Acute Appendicitis: Introduction

Acute   appendicitis is a rapidly progressing inflammation of a small part of the large intestine called the appendix. Acute appendicitis is a medical   emergency that generally requires prompt removal of the appendix to prevent life-threatening complications, such as ruptured appendix and peritonitis.

In contrast, chronic appendicitis develops slowly, has milder symptoms, and can often be treated with antibiotics. Chronic appendicitis is far less common than acute appendicitis.

The appendix is a pouch-like structure located in the lower right quadrant of the abdomen near the area where the small   intestine links into the large intestine. The exact function of the appendix is not known, although it might be useful in protecting beneficial bacteria of the colon.

Acute appendicitis can occur when a piece of food, stool or object becomes trapped in the appendix. Acute appendicitis can also happen after a gastrointestinal infection. A tumor may also cause acute appendicitis in rare cases. Sometimes the cause of acute appendicitis isn't known.

Any of these conditions result in the abnormal growth of bacteria, swelling and inflammation of the appendix. The appendix then fills with pus, resulting in the typical symptoms of acute appendicitis. Symptoms of acute appendicitis include abdominal pain in the right lower area of the abdomen, fever, nausea, vomiting and loss of appetite. However, not all people with acute appendicitis will experience typical symptoms. Acute appendicitis can also lead to serious complications, especially if left untreated. For more details on symptoms and complications, refer to symptoms of acute appendicitis.

Acute appendicitis is a very common condition and a frequent cause of emergency surgery. Acute appendicitis can occur in any age group or population. However, it most often occurs in teens and young adults. It is rare in children under two years of age.

Making a diagnosis of acute appendicitis begins with taking a thorough medical history, including symptoms, and completing a physical examination. Examination of the abdomen frequently reveals severe pain and tenderness in the right lower area of the abdomen. This area is where the appendix is located and is called McBurney's   point .

Diagnostic   testing includes a blood test called a complete   blood count with differential (CBC). A CBC can determine if there is a rise in the number of certain types of white blood cells, which indicates that an inflammatory and/or infectious process, such as acute appendicitis, is occurring in the body.

More specific diagnostic   imaging tests may include an abdominal ultrasound and/or abdominal CT scan, which may reveal the inflamed appendix. These imaging tests are not always conclusive, and in some cases, a surgery called a diagnostic laparoscopy may be needed to look inside the abdomen and make the diagnosis. Other tests, such as urinalysis, are also done to rule out other common diseases and conditions that have similar symptoms, such as a kidney stone.

It is possible that a diagnosis of acute appendicitis can be missed or delayed because symptoms can vary amongst individuals. In addition, some symptoms of acute appendicitis are also common to other conditions, such as gastroenteritis or pelvic inflammatory disease. For more information on misdiagnosis, refer to misdiagnosis of acute appendicitis.

Acute appendicitis is treated by the surgical removal of the appendix. If the appendix has ruptured, more intensive treatment and longer hospitalization is necessary. For more information on treatment, refer to treatment of acute appendicitis. ...more »

Acute Appendicitis: The main symptom of acute appendicitis is abdominal pain or abdominal sensitivity. However, abdominal pain occurs with many conditions and only an estimated 5% of cases of abdominal pain are actually appendicitis. Although uncommon, appendicitis is very serious, and difficulty in diagnosing appendicitis in the emergency   department makes appendicitis the 3rd leading cause of malpractice lawsuits. Misdiagnosis of appendicitis is particularly common in children and infants with abdominal pain with estimates of initial misdiagnosis rates from 28% to 57% for under age 2-12 and almost 100% misdiagnosis for appendicitis in infants. ...more »

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Symptoms of Acute Appendicitis: Introduction

The symptoms of acute   appendicitis can vary between individuals. The well-known classic symptoms of acute appendicitis include abdominal pain in the right lower area of the abdomen that gets progressively sharp and more intense. People with acute appendicitis often have tenderness in the right lower area of the abdomen when it is pressed. This area is where the appendix is located and is called McBurney's   point . The pain and tenderness typically increase when a healthcare   provider releases pressure from McBurney's point after pressing. This is called rebound tenderness.

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Not all people with acute appendicitis will experience this type of abdominal   pain . Abdominal pain may also occur in other areas of the abdomen and can vary in severity and type. In early acute appendicitis, the abdominal pain may be located around the navel or belly button area then later move to McBurney's point as acute appendicitis progresses.

Other symptoms of acute appendicitis can include chills, constipation, diarrhea, abdominal distension, bloating, fever, nausea, vomiting, and loss of appetite.

Acute appendicitis can also lead to serious complications, especially if left untreated. These include ruptured appendix, abscess and peritonitis. These complications can lead to sepsis, shock and death if not treated emergently.

Symptoms of ruptured appendix and peritonitis include severe abdominal pain, high fever, chills, change in consciousness, cold, clammy skin, rapid pulse and low blood pressure (hypotension)....more about Acute Appendicitis »

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Symptoms of Acute Appendicitis

The list of signs and symptoms mentioned in various sources for Acute Appendicitis includes the 18 symptoms listed below:

Abdominal pain o Abdominal pain near navel - in earliest stages o Right-side abdominal pain - in later stages o Abdominal pain on activity o Abdominal pain on breathing o Abdominal pain on coughing o Abdominal pain on sneezing o Abdominal sensitivity - touching the area is painful

Nausea Vomiting Constipation Diarrhea Loss of appetite Inability to pass gas Low fever Abdominal swelling Bad breath Constipation more information...»

Research symptoms & diagnosis of Acute Appendicitis:

Overview -- Acute Appendicitis Diagnostic Tests for Acute Appendicitis Home Diagnostic Testing Complications -- Acute Appendicitis Doctors & Specialists Misdiagnosis and Alternative Diagnoses Hidden Causes of Acute Appendicitis Other Causes -- causes of these or similar symptoms

Acute Appendicitis: Symptom Checkers

Review the available symptom checkers for these symptoms of Acute Appendicitis:

Abdominal pain -- Symptom Checker Abdominal sensitivity -- Symptom Checker Nausea -- Symptom Checker Vomiting -- Symptom Checker Constipation -- Symptom Checker Diarrhea -- Symptom Checker Loss of appetite -- Symptom Checker Abdominal swelling -- Symptom Checker Bad breath -- Symptom Checker Constipation -- Symptom Checker

Acute Appendicitis: Symptom Assessment Questionnaires

Review the available Assessment Questionnaires for the symptoms of Acute Appendicitis:

Abdominal pain -- Assessment Questionnaire Abdominal sensitivity -- Assessment Questionnaire Nausea -- Assessment Questionnaire Constipation -- Assessment Questionnaire Diarrhea -- Assessment Questionnaire Loss of appetite -- Assessment Questionnaire Abdominal swelling -- Assessment Questionnaire Constipation -- Assessment Questionnaire

Acute Appendicitis: Complications

Review medical complications possibly associated with Acute Appendicitis:

Appendix abscess (type of Abscess) Ruptured appendix - often fatal if this occurs.

Peritonitis Death more complications...»

Acute Appendicitis Symptoms: Book Excerpts

Signs and symptoms - Appendicitis Signs and symptoms - Appendicitis

Diagnostic Testing

Diagnostic   testing of medical conditions related to Acute Appendicitis:

Physical exam Blood tests CBC Urine tests more tests...»

Read more at http://www.wrongdiagnosis.com/a/acute_appendicitis/symptoms.htm?ktrack=kcplink#symptom_list

Complete blood count

Complete   blood count : A complete blood count is a test that measures the levels of different blood cells in the blood.

Symptoms Associated with Complete blood count

These symptoms may be diagnosed by, screened for, or associated with Complete blood count:

Fever Fatigue Tiredness

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Introduction: Blood tests

Many conditions can be confirmed by testing the blood for numerous substances and properties. There are literally hundreds of different types of blood   tests .

Complications of blood tests: The actual collection of blood for a blood test rarely causes any complications beyond some minor bruising at the insertion site. A good attendant can reduce the amount of pain from insertion, but a common cause of pain is uncontrolled or sideways removal of the needle after blood is collected. For example, the nurse may forget to take care with the very last step and this can actually cause the worst pain and bruising.

Infant blood tests: Collecting infant blood is far more difficult than for older children or adults. In some cases, a blood drop may be adequate, such as from the heel of an infant as done for infant screening tests.

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Introduction: Urine tests

The urine may contain various substances for different types of disease. For example, sugar in urine may mean diabetes and blood in urine may mean various kidney conditions. Thus, a variety of diseases have urine tests.

There are several types of different urine tests.

Fasting urine test Random urine test Mid-stream urine test 24-hour urine test

Infant urine tests: Collecting urine from an infant is more difficult than for older children or adults. However, collection can be done via a strap-on urine collector worn underneath the diaper. Although more convenient than following your toddler around with a jug, this method does cause higher rates of contamination.

