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Clinical perspectives of knee joint

Clinical perspectives of knee joint






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  • Plain radiographs are the most useful form of imaging, although not necessarily the most sensitive. So characteristic are the radiographic appearances that other forms of imaging are seldom necessary. The cardinal features are asymmetric narrowing of the joint space, sclerosis of the subchondral bone under the area of cartilage loss, cysts close to the subchondral bone plate, osteophytes at the joint margins, and bone remodeling (Figs. 92-1 and 92-2) . There also may be tell-tale signs of previous disorders (e.g., an old fracture, osteonecrosis, congenital dysplasia) (Fig. 92-3) or features that suggest a generalized condition (e.g., hemochromatosis, acromegaly) of which osteoarthritis is merely one manifestation. <br />
  • Just as diabetes has many systemic, genetic and local factors involved in it’s pathogenesis, so a correct understanding of OA begins with understanding the interplay of stystemic biochemical and local biomechanical factors <br />
  • Inescapable <br /> Good news is that this data point is symmetric <br /> Don’t need a metamorphasis, only 10 lbs. <br />
  • Participation in contact/collision sports associated with increased OA. <br /> “Associated” unclear whether loading and twisting or inevitable injuries that causes OA <br /> We’ll talk more about this later <br /> Some sports have no increased risk of OA <br />
  • Mechanics, carpet layers, plumbers <br />
  • Quad strength exercises: Increase strength 20% = Decrease OA 30% <br />

Clinical perspectives of knee joint Clinical perspectives of knee joint Presentation Transcript

  • Tibiofemoral Joint – formed between tibia and femur A HINGE JOINT Patellofemoral joint – formed between the patella and the femur A GLIDING JOINT
  • Femur proximal – head and neck of femur, greater trochanter distal – medial and lateral condyles and epicondyles
  • Patella – largest sesamoid bone in body Tibia – tibial plateau forms knee joint with femur The fibula is not a part of the knee joint
  • The Quadriceps – Knee Extension 1. Vastus Medialis 2. Vastus Lateralis 3. Vastus Intermedius 4. Rectus Femoris – 2 joint muscle that also acts as a hip flexor
  •  
  • The Hamstrings- knee flexion 3 muscles: 1. Biceps Femoris 2. Semimembranosus 3. Semitendinosus
  • The Adductors (Groin) Adduct the thigh 1. Adductor Longus 2. Adductor Magnus 3. Adductor Brevis 4. Gracilis
  •  The Sartorius: - flexes, abducts, and laterally rotates thigh - longest muscle in the body, “tailor’s muscle” - Crosses hip and knee joint
  • The Iliotibial Tract (IT Band) - neither a muscle or tendon, but a long, thick band of tissue that inserts into the lateral tibia (Gerdy’s Tubercle) 
  • 1. 2. 3. 4. ACL – Anterior Cruciate Ligament PCL – Posterior Cruciate Ligament MCL – Medial Collateral Ligament LCL – Lateral Collateral Ligament
  • MCL: - Medial Collateral Ligament - Runs from medial femur to medial tibia LCL: - Lateral Collateral Ligament - Runs from lateral femur to head of fibula
  • A “c”-shaped piece of fibrocartilage located in the knee joint between the femur and attached to the top of the tibia Cartilage = meniscus
  • Medial - larger and more Cshaped - more firmly attached to tibia - has attachments to MCL Lateral - smaller and more round or O-shaped - not firmly attached to tibia and LCL
