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B. Uruk, M.B. B.CH. B.A.O., Ph.D.

Clinical Director, Philadelphia College of Osteopathic Medicine

The anxiety must be accompanied by at least three of the following symptoms: restlessness, easy fatigability, difficulty concentrating, irritability, muscle tension, and disturbed sleep. Eight times more common and of early onset in family members of affected individuals than general population. Increased risk of specific phobias in first-degree relatives of patients with specific phobias. Other anxiety disorders, anorexia nervosa, somatoform disorders, and major depression. Other anxiety disorders, adjustment disorders, psychotic disorders, and substance-induced disorders. Prognosis One study showed that 65% of children cease to have the diagnosis in 2 years. Affected children are likely to develop panic disorder, agoraphobia, or depressive disorders later in life. Social phobia in childhood may become associated with alcohol abuse in adolescence. The panic attacks are not due to direct physiologic effects of drugs or abuse or medication or a general medical condition (e. The panic attacks are not better accounted for by another mental disorder, such as social phobia, specific phobia, obsessive-compulsive disorder, posttraumatic stress disorder, or separation anxiety disorder. Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months, about numerous events or activities B. The anxiety and worry are associated with three or more of the following six symptoms (with at least some symptoms present for more days than not for the past 6 months). Sleep disturbance (difficulty falling or staying asleep or restless, unsatisfying sleep) D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. The disturbance is not due to the direct physiologic effects of a drug or a general medical condition (e. Table 17-3 Criteria for Diagnosis of a Panic Attack A discrete period of intense fear or discomfort, in which four or more of the following symptoms developed abruptly and reached a peak within 10 minutes: Palpitations, pounding heart, or accelerated heart rate Sweating Trembling or shaking Sensations of shortness of breath or smothering Feeling of choking Chest pain or discomfort Nausea or abdominal distress Feeling dizzy, unsteady, lightheaded, or faint Derealization (feelings of unreality) or depersonalization (being detached from oneself) Fear of losing control or going crazy Paresthesias (numbness or tingling sensations) Chills or hot flashes including shakiness, trembling, and myalgias. Gastrointestinal symptoms (nausea, vomiting, diarrhea) and autonomic symptoms (tachycardia, shortness of breath) commonly coexist. In children and adolescents, the specific symptoms of autonomic arousal are less prominent, and symptoms are often related to school performance or sports. Care must be taken to elicit internalizing symptoms of negative cognitions about the self (hopelessness, helplessness, worthlessness, suicidal ideation), as well as those concerning relationships (embarrassment, self-consciousness) and associated with anxieties. Inquiry about eating, weight, energy, and interests should also be carried out to eliminate a mood disorder. The reexperiencing is accompanied by avoidance of stimuli that remind the person of the trauma and by autonomic hyperarousal (Table 17-5). In preverbal children, there are changes in behavior: regressed clingy behavior, increased aggression, unwillingness to explore the environment, alterations in feeding, sleeping behaviors, and difficulty soothing child. Preschool children may display rapidly changing emotional states like anger, sadness, and excitement and play may have compulsive reenactments linked to the traumatic event. Dissociative states lasting a few seconds to many hours, in which the person relives the traumatic event, are referred to as flashbacks. In adolescents anticipation of unwanted visual imagery increases the risk of irritable mood, anger, and voluntary sleep deprivation. When faced with reminders of the original trauma, physical signs of anxiety or increased arousal occur, including difficulty falling or staying asleep, hypervigilance, exaggerated startle response, irritability, angry outbursts, and difficulty concentrating. The person has been exposed to a traumatic event in which both of the following were present: 1. The person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury or a threat to the physical integrity of self or others.