Mortality after hip fracture in Japan: the roleof nutritional statusKeita Miyanishi, Seiya Jingushi, Takehiko TorisuDepartment of Orthopaedic Surgery, Kyushu Rosai Hospital, Kitakyushu, JapanAddress correspondence and reprint requests to: Dr Keita Miyanishi, Department of Orthopaedic Surgery, Kyushu Rosai Hospital,1-3-1, Kuzuharatakamatsu, Kokuraminami-ku Kitakyushu, 800-0296, Japan. E-mail: keitam@major.ocn.ne.jpJournal of Orthopaedic Surgery 2010;18(3):265-70ABSTRACTPurpose. To assess factors that influence 4-yearmortality following hip fracture surgery in a Japanesepopulation.Methods. Records of 129 hips in 24 men and 103women aged 50 to 103 (mean, 79) years who underwentsurgery for femoral neck or trochanteric fractureswere reviewed. Clinical data reviewed includedage, gender, body mass index (BMI), side of fracture,fracture type, fracture stability, surgery type, intervalfrom admission to surgery, length of hospital stay,number of pre-fracture comorbidities, pre-fractureambulatory level, pre-fracture place of residence,preoperative dementia, preoperative skeletaltraction, blood haemoglobin level, serum albuminlevel, number of postoperative complications, andpostoperative delirium. Univariate and multiplelogistic regression analyses were performed toidentify the relative contribution of the variables tomortality. Receiver operating characteristic (ROC)curves were used to identify optimal cut-off levels.Results. The 4-year mortality was 48%. Multiplelogistic regression analysis showed that serumalbumin level (p=0.0004, odds ratio [OR]=5.8541) andBMI (p=0.0192, OR=1.1693) significantly influencedmortality; the cut-off points were 36 g/l and 18.9kg/m2, respectively, based on the ROC curves.Kaplan-Meier curves showed that survival rates weresignificantly worse in patients with values belowthese cut-off points.Conclusion. Serum albumin level and BMI onadmission are predictive of mortality after hipfracture surgery.Key words: body mass index; hip fractures; mortality;risk factors; serum albuminINTRODUCTIONHip fractures are a major cause of morbidity andmortality in osteoporotic elderly people. Over90 000 cases of hip fractures were reported in Japanin 19971; the incidence has increased from 2004to 2006.2 Patients with a history of hip fracture266 K Miyanishi et al. Journal of Orthopaedic Surgery

have a significantly higher mortality rate in thefollowing year than age-matched controls.3 Factorsaffecting ambulatory ability and mortality afterhip fracture include delirium, delayed surgery,comorbidities, gender, and nutritional state,4–8

whereas cerebrovascular accidents and Parkinson’sdisease have no significant effects.9,10 Most studiesfocused on one-year mortality after hip fracture; weassessed factors that affect 4-year mortality followinghip fracture surgery in a Japanese population.MATERIALS AND METHODSBetween April 2002 and March 2004, records of 129hips in 24 men and 103 women aged 50 to 103 (mean,79) years who underwent surgery for femoral neckor trochanteric fractures were reviewed. The meanfollow-up duration was 64 (range, 52–76) months.Clinical data reviewed included age, gender,body mass index (BMI), side of fracture, fracturetype (femoral neck or intertrochanteric), fracturestability (stable femoral neck fractures includeGarden types 1 and 2 and stable intertrochantericfractures include Evan type 1, groups 1 and 2,whereas unstable femoral neck fractures compriseGarden types 3 and 4 and unstable intertrochantericfractures comprise Evan type 1, groups 3 and 4and type 211,12), surgery type (hemiarthroplasty orinternal fixation using cannulated cancellous screwsalone, compression hip screws or intramedullarynails), interval from admission to surgery, length ofhospital stay, number of pre-fracture comorbidities(Parkinson’s disease, diabetes mellitus, asthma,congestive heart failure, cardiac arrhythmias,ischaemic heart disease, previous cerebrovascularaccident, renal disease, cancer, hypertension, chronicobstructive pulmonary disease, and rheumatoidarthritis), pre-fracture ambulatory level (able to walkalone with or without an assistive device or a helper,or bedridden or unable to ambulate but able to siton a chair13), pre-fracture place of residence (homeor geriatric hospital/nursing home), preoperativedementia (loss of function in multiple cognitivedomains severe enough to cause impairment insocial and occupational functioning14), preoperativeskeletal traction (performed at the proximal tibia forrepositioning of the fracture), blood haemoglobinlevel (fasting), serum albumin level (fasting), numberof postoperative complications (namely deep venousthrombus, wound infection, urinary tract infection,decubitus ulcers, and pneumonia), and delirium(reversible changes in mental status characterisedby confusion, disorientation and impaired realitytesting, as well as in consciousness and sleep andwake cycle14).Survivorship and the ambulatory level ofthe patients at the final follow-up were assessed

via telephone, using a standardised checklist. Ifthe patient was unavailable, a family member orcaregiver was interviewed instead. If the patient wasdead, the interval between surgery and death wasrecorded. Annual mortality rates were comparedwith those of the general population in Japan (basedon the Ministry of Health, Labour, and Welfare15).A univariate analysis of variables in patientswho survived to year 4 and those who did not wasperformed. Categorical variables were tested usingChi squared or Fisher’s exact probability tests.Continuous variables were tested using Student’st test. The relative contribution of the variables tomortality was identified using a multiple logisticregression analysis with stepwise variable selection.The optimal cut-off points of the significantfactors were determined using receiver operatingcharacteristic (ROC) curves.16 This involved plottingthe true-positive rate (sensitivity) against the falsepositiverate (1-specificity) for possible cut-off scores.Each point on the ROC plot represented a sensitivity/specificity pair corresponding to a particular decisionthreshold. A Kaplan-Meier curve was produced witha threshold level, defined as the highest sensitivity/specificity combination based on the ROC curvefor the most capable predictor of mortality afterFigure 1 Four-year survival rates for patients with hipfracture surgery and the general population.General populationPatients with hip fracture surgerySurvivalTime after surgery (years)1.00.40.80.20.60.00 1 2 3 4 5Vol. 18 No. 3, December 2010 Mortality after hip fracture in Japan 267hip fracture. Death was the end point. Statisticalsignificance was evaluated by the log rank test, and ap value of <0.05 was considered significant.RESULTSThe survival rates of our hip fracture patients atpostoperative year one, 2, 3, and 4 were 90%, 76%,63%, and 52%, respectively, which were lower thanthose of the general population (Fig. 1). Of the 66living patients at year 4, 25 (38%) were classified asnon-walking and 41 (62%) as walking.Compared to patients who survived to year 4,those who did not differed significantly with respectto BMI (p=0.0005), preoperative dementia (p=0.04),blood haemoglobin level (p=0.002), serum albuminlevel (p=0.0001), and number of postoperativecomplications (p=0.04) [Table 1].Multiple logistic regression analysis withstepwise variable selection showed that serum

albumin level (p=0.0004, odds ratio [OR]=5.8541) andBMI (p=0.0192, OR=1.1693) significantly influencedmortality (Table 2).Based on the ROC curves, the cut-off points forserum albumin level and BMI were 36 g/l (sensitivity,75%; specificity, 65%) and 18.9 kg/m2 (sensitivity,78%; specificity, 50%), respectively (Fig. 2).Kaplan-Meier curves with threshold levels basedon the ROC curves showed that survival rates weresignificantly worse in patients with a serum albuminlevel of <36 g/l (p<0.0001, log-rank test) or a BMI of<18.9 kg/m2 (p<0.01, log-rank test) [Fig. 3].DISCUSSIONOne-year mortality rates after hip fracture rangeTable 1Univariate analysis comparing survivors and non-survivors 4 years after hip fracture surgeryVariable Survivor(n=67 hips)Non-survivor(n=62 hips)p ValueMean±SD age (years) 78±11 81±10 0.11Gender (male, %) 15 23 0.26Body mass index (kg/m2) 21.0±2.9 18.9±3.5 0.0005Side of fracture (right, %) 51 47 0.65Fracture type (femoral neck fracture, %) 54 56 0.76Fracture stability (stable, %) 45 55 0.25Surgery type (hemiarthroplasty, %) 39 32 0.44Mean±SD interval from admission to surgery (days) 3.5±5.4 3.5±4.6 0.95Mean±SD length of hospital stay (days) 43±23 39±21 0.31Mean±SD no. of pre-fracture comorbidities 1.1±0.9 1.4±0.9 0.10Pre-fracture ambulatory level (walking, %) 99 92 0.10Pre-fracture place of residence (home, %) 88 76 0.07Preoperative dementia (%) 21 37 0.04Preoperative skeletal traction (%) 70 66 0.62Mean±SD blood haemoglobin level on admission (g/l) 118±15 109±19 0.002Mean±SD serum albumin level on admission (g/l) 38±04 34±05 0.0001Mean±SD no. of postoperative complications 0.34±0.54 0.57±0.69 0.04Postoperative delirium (%) 22 34 0.15Table 2Multiple logistic regression analysis on mortality 4 years after hip fracture surgeryVariable MaximumlikelihoodestimationStandard error Chi-square p Value Odds ratio (95% CI)Body mass index 0.1564 0.0668 5.4864 0.0192 1.1693 (1.0307–1.3419)Serum albumin level 1.7671 0.4988 12.5509 0.0004 5.8541 (2.3083–16.5277)Surgery type -0.4383 0.2722 2.5920 0.1074 0.6451 (0.3729–1.0914)Fracture type -0.5602 0.2792 4.0274 0.0448 0.5711 (0.3231–0.9723)268 K Miyanishi et al. Journal of Orthopaedic Surgeryfrom 11 to 33%.7,8,13,17 The impact of hip fracture onmortality is primarily in the first year.18 Survivalcurves after hip fracture reveal a dramatic decline atthe beginning and thereafter ran almost parallel tothe expected curves of the general population.15,19,20 Inour study, the survival curve declined gradually andcontinued to diverge from the expected curve duringthe study period, indicating that the mortality risk

continued even after the early period. Such a gradualdecline in survival has also been reported.21,22