  • Mostly avascular – little or no blood supply Only the outer 20% has a blood supply * Does not have the ability to heal itself unless there is a small tear in the outer 20%
  • 1. 2. 3. 4. Stability Shock absorption Lubrication and nutrition Allows adequate weight distribution
  • Normal Torn
  • Trauma  Fractures around knee  Ligamentous sprains  Muscular strains Degenerative conditions  Osteoarthritis of knee joint  Osteochondritis dessicans  Traumatic arthritis
  • Inflammatory conditions  Rheumatoid arthritis  Juvenile Rheumatism  Neuropathic joint  Hemophilic arthritis  Bursitis  Other conditions Infection  Suppurative arthritis  Tuberculosis
  • Tumors around knee joint  Tumors of bone  Tumors of soft tissue Metabolic conditions  Rickets  Scurvy  Gout  Ochronotic Arthritis  Osteoporosis
  • Congenital and Developmental conditions  Genu valgum  Genu varum  Genu recurvatum  Congenital dislocation of patella  Congenital discoid meniscus
  • Fractures around knee  Supra condyler femur fracture  Fractures of the isolated condyle  Tibial condyle and plateau fracture  Fracture patella  Tibial tuberosity avulsion
  • Fractures of the femoral condyle at metaphysis level extending in to knee joint Fractures of the isolated condyle Hoffa’s Fracture Epicondyler avulsions
  • Both condyle fractures  Isolated condyle fractures Tibial spine fracture
  • >200,000 injuries/year >100,000 reconstructions/year Higher incidence in females Males = contact Females = noncontact
  • 1. MOI: twisting of knee forced hyperextension lateral blow to knee *foot must be firmly anchored to playing surface 2. 50% of people describe a “pop” in knee 3. Knee fills with blood quickly Hemarthrosis 4. Usually immediate loss of motion 5. Knee feels unstable
  • Anterior Drawer Test: examiner attempts to slide the tibia forward which may indicate a torn ACL ligament
  • Who needs surgery? - Activity level? - Level of Competition - Age?
  • Arthroscopic Graft options Patellar Tendon Semitendinosus Gracilis Cadaver Synthetic
  • 1. MOI: excessive hyperextension hyperflexion tibia forced posteriorly (blow to front of knee) “dashboard knee” Possibly 90% of all PCL injuries due to motor vehicle accidents?
  • 2. 3. 4. 5. 6. Mild hemarthrosis Posterior knee pain Walk with knee slightly flexed, avoid full extension Posterior sag of tibia Surgery?
  • MOI: Blow to the outside of the = Valgus Force Possible overuse – breaststroke in swimmers Commonly associated with meniscal injuries – attached to medial meniscus No surgery knee
  • Valgus Stress Test: tests for injury to the MCL ligament
  • MOI: Blow to inside of the knee – Varus force Grade III tear may require surgery
  • Varus Stress Test: tests for injury to the LCL ligament
  • 1. MOI: Rotation of the knee as the knee extends during rapid cutting or pivoting
  • 2. Signs and Symptoms: - pain - joint line tenderness - catching or locking - knee buckling or giving way - swelling - incomplete flexion - clicking on stair climbing
  • 3. Surgery? Meniscectomy: removal of the meniscus - Total meniscectomy = osteoarthritis Depends on location of tear, type of tear, and blood supply
  • - bucket handle - Flap tear - Transverse tear - Horn tear
  • Apley’s Compression 
  • Tear of the medial meniscus, anterior cruciate ligament (ACL), and medial collateral ligament (MCL)
  •  Osteoarthritis of knee joint  Osteochondritis dessicans  Traumatic arthritis
  • Disease of the joints characterized by: – Progressive articular cartilage loss – New subchondral bone formation – New bone and cartilage formation at joint margins – Low level synovitis & PAIN!
