliable clinical diagnostic maneuver. Tenderness upon calf or thigh muscle compression is a more specific test for DVT, when associated with edema and local increase in skin temperature. Superficial thrombophlebitis, which conveys a lower likelihood of PE, more commonly displays local heat, edema, erythema, and a palpable cord consistent with the thrombosed vein. Application of a tourniquet above the suspectedthrombosis may cause pain atthe level ofthrombosis within 30-45 seconds, and is stronglysuggestive of DVT. Comparison of calf circumference will often show enlargement of theaffected side. Constitutional findings may include temperature elevation (39.5°-40.5° C), chills,and malaise. Arterial embolism is usually more painful early on, with less swell ing,exaggerated distal temperature decrease, and early sensory deficit. Severe venousthrombosis effecting retrograde arterial flow decrease may result in phlegmasia ceruleadolens, which can result in pedal ischemia and gangrene. Coagulation studies are usually normal unless full blown disseminated intravascular coagulation (DIC). familial antithrombin III deficiency, or lupus erythematosus clotting inhibitors exist. The laboratory diagnosis of DVT hinges on venous non-invasive duplex Doppler examination, andmagnetic resonance venography or contrast venography may be employed if ultrasound isequivocal. Radioactive 1251-fibrinogen scanning, in conjunction with occlusion impedence plethysmography is also a sensitive combination for DVT ofthe calf. Use ofthe D-dimer
testmay also be useful, however combined clinical and venographic tests are more reliable. An accurate diagnosis of DVT is made upon identification of predisposing factors and clinicalobservation, combined with duplex Doppler ultrasound
and, perhaps, magnetic resonancevenogram or contrast venography.Prevention of DVT is recommended, and can be achieved in several different ways (Tables3-6 and 3-7). Prophylactic therapy in the low-risk patient involves mini-dose subcutaneousadministration of 5000 units of heparin every 8 or 12 hours beginning about 60 minutespreoperatively. Adjunct physical measures include support hose, intermittent sequentialpneumatic compression of the lower extremity, leg elevation with the knee flexed, andout-of-bed activity at an early stage after surgery. In high-risk patients, DVT prophylaxis isadministered preoperatively with mini-dose heparinization, however in the postoperativephase, the heparin dose is adjusted upward to keep the PH within 4 seconds of highnormal. Despite statistically more postoperative hemorrhage, this form of DVT prophylaxis appears to be worthwhile in the high-risk patient. A baseline platelet count is recommended prior to mini-dose heparinization, and should be monitored periodically if it is observed tobe low. High-risk patients may also be prophylaxed with a combination of mini-doseheparin and dihydroergotamine, which causes venular constriction and rapid venous return.Other prophylactic combinations include heparin and antithrombin III administration, and theuse of low molecular weight heparin administered once daily has been shown to beeffective and popular (see risk stratification and guidelines for prophylaxis, below).Goumadin, which inhibits the vitamin K-dependent clotting factors II, VII, IX, X, and proteinsG and S, can also be administered preoperatively and during the postoperative phase toeffect DVT prophylaxis.
- Death of tissue, associated with loss of vascular supply. Dry gangrene occurs gradually as a result of occlusion of blood supply and is not usually associate with bacterial infection.
- Wet gangrene-result of sudden stoppage of blood (burns, freezing, embolism) with subsequent bacterial infection.
- WOUND CLASSIFICATIONS
- Wagner's Diabetic Ulcer ClassificationGrade 0 intact skin(cellulitis, erythema)Grade 1 superficial ulcer involving the skin(no subQ involvement)Grade 2 ulcer extending to tendon capsule or bone(through subQ)Grade 3 more extensive ulcer with associated abscess, osteomyelitis,or joint sepsis
- Grade 4 local gangrene of the toes or forefoot
- Grade 5 gangrene of entire foot
- Knighton ClassificationI Partial thickness ulcer-extends through the epidermis and into, but not through, the dermisII Full thickness ulcer-ulcer extending to sub-cutaneous tissue onlyIII Full thickness ulcer-ulcer extending to tendon, ligament, joint, and/or boneIV Full thickness ulcer-level III ulcer with abscess and/or osteomyelitisV Full thickness ulcer-level III ulcer with necrotic tissue in wound
- VI Full thickness ulcer-level III ulcer with gangrene
- Ankle/Arm Ratio>0.96 0.31 - 0.95 0.25 -0.3 Clinical FindingNormalIntermittent claudicationRest Pain
- 0-0.3 Impending gangrene
- What is another name for clostridial myonecrosis? Gas gangrene.
- What is the role of surgical debridement in frostbite injuries?
- It is difficult to assess the depth and extent of tissue injury so it is best to avoid early surgical debridement and instead allow the tissue to demarcate over several months. Amputations can then be performed. Ifinfection and wet gangrene is present, however, early surgical intervention is necessary.
Why is the fact that a wound was due to a farm injury such an important consideration? This wound is Clostridial
prone and can causc gas gangrene