Factors influencing mortality after hip fractureinclude gender,5 systemic disease,17 delayed surgery,7

comorbidities,8 nutritional status,6 postoperativedelirium,4 and postoperative complications.8 Most ofFigure 2 Receiver operating characteristic curves for (a) serum albumin level and (b) body mass index. Arrows indicate theoptimal cut-off points of 36 g/l for serum albumin level and 18.9 kg/m2 for body mass index, corresponding to the highestsensitivity/specificity combination. Dotted line indicates reference line (0 diagnostic efficiency).SensitivitySensitivity1-Specificity 1-Specificity0.0 0.00.4 0.40.2 0.20.6 0.60.9 0.90.1 0.10.5 0.50.8 0.80.3 0.30.7 0.71.0 1.00.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0(a) (b)Figure 3 Kaplan-Meier survival curves for patients with (a) a serum albumin level above and below 36 g/l and (b) a body massindex (BMI) above and below 18.9 kg/m2. Death is an end point.Time after surgery (years) Time after surgery (years)p<0.0001Serum albuminlevel <36 g/lBMI <18.9 kg/m2 Serum albuminlevel ≥36 g/lBMI ≥18.9 kg/m2

p<0.01SurvivalSurvival1.0 1.00.8 0.80.6 0.60.4 0.40.2 0.20.0 0.00 1 2 3 4 5 0 1 2 3 4 5(a) (b)Vol. 18 No. 3, December 2010 Mortality after hip fracture in Japan 269REFERENCES1. Orimo H, Hashimoto T, Sakata K, Yoshimura N, Suzuki T, Hosoi T. Trends in the incidence of hip fracture in Japan, 1987-1997: the third nationwide survey. J Bone Miner Metab 2000;18:126–31.2. Hagino H, Furukawa K, Fujiwara S, Okano T, Katagiri H, Yamamoto K, et al. Recent trends in the incidence and lifetime riskof hip fracture in Tottori, Japan. Osteoporos Int 2009;20:543–8.3. Roberts SE, Goldacre MJ. Time trends and demography of mortality after fractured neck of femur in an English population,1968-98: database study. BMJ 2003;327:771–5.4. Edelstein DM, Aharonoff GB, Karp A, Capla EL, Zuckerman JD, Koval KJ. Effect of postoperative delirium on outcome afterhip fracture. Clin Orthop Relat Res 2004;422:195–200.5. Endo Y, Aharonoff GB, Zuckerman JD, Egol KA, Koval KJ. Gender differences in patients with hip fracture: a greater risk of

morbidity and mortality in men. J Orthop Trauma 2005;19:29–35.6. Koval KJ, Maurer SG, Su ET, Aharonoff GB, Zuckerman JD. The effects of nutritional status on outcome after hip fracture. JOrthop Trauma 1999;13:164–9.7. Moran CG, Wenn RT, Sikand M, Taylor AM. Early mortality after hip fracture: is delay before surgery important? J Bone JointSurg Am 2005;87:483–9.8. Roche JJ, Wenn RT, Sahota O, Moran CG. Effect of comorbidities and postoperative complications on mortality after hipfracture in elderly people: prospective observational cohort study. BMJ 2005;331:1374.9. Idjadi JA, Aharonoff GB, Su H, Richmond J, Egol KA, Zuckerman JD, et al. Hip fracture outcomes in patients with Parkinson‘sdisease. Am J Orthop (Belle Mead NJ) 2005;34:341–6.10. Youm T, Aharonoff G, Zuckerman JD, Koval KJ. Effect of previous cerebrovascular accident on outcome after hip fracture. JOrthop Trauma 2000;14:329–34.11. Evans EM. The treatment of trochanteric fractures of the femur. J Bone Joint Surg Am 1949;31:190–203.12. Garden RS. Low-angle fixation in fractures of the femoral neck. J Bone Joint Surg Br 1961;43:647–63.13. Kitamura S, Hasegawa Y, Suzuki S, Sasaki R, Iwata H, Wingstrand H, et al. Functional outcome after hip fracture in Japan.Clin Orthop Relat Res 1998;348:29–36.14. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: AmericanPsychiatric Association; 1994:136–41.15. Tsuboi M, Hasegawa Y, Suzuki S, Wingstrand H, Thorngren KG. Mortality and mobility after hip fracture in Japan: a ten-yearfollow-up. J Bone Joint Surg Br 2007;89:461–6.16. McNeil BJ, Keller E, Adelstein SJ. Primer on certain elements of medical decision making. N Engl J Med 1975;293:211–5.17. Kenzora JE, McCarthy RE, Lowell JD, Sledge CB. Hip fracture mortality. Relation to age, treatment, preoperative illness, timethese studies examined factors influencing one-yearmortality. In our study, low serum albumin level andBMI were significant factors influencing the 4-yearmortality after hip fracture, with cut-off levels of 36g/l and 18.9 kg/m2, respectively. Both factors areconsidered markers of poor health (malnutrition).There is a close association between malnutritionand outcome following hip fractures. Elderly patientswith femoral neck fractures are often malnourished.23

A low serum albumin level is a major risk factorfor hip fracture.24 A serum albumin level of <35 g/lwas predictive of increased in-hospital mortality.6

Patients with albumin gain during rehabilitation hadbetter functional outcomes on discharge according toFunctional Independence Measure scores.25

Dietary intervention may favourably affectlonger-term outcomes after hip fracture. The ratesof complication and death were significantly lower6 months after femoral neck fracture in patientsreceiving daily oral nutrition supplement than inthose who did not.26

The serum albumin level is a marker of thebody’s protein status, and low levels increase the riskof poor outcomes from various medical conditions,such as coronary heart disease, cardiac surgery, and

pneumonia.27–29 In older persons, low albumin levelsare associated with loss of appendicular skeletalmuscle mass,30 and in particular immobilisation afterhip fracture surgery leads to a decline in muscle mass,strength and function.31 Such adverse systemic effectson health (including functional decline) resulting fromlow serum albumin levels may increase mortality.Limitations of this study were the small numberof patients reviewed and the retrospective nature ofanalysis. Further prospective multi-centre studies areneeded to confirm our results.ACKNOWLEDGEMENTSThis research was supported by research funds topromote the hospital functions of Japan LabourHealth and Welfare Organization and a Grant ofJapan Orthopaedics and Traumatology Foundation,Inc. (No. 0165). We thank Mr Masahiro Kaneseki(Internet Computer Network Laboratory, Takamatsu,Japan) for his advice on the statistical analysis.270 K Miyanishi et al. Journal of Orthopaedic Surgeryof surgery, and complications. Clin Orthop Relat Res 1984;186:45–56.18. White BL, Fisher WD, Laurin CA. Rate of mortality for elderly patients after fracture of the hip in the 1980‘s. J Bone JointSurg Am 1987;69:1335–40.19. Jalovaara P, Virkkunen H. Quality of life after primary hemiarthroplasty for femoral neck fracture. 6-year follow-up of 185patients. Acta Orthop Scand 1991;62:208–17.20. Richmond J, Aharonoff GB, Zuckerman JD, Koval KJ. Mortality risk after hip fracture. J Orthop Trauma 2003;17:53–6.21. Kanis JA, Oden A, Johnell O, De Laet C, Jonsson B, Oglesby AK. The components of excess mortality after hip fracture. Bone2003;32:468–73.22. Muraki S, Yamamoto S, Ishibashi H, Nakamura K. Factors associated with mortality following hip fracture in Japan. J BoneMiner Metab 2006;24:100–4.23. Older MW, Edwards D, Dickerson JW. A nutrient survey in elderly women with femoral neck fractures. Br J Surg1980;67:884–6.24. Thiebaud D, Burckhardt P, Costanza M, Sloutskis D, Gilliard D, Quinodoz F, et al. Importance of albumin, 25(OH)-vitaminD and IGFBP-3 as risk factors in elderly women and men with hip fracture. Osteoporos Int 1997;7:457–62.25. Mizrahi EH, Fleissig Y, Arad M, Blumstein T, Adunsky A. Rehabilitation outcome of hip fracture patients: the importance ofa positive albumin gain. Arch Gerontol Geriatr 2008;47:318–26.26. Delmi M, Rapin CH, Bengoa JM, Delmas PD, Vasey H, Bonjour JP. Dietary supplementation in elderly patients withfractured neck of the femur. Lancet 1990;335:1013–6.27. Corti MC, Salive ME, Guralnik JM. Serum albumin and physical function as predictors of coronary heart disease mortalityand incidence in older persons. J Clin Epidemiol 1996;49:519–26.28. Dey AB, Nagarkar KM, Kumar V. Clinical presentation and predictors of outcome in adult patients with community-acquiredpneumonia. Natl Med J India 1997;10:169–72.29. Rady MY, Ryan T, Starr NJ. Perioperative determinants of morbidity and mortality in elderly patients undergoing cardiacsurgery. Crit Care Med 1998;26:225–35.30. Visser M, Kritchevsky SB, Newman AB, Goodpaster BH, Tylavsky FA, Nevitt MC, et al. Lower serum albumin concentration

and change in muscle mass: the Health, Aging and Body Composition Study. Am J Clin Nutr 2005;82:531–7.31. Bloomfield SA. Changes in musculoskeletal structure and function with prolonged bed rest. Med Sci Sports Exerc1997;29:197–206.