  • – Joint Pain – Typical Pain Pattern – Xray Findings  Standing films  AP with 30 deg flexion – No Sign of Zebras
  • Pathogenesis of Osteoarthritis An Interplay of Factors Dieppe, American Academy of Orthopaedic Surgeons, 1995
  • Joint Biomechanical Risk Factors Age  10-fold increase from 3065 Genetics (generalized) Gender  Men <50: higher risk  Women >50: higher risk Nutritional  Low vitamin C and D intake  Joint trauma  Obesity (knee, hip, hand)  Occupation  Abnormal joint biomechanics  Dysplasia, malalignment, instability, abnormal innervation  Knee extensor wkness  Sports w/ joint risk
  • 50% decrease in OA with with 11# wt loss Larger effect in women (Felson et. al. Ann Int Med 1992, Framingham Heart Cohort data)
  • Jobs requiring repetitive knee bending/moderate activity predict higher rates of osteoarthritis Felson et al Annals of Int Med 1992
  • 11 lb / 50% risk reduction rule Break that vicious cycle: Team approach is critical Pain and stiffness Disuse Weight Gain
  •  Regular aerobic walking for knee OA  LOE 1a for knee OA  LOE IV for hip OA  Home-based quad strength exercises  LOE 1a for knee OA  LOE IV for hip OA  Water-based exercise for hip OA  LOE 1b
  • Medial or lateral unloading
  • Medial tibio-femoral OA
  •  TENS effective in some with knee or hip OA  Short-term, 2-4 weeks  Acupuncture relieves pain (no effect on function)  Pulsed Electromagnetic Field Therapy  Meta-analysis 2009  Thermotherapies
  • No disease modifying drug for OA (yet) Tylenol, max 4 gm/day  analgesic of choice  LOE 1a, but modest pain relief if OA mild/mod NSAIDs—LOE 1a Tramadol: LOE 1a in short-term trials  No long-term trials  More side-effects than Tylenol Glucosamine
  • Considerations before treatment:  Surgical candidate? Don’t waste the time  Previous injections?
  • Beneficial in KNEE Beneficial in HIP Short-duration benefits: 2-4 weeks
  • Effective in knee and hip (LOE 1a) Delayed effect (1-3 weeks) Long duration (6 months) Weekly injections, 3-5x Might delay need for joint replacement
  • X
  • Arthroscopy Joint replacement Cartilage transplantation
  • Cochrane review 2008: NO BENEFIT for undiscriminated OA (mechanical or inflammatory causes)
  • LOE III Universally recommended to improved pain, function, QOL  Unicompartmental  Total joint replacement
  • Osteo-Articular Transplant (OAT) procedures Autologous Chondrocyte Implantation (ACI) Cadaver allografts
  • Due to intraarticular fractures Malunions lead to joint arthrosis Primary cartilage insult leading to repair by fibrocartilage and arthrosis Treatment is TKR if tri compartmental OA
  • In children and adolescents Small segments of nactrotic subchondral bone Pain stiffness and locking Rest/ debridment of joint/ replacment
  •  Rheumatoid arthritis  Juvenile Rheumatism  Neuropathic joint  Hemophilic arthritis  Bursitis  Other conditions
  • Synovitis chronic infl, synovial hypertrophy, effusion Destruction proteolytic enzymes, pannus Deformity articular destruction, capsular stretching, tendon rupture
  • nodules tendon sheath vasculitis myopathy and neuropathy reticulo-endothelial system visceral - lungs, heart, kidneys, brain, GI
  • myopathy, tiredness, weight loss, malaise proximal finger joints wrists, feet, knees, shoulders start up pain tendon crepitus
  • joint destruction pain deformity instability
  • joint space narrowing peri-articular osteopenia erosions
  • stop synovitis prevent deformity reconstruct rehabilitate
  • 10% improve 60% intermittent, slowly worsening 20% severe joint erosion, multiple surgery 10% completely disabled
  • Diabetes is the leading cause:  1/700, 0.16-2.5% of all diabetics  Usually in the 5th or 6th decade of life  Related to duration and control of diabetes  Involvement includes: Tarsometatarsal/metatarsophalangeal joints  Ankles  Knees  Upper limbs (rare)  Giurini. Charcot's disease in diabetic patients. Postgrad Med 1991; Brower. Sinha. Neuro-arthropathy (Charcot joints) in diabetes mellitus (clinical study of 101 cases). Medicine (Baltimore) 1972; 51:191 .
  •  Reported associations:  Leprosy  Alcoholism  Uremia     Amyloidosis   Pernicious anemia   Syphillis (tertiary)   Syringomyelia   Spina Bifida   Myelomeningocele   Cord compression  Cauda Equina lipoma MS Poliomyelitis Connective Tissue disorder Charcot-Marie-Tooth disease Congential sensory neuropathies Ehlers-Danlos syndrome Familial dysautonomia Thalidomide embryopathy Intraarticular steroids
  • Radiographics. 2000;20:S279S293
  • Storey GO.Charcot joints. Rheumatol Phys Med. 1970 Aug;10(7):312-20.