Sinus radiography and computed tomography may be useful, but when these images are abnormal, they do not distinguish allergic disease from nonallergic disease. Inflammation contributes to airway hyperresponsiveness (airways constricting in response to allergens, irritants, viral infections, and exercise). It also results in edema, increased mucus production in the lungs, influx of inflammatory cells into the airway, and epithelial cell denudation. Chronic inflammation can lead to airway remodeling, which results from a proliferation of extracellular matrix proteins and vascular hyperplasia and may lead to irreversible structural changes and a progressive loss of pulmonary function. Asthma is the most common chronic disease of childhood in industrialized countries, affecting nearly 7 million children younger than 18 years of age in the United States. One in 5 children went to the emergency department for an asthma-related visit in 2009. Women are more likely than men to have asthma, and boys are more likely than girls to have asthma. These tests are indicated for patients who have dermatographism or extensive dermatitis; who cannot discontinue medications, such as antihistamines, that interfere with skin test results; who are very allergic by history, where anaphylaxis is a possible risk; or who are noncompliant for skin testing. The presence of specific IgE antibodies alone is not sufficient for the diagnosis of allergic diseases. Exacerbating factors include viral infections, exposure to allergens and irritants (e. Rhinosinusitis, gastroesophageal reflux, and nonsteroidal anti-inflammatory drugs (especially aspirin) can aggravate asthma. Treatment of these conditions may lessen the frequency and severity of the asthma. During acute episodes, tachypnea, tachycardia, cough, wheezing, and a prolonged expiratory phase may be present. Classic wheezing may not be prominent if there is poor air movement from airway obstruction. As the attack progresses, cyanosis, diminished air movement, retractions, agitation, inability to speak, tripod sitting position, diaphoresis, and pulsus paradoxus (decrease in blood pressure of >15 mm Hg with inspiration) may be observed. Physical examination may show evidence of other atopic diseases such as eczema or allergic rhinitis. A chest radiograph should be performed with the first episode of asthma or with recurrent episodes of undiagnosed cough or wheeze to exclude anatomic abnormalities. Repeat chest radiographs are not needed with new episodes unless there is fever (suggesting pneumonia) or localized findings on physical examination. Two novel forms of monitoring asthma and airway inflammation directly include exhaled nitric oxide analysis and quantitative analysis of expectorated sputum for eosinophilia. Spirometry is used to monitor response to treatment, assess degree of reversibility with therapeutic intervention, and measure the severity of an asthma exacerbation. Variability in predicted peak flow reference values make spirometry preferred to peak flow measures in the diagnosis of asthma. For younger children who cannot perform spirometry maneuvers or peak flow, a therapeutic trial of controller medications helps in the diagnosis of asthma. Allergy skin testing should be included in the evaluation of all children with persistent asthma but not during an exacerbation of wheezing. Misdiagnosis delays correcting the underlying cause and exposes children to inappropriate asthma therapy (Table 78-2). Allergic bronchopulmonary aspergillosis is a hypersensitivity type of reaction to antigens of the mold Aspergillus fumigatus. It occurs primarily in patients with steroid-dependent asthma and in patients with cystic fibrosis. Because many children with asthma have coexisting allergies, steps to minimize allergen exposure should be taken (Table 78-3). For all children with asthma, exposures to tobacco and wood smoke and to persons with viral infections should be minimized.

Stab wound may be small on body surface but damage to the deeper organs like liver, spleen, major vessels like inferior vena cava / mesenteric vessels or intestines may be extensive and life threatening. Closed wounds ­ · Contusion · Abrasion · Haematoma Open wounds ­ · Incised wounds · Lacerated wounds · Crush injuries · Penetrating wounds · Clean wound · Clean contaminated wound · Contaminated wound · Dirty wound. Our body loves us, and, even while the spirit drifts dreaming, works at mending the damage that we do. Primary Healing (First intention) It occurs in a clean incised wound or surgical wound. Secondary Healing (Second intention) It occurs in a wound with extensive soft tissue loss like in major trauma, burns and wound with sepsis. Secondary suturing is done after 10-14 days, once wound granulates well with proper control of infection. Here due to fibroblastic activity synthesisation of collagen and ground substance occurs. Wounds and Wound Healing Phases of Wound Healing 5 Inflammatory Phase (Lag or Substrate or Exudative phase) · It begins immediately after wound healing. Proliferative Phase (Collagen/Fibroblastic phase) · Collagen and glycosamines are produced by fibroblasts. Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube drainage, intraabdominal by laparotomy) has to be dealt with accordingly. Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid, (0. Wound debridement (wound toilet, or wound excision) is liberal excision of all devitalized tissue at regular intervals (of 48-72 hours) until healthy, bleeding, vascular tidy wound is created. If it is a lacerated wound then the wound is excised and primary suturing is done. If it is a crushed or devitalised wound there will be oedema and tension in the wound. So after wound debridement or wound excision by excising all devitalised tissue, the oedema is allowed to subside for 2-6 days. If it is a deep devitalised wound, after wound debridement it is allowed to granulate completely. If the wound is large a split skin graft (Thiersch graft) is used to cover the defect. In a wound with tension, fasciotomy is done so as to prevent the development of compartment syndrome. If the nerves are having clean cut wounds it can be sutured primarily with polypropylene 6-zero or 7-zero suture material. If there is difficulty in identifying the nerve ends or if there are crushed cut ends of nerves then marker stitches are placed using silk at the site and later secondary repair of the nerve is done. It is done as single layer