http://www.josonline.org/pdf/v18i3p265.pdf

ABSTRACTPurpose. To evaluate outcomes of 28 patients whounderwent intramedullary nailing for displacedproximal humeral fractures.Methods. 24 women and 4 men aged 38 to 87 (mean,65) years underwent intramedullary nailing fordisplaced proximal humeral fractures. 17 (61%) ofthem were aged >70 years. Fractures were classified

into 2-part (n=8), 3-part (n=17), and 4-part (n=3), andcorresponded to AO 11 A3 (n=8), B1 (n=3), B2 (n=9),and C2 (n=8) types. The Constant and Oxford scoreswere assessed at the final follow-up.Results. All patients had bone union except for onewho had tuberosity failure. 23 (82%) patients hadsatisfactory-to-excellent and 5 had poor Constantscores; outcomes were worse with more complexfractures. 20 (71%) patients had satisfactory Oxfordscores. Seven (25%) patients had impingement of anail tip. Other complications included avascularnecrosis (n=1), proximal locking screw back-out(n=1), and screw penetration into the joint (n=1).Conclusion. Intramedullary nailing provides astable fixation with minimal soft tissue dissection

Intramedullary nailing for displaced proximalhumeral fracturesVinod Kumar, Sandeep Datir, Balachandran VenkateswaranDepartment of Trauma & Orthopaedic Surgery, Dewsbury and District Hospital, Dewsbury, West Yorkshire, UnitedKingdomAddress correspondence and reprint requests to: Mr Vinod Kumar, 31 Holt Park Crescent, Leeds, LS16 7SL, United Kingdom.E-mail: geo_bug@yahoo.comJournal of Orthopaedic Surgery 2010;18(3):324-7for displaced proximal humeral fractures. It enablesearly mobilisation and functional recovery.Key words: bone nails; fracture fixation, intramedullary;humeral fracturesINTRODUCTIONProximal humeral fractures account for 5% of allfractures and are the third most common fracturein elderly patients.1 The incidence of such fracturesincreases exponentially from the fifth decade oflife, being almost twice as common in women thanmen.2 This type of fracture affects quality of life,making elderly patients dependent on others for theiractivities of daily living.Most proximal humeral fractures are undisplacedor minimally displaced and can be managed nonoperativelywith satisfactory outcomes.3,4 Displacedfractures almost always require surgical interventionto obtain a favourable outcome.3,5–7 Intramedullarynailing enables closed reduction, less-invasiveimplantation, and minimal disruption of the softtissues. We evaluated outcomes of 28 patients whounderwent intramedullary nailing for displacedVol. 18 No. 3, December 2010 Intramedullary nailing for displaced proximal humeral fractures 325and distal locking.Patients were placed in a beach chair position. Asuperior deltoid-split approach was used; the entry

point of the nail was posterior to biceps tendonand medial to the greater tuberosity. The entry holewas hand reamed and the nail inserted after closedreduction. In cases with displaced tuberosities, thetuberosities with the rotator cuff attachment wererepaired using ethibond sutures (Fig. 1), after fixing2 proximal locking screws and a single dynamicdistal locking screw. The shoulders were supportedin a sling and gentle pendulum exercises commencedas comfort allowed. Assisted exercises followed byactive exercises were commenced at week 2.Patients were followed up at weeks 2 and 6,month 6, and every 6 months thereafter. Radiographswere obtained at each follow-up to assess bone unionand complications. The Constant8 and Oxford9 scoreswere assessed at the final follow-up. The Constantscore assesses pain, activities of daily living (ADL),range of motion, and power. The Oxford scoreassesses subjective pain and impairment of ADL; 33%of the score is derived from 4 pain-related questionsand 67% from 8 ADL-related questions. Higher scoresindicate worse outcomes.RESULTSThe mean follow-up period was 25 (range, 9–39)months. All patients had bone union except for onewho had tuberosity failure. The mean Constant scorewas 65 (range, 30–86); 23 (82%) of the patients hadsatisfactory to excellent results and 5 had poor results(Table). According to age-related analysis, 9 (82%) outof 11 patients aged ≤70 years and 14 (82%) out of 17patients aged >70 years had satisfactory to excellentoutcomes. The mean score was 71 in patients with2-part fractures (n=8), 65 in those with 3-part fractures(n=17), and 44 in those with 4-part fractures (n=3).Outcomes were worse with more complex fractures.The mean Oxford score was 17 (range, 12–34). 20(71%) out of 28 patients had satisfactory outcomes(Table).Impingement of a nail tip (Fig. 2a) or a lockingscrew head occurred in 7 (25%) patients. Thiscomplication was not always radiologically evident.Following removal of the hardware after bone union,5 patients had improvement of symptoms, whereas 2still had residual symptoms. Avascular changes werenoted in the humeral head of a 71-year-old asthmaticand diabetic woman with a 3-part fracture (Fig. 2b).She had marked stiffness and a low Constant score.Proximal locking screw back-out was noted in onepatient (Fig. 2c). This occurred after radiologicalbone union and was attributed to a surgical errorproximal humeral fractures.MATERIALS AND METHODSBetween October 2004 and January 2007, 24 womenand 4 men aged 38 to 87 (mean, 65) years underwentintramedullary nailing for displaced proximal

humeral fractures. 17 (61%) of them were aged >70years. Fractures were classified into 2-part (n=8),3-part (n=17), and 4-part (n=3), and correspondedto AO 11 A3 (n=8), B1 (n=3), B2 (n=9), and C2 (n=8)types.The T2 proximal humeral nail (Stryker) is madeof titanium alloy and has a maximum diameterof 10 mm. It enables static or dynamic locking of 4multi-directional proximal locking screws and 2distal locking screws. The proximal locking holesare threaded and have nylon bushings to enhancethe hold of the screws in the humeral head. It has aradiolucent targeting device to facilitate proximalFigure 1 The tuberosities with the rotator cuff attachmentare repaired using ethibond sutures, after fixing 2 proximallocking screws and a single dynamic distal locking screw.326 V Kumar et al. Journal of Orthopaedic Surgery(applying a 4-mm instead of a 5-mm diameter screw).Screw penetration into the joint was seen in anotherpatient. Overall, 8 nails had to be removed after 5 to16 months.DISCUSSIONNon-operative treatment for proximal humeralfractures does not provide adequate stability or painrelief and hence does not allow early mobilisation.Surgical management is difficult when fracturesoccur in elderly patients with osteoporotic bone andpoor bone stock, a high degree of comminution, anddisplacement. Injury to blood supply can result inosteonecrosis. The proximity to the shoulder jointand injury to the rotator cuff leads to severe stiffnessof the shoulder and hence an intensive rehabilitationprogramme is required to optimise return of function.There is insufficient evidence to determinethe best surgical treatment for displaced proximalhumeral fractures. Tension band fixation requiresan extended approach for reduction and fixation6

and may cause posteromedial gapping and cutout.10 Transosseous suture fixation also requires anextended approach and may not provide enoughstability. Transcutaneous pinning may cause skinirritation, pin-tract infections, and loss of reduction,and requires demanding techniques.11,12 The pitfallsof retrograde flexible nailing are unstable fixation,angulation, and perforation of the humeral head.Fixation using locking plate and screws is one optionif the bone is osteoporotic. However, it requires anextensive soft tissue dissection and carries the riskof avascular necrosis, impingement and poor screwpurchase in the osteoporotic bone.13 Inadequatereduction and fixation results in deformity andfunctional disability. A displaced greater tuberositymay cause impingement and rotator interval tear. TheTableOutcome of patientsParameter No. of patients

Constant score>75 (excellent) 850–75 (satisfactory) 15<50 (poor) 5Oxford score12–20 (satisfactory) 20>20 (unsatisfactory) 8ComplicationTuberosity malunion 1Impingement 7Avascular necrosis 1Screw back-out 1Screw tip into joint 1Figure 2 (a) Impingementof a prominent nail tip,(b) avascular changes inthe humeral head, and (c)proximal locking screwback-out.Figure 3 The proximal nail tip is buried below the corticalsurface to prevent impingement.(a)(c)(b)Vol. 18 No. 3, December 2010 Intramedullary nailing for displaced proximal humeral fractures 327rotated articular fragment may result in secondaryshoulder arthritis or humeral neck non-union.Good surgical fixation should entail anatomicreduction of the tuberosities and restoration of thelength, alignment and rotation of the fragments. Thisshould be achieved with minimal soft tissue trauma,and with preservation of the medial periosteal hingeand blood supply. To prevent impingement, theamount of hardware at the cortical surface shouldbe minimal. Stable fixation enables good pain reliefand early mobilisation together with restoration offunction.In a cadaver biomechanical study, intramedullaryfixation has been shown to be more stable andstronger than locked plating or traditional plate andscrews.14 It enables stable fixation through a smallincision with minimal soft tissue disruption, andfacilitates early mobilisation of the shoulder andfunctional recovery.21 out of 27 patients with displaced 3-partfractures achieved satisfactory to excellent resultsafter locking nail fixation; no patients had fixationor hardware failure.15 The Polarus nail also achievedgood results for displaced 2-, 3- and 4-part fractures16;77%17 and 80%18 of such patients achieved satisfactoryto excellent outcomes, and those younger than 65years achieved better functional outcomes.17 The Sirusproximal humeral nail achieved good to very goodresults in 75% of the patients.19 In our study, 82% ofthe patients had satisfactory to excellent outcomes.Loss of fixation or nail breakage after rigidintramedullary nailing was not observed in any ofthe studies. The common complications were lateral