  • Problems with patella – most common cause of knee pain Anatomy: - Patella is a sesamoid bone formed in Quad tendon - Patellofemoral joint – patella and femur - Compression forces – <body weight during walking 2.5 x body weight during stairs
  • “Jumper’s Knee” Inflammation and degeneration of the tendon that connects the kneecap (Patella) to the shin bone (Tibia).
  • A gradual degenerative change that occurs beneath the patella Caused by acute trauma, repeated microtrauma, or improper alignment of the patella in the trochlear groove Weak vastus medialis (VMO) can cause improper alignment Prevention: strengthen quads Minimize squats, downhill running, biking with low seat
  •  
  • 1. Painful swelling over tibial tuberosity (patellar tendon insertion) 2. Usually occurs between 9-13 years of age 3. Pain increases with activity
  • Occurs where IT Band rubs over femur at the knee joint Common in running (esp. downhill) or any activity with repetitive flexion Hills or stairs increase pain Lots of IT Band stretching
  • “Baker’s Cyst” Fluid accumulation in posterior knee (popliteal space) Patient usually complains of a mass behind the knee
  • “Housemaid’s Knee” Tender swelling over the kneecap (prepatellar bursa) 
  •  Pes anserine bursitis is an irritation or inflammation of a bursa in your knee. The pes anserine bursa is located on the inner side of the knee just below the knee joint.  Tendons of three muscles attach to the shin bone (tibia) over this bursa
  •  Suppurative arthritis  Tuberculosis
  •  Bacterial: staphylococcus streptococcus Gonococcus H. pneumonia gram negative organisms  Mycobacterium:TB, atypical TB  Fungi: candida  Spirochete: lyme (borrelia burgdorfi)  Viral: HIV, Hepatitis B, C
  •  Tumors of bone  Tumors of soft tissue
  • Signs/Symptoms:  Pain, characteristically more intense at night, relieved by NSAIA and eliminated by excision  Vertebral lesions may cause scoliosis Age:  10-30 years Sex:  M > F (2:1) Anatomic Distribution:  Nearly every location, most frequent in femur, tibia, humerus, bones of hands and feet, vertebrae and fibula  Over 50% of cases in femur or tibia  Metaphysis of long bones
  • Central radiolucent nidus with or without a radiodense center; surrounded by thickened sclerotic bone
  • Central hemorrhagic nidus surrounded by dense rim of sclerotic bone
  • Nidus contains interlacing network of osteoid and bony trabeculae with variable amount of mineralization, lying in vascular fibrous tissue
  • Signs/Symptoms:  Pain  Gait disturbances Age:  80% of patients < 30 years Sex:  M >> F (3:1) Anatomic Distribution:  Predilection for vertebral column  Metaphysis of long bones
  • Radiographic Findings:  Similar to osteoid osteoma, though much larger (up to 11.0 cm) Gross and Microscopic Findings:  Similar to osteoid osteoma, though much larger nidus Ancillary Testing:  N/A Prognosis/Treatment:  Curettage followed by bone grafting  If incompletely removed, tumor may recur  Malignant change to osteosarcoma has been rarely reported
  • Most frequent primary malignant bone tumor Malignant cells must produce osteoid Most tumors arise de novo, though others arise in the setting of:  Paget’s disease  Previous RT  Previous chemo (especially alkylating agents)  Fibrous dysplasia  Osteochondromatosis  Chondromatosis  Chronic osteomyelitis
  • Signs/Symptoms:  Pain and swelling  Pathologic fracture is uncommon Age:  Peak in 2nd decade with gradual decrease thereafter Sex: M > F Anatomic Distribution:  50% arise around the knee  Metaphysis of long bones
  • An 11-year-old male was seen in consultation for an increasingly painful distal femoral lesion associated with a soft tissue mass. Plain radiograph shows an ill-defined destructive tumor in the distal femur. Fluffy radiodense infiltrates represent malignant tumor osteoid. Biopsy material shows two major components of this neoplasm: highly pleomorphic cells and haphazard deposits of osteoid. Note that the malignant cells fill the spaces between osteoid deposits. Lace-like osteoid deposition is very characteristic of this neoplasm.