interrupted deep sutures using monofilament polypropylene or polyethylene. After the control of infection, once healthy granulation tissue appears, secondary suturing is done. Wounds and Wound Healing Principles of wound suturing · Primary suturing should not be done if there is oedema/infection/devitalised tissues/haematoma · Always associated injuries to deeper structures like vessels/nerves or tendons should be looked for before closure of the wound · Wound should be widened by extending the incision whenever needed to have proper evaluation of the deeper structures ­ proper exploration · Proper cleaning, asepsis, wound excision/debridement · Any foreign body in the wound should be removed · Skin closure if it is possible without tension · Skin cover by graft/flap ­ immediate or delayed · Untidy wound should be made tidy and clean before suturing · Proper aseptic precautions should be undertaken · Antibiotics/analgesics are needed · Sutured wound should be inspected in 48 hours · Sutures are removed after 7 days Remember · Wound toilet is washing the wound thoroughly using normal saline · Wound debridement (french- letting loose) is allowing content to come out by release incisions or faciotomies. It is often associated with fracture of the underlying bone which in turn compresses the major vessel further aggravating the ischaemia causing pallor, pulselessness, pain, paraesthesia, diffuse swelling and cold limb. If allowed to progress it may eventually lead to gangrene or chronic ischaemic contracture with deformed, disabled limb. Problems with the compartment syndrome · Infection, septicaemia and abscess formation · Renal failure · Gangrene of the limb · Chronic ischaemic contracture · Disabled limb Muscle necrosis releases myoglobulin which is excreted in the urine, damages the kidneys leading into renal failure. Note: Affected muscle when passively stretched worsens the pain ­ the most reliable clinical sign. It can be measured by placing a fine catheter in the compartment and using a pressure monitor. Adequate lengthy incision involving skin, fat and deep fascia should be done until underneath muscle bulges out properly. Clinical diagnosis is an art, and the mastery of an art has no end: you can always be a better diagnostician. Note: Doing fasciotomy several days after crush injury may not be safe as it may lead to sudden release of myoglobulin causing myoglobulinuria and renal failure. It causes extensive lacerations, bruising, compartment syndrome, crush syndrome, fractures, haemorrhage etc.

Occasionally toxic megacolon can occur in pseudomembranous colitis, amoebic colitis or typhoid colitis. Fulminant type, 5% common · It is a severe form, with continuous diarrhoea with passage of blood, mucus and pus. Chronic type (95%): · Lasts for months to years with diarrhoea, blood loss, anaemia, invalidism, abdominal discomfort and pain. Investigations · Barium enema-shows loss of haustrations, narrow contracted colon (hose pipe colon), mucosal changes, pseudo polyps. Clinical Features Disease usually begins in rectum as proctitis later becomes left sided colitis and eventually causes severe total proctocolitis. Due to very high incidence of malignant transformation in ulcerative colitis (10-20%), multiple biopsies should be taken from suspected areas of the colon. Sigmoidoscopic grading of ulcerative colitis 0-Normal mucosa 1-Loss of vascular pattern 2-Granular, non-friable mucosa 3-Friability on rubbing 4-Spontaneous bleeding, ulcerations · Plain X-ray abdomen is useful in obstruction, toxic megacolon, perforation. Later drugs also should be given for maintenance of remission and to prevent relapses. Side effects are skin rashes, bone marrow suppression, folic acid deficiency, haemolysis in glucose 6 phosphate dehydrogenase deficiency patients, temporary fertility problems in men. It is also used as retention enema which is better than steroid enema in left sided ulcerative colitis/proctitis. Other measures are using sucralfate, short chain fatty acids, probiotics, antidiarrhoeal drugs (diphenoxylate, loperamide, codeine), avoiding milk products, fibre, fruits. Proper follow-up at regular intervals by regular sigmoidoscopy evaluation should be done as rectum is also diseased and vulnerable for complications. Total colectomy with rectal mucosectomy and anastomosis above the dentate line on posterior aspect is also occasionally used. Pouchitis disease activity scoring index is at present used which is based on clinical, endoscopic and histological inflammatory features. Splenic flexure is the water shed area of colon, receiving blood supply from terminal branches of superior and inferior mesenteric arteries. It forms trophozoite which multiplies and causes inflammation and flask shaped ulcers in the rectosigmoid, caecal and often in the terminal ileal region. Acute fulminant amoebic colitis is a severe type with sloughing of colonic and rectal mucosa causing torrential bleeding, toxicity which can be lifethreatening. Others are cutaneous amoebiasis, amoebic empyema, and very rarely amoebic brain abscess, amoebic pericarditis. Amoeboma can occur in caecal region where it forms granuloma in pericolic area presenting as mass abdomen. Amoebic typhlitis (inflammation of caecum) presentation with pain and tenderness in right iliac fossa and often also as a mass in the right iliac fossa mimicking carcinoma caecum called as amoeboma (amoebic granuloma) (1. Differential diagnosis for amoeboma · · · · · Appendicular mass Ileocaecal tuberculosis Carcinoma colon Retroperitoneal tumour Lymph node mass. Metaplastic/hyperplastic Polyp · Metaplastic- indicates a difference in appearance from normal mucosa. Complications Bleeding or intussusception, when occurs requires surgery either resection-anastomosis or colonoscopic removal. If size of adenoma is > 2 cm ­30 - 50% chances of developing carcinoma; 1-2 cm -10% chances of carcinoma; < 1 cm -1% chances of carcinoma. Problems in therapeutic colonoscopy · · · · Perforation due to necrosis Haemorrhage- secondary Intracolonic explosions Sepsis. Alternatively a conservative total colectomy with ileo rectal anastamosis can be done, but with a regular follow-up with sigmoidoscopy for any rectal polyps. It directly acts on the colonic mucosal cells to reduce their proliferative potential. Crohn`s disease is a premalignant condition but not as much as ulcerative colitis. Colonic cancer may be Non hereditary colon cancer · It can be sporadic colon cancer ­ 60%.