migration of the proximal screw causing irritationand impingement, non-union, avascular necrosis,and shoulder stiffness. In our series, impingementwas avoided in patients operated on in the later yearsof the study, in whom placement of the most proximallocking screw was avoided and their Constant scoresimproved. The distal locking screw was placed inthe dynamic mode to enable a small amount offracture collapse as the metaphysical bone heals. It isimperative to reduce the tuberosity and to bury theproximal nail tip well below the cortical surface toprevent impingement (Fig. 3).REFERENCES1. Kristiansen B, Barfod G, Bredesen J, Erin-Madsen J, Grum B, Horsnaes MW, et al. Epidemiology of proximal humeralfractures. Acta Orthop Scand 1987;58:75–7.2. Lind T, Kroner K, Jensen J. The epidemiology of fractures of the proximal humerus. Arch Orthop Trauma Surg 1989;108:285–7.3. Neer CS 2nd. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am 1970;52:1077–89.4. Young TB, Wallace WA. Conservative treatment of fractures and fracture-dislocations of the upper end of the humerus. JBone Joint Surg Br 1985;67:373–7.5. Cofield RH. Comminuted fractures of the proximal humerus. Clin Orthop Relat Res 1988;230:49–57.6. Hawkins RJ, Angelo RL. Displaced proximal humeral fractures. Selecting treatment, avoiding pitfalls. Orthop Clin NorthAm 1987;18:421–31.7. Neer CS 2nd. Displaced proximal humeral fractures. II. Treatment of three-part and four-part displacement. J Bone JointSurg Am 1970;52:1090–103.8. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res 1987;214:160–4.9. Dawson J, Fitzpatrick R, Carr A. Questionnaire on the perceptions of patients about shoulder surgery. J Bone Joint Surg Br1996;78:593–600.10. Koval KJ, Blair B, Takei R, Kummer FJ, Zuckerman JD. Surgical neck fractures of the proximal humerus: a laboratoryevaluation of ten fixation techniques. J Trauma 1996;40:778–83.11. Hawkins RJ, Kiefer GN. Internal fixation techniques for proximal humeral fractures. Clin Orthop Relat Res 1987;223:77–85.12. Jaberg H, Warner JJ, Jakob RP. Percutaneous stabilization of unstable fractures of the humerus. J Bone Joint Surg Am1992;74:508–15.13. Wachtl SW, Marti CB, Hoogewoud HM, Jakob RP, Gautier E. Treatment of proximal humerus fracture using multipleintramedullary flexible nails. Arch Orthop Trauma Surg 2000;120:171–5.14. Hessmann MH, Hansen WS, Krummenauer F, Pol TF, Rommens PM. Locked plate fixation and intramedullary nailing forproximal humerus fractures: a biomechanical evaluation. J Trauma 2005;58:1194–201.15. Lin J. Effectiveness of locked nailing for displaced three-part proximal humeral fractures. J Trauma 2006;61:363–74.16. Adedapo AO, Ikpeme JO. The results of internal fixation of three- and four-part proximal humeral fractures with the Polarusnail. Injury 2001;32:115–21.17. Kazakos K, Lyras DN, Galanis V, Verettas D, Psillakis I, Chatzipappas CH, et al. Internal fixation of proximal humerusfractures using the Polarus intramedullary nail. Arch Orthop Trauma Surg 2007;127:503–8.18. Rajasekhar C, Ray PS, Bhamra MS. Fixation of proximal humeral fractures with the Polarus nail. J Shoulder Elbow Surg2001;10:7–10.

19. Fuchtmeier B, Brockner S, Hente R, Maghsudi M, Nerlich M, Prantl L. The treatment of dislocated humeral head fractureswith a new proximal intramedullary nail system. Int Orthop 2008;32:759–65.

ABSTRACTPurpose. To evaluate the characteristics of bicyclespokeinjuries in a suburban Indian population.Methods. 30 male and 11 female children aged 4 to12 (mean, 6) years with bicycle-spoke injuries wereprospectively studied. Data collected includedpatient age, gender, position at the time of injury, site,type, and characteristics of the injury. According tothe Oestern and Tscherne classification, soft-tissueinjuries were classified into grades 0 to 3.Results. 37 patients injured the right foot, and 4the left foot; 34 by the rear wheel and 7 by the front

wheel. All front-wheel injuries involved the forefootand midfoot. 73% of injuries involved the lateralaspect of the ankle. The most common injury sitewas the posterior ankle (n=30), followed by themedial midfoot (n=7), and the forefoot (n=3). Partialavulsion of heel flap and an exposed Achilles tendonwere each noted in 2 patients. 10, 13, 14, and 4patients sustained soft-tissue injuries of grades 0, 1,2, and 3, respectively. Eight patients had associated

Bicycle-spoke injuries of the foot in childrenAnil Agarwal,1 Manish Pruthi2

1 Department of Orthopaedics, Chacha Nehru Bal Chikitsalaya, Delhi, India2 Department of Orthopaedics Surgery, Government Medical College and Hospital, Chandigarh, IndiaAddress correspondence and reprint requests to: Dr Anil Agarwal, 4/103, East End Apartments, Mayur Vihar Ph-I Extension, Delhi,110096, India. E-mail: rachna_anila@yahoo.co.inJournal of Orthopaedic Surgery 2010;18(3):338-41fractures. All fractures healed uneventfully. Marginalnecrosis of the wound was noted in 5 patients, butnone required a skin graft. No patient had functionalimpairment or residual tenderness of the foot.Conclusion. Bicycle-spoke injuries usually affectedthe ankle region, and the wound was usually deeperthan it appeared on initial examination. Reassessmentof the wound after 48 hours is recommended.Severity of soft-tissue injury was the determinant ofoverall function; bone fractures by themselves didnot alter the duration of recovery. To prevent bicyclespokeinjuries, spoke guards and foot rests should beused, and children being carried on a bicycle shouldwear proper shoes. Education on injury mechanism,severity, and preventive measures is also important.Key words: ankle injuries; bicycling; child; foot injuriesINTRODUCTIONBicycles are a common mode of transport in suburbanIndia. 52% of bicycle-spoke injuries involve childrenaged 3 to 5 years.1,2 Such injuries occur when theVol. 18 No. 3, December 2010 Bicycle-spoke injuries of the foot in children 339foot of a passenger (usually a child) is caught in thespokes of a rotating wheel. The passenger usuallysits on the handle bar, the bar connecting the handleand the seat, or the pillion, with feet dangling on oneside (side-saddle position) or both. The right foot isusually closer to the wheel in the side-saddle positionand hence more commonly injured (Fig. 1). The modeof injury is comparable to human tooth clenched fistbites, which cut deep and inoculate the stretchedand devascularised tissue.3 The usual injuries are:(1) lacerations of the tissue, (2) crushing of the foot,and (3) shearing injuries due to these 2 forces.4–6 Weevaluated the characteristics of bicycle-spoke injuries

in a suburban Indian population.MATERIALS AND METHODSBetween June 2005 and May 2009, 30 male and11 female children aged 4 to 12 (mean, 6) yearswho presented with bicycle-spoke injuries wereprospectively studied. Data collected includedpatient age, gender, position at the time of injury, site,type, and characteristics of the injury.According to the Oestern and Tscherneclassification,7 soft-tissue injuries were classified intograde 0 (closed, only soft-tissue swelling), grade 1(superficial abrasion or contusion/bruising), grade 2(deep abrasion or laceration with full thickness skinloss), and grade 3 (extensive soft-tissue injury and/or open fracture, with damage to the vessels/nerves/tendons and/or exposure of bone) [Fig. 2].Grade 0 injuries were treated conservatively withcrammer wire splintage and limb elevation, and werereassessed after 48 hours. Grade 1 injuries were treatedwith thorough wound washing (with 0.9% saline)followed by dressing (with an antibiotic-vaselinegauze), crammer wire splintage, and limb elevation.The wounds were reassessed after 48 hours for signsof local infection and to reassess severity. Splintageof the ankle in neutral position was maintained untilthe abrasions were dressed. A below-knee plasterof-Paris backsplint was applied for 2 weeks. Grade 2injuries were treated with thorough wound washing(sometimes under anaesthesia) and dressing. Thewounds were reassessed after 48 hours and abelow-knee backsplint was applied for 3 to 4 weeks,depending on the condition of the wound. Grade 3injuries were treated with thorough debridementunder anaesthesia with tendon repair if required.After 48 hours, a second debridement was carriedout if necessary. As soon as the wound conditionpermitted, a supervised rehabilitation programmewas started to regain ankle motion. An ankle footorthosis enabled exercises while the dressings werestill in place.In patients with associated fractures, closedreduction was attempted. If that failed, openreduction and internal fixation was performed. Openfractures were treated with debridement, lavage,and external fixation. Broad spectrum antibioticswere administered as appropriate to patients withgrade 2 or 3 injuries. The duration of wound healing,residual tenderness in the foot/heel, range of anklejoint motion, and difficulty in walking were assessedat the final follow-up.Figure 1 The passenger usually sits on the pillion or the bar connecting the handle and the seat. The right foot is usually closerto the wheel in the side-saddle position.340 A Agarwal and M Pruthi Journal of Orthopaedic SurgeryRESULTSThe mean interval from injury to presentation was