  • The tan-white tumor fills most of the medullary cavity of the metaphysis and proximal diaphysis. It has infiltrated through the cortex, lifted the periosteum, and formed soft tissue masses on both sides of the bone.
  • Benign: Chondroma Osteochondroma Chondroblastoma Chondromyxoid Fibroma Malignant: Chondrosarcoma
  • Benign tumor of mature hyaline cartilage Most within bone (enchondroma) 2 syndromes characterized by multiple chondromas:  Ollier’s disease  Multiple enchondromas, usually unilateral  Maffucci’s syndrome  Multiple enchondromas associated with soft tissue hemangiomas  Both disorders have 25% risk of malignant transformation to chondrosarcoma Enchondroma is the most common tumor of the bones of the hand
  • Signs/Symptoms:  Usually asymptomatic lesions; pain with pathologic fracture Age:  Evenly distributed Sex: F > M Anatomic Distribution:  50% of lesions within small bones of hands and feet (mostly the phalanges)
  • Localized central lytic lesion surrounded by sharp rim of sclerosis; cortex usually not involved, though may be thin
  • An incidental finding of a bone lesion in the distal femur of a 38-year old female. The lesion was completely asymptomatic. Plain radiograph showed an intarmedullary zone of stippled and ring-shaped calcifications in the distal femoral metaphysis. This mineralization pattern with Low-power microscopic radiodense stipples andexamination of the biopsy rings is characteristic of mature specimen shows three hyaline cartilage. characteristic features of this lesion: a) vague lobularity; b) abundant cartilaginous matrix, which can be focally High-power view shows calcified; c) low cellularity. clustered and scattered chondrocytes with small, uniform, darkly stained nuclei. Occasional binucleated chondrocytes are present. Importantly, there were no mitotic figures.
  • Ollier’s disease
  • Composed of mature lobules of hyaline cartilage with foci of myxoid degeneration, calcification and endochondral ossification; may be quite cellular
  • Ancillary Testing: N/A Prognosis/Treatment: Solitary chondromas of long or flat bones need no treatment If fracture occurs, treat with curettage and bone grafting Recurrence unusual
  • Most frequent benign bone tumor Probably not a true neoplasm, but rather a tumor produced by growth of aberrant foci of cartilage on the surface of bone Autosomal dominant disorder of osteochrondromatosis with risk of malignant transformation to chondrosarcoma
  • Signs/Symptoms:  Palpable mass of long duration  Pain from compression of regional structures Age:  60% of patients < 20 years  Average age 10 years Sex: M > F Anatomic Predilection:  May occur in any bone; usually metaphysis of long bones (lower end of femur, upper end of humerus and upper end of tibia are most frequent)
  • Projection with cortex continuous with underlying bone; may be pedunculated; cartilaginous cap with frequent calcification
  • A 20-year-old male presented with a painless, hard subcutaneous mass in the popliteal fossa. He stated that the mass had been present for several years and did not change in size. Two words, "painless" and "non-growing" (or very slow growing), suggest that the lesion Plain radiograph described here is probably benign. demonstrated a pedunculated bony outgrowth at the proximal tibial metaphysis. The lesion had a uniform, The cartilagenous cap with specimen consisted of a stippled calcifications. pedunculated The tibial cortex and lesion, 3 x 3 x 2cm, medulla were with continuous with those a lobulated cartilage cap of the lesion. Osteochondroma, the most common benign measuring up to bone tumor, is not a neoplasm but a hamartoma. It is thought to arise from a 0.9cm in thickness portion of growth plate cartilage entrapped beneath the periosteum during skeletal growth. These entrapped pieces continue to grow and ossify at the same rate as the adjacent bone. When skeletal maturity is reached, osteochondromas usually stop growing.