The main drugs used for therapy are albendazole, mebendazole, and more recently ivermectin. Travelers returning from tropical countries should be thoroughly examined for Strongyloides infections before any immunosuppressive measures are initiated (e. Enterobius Enterobius vermicularis (Pinworm) Causative agent of enterobiosis (oxyuriosis) Occurrence. The pinworm occurs in all parts of the world and is also a frequent parasite in temperate climate zones and developed countries. The age groups most frequently infected are five- to nine-year-old children and adults between 30 and 50 years of age. Enterobius vermicularis which belongs to the Oxyurida has a conspicuous white color. Sexually mature pinworms live on the mucosa of the large intestine and lower small intestine. The females migrate to the anus, usually passing through the sphincter at night, then move about on the perianal skin, whereby each female lays about 10 000 eggs covered with a sticky proteinaceous layer enabling them to adhere to the skin. In severe infections, numerous living pinworms are often shed in stool and are easily recognizable as motile worms on the surface of the feces. The eggs (about 50 В 30 lm in size) are slightly asymmetrical, ellipsoidal with thin shells. Freshly laid eggs contain an embryo that develops into an infective first-stage larva at skin temperature in about two days. Eggs that become detached from the skin remain viable for two to three weeks in a moist environment. Infection occurs mainly by peroral uptake of eggs (each containing an infective larva) that are transmitted to the mouth with the fingers from the anal region or from various objects. The sticky eggs adhere to toys and items of 10 Kayser, Medical Microbiology © 2005 Thieme All rights reserved. In the intestinal tract, larvae hatch from the ingested eggs, molt repeatedly, and develop into sexually mature pinworms in five to six weeks. Occasionally, different stages of the pinworm penetrate into the wall of the large intestine and the appendix or migrate into the vagina, uterus, fallopian tubes, and the abdominal cavity, where they cause inflammatory reactions. The females of Enterobius produce in particular a very strong pruritus that may result in nervous disorders, developmental retardation, loss of weight and appetite, and other nonspecific symptoms. Scratch lesions and eczematous changes are produced in the anal area and can even spread to cover the entire skin. A tentative diagnosis based on clinical symptoms can be confirmed by detection of pinworms spontaneously excreted with feces and eggs adhering to the perianal skin. Reinfections are frequent, so that treatment usually should be repeated once or more times, extended to include all potential parasite carriers (e. Nematoda (Roundworms) 587 Nematodal Infections of Tissues and the Vascular System Filarial nematodes, the Medina worm, and Trichinella are discussed in this section along with infections caused by the larvae of various nematode species. Filarioidea (Filariae) Causative agents of filarioses & the nematode genera of the superfamily Filarioidea (order Spirurida) will be subsumed here under the collective term filariae, and the diseases they cause are designated as filarioses. In the life cycle of filariae infecting humans, insects (mosquitoes, blackflies, flies etc. Filarioses are endemic in subtropical and tropical regions; in other regions they are observed as occasional imported cases. The most important filariosis is onchocercosis, the causative agents of which, Onchocerca volvulus, is transmitted by blackflies. Microfilariae of this species can cause severe skin lesions and eye damage, even blindness. Diagnosis of onchocercosis is based on clinical symptoms, detection of microfilariae in the skin and eyes, as well as on serum antibody detection. Other forms of filarioses include lymphatic filariosis (causative agent: Wuchereria bancrofti, Brugia species) and loaosis (causative agent: Loa loa). Dirofilaria species from animals can cause lung and & skin lesions in humans (see p. The length of the adult stages (= macrofilariae) of the species that infect humans varies between 2­50 cm, whereby the females are larger than the males. Based on the periodic appearance of microfilariae in peripheral blood, periodic filaria species are differentiated from the nonperiodic ones showing continuous presence.