6 (range, 2–24) hours. 37 patients injured the rightfoot, and 4 the left foot; 34 by the rear wheel and 7by the front wheel. All front-wheel injuries involvedthe forefoot and midfoot. 73% of injuries involved thelateral aspect of the ankle, with equal involvementof the anterolateral and posterolateral regions. Themost common injury site was the posterior ankle(n=30), followed by the medial midfoot (n=7), and theforefoot (n=3). There was one patient with a fingerentrapment injury. Partial avulsion of the heel flapand an exposed Achilles tendon were each noted in2 patients.10, 13, 14, and 4 patients sustained soft-tissueinjuries of grades 0, 1, 2, and 3, respectively. Thegrading changed to a higher grade on reassessmentin 8 patients (5 from grade 0 to 1 and 3 from grade 1to 2), owing to the presence of tissue necrosis and/or superimposed infection. Patients with grade 0 or1 injuries returned to function and weight bearingearlier than those with grade 2 or 3 injuries (mean,28 [range, 5–40] vs. 40 [range, 14–90] days). Marginalnecrosis of the wound was noted in 5 patients, butnone required a skin graft. No patient had functionalimpairment or residual tenderness of the foot.Eight patients had associated fractures: 3 sustainedmedial tibial epiphyseal fractures (2 of whom weretreated conservatively and one with open reductionand Kirschner wire fixation), 4 sustained distal tibialfractures (3 of whom were treated conservatively andone with debridement and external fixation), andone sustained a fracture of the proximal phalanx ofthe fourth toe and was treated conservatively. Allfractures healed uneventfully. The mean healing timewas 18 (range, 5–66) days.DISCUSSION63% of bicycle-spoke injuries occur in the area aroundthe Achilles tendon.8 More severe soft-tissue injuriesaffect the posterolateral aspect of the ankle and extendto the Achilles tendon,6 which is consistent with ourseries. There is no universally accepted classificationfor such injuries. Besides the Oestern and Tscherneclassification,7 soft-tissue injuries can be classified intosimple abrasions or laceration with partial avulsion,8

or oedema and bruising, bruising with abrasions orfull thickness skin defects.6 In our study, treatmentand prognosis correlated with the classification.Abrasions and ecchymoses usually affect theankle region and appear deeper on re-examination.Figure 2 Oestern and Tscherne classification of soft-tissue injuries of grades 0, 1, 2 and 3.Vol. 18 No. 3, December 2010 Bicycle-spoke injuries of the foot in children 341REFERENCES1. Sankhala SS, Gupta SP. Spoke-wheel injuries. Indian J Pediatr 1987;54:251–6.2. Jaiswal A, Nigam V, Jain V, Kapoor S, Dhaon BK. Bicycle and cycle rickshaw injury in suburban India. Injury 2006;37:423–7.3. Phair IC, Quinton DN. Clenched fist human bite injuries. J Hand Surg Br 1989;14:86–7.

4. Izant RJ Jr, Rothmann BF, Frankel VH. Bicycle spoke injuries of the foot and ankle in children: an underestimated “minor”injury. J Pediatr Surg 1969;4:654–6.5. Ahmed M. Motorcycle spoke injury. Br Med J 1978;2:401.6. Segers MJ, Wink D, Clevers GJ. Bicycle-spoke injuries: a prospective study. Injury 1997;28:267–9.7. Oestern HJ, Tscherne H. Pathophysiology and classification of soft issue injuries associated with fractures. In: Tscherne H,editor. Fractures with soft tissues injuries. New York: Springer-Verlag; 1984:1–9.8. Mine R, Fukui M, Nishimura G. Bicycle spoke injuries in the lower extremity. Plast Reconstr Surg 2000;106:1501–6.9. Lodha SC. Spoke wheel injuries in children. Indian J Surg 1973;35:92–5.10. Suri MP, Naik NR, Raibagkar SC, Mehta DR. Heel flap injuries in spoke wheel accidents. Injury 2007;38:619–24.The skin and soft-tissue vascularity is poor becauseof underlying internal degloving, with a high riskof wound infection. It is therefore mandatory toreassess the wound for infection and necrosis after 48hours, and adjust the wound grade and managementaccordingly. Below-knee backsplints applied for 2to 3 weeks with the ankle in a neutral position arerecommended. An ankle foot orthosis enables bothwound care and exercise to be performed. Despiteleaving large uncovered areas, debridement (evendelayed) is also recommended, as is split skin graftingto hasten healing in cases of wound necrosis.4,9

Lacerations of the posterior ankle region withexposure of the Achilles tendon or heel flap avulsionsresulting from the shearing effect of spokes riskbecoming necrotic. Heel flap avulsions requirethorough lavage, debridement, suturing, andsplintage. In cases of heel flap necrosis or developmentof painful contractures, it may be necessary to delaycovering the injury with a flap.8,10

In our study, the severity of the soft-tissue injurywas the determinant of overall function; bone fracturesby themselves were simple and healed uneventfullyand did not alter the duration of recovery in eachgrade. Nonetheless, radiological screening and longtermfollow-up are recommended for patients withassociated fractures, as growth disturbances arepossible.To prevent bicycle-spoke injuries, spoke guardsand foot rests should be used (Fig. 3), and childrenbeing carried on a bicycle should wear propershoes. Education on injury mechanisms, severity,and preventive measures is also important. Bicyclespokes can cause injuries resulting in a combinationof devascularisation, internal degloving, andcontamination. Such injuries may be deeper thanthey first appear. Reassessment after 48 hoursprovides better evaluation of the wound. Multipledebridements may be necessary to preventcontamination.Figure 3 Spoke guards and foot rests should be attached to prevent bic

ycle-spoke injuries.

ABSTRACTPurpose. To assess the effects of tranexamic acid (TA)in patients undergoing total hip arthroplasty (THA)for osteoarthritis.Methods. 42 patients underwent primary THA forosteoarthritis by a single surgeon. 10 men and 11women who did not receive TA were controls, whereas9 men and 12 women who received TA constitutedthe treatment group. Both groups were matched forage, gender, body mass index, and American Societyof Anesthesiologists grading. The type of prosthesisused (cemented or uncemented) was based on thesurgeon’s preference and patient age, activity level

and demands. No hybrid prosthesis was used. 10minutes prior to incision, a single dose of intravenousTA (10 mg per kg body weight) was given to patientsin the treatment group. Comparison was madebetween both groups with regard to intra-operativeblood loss, postoperative reduction in haemoglobinand haematocrit levels, blood transfusion, incidenceof deep vein thrombosis, and the length of hospital

Effects of tranexamic acid on blood loss duringtotal hip arthroplastyJagwant Singh,1 Moez S Ballal,2 P Mitchell,1 PG Denn1

1 Macclesfield District General Hospital, Cheshire, United Kingdom2 Leighton Hospital, Crewe, United KingdomAddress correspondence and reprint requests to: Mr Jagwant Singh, 52 Rosedale mansions, Malm street, Boulevard Hull, EastYorkshire, HU32TF, United Kingdom. E-mail: drjagwant@gmail.comJournal of Orthopaedic Surgery 2010;18(3):282-6stay.Results. The mean intra-operative blood loss(489±281 vs. 339±184 ml, p=0.048) and the decreasein haemoglobin level (38±12 vs. 29±10 g/l, p=0.014)were significantly higher in the control than thetreatment group. Two patients among the controlsreceived a transfusion, compared to none in the TAgroup (p=0.49, Fisher’s exact test). The 2 patientswho needed blood transfusion had blood losses of600 and 690 ml, compared to a mean of 489 ml in thewhole group. No patient in either group developeddeep vein thrombosis or pulmonary embolism up to3 months.Conclusion. A single dose of intravenous TA (10 mgper kg body weight) given 10 minutes prior to THAis a cost-effective and safe means of minimising bloodloss and reduction in haemoglobin concentrationsas well as the need for allogenic blood transfusion,without increasing the risk of thromboembolic events.Key words: arthroplasty, replacement, hip; blood loss,surgical; postoperative hemorrhage; tranexamic acidVol. 18 No. 3, December 2010 Effects of tranexamic acid on blood loss during THA 283INTRODUCTIONTo avoid allogenic blood transfusions in total hiparthroplasty (THA), various blood-conservationtechniques have been developed. Tranexamic acid(TA) has been widely used in surgeries involvingfields of gynaecology, cardiology, urology, livertransplant, and dentistry. It inhibits fibrinolysisand reduces blood loss, minimising the need forallogenic blood transfusions after joint arthroplastyand spinal surgery.1 The effects of TA on intra- andpost-operative blood loss in patients undergoingcemented or uncemented THA have been reported.1–9

We assessed the effects of a single dose of intravenousTA in patients undergoing THA on intra-operativeblood loss, postoperative reduction in haemoglobinand haematocrit levels, blood transfusion, incidenceof deep vein thrombosis, and the length of hospitalstay.MATERIALS AND METHODSBetween May 2006 and March 2007, 42 patientsunderwent primary THA for osteoarthritis by asingle surgeon. 10 men and 11 women who did notreceive any TA were considered as controls, whereas9 men and 12 women who received TA constitutedthe treatment group. Both groups were matched forage, sex, body mass index, and American Society ofAnesthesiologists grading. Patients with a history ofsevere ischaemic heart disease, pulmonary embolism,deep vein thrombosis, hepatic or renal failure, orallergy to TA were excluded.Four to 6 weeks before surgery, haemoglobin andhaematocrit values, platelet counts, and coagulationprofiles of the patients were assessed. 10 days beforesurgery, oral anticoagulants, aspirin, and nonsteroidalanti-inflammatory drugs were stopped.On the evening before surgery, thromboprophylaxis(enoxaparin sodium 0.4 ml) was given subcutaneouslyand continued after surgery.Patients were operated on under spinalanaesthesia by a single surgeon using the anterolateralapproach. The type of prosthesis used (cemented oruncemented) was based on the surgeon’s preferenceand patient age, activity level and demands. Nohybrid prosthesis was used. In cemented THA, theExeter femoral stem and the Pinnacle acetabular cupsystems were used, whereas in uncemented THA, thehydroxyapatite-coated Corail femoral stem and thePinncale DuoFix acetabular prosthesis were used.In the treatment group, 10 minutes prior toincision, a single dose of intravenous TA (10 mg perkg body weight) was administered. In both groups,prophylactic antibiotic (cefuroxime) was givenintravenously before and after surgery.Intra-operative blood loss was measured bycollection of suction volume and change in the weight(wet vs. dry) of the sponges. No drains were used.Postoperative haemoglobin and haematocrit valueswere recorded on the morning of postoperative day2. The decision to transfuse was not entirely based onblood loss or a haemoglobin concentration of <85 g/l;patient age, cardiovascular status and symptoms (ifany) were also considered.For deep vein thrombosis, the patients wereassessed clinically for calf swelling, tendernessand oedema of the leg. When clinically indicated,duplex ultrasonography was performed and lowmolecular-weight heparin prescribed. Warfarin was