  • Rare benign tumor Most common primary epiphyseal tumor in children Signs/Symptoms:  Local pain and swelling; tumors 1.0 to 7.0 cm Age:  2nd decade of life Sex: M > F Anatomic Distribution:  Epiphysis of long bones  40% in distal femur or proximal tibia
  • Lytic lesion of epiphysis with thin sclerotic rim; thinning without destruction of cortex
  • Rare benign tumor Signs/Symptoms:  Pain and swelling Age:  2nd and 3rd decades Sex: M > F Anatomic Distribution:  Metaphysis of long bones, though may abut the epiphysis  30% of tumors in tibia
  • Eccentric, sharply defined radiolucency in metaphysis of long bones; may destroy cortex
  • Signs/Symptoms:  Local swelling and pain Age:  Adulthood (60% between 30-60 years)  Rare in childhood Sex: M > F Anatomic Distribution:  Trunk, shoulder girdle, upper ends of femur and humerus
  • Ill-defined margins; fusiform thickening of shaft; perforation of cortex
  • Mesenchymal Chondrosarcoma Myxoid Chondrosarcoma
  • Ancillary Testing:  IHC  S100 – positive Prognosis/Treatment:  Must completely excise; biopsy leads to soft tissue implantation  RADIORESISTANT; surgery is Tx of choice  Recurrence may occur 5-10 years after primary  5-year survival 80%  Hematogenous metastasis to lung in high grade lesions
  • Giant Cell Tumor Ewing’s Sarcoma / Primitive Neuroectodermal Tumor (PNET) Chordoma
  • Signs/Symptoms:  Pain, loss of mobility, fracture Age:  80% of patients > 20 years Sex: F > M Anatomic Distribution:  Epiphysis of long bones  50% around knee with most in distal femur  Most common primary epiphyseal tumor of adults
  • A 45-year old female presented with increasing pain and swelling around the knee. She mentioned that the symptoms had progressed over a 4-month period. Age of the patient is an important diagnostic clue. If a pathologic fracture is excluded, pain and swelling imply active growthdemonstrates a Plain film of the lesion. large, lobulated, ill-defined lesion centered in the distal femoral metaphysis. There is endosteal scalloping and periosteal thickening. Central stippled and "ring and arc" calcifications are apparent and are typical of cartilaginous matrix. Small Low magnification seen radiolucent areas are shows a moderately cellular, at the periphery of the lesion. lobulated cartilaginous tumor. High-power view shows scattered plump, moderately pleomorphic chondrocytes. Binucleated cells are
  • Tumor Geographic and Expansile Sharp Zone of Transition between Tumor and Normal Bone/Fibula
  • CT scan shows a thin cortical shell around the tumor indicating the periosteum is intact and the tumor is likely benign There was no ossification or calcification within the tumor indicating that the tumor was probably not a bone or cartilage producing tumor
  • Tumor Peroneal Muscles Peroneal Nerve Soleus Muscle
  • Signs/Symptoms:  May simulate osteomyelitis as patients often present with pain, fever and leukocytosis Age:  5-20 years Sex: M > F Anatomic Distribution:  Long bones of extremities Gross Findings:  Solid masses of degenerating gray-white tumor
  • Signs/Symptoms: Usually found incidentally; may cause pain Age: Children and adolescents Sex: M > F Anatomic Distribution: Metaphysis of long bones, usually distal femur and tibia
  •  Genu valgum  Genu varum  Genu recurvatum  Congenital dislocation of patella  Congenital discoid meniscus
  • Genu Valgum: “knock knees”
  • Genu Varum: “bowlegs”
  • Genu Recurvatum: hyperextension of the knee joint
  • Dislocation usually occurs as a result of sudden direction changes while running and the knee is under stress or it may occur as a direct result of injury. Usually lateral
  • Rehab: strengthen quads, especially VMO to hold patella in place Each dislocation will damage cartilage which can eventually lead to traumatic arthritis
  •  Rickets  Scurvy  Gout  Ochronotic Arthritis  Osteoporosis
  •  Mineralization defect are classified according to the mineral deficiency.  Calcipenic rickets ( vit D↓, 1-alpha hydroxylase defect, vit D receptor dysfunction, dietary Ca ↓, CRF) .  Phosphopenic ricket: Inadequate intake (Premature infants (rickets of prematurity) , Aluminum-containing antacids).