prescribed if deep vein thrombosis was confirmed.At postoperative month 3, patients were assessedfor any wound problems or incidence of deep veinthrombosis.The sample size was determined using data of2 pilot studies.2,10 To detect a mean difference of 225ml of blood loss with a standard deviation of 200 ml,with a power of 90% and a type-one error probabilityof 5%, a minimum of 18 patients in each group wereneeded. Differences between groups were comparedusing the Chi squared test, Fisher’s exact test, t testand Mann-Whitney U test where appropriate. Preandpost-operative blood indices were comparedusing the paired t test. A p value of <0.05 wasconsidered significant.RESULTSThe mean intra-operative blood loss (489±281 vs.339±184 ml, p=0.048) and the decrease in haemoglobinlevel (38±12 vs. 29±10 g/l, p=0.014) were significantlyhigher in the control than the treatment group(Table). Two patients among the controls receiveda transfusion, compared to none in the TA group(p=0.49, Fisher’s exact test). The 2 patients whoneeded blood transfusion had blood losses of 600 and690 ml, compared to a mean of 489 ml in the wholegroup. No patient in either group developed deepvein thrombosis or pulmonary embolism up to 3months.DISCUSSIONTA inhibits fibrinolysis mainly by blocking the lysinebindingsites of plasminogen.11 Plasminogen binds to284 J Singh et al. Journal of Orthopaedic Surgeryfibrin at this site and results in clot breakdown. Tissueplasminogen activator is a major enzyme responsiblefor conversion of plasminogen into active plasmin.Surgery and venous stasis increase the release of tissueplasminogen activator and activate the fibrinolyticsystem. Binding of TA to plasminogen preventsthe breakdown of fibrin even though plasmin isgenerated.11 For TA to be effective, it has to interactwith the plasminogen binding site before binding tofibrin takes place.10,12 The fibrinolytic response aftersurgery is biphasic.4,13 The initial phase of increasedfibrinolytic activity lasts one hour and is followed byfibrinolytic shutdown, which peaks again after about24 hours. This is a consequence of increased release ofplasminogen activator inhibitor.The elimination half life of intravenous TA is2 hours, and it has a volume of distribution of 9 to12 litres.11 Once plasminogen is bound to the fibrinsurface, TA is no longer effective.13 TA had little effectwhen administered at the end of surgery and 3 hourslater; reduction in blood loss after THA was notsignificant.10,11 TA inhibited clot lysis more effectivelywhen it was added before clot formation.12

TA reduced blood loss during and after THAwhen 2 doses of TA (10 mg/kg) were administeredjust before incision and 3 hours later (and continuedfor 10 hours at a dosage of 1 mg/kg/h), together withintra-operative autotransfusion.8 Nonetheless, otherstudies reported no significant reduction in intraoperativeblood loss.3,5

Significant reduction in postoperative (but notintra-operative) blood loss was associated witha single bolus of TA (10 mg/kg) administeredimmediately before the operation,2 or 3 doses (each of10 mg/kg) given at the operation, and 8 and 16 hourslater.9 In uncemented THA patients, a TA bolus of 1000mg 5 minutes before the operation was associatedwith reduced postoperative (but not intra-operative)blood loss in the first 4 hours.14 There was no definiteanswer with regard to effective dosage and pattern.Nonetheless, its use significantly reduced intra- andpost-operative blood loss,6 and the need for bloodtransfusions.2–5,9,15 TA was associated with lowerallogenic blood transfusion rates and blood loss in hipand knee arthroplasty patients.6,7 1000 mg of TA costs£1.55, whereas a unit of blood costs £133. Avoidanceof allogenic blood transfusions has economic benefitsand minimises the risk of related infections and otheradverse reactions,16–19 and is associated with reducedmorbidity and shorter hospital stays.18,20,21

The use of TA increases the risk of thromboembolicevents (especially deep vein thrombosis). Nonetheless,in our study, such increases were not observed,which is consistent with other findings reported in* Mann-Whitney U testTableDemographics and pre- and post-operative parameters of both groupsVariable Controls (n=21) Tranexamic acid (n=21) p ValueMean±SD age (years) 73±7 69±6 0.116No. of males/females 10/11 9/12 0.756Mean±SD weight (kg) 80±14 73±14 0.131Mean±SD body mass index (kg/m2) 29±4 28±5 0.301American Society of Anesthesiologists grading(no. of patients)0.276I 2 5II 14 14III 5 2Type of prosthesis (no. of patients) 0.041Uncemented 5 11Cemented 16 10Mean±SD preoperative haemoglobin level (g/l) 140±13 139±12 0.728Mean±SD preoperative haematocrit level (g/l) 0.414±0.038 0.405±0.036 0.437Mean±SD preoperative platelet count (x109/l) 268±72 280±53 0.571Mean±SD (range) intra-operative blood loss (ml) 489±281 (126–1300) 339±184 (112–836) 0.048Mean±SD decrease in haemoglobin level (g/l) 38±12 29±10 0.014Mean±SD decrease in haematocrit level (g/l) 0.149±0.175 0.085±0.031 0.014*Mean±SD decrease in platelet counts (x109/l) 64±40 65±32 0.86*Mean±SD blood transfused (units) 2±0 0±0 0.49No. of patients having blood transfusions 2 0 0.49Mean±SD length of hospital stay (days) 6.4±1.9 5.9±1.5 0.34

No. of patients with deep vein thrombosis 0 0 -Vol. 18 No. 3, December 2010 Effects of tranexamic acid on blood loss during THA 285REFERENCES1. Lemaire R. Strategies for blood management in orthopaedic and trauma surgery. J Bone Joint Surg Br 2008;90:1128–36.2. Benoni G, Fredin H, Knebel R, Nilsson P. Blood conservation with tranexamic acid in total hip arthroplasty: a randomized,double-blind study in 40 primary operations. Acta Orthop Scand 2001;72:442–8.3. Husted H, Blond L, Sonne-Holm S, Holm G, Jacobsen TW, Gebuhr P. Tranexamic acid reduces blood loss and bloodtransfusions in primary total hip arthroplasty: a prospective randomized double-blind study in 40 patients. Acta OrthopScand 2003;74:665–9.4. Claeys MA, Vermeersch N, Haentjens P. Reduction of blood loss with tranexamic acid in primary total hip replacementsurgery. Acta Chir Belg 2007;107:397–401.5. Johansson T, Pettersson LG, Lisander B. Tranexamic acid in total hip arthroplasty saves blood and money: a randomized,double-blind study in 100 patients. Acta Orthop 2005;76:314–9.6. Gill JB, Rosenstein A. The use of antifibrinolytic agents in total hip arthroplasty: a meta-analysis. J Arthroplasty 2006;21:869–73.7. Ho KM, Ismail H. Use of intravenous tranexamic acid to reduce allogeneic blood transfusion in total hip and kneearthroplasty: a meta-analysis. Anaesth Intensive Care 2003;31:529–37.8. Ekback G, Axelsson K, Ryttberg L, Edlund B, Kjellberg J, Weckstrom J, et al. Tranexamic acid reduces blood loss in total hipreplacement surgery. Anesth Analg 2000;91:1124–30.9. Niskanen RO, Korkala OL. Tranexamic acid reduces blood loss in cemented hip arthroplasty: a randomized, double-blindstudy of 39 patients with osteoarthritis. Acta Orthop 2005;76:829–32.10. Benoni G, Lethagen S, Nilsson P, Fredin H. Tranexamic acid, given at the end of the operation, does not reduce postoperativeblood loss in hip arthroplasty. Acta Orthop Scand 2000;71:250–4.11. Mahdy AM, Webster NR. Perioperative systemic haemostatic agents. Br J Anaesth 2004;93:842–58.12. Krishnamurti C, Vukelja SJ, Alving BM. Inhibitory effects of lysine analogues on t-PA induced whole blood clot lysis.Thromb Res 1994;73:419–30.13. Eriksson BI, Hultman E, Martinell S, Eriksson E, Tengborn L, Risberg B. Regional fibrinolysis following total hip replacement.Thromb Res 1991;62:441–7.14. Yamasaki S, Masuhara K, Fuji T. Tranexamic acid reduces postoperative blood loss in cementless total hip arthroplasty. JBone Joint Surg Am 2005;87:766–70.15. Lemay E, Guay J, Cote C, Roy A. Tranexamic acid reduces the need for allogenic red blood cell transfusions in patientsundergoing total hip replacement. Can J Anaesth 2004;51:31–7.16. Hill GE, Frawley WH, Griffith KE, Forestner JE, Minei JP. Allogeneic blood transfusion increases the risk of postoperativebacterial infection: a meta-analysis. J Trauma 2003;54:908–14.17. Edna TH, Bjerkeset TB. Association between blood transfusion and infection in injured patients. J Trauma 1992;33:659–61.18. Fernandez MC, Gottlieb M, Menitove JE. Blood transfusion and postoperative infection in orthopedic patients. Transfusion1992;32:318–22.19. Bierbaum BE, Callaghan JJ, Galante JO, Rubash HE, Tooms RE, Welch RB. An analysis of blood management in patientshaving a total hip or knee arthroplasty. J Bone Joint Surg Am 1999;81:2–10.20. Newman JH, Bowers M, Murphy J. The clinical advantages of autologous transfusion. A randomized, controlled study afterknee replacement. J Bone Joint Surg Br 1997;79:630–2.