  •  Deficient Intake: Ca, Ph, Vit D.  Poor absorption: vit D ↓, pseudo vit D↓, vit D resistance, high phytin content( soy formula), antacids, anticonvulsants, renal insufficiency, Fanconi syndrome, hepatic insufficiency, fat malabsorption (cystic fibrosis).  Increased excretion: furosemide, renal tubular dysfunction( phosphaturia, RTA with hypercalciuria), renal tubular damage e.g. cystinosis, tyrosinosis, galactosemia, fructose intolerance, wilson disease.  Local effect on bone matrix: hypophosphatasia(alp↓)
  •  VITAMIN D DISORDERS Nutritional vitamin D deficiency; Congenital vitamin D deficiency; Secondary vitamin D deficiency; Malabsorption ; Increased degradation; Decreased liver 25hydroxylase; Vitamin D-dependent rickets type 1; Vitamin D-dependent rickets type 2 ;Chronic renal failure.  CALCIUM DEFICIENCY Low intake Diet Premature infants (rickets of prematurity) Malabsorption Primary disease Dietary inhibitors of calcium absorption  PHOSPHORUS DEFICIENCY Inadequate intake Premature infants (rickets of prematurity) Aluminum-containing antacids  RENAL LOSSES X-linked hypophosphatemic rickets; Autosomal dominant hypophosphatemic rickets; Hereditary hypophosphatemic rickets with hypercalciuria; Overproduction of phosphatonin ( Tumor-induced rickets, McCune-Albright syndrome’ Epidermal nevus syndrome, Neurofibromatosis) ,Fanconi syndrome, Dent disease  DISTAL RENAL TUBULAR ACIDOSIS
  • Skeletal findings: 1. Delay in closure of the fontanelles. 2. Parietal & frontal bossing. 3. Craniotabes ( soft skull bones). 4. Enlargement of the costochondral junction (rachitic rosary). 5. The development of Harrison sulcus ( caused by pull of the diaphragmatic attachments to the lower ribs). 6. Enlargement of the wrist & bowing of the distal radius & ulna. 7. Progressive lateral bowing of the femur & tibia.
  •  GENERAL Failure to thrive; Listlessness; Protuding abdomen; Muscle weakness (especially proximal); Fractures.  HEAD Craniotabes; Frontal bossing; Delayed fontanelle closure; Delayed dentition; caries; Craniosynostosis  CHEST Rachitic rosary; Harrison groove; Respiratory infections and atelectasis  BACK Scoliosis ,Kyphosis ,Lordosis  EXTREMITIES Enlargement of wrists and ankles; Valgus or varus deformities Windswept deformity (combination of valgus deformity of 1 leg with varus deformity of the other leg); Anterior bowing of the tibia and femur; Coxa vara; Leg pain.  HYPOCALCEMIC SYMPTOMS Tetany ; Seizures; Stridor due to laryngeal spasm
  •  Extraskeletal manifestation of rickets vary depending upon the 1ry mineral deficiency.  Hypoplasia of the dental enamel is typical for hypocalcemic rickets, whereas abscesses of the teeth occur more often in phosphopenic rickets.  Hypocalcemic seizures, decreased muscle tone leading to delayed motor milestones, recurrent infections, increased sweating.
  • Antioxidant Not produced in the human body Necessary for collagen synthesis Prolyl and lysyl hydroxylase Procollagen triple helix 4-8 months of deficiency to develop clinical signs
  • Figure 2 : Corkscrew hair [3] Figure3: gingivitis
  • Male>>>Female Associated conditions  Hyperlipidemia, obesity, HT, CAD, DM Precipitating Conditions  ETOH, dietary excess, trauma  Stress: surgery, GI bleed, MI  Drugs: low dose ASA, diuretics, allopurinol
  • Clinical:  Monoarticular ->Cluster ->Polyarticular  1st MTP > 90%; any joint  Peaks in 12 hours  Red, hot, swollen  Very painful  Desquamation of skin  Tophi
  • Soft tissue swelling; tophi 1st MTP -> any joint Overhanging edge Destructive +++ if not treated
  • Aspirate the joint and look for MSU crystals under polarized microscopy