21. Hynes MC, Calder P, Rosenfeld P, Scott G. The use of tranexamic acid to reduce blood loss during total hip arthroplasty: anobservational study. Ann R Coll Surg Engl 2005;87:99–101.22. Clarke AM, Dorman T, Bell MJ. Blood loss and transfusion requirements in total joint arthroplasty. Ann R Coll Surg Engl1992;74:360–3.23. Trice ME, Walker RH, D’Lima DD, Morris BA, Colwell CW Jr. Blood loss and transfusion rate in noncemented andrandomised trials2,8 and meta-analyses.6,7 The use ofTA is not associated with increased thromboembolicevents, because the effects of TA are more pronouncedin operative wounds than in peripheral venous blood.This is because generation of tissue plasminogenactivator (activating the fibrinolytic pathway) ensuesin wounds.2,11,21 Thus, TA acts as a clot stabiliser andnot a clot promoter.Cemented prostheses are associated with lessblood loss,6,22 as cement prevents bleeding from themedullary canal. Nonetheless, blood transfusionin patients treated with cemented or uncementedprostheses were similar.23

TA has also been shown to reduce blood lossassociated with cardiopulmonary bypass surgeryby 30 to 40%.11,24 In cardiac surgery its use wasassociated with a reduction in peri-operative bloodloss and allogenic transfusion.25 Most studies used 10mg/kg bolus injections immediately before surgery,and continued at a rate of 1 mg/kg for 10 to 12hours. TA administered before and during in primarycoronary artery bypass operations was associatedwith more effective reduction in blood loss andtransfusions.26 Thus, TA is a cost-effective and safemeans of minimising blood loss and reductions inhaemoglobin concentrations, as well as the need forallogenic blood transfusion, without increasing therisk of thromboembolic events.286 J Singh et al. Journal of Orthopaedic Surgerycemented/hybrid total hip arthroplasty. Is there a difference? A comparison of 25 matched pairs. Orthopedics 1999;22(1Suppl):S141–4.24. Levi M, Cromheecke ME, de Jonge E, Prins MH, de Mol BJ, Briet E, et al. Pharmacological strategies to decrease excessiveblood loss in cardiac surgery: a meta-analysis of clinically relevant endpoints. Lancet 1999;354:1940–7.25. Laupacis A, Fergusson D. Drugs to minimize perioperative blood loss in cardiac surgery: meta-analyses using perioperativeblood transfusion as the outcome. The International Study of Peri-operative Transfusion (ISPOT) Investigators. Anesth Analg1997;85:1258–67.26. Brown RS, Thwaites BK, Mongan PD. Tranexamic acid is effective in decreasing postoperative bleeding and transfusionsin primary coronary artery bypass operations: a double-blind, randomized, placebo-controlled trial. Anesth Analg1997;85:963–70.

Appendicitis AnatomyTo better understand appendicitis, it helps to understand the anatomy of the intestines and the appendix.

The intestine absorbs nutrients from food and liquids. The intestine is about 22 feet long in an adult. It includes the large intestine and the small intestine.

The small intestine has three parts:

Duodenum:o Connects to the stomach

Jejunum:o Middle portion of the small intestine

Ileum:o Lower portion of the small intestine that connects to the cecum (first part of the large

intestine)

The large intestine is also known as the colon. It is the last portion of the intestine.

The colon has several parts, including:

Cecum:o The portion of the colon that connects to the ileum (small intestine). The appendix is a

finger-like pouch that comes off of the cecum. Ascending colon:

o The first section after the small intestine, located on the right side Transverse colon:

o Sits horizontally across the upper abdomen Descending colon:

o Located on the left side of the abdomen Sigmoid:

o A short, S-shaped section above the rectum Rectum:

o The lowest internal part of the colon

Intestinal anatomy:

Entire gastrointestinal tract Intestines and other abdominal organs Blood vessels of the intestines The appendix is a small pouch that protrudes from the wall of the large intestine. It is located at

the point where the small intestine turns into the large intestine.

The anatomy of appendicitis.

Guidry SP, Poole GV.

Dept. of Surgery, University of Mississippi Medical Center, Jackson 39216-4505.

Abstract

Acute appendicitis is a common disorder and, ideally, should be diagnosed prior to the onset of gangrene or perforation. Nonetheless, the goal of early diagnosis remains elusive. In a prospective study, 100 appendectomies were performed for suspected acute appendicitis over 19 months. The location of the appendix was noted by the operating surgeon and was listed as anterior intraperitoneal, retrocecal, pericolic gutter, retroileal, pelvic, or retroperitoneal. The

latter four positions were regarded as sites in which the appendix was hidden from the anterior parietal peritoneum. Fifteen patients did not have appendicitis. Of the 85 inflamed appendices, 25 were indurated, 19 were suppurative, and 41 were gangrenous or perforated. Patients with gangrene or perforation were more likely to have pain and tenderness at a site other than the right lower quadrant and had a higher mean heart rate on admission than patients with simple appendicitis, but there were no other differences in symptoms, signs, or laboratory findings among the groups. The appendix was in a hidden location in 15 per cent of patients with simple appendicitis or without appendicitis, compared with 68 per cent of patients with gangrenous or perforative appendicitis (P < 0.001). Complications were more frequent, and hospital stays were longer in patients with advanced appendicitis (P < 0.001). Patients and physicians were equally responsible for delays in treatment, but the high incidence of hidden appendices in those with advanced appendicitis resulted in less severe symptoms and signs than expected. Anatomic variations in the location of the appendix are often responsible for delays in the diagnosis of appendicitis.

The appendix is a narrow, muscular tube. One end is attached to the first part of the large intestine, while the other end is closed. The position of the appendix in the body can vary from person to person.

An average adult appendix is about 4 inches (10cm) long. However, it can vary in length from as less as an inch to 8 inches. Its diameter is usually about about 6 to 7 mm.

The function of the appendix is unknown.

Foods that have not been digested tends to move into the appendix and are forced out again by the contractions of appendix. In herbivorous animals like cow and goat, the appendix can function. In man, this has become what is called as a vestigial organ (an organ that is no more required)..

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ATHOPHYSIOLOGY OF APPENDICITIS

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The pathophysiology of appendicitis is the constellation of processes that leads to the development of acute appendicitis from a normal appendix.

Understanding the pathophysiology of appendicitis helps to explain all the signs and symptoms as well as complications seen in appendicitis.

The main thrust of events leading to the development of acute appendicitis lies in the appendix developing a compromised blood supply due to obstruction of its lumen and becoming very vulnerable to invasion by bacteria found in the gut normally.

Obstruction of the appendix lumen by faecolith, enlarged lymph node, worms, tumour, or indeed foreign objects, brings about a raised intra-luminal pressure, which causes the wall of the appendix to become distended.

Normal mucus secretions continue within the lumen of the appendix, thus causing further build up of intra-luminal pressures. This in turn leads to the occlusion of the lymphatic channels, then the venous return, and finally the arterial supply becomes undermined.

Reduced blood supply to the wall of the appendix means that the appendix gets little or no nutrition and oxygen. It also means a little or no supply of white blood cells and other natural fighters of infection found in the blood being made available to the appendix.

The wall of the appendix will thus start to break up and rot. Normal bacteria found in the gut gets all the inducement needed to multiply and attack the decaying appendix within 36 hours from the point of luminal obstruction, worsening the process of appendicitis.

This leads to necrosis and perforation of the appendix. Pus formation occurs when nearby white blood cells are recruited to fight the bacterial invasion.

A combination of dead white blood cells, bacteria, and dead tissue makes up pus.

The content of the appendix (faecolith, pus and mucus secretions) are then released into the general abdominal cavity, bringing causing peritonitis.

So, in acute appendicitis, bacterial colonisation follows only when the process have commenced.

These events occur so rapidly, that the complete pathophysiology of appendicitis takes about one to three days. This is why delay can be deadly!

Contents

Overview History Causes Pathophysiology Signs & Symptoms Lab Test Differentials Complications Treatment Recovery prevention In Pregnancy In Children

Pain in appendicitis is thus caused, initially by the distension of the wall of the appendix, and later when the grossly inflamed appendix rubs on the overlying inner wall of the abdomen (parietal peritoneum) and then with the spillage of the content of the appendix into the general abdominal cavity (peritonitis).

Fever is brought about by the release of toxic materials (endogenous pyrogens) following the necrosis of appendicael wall, and later by pus formation.

Loss of appetite and nausea follows slowing and irritation of the bowel by the inflammatory process.

The pathophysiology of appendicitis obviously correlates with the clinical picture.

Acute appendicitis pathophysiology follows the same pattern, even in children and pregnant women.

In the elderly, the pathophysiology of appendicitis remains unaltered, but the inflammatory response generated by the elderly is often less than that seen with young fit individuals, accounting for the often benign presentation froth with a tendency to miss the diagnosis, thus courting more complications.